Step Up to Medicine

Ulcers that do not heal with unna boot in CVI results in use of
split thickness skin grafts +/- ligation of adjacent perforation veins

Pericardial friction rub sounds = (3)

ECG changes in acute pericarditis = (4)

1. Scratching between atrial systole (pre systole)
2. Ventricular systole post S2
3. Early diastole between S2–>S1Heard best sitting up and leaning forward

1. ST segment elevatin and PR segment depression
2. ST returns to normal
3. T wave inverts
4. T wave normalizes

WPW syndrome on the EKG will show?


Narrow complex tachycardia
Short PR
Delta wave (will upward deflect seen before QRS)RX: Radiofreq ablastion of one arm of reentrant loop; avoid drugs active on AV node that prolongs QT and can accelerate conduction through accessory.

Medication: Type IA (Procainamide) and Type IC good

Complications of acute MI?
1. Pump failure (CHF) – if mild, ACEi; if severe, cardiogenic shock
2. Arrhythmias = PVCs, Afibb, VT, Vfibb, AIR PSVT, STachy, SBrady, Asystole, AVBk
3. Recurrent infarctions
4. Mechanical complication
5. Acute pericarditis
6. Dresslers syndrome
Chest pain differential diagnosis?

1. HEART/pericardium/vascular causes: stable angina, USA, variant angina; MI; pericarditis, aortic dissection

2. Pulmonary: Pulmonary embolism (pain and pulm infarct); pneumothorax; pleuritis (pleural pain); pneumonia/status asthaticus

3. GI: GERD; diffuse esophageal spasms, PUD, esophageal rupture

4. Chest wall

5. Psychiatric

6. Cocaine

IF not thrombus is found subsequent to performing a TEE in a patient that is in Afibb, what therapy (anti-coag_ should be started if < 48hr since diagnosis?
Start IV heparin and cardiovert within 24 horus. Continue anticoag for 4 weeks post A fibb episode
Causes of Systolic DYS v. Causes of Diastolic DYS
1. Systolic: impaired contractility (post MI, Cardiomyopathy, Myocarditis)
2. Diastolic: imparired ventricular filling during diastole: HTN –> hypertrophy’ valvular diseases (AS, MS, AR); restrictive CM
NBTE Marantic Endocarditis refers to?
What types of deposits are often found?

Endocarditis associated with debilitating illnesses like metastatic cancer found in up to 20% of cancer patients.

1. Sterile deposits of fibrin and platelets forming along closure line of valve leaflets.

Embolize to brain/periphery therefore requires the use of heparin.

Treatment of AORTIC dissection
Immediate therapy
1. IV – BB to decrease HR and decrease force of LV ejection
2. IV – nitroprusside to decrease systolic BP decreased 120 mm HgIf type A: surgical management = ant chest pain
If type B: medical management = interscapular pain

When superficial thrombophlebitis occurs over different locations over short period of time –> think of migratory superficial thrombophelbitis –> caused by?
Secondary to occult malignancy of pancreatic origin
When is pulses paridoxicus seen?
1. exaggerated decrease in arterial pressure during inspiration (> 10 mm Hg drop). Detected by decrease in amplitude of femoral/carotid pulse during inspiration. Stronger when expiring.
SIgns of HCM
2. S4 (precedes S1) – loud at the LL border
3. SYSTOLIC ejection murmor (inc with standing, valsalva, leg raise) and decreases with squatting and handgrip)
4. Increase pulse @ carotid with 2 upstrokes with BISFERIOUS pulse
What mechanical complications occur subsequent to MI
1. Free wall rupture
a. Catastrophic, usually fatal event that occursduring the first 2 weeks post MI (905 will occur within 2 weeks, 1-4 days after MI)
b. 90% mortality
c. Leads to hemipericardium and cardiac tamponade
d. Hemodynamic stability; immediate pericardiocentesis; surgical repair
Ventricular septal defect (VSD)
Most common congenital malformation of the heart
1. Blood flows from the LV to the RV (low pressure) causing an increase in pulmonary blood flow.
2. If PVR < SVR, shunt is always L –> R. But if the PVR > SVR, shunt will then be R –> L.Therefore is patient with VSD has L to R shunt: CHF, dec growth, elevated LRI
Therefore if patient with VSD has a R to L shunt: SOB, chest pain, dyanosis

Ventricular fibrillation

Multiple focal depolarizations in ventricles that fire rapidly that cause quivering ventricles with little to NO output –> most start as ventricular tachycardia.

VFIBB + MI post 48 hours (low recurrence)
VFIBB (-) MI; increase in recurrence of VFIBB episode

Cholesterol embolization syndrome

Syndrome due to “showers” of cholesterol crystals originating from proximal source (most common the abdomial aorta, iliacs, femorals) – triggered by surgical/radiographic intervention (arteriogram) or thrombolytic therapy

“Blue toe syndrome”

A myocardial infarction is due to the necrosis of ______ as a result of an interruption of blood supply.

Number one cause:


Acute coronary thrombosis = atheromatous plaque ruptures into the vessel lumen and thrombus formed ontop of lesion. Occlusion of vessel results.

What is the diastolic dysfunction seen in CONSTRICTIVE PERICARDITIS

Early diastole will be unimpeded because volume during filling threshold has not yet been impeded

early diastole – unimpeded
late diastole – halted filling

Decreased and delayed upstrokes of carotid artery seen in AV stenosis
Treatment of DVT
1. Anticoagulation
a. Prevents further propagation of thrombus
b. IV heparin at constant to maintain PTT of 1.5-2 times aPTT
c. Start warfarin once aPTT theraptuc and continue 3-6 mo. INR 2-3
2. Thrombolytic therapy (streptoK; uroK; tPA (alteplase))
3. IVC filter placement (Greenfield filter in patients) if other prophylaxis isnt working. PE prevention, NOT DVT prevention
What are the side effects of nitrates?
Orthostatic hypotension

Rheumatic heart disease: Characteristics
Occurs as a complication of streptococcal pharyngitis (GAS)
-acute RF immunologically mediated systemic process (RHD)
-most common valvular abnormality 2ndary to ARF is MV stenosis; AV or TV can be affected too.
Chronic venous insufficiency (venous stasis DZ)
1. Postphlebitic syndrome (superficial, deep, both)
2. Anatomy = lower extremity venous system consists of deep, superfiial and perforating which connects valves allow super –> deep
3. Pathophysiology = hisotry of dvt is the underlying cause
How is cardiac tamponade treated?

1. Nonhemorrhagic tamponade = if stable, monitor with ECHO, EXR, EKG (dialysis > pericentesis if renal failure present)

2. Hemorrhagic tamponade = emergent surgery pericardiocenttesis only temporizing measure is not definitive treatment

What is the treatment for VFIBB?
1. Unsynchronized cardioversion – start CPR
2. Give 3 sequential shocks (120, 150, 180); assess rhythm
3. IF VF persists –> do CPR and intubate
4. Admin 2 doses amiodarone 2-4 min. Admin 1 mg IV bolus epi every 3-5 minutes (will increase myo and dec cerebral blood flow and dec defib threshold)
Substernal chest pain (“crushing”) lasting > 30 minutes + diaphoresis strongly suggests ______ _______
myocardial infarction (ACUTE)
LMWH versus UF Heparin
Longer 1/2 life than UF heparin – 1 dose daily (lovenox).
1. Admin outpt basis
2. No need to follow aPTT
3. More $$ than UF Hep
Orthodromic AV reentrant tachycardia as a PVST
Accessory pathway between the atria/ventricles that conducts regradly (concealed bypass tract) common cause of SVTs
Treatment of Rheumatic Heart Disease
1. Penicillin/erythromycin to prevent RF – by GAS
2. Acute RF treat with NSAIDS. Look at CRP for monitoring treatment (patients with a history of HD by RF should get prophylactic treatment of erythro/amoxacillin for dental/GI/GU procedures
____ ______ IS IMPORTANT clinically when it develops rapidly because it can become cardiac tamponade
Pericardial effusion (if >250mL fluid accumulates, can see on CXR as “water bottle” silhouette)
Second degree AV heart block
Mobitz type I v. type II

Mobitz type I – Wenchbach – progressive prolongation of PR interval until the p wave fails to conduct suddenly. Site of block is at the AV node – no treatment needed but will have a dropped QRS complex.

Mobitz type II – Pacement implant for Rx – P waves fails to conduct suddenly, without a preceding PR interval prolong therefore QRS is dropped randomly. Site of block is @ the BUNDLE OF HIS

Sustained handgrip increases the intensity of a ____ murmor while _____ the intensity of HCM murmor. WHY?

Handgrip increases the MVP murmur and decreases the HCM murmor.

This is due to tht of increase in systemic vascular resistance

Clinical features of Vtachycardia
1. Palpitations SOB, lightheadedness
2. Sudden cardiac death
3. Cardiogenic shock
4. Canon “a” waves in neck (secondary) to AV dissociation resulting in atrial contraction during ventricular contraction and an S1 that varies in intensity.
Signs of serum digitoxin toxicity
GI: N/V, anorexia
CARDIAC: Ectopic ventricular beats, AV block, Afibb
CNS: disorientation (visually)
What is a hypertensive emergency? What is hypertensive urgency?

1. Systolic BP > 220 +/- diastolic BP > 120 in addition to end organ damage whereas urgency is only elevated BP alone.

2. End organ damage assessment
a. EYES (papilledema)
b. CNS (altered mental status; intracranial hemorrhage; HTN encephalopathy can develop)
c. KIDNEY (renal failure/hematuria)
d. HEART = USA; CHF with pulm edema; aortic dissection

Clinical features of hypertrophic cardiomyopathy?


SOB on exertion
Chest pain (angina)
Syncope (dizziness) post valsava
Arryhymias (Afibb/V arrhythmia)
Cardiac failure d/t stiffness during diastole – do not fill – hypoxemia – cor pul
SUDDEN death
For treatment in hypovolemic shock


Circulation: Iv hydration –> class I no fluid II benefits with fluid III/IV requires it

Causes of HIGH output heart failure

Increased cardiac output needed for req of peripheral tissue for O2

1. Chronic anemia
2. Pregnancy
3. Hyperthyroid
4. AV fistula
5. Wet beriberi
6. Paget’s disease of the bone
7. MVR
8. Aortic insufficiency (stenosis too)

Asystole post MI
VERY HIGH MORTALITY RATE. Treatment should begin with electrical defibrillation for Vfib which is more common in cardiac arrest and may be difficult to clearly differ from asystole
Which Rx options for psvt
Manevers that stimulate vagus to delay AV condunction and block re-entry
1. Valsalva maneuver
2. Carotid sinus massage
3. Breath holding
4. Head immersion in H2O (cold)ACutely: IV adenosine (short duration of action and effective at dec SA and AV node); IV verapamil/esmolol

Diagnosis of the PVD
ABI = ratio of systolic BP at ankle to the systolic BP @ arm. Normal ABI >/= 1.0
1. Claudication ABI < 0.7
2. Rest pain ABI < 0.4Pulse volume recordings
1. Assessment of segmental limb perfusion
2. Pulse wave form represents volume of blood/B @ sequential sites down leg.

Arteriography = GOLD STANDARD

Causes of TVR
1. Secondary to RV dilitation resulting in enlargment of TV orifice
-LVF is number 1 cause
-RV infarction
-Inferior wall MI
-COR pulmonale; secondary pulm HTN
2. Tricuspid endocarditis due to IV drug users
3. Secondary to RHD; accompanied by mitral and AV disease
4. EPSTEINS anomaly = congenital malformations
5. Carcinoid syndrome, SLE, myxematous valve
What can cause atrial fibrillation?
1. Heart DZ (CAD, MI, HTN, MV dysfunction)
2. Pericarditis/Pericardial trauma
3. Pulmonary disease (PE)
4. Hyper/hypothyroid
5. Sepsis
6. Stress
7. Alcohol
8. Sick sinus syndrome (sinus node dysfunction -SND)
9. Pheochromocytoma

Chronic stable angina verusus USA


ECG + cardiac enzymes
Give ASA
Begin IV heparin
What is the treatment for MV stenosis
1. Medical: diuretics if (CHF); infective endocarditis prophylaxis; anti-coag therpy
2. Surgical: percutaneous ballooning valculoplasty usually producing excellent results and open commissurotomy and MV replacement
3. Management: no therapy if asymptomatic; diuretics can be used if mild symptoms of edema show (pulmonary)

DVT = causes (VIRCHOWS)

DVT Risk factors:

Virchows: 1. hypercoaguability 2. stasis 3. trauma

Risk factors: >60YO, malignancy, prior DVT/PE/Varicose veins, factor v leiden, PC or S def, AT3 def, prolonged immobilization, cardiac disease, estrogen use, obesity, pelvic surgery

Evaluation of patient with PVD or chronic arterial insufficiency
PVD is an occlusive, atherosclerotic disease of the lower extremities.
1. CAD, CHF, Hx of MI
2. DM, Lung DzSites of occlusion/stenosis is after the superficial femoral artery (Hunter’s canal) – most common site

Popliteal artery/aortoiliac occlusive disease

Hypovolemia shock = decreases circulatory BV — decrease preload, decrease CO
The slower the loss the better the compensatory mechanisms. These fall when > 20%-25% of blood volume lost. If CVP low, hypovolemic shock is present
How is AVR diagnosed? How is it treated for?
1. CXR should should LVH, dilated aorta
2. ECG should show LVH
3. ECHO should be performed serially in stable patients with needs to assess surgery.
4. Cardiac cath = assess severityTreatment:
1. Conservative if stable
2. Definitive Rx = AV valve replacement
3. Acute AR post MI = do immediate replacement

Acute pericarditis causes:
1. Postviral preceded by recent flu like illness; URI; UGI
2. Infectious = viral (coxsackie, ECHO, HIV); bacterial (TB)
3. 1st 24 hours or in dresslers syndrome (wks – mo) post MI
4. Uremia
5. Drug-induced lupus (SHIPP)
What is the treatent for patients with chronic A fibb?
1. Rate control (BB or CCB)
2. Anticoagulation therapy: patients with LONE Afib, no hemodialysis or cardiovascular risks < age 60 do not require antigoags due to low risk for embolism. Thus use of ASA is warranted. Pateints who have risk should continue on lifelong WARFARIN post bridging of enoxaparin
Leading cause of death in patients with PDA
Heart failure
Revascularization: Percutaneous tranluminal coronary angioplasty (PTCA) v. CABG

PTCA: 1 or 2 vessel dx if proximal lesion; restenosis significant issue up to 40% in 6 months (if cannot/doesnt happen then likely not to) – stent placement dec rate of stenosis

CABG: Treatment of choice with HIGH RISK DZ; if L main coronary (CCA); 3 vessel disease with decreased EF or proximal LAD stenosis –> SEVERE STENOSIS

Surgical treatment in patients diagnosed with PVD and have severe claudication?

Surgical bypass grafting (most common procedure with 5 year patency rate of 70%)

1. Angioplasty – ballooning

MVP is most common in which patients?
Patients with a genetic tissue disorder:
1. Marfans syndrome (fibrillin)
2. Ehlers danlos syndrome (collagen III)
3. Osteogenesis imperfection (collage I)
Longterm treatment of USA
BB (metoprolol)
Nitrates (SL)Decrease risk factors = smoking cessation/wt loss; treat DM and HTN; hyperlipidemia (use statins); folic acid

Three classic symptoms of AV stenosis and survival rates
1. Angina (35%) – avg = 3 years
2. Syncopy (15%) – avg = 2 years
3. Heart failure (50%) – avg = 1.5 years
How is a DVT diagnosed (next step if suspected)

Step 1: Doppler analysis and duplex US; operater-dependent (good for proximal) veins like popliteal and femoral

Step 2: Venography = most accurate dx in DVT in CALF. Invasive

Step 3: Impedence plethsmography noninvasive alt to doppler

Step 4: D-dimer testing (95% sensitive) RULE OUT; 50% specific

CAUSES of hypertensive emergency
1. Noncompliance with antiHYP therapy
2. Cushings syndrome (inc cortisol)
3. Drugs: cocain/LSD/methamphetamine
4. Hyperaldosteronism (Conn’s disease)
5. Ecclampsia: gestational HTN and serizures
6. Vasculitis
7. Alcohol withdrawal
8. Pheochromocytoma
9. Noncompliance with dialysis
Features of chronic venous insufficiency
1. Swelling of lower leg (leg elevation relieves it)
2. Skin change (skin thin, atrophic, shiny, cyanotic, browny induration develops with chronicity)
3. Venous ulcers (above medial malleolus; rapidly occuring)
Two major complications associated with acute pericarditis:
1. Pericardial effusion
2. Cardiac tamponade
Clinical features of PDA
Normal pulmonary pressures
Signs of HF
Loud P2 = pulm HTN bc is a L-R shunt through DA.
Will have LVH secondary to L-R shunt
RVD secondary to pulm HTN
Machinery murmor at L intercostal (2nd) space
Lower extremity clubbing
(-) Cardiac enzymes + ST segment depression
Unstable angina
What are the causes of chest wall pain?
Muscle strain
Rib fracture
Herpes zoster
Thoracic outlet syndrome
Cardioversion versus defibrillation

Cardioversion: delivery of shock synchronous with QRS complex to terminate dysarrythmias like PSVT or VT so shock timed NOT to hit T wave because would otherwise cause Vfib. Use with Afibb, A fluttle, VT with pulse, SVT

Defibrillation: delivery of shock not synchronous with QRS. Converts the dysrhythmia to normal sinus rhythm (Vfibb, VT without pulse)

What is cardiac heart failure

Hearts inability to meet the bodys demand under normal physiological conditions.

1. Dec cardiac output, activates (RAAS at kidneys) and SYMP nervous system, activates (vasoconstricts) the peripheral vessels by release of EPI and NE causing volume retention, this increase vascular resistance and maintains CO but will INCREASE preload without increasing CO, thus –> will have an elevated LVEDV –> inc LVEDP –> transmitted to the pulmonary veins –> leads to pulmonary congestions and effusions/”CARDIO FLASH PULMONARY EDEMA)

NBVE Endocarditis “Libmann Sacks”

Involves AV in patients with SLE. Small warty vegetations bilaterally causing AVR or AVS. Rarely infective but CAN lead to embolization

Rx: SLE and anti-coag therapy

Symptoms of stable angina and diagnosis
1. Chest pain.substernal
2. <10-15 minutes
3. Heaviness, pressure, squeezing
4. Can be induced by emotion/exertion
5. Relieved with rest or nitroglycerinDx: resting ECG – normal in pts with stable angina; Q waves consistant with prior MI if ST depression, treat for USA

Exercise stress test (stress ECG or echo)

Signs and symptoms of SHOCK
1. Hypotension (dec CO dec SVR)
2 Oliguria
3. Tachycardia
4. Altered mental status
What are the causes of cardiac tamponade?
1. Penetrating trauma to the thorax such as a gunshot and stab wound
2. Iatrogenic – central line placement; pacemaker insertion; pericardiocentesis
3. Pericardition – idiopathy, neoplastic, uremic
4. Post MI – free wall rupture
Post MI: Rupture of IV septum versus Papillary muscle rupture

Rupture of IV: greater potential for successful therapy than with a free wall rupture, although state of critical event –> occurs within 10 days after MI.

Mitrial valve REGURGITATION will be heard. Get an echocardiogram, perform surgery with MV replacement. Administer intr-aortic balloon pump (IABP)

Harsh blowing holosystolic murmor at the 4th L intercostal space with sternal lift (d/t RV enlargment) and as the PVR increase, S2 increases with intensity
VSD – murmur will decrease with valsalva and decrease with handgrip
What causes VFIBB?
1. Ischemic heart disease
2. Antiarrhythmics (esp those causing torsades that PROLONG QT)
3. A fibb with rapid ventricular rate due to accessory reeentrant pathways (WFW is a good example)
How does ventricular filling in costrictive pericarditis differ from that of cardiac tamponade?

Constrictive pericarditis: inflammation and thickening of the pericardium that results in decreased volume filling and decreased cardiac output during systole. Early fills rapid and late fills slowly

Cardiac tamponade: ventricular filling is impeded throughout diastole

Variant (prinzmetal’s) angina

ST segment elevation on ECG during chest pain representing transmural ischemia

-this is a coronary vasospasms that is accompanied by a fixed, sclerotic lesion in 75% of cases but can occur in a normal coronary artery

Lateral infarction with ECG changes
Will show change in leads aVL, I, II in Q wave
Which cardiac enzymes is most important in MI dx?
Troponin I and T
1. Increases within 5-14 days and peaks 1-2 days
2. Greater sensitivity/specificity than CKMB for MI
3. Obtain on admission and again in cycles of 8 hours for 24 hours
4. Can be falsly elevated in renal F patients (thus isnt specific to heart)
Patients with a positive echo or stress ECG should undergo ____ ___.
Cardiac catheterization
Sustained VT versus NONsustained VT
Sustained VT = persists in absense of intervention
->30 seconds, hypotension or MI, life threatening, progress to VFIBBNONsustained VT = breif and self-limited runs of asymptomatic VTACH
-if CAD or LVF present can cause sudden cardiac death

Ventricular fibrillation as a complication post MI:
Immediate unsynchronized defibrillation and CPR

Interpretation of diagnositic tests for DVT:

Pretest probability = Intermediate –> HIGH
Low –> intermediate

Doppler (+) – begin anticoag
Doppler not diagnostic then repeat the US in 2-3 daysDoppler (-); no need for anticoag; observe repease US 2 days

Systolic click with midsystolic rumble when standing/valsalva and decreases with squatting:

Cardiac arrest versus SCD

Dx of Vfibb (leads to cardiac arrest)

Cardiac arrest: loss of CO; reversible with ABCs promptly restored
SCD: unexpected death within 1 hour of symptom onset secondary to cardiac etiologyRx: No atrial p waves, no QRS waves identified

Triad of AAA
-Abdominal pain
-Palpable pulsatile abdominal mass
-HypotensionEmergent laparatomy

Diagnosis of restrictive CM?
1. Echocardiogram will show thickened mycardium and SYS ventricular dysfunction (both LV and RV)
a. Increased RA and LA size with normal LV and RV size
b. If amyloid, myocardium bright
2. ECG shows low voltages, arrhythmias, afibb, endomyocardial biopsy is DIAGNOSTIC
Multifocal atrial tachycardia
Most common to COPD patients!
-Variable p waves morphology (PR segment and RR interval)
-Vagal maneuvers and adenosine shows AV block without a change in atrial tachycardia
-Treatment is to improve O2 and CO2 ventilation. If LV good, use CCB/BB, digotoxin, amiodarone, IV fluconide and IV propafenone
Leutic heart v. Mycotic Aneurysm

Complication of syphilitic aortitis affecting men in 40-50s. Aneurysm of aortic arch with retrograde extention backwards to cause AVR and stenosis of aortic branches (coronary) Rx: IV penicillin and surgical repair

Mycotic aneurysm (secondary to infection)

Atrial myxoma

benign gelatinous growth arising from intratrial septum of heart in region of fossa ovalis – primary cause of cardiac neoplasm that can embolize leading to metastatic disease or can cause relative valve dysfunction

Treatment: surgical excision

What is the diagnosis of constrictive pericarditis? Treatment?
ECG: Low QRS voltages, generalized Twave flattening and inversion, atrial fibrillation.
ECHO: Thickened pericardium
CT Scan/MRI = better accuracy than an ECHO
Cardiac cath = elevated and equal diastolic pressures in all 4 chambers.
Ventricular tracing = rapidly decent (will see a “square root sign”Rx: Surgical resection of the pericardium

3rd degree HEART BLOCK

NO conduction of atrial impulses to ventrcles, no correspondence between P waves and QRS complexes

ventricular pacemaker (escape rhythm) maintains rate of ~25-40 bpm but #1 = AV dissociation

Medical therapy for stable angina or CAD
ASA – all patients with CAD; decreased morbidity and risk of MI
BB – blocks symp system on heart (dec CO dec HR dec SVR)
Nitrates – generalized vasodilation (decreases preload)
CCB – causes coronary vasodilation and afterload reduction (amylodipine)
What are the physical findings of aortic insufficiency
De musset sign = headbobbing
Muller’s sign = uvula bobs
Duroziez’s sign = pistol shot sound at the femoral arteries
What is BNP?

Brain natriuretic peptide that is released from the venctricles in resposne to elevated ventricular volume/volume expansion and pressure overload

BNP > 100 = decompensated CHF. Deciphers whether the CHF due to COPD or HF

Inferior infarction with ECG changes?
Leads II, III, aVF will show pathologic Q waves
HOW is hypertrophic CM diagnosed and treated if asymptomatic versus symptomatic?
Diagnosis of HCM is by that of ECHO, clinical, family history
1. Asymptomatic: no Rx, avoid vigorous exercise – BB #1 choice, then CCB
2. Symptomatic:
a. BB – reduces symptoms by improving diastolic filling (HR dec, duration in diastole increases) and decrease mycontracting and O2 consumption.
b. CCB (verapamil)
c. Diuretics
d. Afibb – treat with BB
e. Surgery – myomectomy, MV replacement
f. Pacemaker
Septic shock

Hypotention despite fluids –> hypoperfusion –> organ failure –> death

Causes: pneumonia, pyelonephritic, meningitis, cholangitis, cellulitis, peritonitis
Timeline: SIRS –> Sepsis –> Shock –> MODS
Pathophysiology: Decreased SVR secondary to peripheral vasodilation, increased CO (maintains SV/tachy); EF decreases secondary to decreased contract.

Which Rx can be helpful adjuvant in USA, especially if undergoing PTCA or stenting?
1. Abiximab
2. TirofibanGlycoprotein IIb/IIIa

Symptoms of LEFTSIDED heart FAILURE
1. SOB – dyspnea secondary to pulmonary congestions on exersion
2. Orthopnea – diffculty breathing supine
3. PND – awakening 1-2 hrs of sleep with difficulture of SO
4. Nocturnal cough – nonproductive, worse supine
5. Confusion/memory loss – decreased brain perfusion
6. Diaphoresis and cool
Sinus tachycardia post MI
Caused by pain and anxiety, fever, caffeine, pericarditis, medications
-worsens ischemia (increased myocardial O2 consumption)
-treat underlying cause (analgesics for pain ASA for fever)
Pharmacologic Rx of PSVT
1. IV adenosine due to SA-duration of action (~15 seconds and terminates STs by decreasing SA node and AV)
2. IV verapamil (CCB) OR IV esmolol –> use digoxin in patients with LV functionPrevent with = digoxin, verapamil, radiofrequency ABLATION of AV/accessory loop

Patients with PVD should be evaluated with:
2. Assess arterial pulses
3. Inspect the lower pulses, color change, ulcers, atrophy, hair loss, thick toenails
4. Do a ECG, CBC, RFT, coagulation profile (Factor V leiden, AT3, PC and PS)
Holosystolic murmur that starts at S1 and continues to S2 at the apex, radiating to back and clavicular area depending upon the leaflet wound
Preventricular Contraction

Early beat that fires on own from a focus in ventricle and spreads to other ventricle. Doesnt occur through normal contraction but through muscle and is much slower so QRS is slow and WIDE

Couplet: two successive PVCs
Bigeminal = sinus followed PVC
Trigeminal = sinus followed by two PVCs

MV Stenosis murmur:

Diastolic murmur: S2 with an opening snap with a low pitch diastolic rumble and is followed by S1 that is LOUD.

LOUD S1 is the most prominent and GETS WORSE in the LL decubitus position

Diagnosis of AAA

US = #1choice to evaluate location and size of AAA; 100% sensitive

CTscan = 100% sensitive to detect AAA takes longer than CXR/US; use in hemodynamically STABLE pts only

Abdominal radiographs = shows calcification of dilated segment

New heart murmor with unexplained fever?
1. Diagnostic: Dukes clinical criteria (2 major/1major+2minor)
2. Parenteral AB based on culture results (4-6 weeks)
-if culture negative, treat empirically with VANCOMYCIN or penicillin + AG
Cardiogenic shock

When heart doesnt generate CO sufficient to maintain tissue perfusion with systolic BP < 90 with urine output < 20 mL/hr and adequate LVFP Causes: acute MI = #1 cause, tamponade, tension pneumothorax, arrhythmias, massive PE –> RVF, CM, Myocarditis

Dx: ECG; ECHO; Swan ganz cath
Rx: ABC; Rx udnerlying pressors (DA, dobutamine, NE), IABP

Due to: hemochromatosis (deferoxiamine and phlebotomy)
sarcoidosis (corticosteroids/glucocorticoids)
Amyloidosis (NO rx) – can usually give digoxin if sys dys unless patient + for amyloid, so if were to adminster would cause tox)If pulm edem/peripheral edema –> Diuretics (loops, thiazine, spironolactone)/vasodilators like clonidine/hydralazine for perpheral edema

Coarctation of the aorta

Increased in L ventricle afterload due to obstruction bt proximal and distal aorta; common in Turners patients

Features: HTN in upper extremities and HYPO tension in lower. Well developed upper body, poorly developed lower body. Headache; cold extremities, clausication with exercise.

Dx: ECG shows LVH and CXR should notching of ribs with “fig 3” appearance of aorta

Treatment if patient has moderate cardiac disease:
1. Normal EF
2. Moderate angina
3. 2 vessel disease
1. Nitrates (nitroprusside, nitroglycerine)
2. BB (metaprolol)
3. CCB if BB are not effective
4. consider PTCA or cabg if above combo doesnt work
What is acute arterial occlusion and how does it differ from PVD
AAO clinically: pallor, pain, pulselessness, paresthesias, paralysis, polar (cold)
PVD clinically: claudication, rest pain, decreased pulses, ischemic ulcersRx: for PVD
Treatment for claudication (conservative therapy)
Treatment for rest pain (surgery)

Rx: for AAO
Diagnosis: arteriogram
Rx: anticoagulation; emergent surgery

Which maneuvers increase the MVP sound?

Standing, valsalva, leg raise increases this heart murmur along with that of handgripping. Why? because decreased LV chamber size, less to fill up due to lower venous return on standing.

Those which decrease the MVP murmor: squatting (increases the chamber size and thus delays click

Treatment of ventricular tachycardia
1. Sustained VTACH if stable: mild symp + SBP >90 admin amiodarone, procainamide, sotalol (ALL IV)
2. Sustained VTACH if unstable: Seroconvert dc immediatiately. Follow with amiodarone IV, placement of ICD will be required unless EF > 50%.1. NONsustained VTACH: if no underlying heart disease, do not treat. If heart disease, consider a ICD placement.

What decreases frequency of cardiovascular events
What complications arise with that of AV stenosis, how does the hearts mechanical ability change?
With AV stenosis, this decreases the LV output due to increased resistence across ths valve, therefore the heart must increase stroke volume by either increasing CO or HR to maintain certain level of arterial pressure. That being said, LVH will occur due to attempted compensation. WHen AV area < 0.7cm2, dec CO and increased exertional angina. THis progressive LV dys can further pull on the MV annulus causing mitral regurgitiation hence why AVS with secondary MVR can be seen.
Treatment of chronic venous stasis disease (CVI)
1. Leg elevation
2. Avoid long periods of sitting/standing
3. Elastic stockings
4. Ulcers = “wet-to-dry” dressings
5. Unna venous boot = change every week –> 10 days
% of patients who improve from medical regimen of (nitrates, enoxparin, BB, ASA) +/- PTCA/CABG?
How is PDA diagnosed?
Echo – patent ductus with turbulent blood flowRx: if PVD not present then LIGATE; if pulm HTN or R to L shunt is present then do not correct.

Unstable angina pectoris

O2 demand unchanged but decreased coronary flow at rest thus indicates a STENOSIS with enlarged d/t thrombosis

Increased and worsening chest pain that is severe AT REST.


Coronary artery disease presents with which of the following
Stable angina
Sudden Cardiac Death
What is Dresslers syndrome?

Occurs post MI, presents within WEEKS to MONTHS with:

1. Fever
2. Malaise
3. Pericarditis
4. Leukocytosis
5. Pleuritis


Imaging/method of obtaining a culture in patients with endocarditis that is infective:
Transesophaeal echo > than a transthoracic echo
2 forms of revascularization of MI
1. Thrombolysis
2. PTCA (if one vessel – CABG if more) *
Superficial thrombophlebitis
Diagnosis: Rx:

Local tenderness, erythema along course of superficial vein

Dx: clinical

Rx: analgesics (ASA); monitor; continue activity if pain and cellulitis (rest with warm compression)

1. hypotension
2. muffled heart sounds
3. JVD ***MOST COMMON FINDING; prominant waveforms (x descent) with absent y descent
What is sick sinus syndrome (now called sinus node dysfunction-SND)

Characterized by a sinus block: syncope, confusion, fatigue, CHF

Rx: Atropine if unstable; pacemaker for LT

Recurrent infarction post MI

Extension of existing infarction/reinfarction of new area

1. Cardiac enzymes will already be elecated from the initial infarct. Troponin levels remian elevated for one week and reutrns to normal faster. re-evaluation of CKMB 26-48 hours later can indicates recurrent infarct.

2. Repeat ST segment levations of EKG on first 24 hours post infarction

Complications of ASD:
Treatment of ASD
1. Pulmonary HTN (<20YO) but common if > 40YO
2. Eisenmengers disease (late comp; irreversible pulm HTN leads to reversal shunt from L –> R) back to R –> L causing HF and cyanosis
3. RHF, AFIBB, STROKE/CVASurgical repair if pulmonary:systemic flow > 1.5:1 or 2:1 or symptomatic

If patient has QRS tachy with wide (>0.12) seconds, then:
Constrictive pericarditis differs from acute pericarditis by what mechanism?

Fibrous scarring of PERICARDIUM leads to thickening and oliteration of the pericardial cavity. This will not only restrict diastolic filling of heart, but it will resulting in an early UNimpeded ventricular filling during diastole because intracardial volume has not yet reached limit defined by stiff pericardium.

LATE diastole WILL BE IMPEDED and halts filling due to (usually) calcifications along the pericardium that can form.

Diagnosis of AORTIC dissection
Widened mediastinum (>8mm on AP view)
1. Transesophageal echocardiogram (TEE) has a very high sensitivity and specificity; noninvasive and done at bedside2. CT scan/MRI highly accurate

3. Aortic angiography – determines the extent of dissection for surgery

Anterior infarction shows changes in the ECG by?
Anterior leads V1, V2, V3, V4 (ST SEGMENT ELEVATION)
Anterior leads V1, V2, V3, V4 (Q Waves show late change)
Neurogenic shock

General characteristics = failure of sympathetic nervous system to maintain adequate vascular tone.

Causes = SC injury/head injury/pharmacologic symptoms/peripheral vasodilation with decreased SVR

Features: warm; well perfused skin, URINE output low, brady cardia/HYPOtn (CO normal, SVR lo, PCWP lo)


What is the treatment of acute pericarditis?
1. Most are self-limited in viral etiology (2-6) weeks
2. NSAIDS good for symptomatic treatment and for pain.
3. Glucocorticoids if NSAIDs do not work
Ventricular tachycardias
Rapid repetitive firing of 3 or greater PVCs in a row @ rate of 100-250 bpm. AV dissociation (sinus P wave cycle) originates @ the bundle of HIS
Arrhythmias post MI: Premature ventricular contractions (PVCs)
Conservative treatment (observe indicated); no need for antiarrhythmic agents
How is cardiac tamponade diagnosed?
Clinically: look for BECKs triad: hypotension, JVD, muffled heart sounds
Diagnostic tests:
1. ECHO – most sensitive and noninvasive
2. CXR – enlargement of cardiac silouette by >250mL
3. ECG – electrical alterans (alt beat variation in direction of ECG waveform) due to swinging of heart with in pericadial space.
4. Cardiac CATH – equal pressures (4 chambers) – loss of y decent
What are the causes of diastolic dysfunction dut to restrictive CM?
Amyloidosis, sarcoidosis, hemachromatosis
Prognostic indicators of CAD
1. Left ventricular function (EF)
2. Vessels occluded

EF: normal > 50%; if EF < 50%, associated with increased mortality

Vessels involved:
1. LMain Coronary Artery = poor prognosis because covers ~2/3 heart
2. 2nd or 3 vessel CAD – worse prognosis

General characteristics of AAA:


Abnormal localized dilitation of aorta occurs between renal arteries and iliac bifurcation; incidence increases with age (AAA < 50 rare) – 65-70 YO common M>F

1. Atherosclerotic weakening of aortic wall (trauma, HTN, vasculitis, smoking, + family Hx)
2. Syphilis and connective tissue abnormalities; Marfans, ehler-danlos syndrome, osteogenesis imperfecta

Restrictive cardiomyopathy
1. Characteristics
2. Causes

Infiltrations of the myocardium resulting in impaired diastolic ventricular filling due to decreased compliance of ventricles.

Cause: amyloid, sarcoid, hemochromatosis, scleroderma, carcinoid syndrome

Paroxysmal SVT (PSVT
#1 cause: reentry by AV node; one fast and one slow within AV node so the reentrant circuit occurs within AV. This results in a narrow QRS with no visible P waves because within that of the QRS. Due to short circuit and rapid conduction so both the atria and ventricles are activated simultaneously.
#2 cause: Orthodromic AV reentrant tachycardia
Small, discrete areas of tissue ischemia, resulting in blue/black toes, renal insufficiency and or abdominal pain/bleeding –> intestinal hypoperfusion
Cholesterol Embolization Syndrome
MI is associated with ___% mortality rate, where 1/2 deaths are pre-hospital

AV block (bradyarrhythmias)

1st degree:

1. PR interval is prolonged (>0.20 sec)
2. A QRS complex follows every P wave, so its normal
3. Delay is in the AV node
4. Benign – no RX
What is the most accurate method of identifying presense and severity of CAD?
Coronary arteriography (angiography)
1. Standard test to delineated coronary artery
2. Purpose is to determine whether revascularization is needed
3. Coronary artery stenosis >70% produces angina

AV Regurgitation:

1. Causes of chronic versus acute:

Acute causes of AVR: Trauma, Infective endocarditis (Staph), Aortic Dissection
Chronic causes of AVR:
1. Primary valvular: RF; bicuspid AV valve; MARFANS; EHLORS-DANLOS; ANK SPA; SLE2. Aortic root disease: Syphilis in tertiary, osteogenesis imperfecta (collagen dz); AD; Reiters syndrome

Post surgical methods of prophylaxis after surgery
1. Mechanical
a. Leg elevation, compression socks, ambulation
b. Pneumatic compression boots
2. Pharmacologic
a. Heparin or LMWH = UFHep or LMWH post op until ambulation
Cardiac catherderization with coronary angiography is used for what purpose?
Cardiac cath:
1. Determines specific cardiac dx (gives hemodynamic, intracardiac pressure, CO, O2 saturdation)
2. Coronary angiography alwyas performed to visualize coronary arteries
3. When to perform cardiac cathederization
-post positive stress test
-patient with angina and noninvasive test are nondiagnostic, angina +/- therapy
-if patient symptomatic + need diag
-evaluate for valvular disease
What is the treatment for systolic dysfunction or (CHF)
1. Restriction of sodium (<4g/day)
2. Diuretics (loops – ferusemide – post potenti)
3. ACEi – venous and arterial dilation (dec preload and afterload) – best in renal failure patients as well
5. BB – good if post mI CHF
If a patient present with severe
1. Headache
2. Markedly elevated BPWhat should next step be?

1st step is to lower BP with antiHTN agent
2nd step is to order CT scan of head to rule out intracranial bleeding (SAH is DDx for headache) – ischemic stroke shows up 24-48 hoursIf CT scan is negative; flu with lumbar puncture

Diagnosis of ARF (Acute Rheumatic Fever)

Require 2 major or one major and 2 minor symptoms/signs:

1. Joint – migrating polyangitis
2. New murmor – CHF
3. N-nodules that are subQ
4. Erythema marginatum
5. Syndynems chorea

1. Fever
2. Elevated ESR
3. Polyarthralgias
4. Prolongs PR
5. Evidence of GAS infection

Causes and diagnosis of hypovolemic shock:
1. Hemorrhagic = trauma, GI bleeding, retroperitoneal
2. Nonhemorrhagic = vomiting, diarrhea, dehydration, burnsDx: central venous line or pulmonary artery cateder gives invaluble information; cvp/PCWP decreases, decrease CO, increases SVR

Treatment for unstable angina
1. IV access
2. 4L o2 by NC
3. Control pain with nitrates and morphine
How does DVT causes CV stasis disease
1. Destruction of venous valves in deep venous system. Valvular in comp causes gravitational pressure of blood column to ankles
2. Valves in perforation veins damage secondary to chronic increases deep venous pressure inhibitory transmission of super –> deep
Hypertrophic cardiomyopathy

Inherited as autodominant but can be spontaneous

Pathophysiology: Diastolic dys due to stiff, hypertrophic ventricle with an elevated LVEDV and LVEDP

Clinically: Pressures in LV increase during exercise or increase with HR/CO activity or dec LV filling (VALSALVA MANEUVER, OUTFLOW OBSTRUCTION OBS d/t hypertrophy of IVS)

Causes of PSVT?
Digitoxin toxicity (2:1) block most common
AV node reentry
Aflutter with rapid ventricular response
AV reciprocating tachycardia excessive caffeine/alcohol
If cardioversion is successful post VFIBB and DC synchronization

Continue IV infusions of the effective antiarrhythmic agent (IV amio has een shown to be most effective)

Implantable defibrillater/LT amio for LT treatment

How might WOMEN (DM, elderly, post-operative) patients with heart ischemia d/t MI present?
Asymptomatic – painless infarcts or atypical presentation
Treatment of MVR medically v. treatment performed surgically
afterload decreases with
Vasodilaters like hydralazine and a-methyldopa, clonidine
Decreased salt reduction
chronic antigoagulation if AFIBB present
IABP as bridge to surgery for acute MVRSurgical: MVR/replacement; done b4 LVFcn severe

Intermittent claudication v. Rest pain (continuous)

Cramping leg pain thats reliably reproduced by same walking distance; relieved by rest. = intermittent claudication

Worse prognosis felt over distal metatarsel, prominent at night awakens pt from sleep, frank gangrene.

Tachyarrhythmias: Atrial fibrillation

Multiple foci in atria firing continuously: total irregularly rapid ventricular rate

Atria are not contracting but instead they are quivering

Atrial rate > 400 bpm but most are blocked at the AV node therefore the ventricular rate will be between 75-175

How might MV stenosis be diagnosed:
CXR: LA enlargement
ECHO: Most important test to confirm (LA thickness); thick calcified MV, narrow fishmouth shaped; RVF
80% of patients with ______ hx will develop chronic venous insufficiency (CVI)
Infective endocarditis:

Infective endocarditis – infection of the endocardium that involves the cusps of the valves

1. Acute endocarditis (S. aureus) – occurs on normal hearts but is fatal in < 6wks without treatment. VIRULENT 2. Subacute endocarditis (S. viridans, enterococcus) – occurs on damaged valves and is not as acutely fatal > 6wks.

Use of IABP improves survival in patient with cardiogenic shock decrease CO, increase SVR, increased PCWP
Intraaortic balloon pump
1. Decreases afterload
2. Increases CO
3. Myo O2 demand
Cardiac tamponade
1. Fluid accumulation:
2. Pathophysiology:
1. 200 mL fluid that develops rapidly can cause cardiac tamponade
2. 2L of fluid may accumulate slowly before cardiac tamponade occurs. When it occurs slowly, the pericardium has opportunity to stretch and adapt to the increased volumePathophysiology of pericardial effusion: it impairs the ability for diastolic filling thus leads to elevation and equalization of intracardial pressures such that all RA, RV, LA, LV are equal in pressure. Pulm artery and pericardium are also equali in pressure and thus during diastole there is difficulty in properly filling ventricles due to little change in pressure.

WHen/what maneuvers increase with HCM?
Standing, valsalva, leg raise = increase HCM murmur and S3 S4 sounds
Complications of coarctation of the AORTA and Rx:
Severe HTN
Ruptured aneuryms within the cerebrum
Infective endocarditis
Aortic dissectionRx: Surgically decompress; percutaneous balloon aortoplasty is common

Management for intermittent claudication
1. Stop smoking
2. Exercise
3. Footcare
4. Atherosclerotic risk factor reduction control of hyperlipidemia/HTN/weight/DM and so on
5. Avoid cold temperatures
6. ASA
7. Trental (pentoxiphylline) decreases blood viscosity
Clinical features of TVR
1. Diagnosis:
2. Rx:
1. RVF (ascites, hepatomeg, edema, JVD)
2. Pulsatile liver
3. V waves in JVP
4. Inspiratory S3 in LLSB
5. Blowing holosystolic murmur
6. AFIBBDx: ECHO (quantifies the amount of TVR) and identifies prolapse/flail TVL and pulmonary pressures

EKG: RA/RV enlargement

Diagnosis of Vtach
ECG: Wide and bizarre QRS
QRS: Monophasic VT = QRS complex identical
Polyphasic VT = QRS complexes differ

If SEVERE CAD: Decreased EF <50%, severe angina, 3 vessel disease + LAD


1. Coronary angiography
2. Consider CABG
When is revascularization preferred in patients with CAD

HIGH risk patients (very low EF or LAD/3 vessel occlusion)


Do not decrease incidence of MI but instead dec symptoms

Aortic Stenosis

Causes: Bicuspid aortic valve; tricuspic aortic valve in elderly; congenital unileaflet valve; rheumatic fever (although dominant in MV stenosis)

Course: Patients asymp for years (40s) until middle ages despite severe obstruction (bicuspid). Development of angina, syncope, HF, poooooor prognosis

Dx: CXR – calcification of AV caused ^ in LA and LV
EKG = LVH/LA abnormality

Rx: Surgical


LSHF: displaced MI; pathologic S3 heard post S2 into a noncompliant ventricular chamber; heart at the APEX. Pathological S4 in atrial systole into noncompliant LV chamber at L sternal border preceededS1. CRACKLES AND RALES HEARD AT BASES OF THE LUNGS SECONDARY TO INCREASED FLUID INTO THE ALVEOLI DUE TO PULMONARY EDEMA. Dullness to percussion over lung bases due to effusion. Increase intensity of pulmonary component of 2nd heart sound.(P2)

RSHF: Peripheral pitting edema; pedal edema (in elderly due to venous insufficiency); nocturia due to increased VR with elevation of legs; JVD; hepatomegaly; ascites

AV block post MI
1st degree
2nd degree
Type I
Type II
1st degree: prolonged PR interval without dropped QRS
2nd degree Type I: Wenkebach (progressive elongated PR interval with a dropped QRS 2:1)
2nd degree Type II: Anterior MI, disregulated randomly dropped QRS
3rd degree: Unrelated p wave and QRS. REQUIRES pacemaker
Clinical features of DVT
1. Lower extremity pain and swelling (worse with walking; better with elevation)
2. Homans sign (calf pain on dorsiflex)
3. Palpabale cord
4. fever
DVT –> CVI –> ambulatory venous HTN
-Interstitial fluid accumulation = edema
-Extravasation of plasma proteins and RBC into subQ tissue resulting in browny black color
PDA = communication between the _____ and the ______ artery that persists post birth

Pulmonary and Aortic

PGE and low O2 fetally mantain the ductus arteriosis. Blood shunting from nonfcning lungs = normally closes within days post birth.
1. Becomes L-R shunt in life outside of womb if patients (aorta –> pulm)
2. Seen in congenital rubella, HIGH altitude, prematurity

+ Cardiac Enzymes + ST segment depression –>
Recovery time for someone with acute pericarditis?
1-3 weeks
Causes of Atrial FLUTTER
1. Irritable automaticity focus in the atria fires ~250-350 bpm giving rise to regular atrial contractions
2. Atrial rate = 250-350 bpm
3. Ventricular rate = 1/3 – 1/2 atrial rateCauses: COPD, CHF, Rheumatic fever, CAD, ASD

____ ______ is impaired during _______ in cardiac tamponade leading to decreased filling, decreased SV, and decreased CO
Ventricular filling
Sinus bradycardia
SInus rate < 60 bpm
Clinical significant if < 45 bpmIschemia, dec vagal tone antiarrhymic drugs (symp: fatigue, no exercise, angina, syncope)

Treatment for hypertensive emergency
Decrease MAP by 25% within 2hrs
-do not immediately acheive normal BP, but get pt out of danger then reduce BP gradually.
-If diastole > 130 or HTN encephalopathy, IV nitroprusside, labetolol, nitroglycerin used
Posterior infarction with ecg changes?
Large R wave in V1 and V2
ST segment depression in V1, V2
Upright T waves in V1 and V2
Cardiac neoplasms
primary tumors of heart are rare
-mets from primary tumors more common (75%) via the lung, breast, skin, kidney, lymphoma, kaposi’s sarcoma in patients with aids
What cardiac enzymes are the golden standard for diagnosing myocardial injury?

CK-MB – creatinine kinase: ^ 4-8 hours and returns to normal 2-3days and peaks in 1 day. If measure betwenn 24-36 hours, then peaks Levels of total CK and CK-MG is measured on admission and every 8 hours for 24 hours (therefore 3x total)

Troponins (troponin I and T) are the most important test to order (enzymes)

Cardinal manifestations of acute pericarditis:
1. Chest pain (pleuritic, retrosternal to ridge/neck) pain is positional and relived by sitting up and forward
2. Pericardial friction rub *viscera and parietal precodial surgaces” Scratching/high pitched sounds
3. ECG changes = ST elevation or PR depression; ST turns normal but T wave with invert then return to normal
Causes of ventricular tachycardia?
1. CAD with prior MI = #1 cause ~2-3 days post M
2. Active inschemia/hypotension
3. Cardiomyopathies
4. Congenital defects
5. Prolonged QT syndrome
6. Drug toxicity
Post MI Arrhythmia Ventricular Tachycardia (VT)
Sustained Vtach needs to be treated
1. If unstable: electrical cardioversion required
2. If stable: antiarrhythmia therapy (amiodarone IV)
What tests should be ordered to diagnose that of CHEST PAIN

1. Ancillary tests:

-Cardiac enzymes *troponin and CKMB
-Workup of PE

MVR pathophysiology (acute v. chronic)

1. ACUTE MVR: abrupt increase in L atrial pressure in normal sized LA and compliance, causing backflow into pulmonary circulation with pulmonary edema. Decreased cardiac output because decreased forward flow so HYPOTENSION and shock results from severe case of MVR.

2. Chronic MVR: gradual change in LA pressure in setting of DILATED LA and LV *unlike that of acute. Increase of LA compliants. Pulmonary HTN (>35 mm Hg on exertion and > 25mm Hg at rest) can result from CHRONIC backflow.

How is atrial fibrillation on EKG treated?

Irregularly irregular rhythm (RR intervals and small erratic spikes without P waves on EKG)


If UNstable: immediately cardioversion to sinus rhythm

If stable: (1) control rate: if AFIBB but pulse >60-100 then use CCB like amlodipine. If L ventricle- use amiodarone/dig. (2) Cardiovert to sinus rhythm (begin anticoagulation prevention if afib > 48hrs. Then get a tracheoesophageal echo (TEE) of the L atrium to check for thrombosis.

Monitoring urine output is most useful indicator of the Rx for _____ shock
Frankstarling relationship

As preload increases or (RV pressure or LVEDV/LVEDP) the CO should also INCREASE as contracitility and stroke volume increases. Preload represents the ability to which the heart is stretched (taut) at steady state. When preload is low, difference in performance between normal and failing heart is minimal

IF systolic dysfunction, there is NOT elevation in CO and EF < 50%

ASD = congenital heart defect
Ostium secundum (80%)
1. O2 blood passes from the LA into the RA and increases the R-Heart OUTPUT and thus increases pulm flow.
2. Increases shunt; increases RA; increases RV, and with pulm to systemic flow ratios of 1.5-1.0 –> pulm htn results
3. Benign until 40YO like that of AV stenosisHeart sounds: midsystolic murmor in pulmonic area secondary to increased pulmonary blood flow. Wide, fixed S2.

Dx: TEE is diagnostic; CXR: large PArteries; ECG: RBBB, RA deviation

For patients with normal resting ECG in diagnosis of CAD, what test should be performed next?
Stress test
1. Exercise stress if patient can do so
2. Stress ECG records before, during, after treadmill exercise at 85% max HR
3. Exercise indiced ischemia results in SE ischeia and thus ST depression
4. + Test = HF, V. arrhythmia, hypotension
5. Stress echo records b4 and after exercise
6. Exercise induced ischemia with wall abnormalities (akinesis/dyskines) not present at rest.
7. Favored over ECG because assess LV size and function
How might AAA present? Diagnosis?
Asymptomatic until abdominal exam or CXR for another reason (incidental diagnosis)
1. Fullness
2. Pulsatile abdominal mass in hypogastrium and lower back-throbbing character
3. “Grey Turners” sign = ecchymosis on back and flanks
4. “Cullen sign” = ecchymosis around umbilicus
Causes of shock and INITAL STEPS TO APPROACH
1. Fever + site of infection ~~ septic
2. Trauma.GI bleed.Vomiting. Diarrhea = hypovolemia
3. History of MI/CHF/Angina ~~cardiogenic
4. JVD ~~cardiogenic
5. SC injury/neuro change ~~ neurogenic1. Establish 2 large venous catheders, central line, arterial line
2. FLuid bolus (1500-1000 mL saline)
3. Draw blood (CBC/RFT/PT/PTT)
5. Pulse ox
6. Pressors

Elevated filling pressures leading to dyspnea/exercise intolerance and RSHF/SIGNS
Restrictive CM
How is Atrial flutter diagnosed?

Sawtooth baseline QRS complex appearing post every 2nd-3rd “tooth” P wave. These are usually seen in leads II, III, and aVF (inferior leads)

Treatment is similar to that of AFIB:
1. Rate control: BB/CCB
2. Cardiovert if unstable to get normal sinus rhythm
3. Anticoagulation therapy starting with ASA if low risk or going WARFARIN if serious complications

Ventricular aneursym can occur post MI by?
Rarely ruptures
-increase ventricular tacharrythmias
-medical management maybe protective
ECHOof patient with severe VSD:

ECG: Biventricular hypertrophy if PVR high because shunt was l to R causing RVH (HIGH P to low P) then once PVR>SVR, shunt was R to L causing LVH

CXR: ^ Pulmonary artery
^ Cardiac silhouette; as pvr ^ (L-R shunt decreases), heart size decreasesm pulmonary artery size increases and R to L shunt increases

ECHO: shows septal defect

Clinical features of ______ _______ include:
1. No BP
2. No heart sounds
3. Patient unconscious
4. If untreated, eventual SUDDEN CARDIAC DEATH
Mycotic aneurysm

Resulting from damage to aortic wall secondary to infection

Blood cultures (+)
Rx: IV AB and excision

SYMPTOMS: Cough, Exertional dyspnea, orthopenia
SIGNS: JVD, kussmauls sign, pericardial knock, ascites, dependent edema
Contrictive pericarditis

What/how can (“PRINZMETAL’S”) ANGINA can be definitively test for?

How is prinzmetals Rx?

IV Ergonovine (provokes chest pain)

Vasodilators = CCB, nitrates

Treatment for CAD/CHD
#1 – Smoking cessation cuts by 50% post 1 year
#2 – HTN
#3 – Hyperlipidemia – decrease serum LDL with statins
#4 – DM – strict glycemic control
#5 – Obesity – wt loss modifiers (DM, HTN)
#6 – Exercise – decreases emotional stress and promotes weight loss
#7 – diet
#8 – hyperhomocysthemia
What are the clinical features of AVR?
1. SOB
2. PND
3. Angina
4. WIdened pulse pressures (elevated systolic and decreased diastolic)
5. Corrigans pulse: water hammer pulse is one in which collapse suddenly as arterial pressures decrease rapidly in late systole and diastole
6. Austin flint murmor
3 complications post DVT
1. Pulmonary embolism
2. Postthrombotic syndrome (CV insufficiency)
3. Phlegmasis cerulea DOLENS
-major venous obstruction, leg edema, compromises arterial supply therefore decreased nerve and decreased sensory motor function.
If the patient with STABLE ANGINA, normal resting ECG and cannot exercise to perform stress test, what Rx should be performed?
Pharmacologic stress test:
1. IV adenosine, dipyramidole, dobutamine –> cardiac stress increases c/out exercise
2. Can be combined with ECG, echo, IV nuclear perfusion
3. Adenosine dypyramidole = coronary vasodilation
4. Dobutamine increases myocardial O2 demand, increases HR, increases CO, increases SVR (BP).
How is heart failure diagnosed?
CXR = Kerley B lines with prominent interstitial markings and pleural effusion.
ECHO = initail chest of choice to determine estimates of the EF both sys/dys
ECG = nonspecific
RADIONUCLEUOTIDE ventriculopathy
Cardiac CATH
Stress testing
Diagnosis and treatment of MVP
Dx: echo most useful
Rx: Reassurance if asymptomatic; BB if chest pain occurs;**administer AB prophylaxis for dental procedures to prevent endocarditis

Aggressive management for patients with Unstable Angina
1. ASA
2. BB
3. LMWH (IV) or UFH for 2 days (PTT at 2-2.5x normal if UFH)
4. Enoxaparin > LMWH because has better coverage with factor X
5. Nitrates = 1st line!!!
6. Glycoprotein IIb/IIIa
DO NOT _____ FOR ASYSTOLE. Try ____ or transcutaneous pacing.

Defibrillate (not for asystole, or PEA)

Admin: amiodarone/CPR

Leriche’s syndrome
Atheromatous occlusion of distal aorta just above the bifurcation causing bilateral claudication, importence, absent/diminished pulses
RIGHT ventricular infarction will present with what clinical changes and EKG changes?
Inferior ECG changes (II, III, aVF)
Elevated JVD/JVP
Clear lungs
Premature atrial complexes as a type of arrhythmia
1. Early in atria, fires on own
-srugs, alcohol, tobacco, electrolyte imbalances, ischemia, infectionSigns on EKG:
1. Early P waves that differ from others (not normal sinue rhythm)
2. QRS complex is normal
3. Found 50% of normal adults with holter monitoring
4. Causes palpitations or PSVTs
5. Assymptomatic

TREATMENT: BB – metoprolol

What are the causes of MVR: *Acute and Chronic
Causes of acute: Endocarditis, Papillary m. rupture, infarction or dysfcn, higher mortality
Causes of chronic: RF, Marfans, Cardiomyopathy
Mitrial Stenosis
Almost all causes are secondary to:
Mitrial valve stenosis: #1 cause due to Rheumatic Heart Disease/Fever
1. Scarring/narrowing of the MV oriface – increase LA pressure and PV press
2. Asymptomatic until MV area < 1.5cm2 normal is (4-5cm2)Clinical features: Exertional dyspnea, orthopnea, PND; Palpitations, chest pain; hemoptysis (because as there is an increase in LA pressure, this ruptures anastomosis of small bronchial veins and thus causes coughing up of blood). Thromboembolism can occur

SIGNS: (MV Stenosis murmur) Heart during diastole between that of S2 and S1 at the apex of the heart. Will be heard best on EXPIRATION because L side heart. Diastolic following S2 with an opening snap.

Native heart valve is most commonly affected by: _____________
Prosthetic heart valve is most commonly affected by : _____________
Endocarditis of IV drug users: _______________
1. S. Viridans most common native valve endocarditis organism but is SUBACUTE
-Staphylococcus (aureus > epi)
-HACEK group = Haemophilus, actinobacillus, cardiobacterium, Eikenella, Kingella
2. Staph epi > aureaus within 60 days of surgery. Streptococcus later onset > 60 days.
3. Right sided; S. Aureus = #1 cause/candida/entero/Pseudo

Treatment of shock

1. Cardiogenic (dec CO inc SVR inc PCWP)
2. Hypovolemic (dec CO, inc SVR dec PCWP)
3. Neurogenic (dec CO dec SVR dec PCWP)
4. Septic (inc CO, dec SVR, dec PCWP)

1. Airways, breathing, circulation
Pericardal effusion
Clinical features:

Characteritistics: Any cause of acute pericarditis leading to exudative fluid into the pericardial space — can occur with ascites, pleural effusion in sodium and water retention states like CHF, cirrhosis, nephrotic syndrome.

Clinical findings: Muffled heart sounds, soft PMI, dullness at L lung base, pericardial fricition rub

Dx: ECHO – most sensitive and specific for effusion (shows 20mL fluid)
CXR – enlargement of the silouette > 250mL fluid

Dilated cardiomyopathy
Clinical features:

#1 type of CM

Cause: CAD (with prior MI) – most common; toxin (alcohol, doxorubicin, adriamycin); metabolic (thiamine/selenium deficiency); infectious (coxsackieBvirus/chagas/lyme/HIV), peripartum; CVD; SLE; COCAINE: idiopathic

Features: LCHF (pulm HTN, pleural effusion, SOB, crackles and rales at lung bases, pulm edema, S3/S4). RCHF (peripheral edema, RVH, JVD, ascites, nocturia)

Acute pericarditis post MI?
ASA is Rx for acute pericardial inflammation = do not administer NSAIDs or CORTICOSTEROIDS because hinders the mycardial scar formation.

Which maneuvers diminish the intensity of ALL murmurs but will increase those of MVP and HCM?


Squatting increases the intensity of all murmose but ___ that of MVP and HCM

Squatting will dec intensity of MVP and HCM

Standing, Valsalva, Leg raise – all decrease murmurs except for MVP and HCM

This is because these all dec the LV volume by decreasing venous return. Thus, HCM is caused by diastolic dys; no change in size, and decreased filling of venticle will result in a increase of sound.

Thus MVP/HCM gets louder with standing, valsava and leg raise. Gets diminished with squatting because inc LV volume, inc filling and thus decreased the murmor.

Complications of VSD and Rx:
Progressive AORTIC regurgitiation
Pulm HTN/shunt reversalRx: Prophylaxis if endocarditis (vanc and amoxicillin and aminoglycosides)
Surgical repair if PVR to SVR flow is >1.5:1 or 2:1

Patients with: Mild disease (CAD)
1. Normal EF (>55%)
2. MILD Angina
3. Single vessel disease
1. Nitrates (symptoms as prophylaxis)
2. BB (metoprolol)
-use CCB if symptoms continue
Which rapid polymorphic VT leads to Vfibb, associates with prolonged AT syndromes, TCAs, anti-ACh and can be treated with IV Mg2+
Torsades de pointes

#1 cause death in ICU =

surgical drainage if necessary
fluid to maintain BP
pressors (DA, dobutamine, NE)

Signs of Left sided HF
Displaced PMI due to cardiomegaly
S3 ventricular gallop
1. Rapid filling into noncomplaint LV, normal in children; adults = CHF
2. Difficult to hear but MOST specific in CHF pateints heard at the apex by following SV
Sinus bradycardia post MI
Common occurance in EARLY stages of acute MI; may be protective mechanism by reducing myocardial O2 consumption. NO treatment (OBSERVE) if mild; if gets severe, administer ATROPINE to increase HR
Wolff-Parkinson-White Syndrome
Bundle of Kent accessory pathway from atria to ventricles causing a premature ventricular excitation because lacks the delay seen in teh AV node. Can result in PSCTs of orthodromic reciprocating tachy (anterograde limb, depolarizing ventricles, then goes back with accessory pathway, retrograde and redepoarizing atria). No hange in wave because conduction retrograde. SVT (afib/flutter) usually AV node only allows certain impulses to vent, but with accessory, all/most get to the ventricles
Treatment of AAA

Consider age as a factor in AAA patients that are assymptomatic

Managment depends on aneurysm size > 5cm in diameter or symptomatic

Surgical resection with synthetic graft placement recommended

What did the HOPE trial show regarding drugs that dec mortality, stroke, AND renal disease in patients with vascular disease?
ACEi = ramipril

Three drugs needed for A fibb:


1. Rate control – CCB
2. Restore normal sinus rhythm (cardiovert)
3. Start coag therapy to avoid clot formation (anticoag therapy)

Myocarditis is caused by _______ which leads to inflammation of the myocardium

Dx by:
Rx by:

Viruses (coxsackie B virus); bacteria (GAS in RF, LYME Dz, MYOCOPLASMA)
IDIOPATHICDx: Look for increased ^CK-MB/TROPONIN; Elevated ESR

Rx: Supportive

Main goal of someone with AAO?
1. Assess viability of tissues to salvage the limb
2. Skeletal muscle tolerates 6 horus of ischemia
3. Amputation necessary
4. IV heparinas anticoagulation
5. Embolectomy indicated via cutdown and fogarty balloon. Bypass reserved for embolectomy failure.
Treatment of sinus bradycardia?
1. Atropine (blocks vagal stimulation) – mad as hat blind as bat
2. Pacemaker if persist
Categories of infarcts include:

1. ST Segment elevation infarct = transmural (involving entire thickness of the wall); tends to be larger; seen in prinzmetals angina as well

2. Non-ST segment elevation infarct: subendocardial involving inner 1/3 of wall; tend to be smaller and presentation of such similar to USA. THus both nonSTEMI and USA have elevated ST only nSTEMI has increased cardiac enzymes

Signs of _____ ______ include:
1. Harsh crescendo-descendo sys murmur
2. Heard in secondary right intercostal space
3. Radiates to the carotid arteries
AV stenosis
Aortic dissections

Characteristics: longstanding HTN (70%);trauma; CTD (Marfans/Ehlers danlos) syndrome; biscuspid valve; coarctation of the aorta; 3rd trimester pregnancy

Type A: proximal involving AA with retrograde extension from descending aorta
Type B: Distal and limited to descending aorta

Treatment of patients with diagnosed MI
Admit patient to CCU and establish IV access
Admin O2 and analgesics (nitrates; morphine)
Medical therapy that dec mortality
1. ASA
2. BB – stimulation HR and contractility, decreases afterload; dec mortality
3. ACEi – initiate within hours of hospitalization
2 symptoms:
1. Fever or hypothermia
2. Hyperventilation (>20 bpm or PaCO2 < 32) 3. Tachycardia (>90 bpm)

Pnematocoeles Are?
Often form secondarily to an uri caus by streptococcus pneumonia. S aureus can result in blood streaked sputum and multiple midfield lung cavity in CXR suggesting an acute necrotizing pnemonia
Which patients are the most sensitive to asthma-like symptoms? (cough, wheeze, SOB, CHEST tightness) in RX?
ASA (aspirin) sensitive asthema – if patient has asthma or a polyp – the use of ASA could force an exacerbation that resembles asthma like symptoms
BERYLLIOSIS can have similar clinical findings to sarcoid. What is the diagnostic test associated with its diagnosis?
Beryllium lymphocyte proliferation test

O2 delivery systems

1. Low flow v. HIGH flow:

Low: nasal cannula (<0.40 FiO2); Simple face mask (0.4-0.6 FiO2)

High: venturi mask (<0.5 FiO2); nonbreathing mask (0.70-0.80 FiO2)

primary pneumothorax versus secondary pneumothorax?
1. Primary: heathy, tall, young, lean male
-spontaneous subpleural bleds at apex, escape of air yeilds collapsed lung
-recurrence rate 50%/2 years
-sufficient pulmonary reserve therefore not life threatening2. Secondary: complicated
-underlying disease like COPD, asthema, ILD, CF< TB, life threateneing bc lack of pulmonary reserve

IN COPD = FEV1 is _____ and the FEV1/FEV ratio is?

Pulmonary symptoms?

FEV1< 70% if mild or <50% if severe.

Decreased FEV1/FEV (<0.75-0.80)
Increased TLC, RV, FRC due to air trapping
Decreased vital capacity

Dyspnea, cough ,sputum production; wheezing

Pathophysiology of ARF
1. V/Q mismatch – hypoxia without hypercapnia is the MOST COMMONY MECHANISM THAT DOES REPOND TO O2 SUPPORT AND SUPPLEMENTAL
2. Shunting – little or no ventilation in perfused areas due to collapsed or fluid filled alveoli – the venous shunts to the arterial circulation without [email protected] ocygenation
3. Hypoventilation leads to hypercapnia
4. Increased CO2 production – hypercarbic
5. Diffusion impairment

How is cor pulmonadle diagnosed?

3 tests:


1. CXR – enlargement of the RA, RV, pulm arteries. Right heart enlargment
2. ECG – right axis deviation, P pulmonale (peaked P waves), right venticular hypertrophy
3. Echo – RV dilitation; normal LV size and function; rule our LV dysfunctionTreatment: underlying pulmonary disorder, diuretic therapy cautiously (if preload dep) O2 therapy

CNS: bilateral bells palse CNVII/ CNI optic
Lungs: dry cough, SOB
Skin: eryethma nodosum; plaques; subq nodules
Eyes: anterior uveitis (75%) > posterior
Heart: arrhythmia, HB, sudden death
MUS: bone lesions
Whiat treatments are used in acute COPD exacerbations?
FLUTICASONEBoth are inhaled steroids that are anti-inflammatory in nature.

symptoms of acute Respiratory FAILURE

SIGNS: Diagnosis:

Signs: elevated HR, elevated RR, cannot speak in full sentences

-SOB is the first symptom
-COUGH (+/-)

Signs: 1. talk in complete sentences depends upon underlying cause; use of accessaory muscle (SCM/trap). 2. Tachypnic (elevated RR). 3. Tachycardic (inc HR). 4. Cyanosis. 4. Impaired mentation

What triggers asthma?

4 classic features of asthmatics (clinically)

1. exercise
2. pollens
3. house dust
5. cockroaches
7. cold air
8. viral infection
9. tobacco smoke
10. BB and ASAFour major presented findings: SOB, COUGH, WHEEZE, CHEST TIGHTNESS

Which pneumoconiosis increases the risk of bronchogenic carcinoma and malignant mesothelioma?



No specific traetment abailable
-bilateral hazy infiltrates with linear, opacities

What is PEEP?

positive pressure applied during mechanical ventilation at the end of passive exhale that keeps alveoli open. differs from CPAP which is used in pts who spontanously breathe. Pts with PEEP are under mechanical ventilation

-2.5-10cm H2o appropriately set
-used in ARDS patients
-good = increases lung compliance/O2 and presvents alveolar collapse

If patient presents with COPD exacerbation – what are the following steps appropriate for its diagnosis?
1. CXR
2. B2 agonist (albuterol)/anticholinergic (ipra)
3. Systemic corticosteroids
4. AB (r/o infection)
5. Supplemental O2 therapy
6. Non-invasive PPV if needed like a CPAP or BIPAP
Parapneumonic effusion treatment:
P effusion + pneumonia
1. uncmplicated = AB alone
2. complicated = EMPYEMA – pus in the effusion
-chest tube draininage
-intrapleural injection of thrombolytic agents (streptokinase, urokinase)
-surgical lysis of adhesions may be required
Acute respiratory failure = either ______ oxygenation or blood or ________ ventilation of _________.
Decrease the O2 of PaO2 (inadequate perfusion)
Decreased the CO2 ventilation of PaCO2Thus hypoxia is PaO2< 60mmHg and PaCOD > 50 mmHg

Thus hypercapnia PaCO2 > 50 mm Hg

What is the number one diagnosis of a mediastinal mass?
CHEST CT – discovered by CXR incidentally
SIMv = synchronous intermittent mandatory ventilation
TV is NOT determined or preset by ventilation but the RATE is.
-breathe on their own above mandatory rate without help from ventilator (TV of extra breaths is not determined by the ventilator)
-delivers mandatory breath in syncrhony with pts intitiated spontaneous breathe so the two dont overlap
-if the patient breathes spontanously – no preset volume (gets it at rate) if doesnt breathe, gets predetermined breath rate

ALL patients, including those who are pregnant with HCV chronically should receive vaccinations against both ____ and _____ if not already immune.


Hepatitis c perinatal transmission is less frequent (2-5%). Increased risk if pt is HIV positive with high HCV viral load. Both interferon and ribairon for the treatment of pts with chronic HCV must be held during pregnancy. Some evidence that sexual transmission of HCV occurs, but the incidence is extremely low. Thus no barrier precaustion between stable monogamous sexual partners is required.

Increased risk of ILD (SOB, later on exertion, COUGH, FIBROSIS) in dividuals with mining, stone cutting

Increased risk of TB

signs of ILD that differs from OLD (COPD/CB)
-rales at lung base
-pulmonary HTN/cyanosis
-CXR with honeycombing = scarred shrunken lung ciliated air spaces, fibro scars in interstitium.
-CT scan show groundglassing
-FEV1/FVC normal – high in restrictive lun disease, has low TLC and low RV unlike that of obstructive. Also has decreased ERC and decreased TV
-decreased diffusion capacity
Key parameteres of mechanical ventilation
minute ventilation (RR x TV)
I:E ratio
EGOPHONY ON Lung auscultation:
Say EEE sounds like AA indicates lung consodidation
When might DIGOXIN be used in patients to treat COR PULMONALE?
only is 2/2 LV failure. Otherwise stick to diuretic therapy cautiously
Treatment of ARDS:
Keep O2 sat > 90%
-mechanical ventilation with PEEP
-increased lung olue by opening collapsed alveoli and decreasing the shunt
-fluid management (PCWP 12-15) maintain vasopressors used to mantain BP
-treat underlying cause
-tube feeding > than parenteral
How is sarcoidosis staged?
Stage I = bilateral hilar LAD without infiltrates
Stage II = hilar LAD+ infiltrate
Stage III = diffuse infiltrate without HILAR –> WORST PROG
Stage IV = fibrosis and honeycoming – this is an ILD and thus has restrictive lung pattern….
Diff diagnosis of hemoptysis
1. Bronchitis (50% of cases viral)
2. Lung CA – bronchogenic carcinoma
3. TB
4. Bronchiectass – seen in CF
5. Pneumonia
6. CVD – good pastures, PE with pulmonary infarct, aspergilloma, mitrial stensosis
Inhalation of coal dust (both carbon and silica) by coal workers can either be assymptomatic or result in respiratory disability by fibrosis (ILD)
coal workers pneumoconiosis

How does CF present:

Most common infections;
Most likely treatment?

#1 AR disease in caucasians that includes a defect in the CL- channel @ F508 chromosome 7. This leads to the dec ablity to secrete Cl- in the mucous glands and dec ability to absorb Cl- in the sweat glands leading to think, nonwatery mucus plugging – bronchiectatsis (obstructive), pancreativ insufficiency, GI complicatiosn and increased Cl- sweat > 65

Infection = Pseudomonas aeruginosa (gram -) and treatment is FLUOROQUINOLONEs

Rx: Pancreatic enzyme replacements; FAT soluble vitamin replacement chest percussions and antibiotics

MORGAGI Hernia v. BOCHDALAK’s Hernia
Congenitdal diaphragmatic hernia (CDH)
1. Morgagi – herniation through foramen (2%) moragni located adjacent to xiphoid process of sternum/anterior defect of the diaphragm2. BOCHdalaks – posteriolateral diaphragmatic hernia (95%)/allows passage of adbominal viscera into chest cavity on L side

What is a pneumoconiosis?

example of “dust” particles?

accumulation of dust in the lungs and the tissue reaction 2.2 to its presense:

1. SIlica
2. Beryllium
3. Asbestos
4. Coal dust
5. Graphite
6. Carbon black
7. Aluminum
8. Talc

FiO2 parameter on ventilator
100% set
-quickly titrate and use lowest possible to maintain paO2 50-60mmHg (or sat 90%) to avoid O2 intox
-FiO2 < 60% safe
-FiO2 of 0.5 doesnt result in adequat PaO2 thus add PEEP or CPAP to reduce FiO2 to suppor PaO2 and lower FiO2

Which environmental causes exposures?

Restrictive interstitial lung disease?

Coal workers pneumoconiosis
1. Status asthmaticus
2. Acute respiratory failure (2/2) respiratory muscle failure
3. Pneumonthorax, atelectasis, penumomediastinum
Incidental discovery of a solitary pulmonary nodule on a radiograph imaging is common. The first step in the workup of such nodules is to:

obtain any previous radiographic lung images.

Absense of growth over time rules out malignancy. If previous radigrpah films are not available thn the nodule is assigned either alow, intermediate or HIGH probability of malignancy based on clinical and radiogrpahic data.

Low: followed by high resolution chest CT
intermediate: further investigated with PET scan and/or biopsy
HIGH probability nodules are removed surgically

Primary lower extremity sites responsible for PE?
Lower extremity DVT
#1 – iliofemoral DVT (area above the knee)
#2 = deep veins of the pelvis
## – calf vein emboli => proximal veins, increase incidence
What is the treatment for NSCLC: SQUAA LC, adenocarcinoma, large cell
1. Surgical removal: if mets out of chest – then not a candidate for removal
2. Radiation therapy prior to surgery – patients with
3. Chemotherapy is of uncertain benefit
NSCLC is staged by TNM, whereas SCLC is staged by?
1. Limited to chest plus supravlacicular node but not cervical/axillary
2. Extensive- outside of chest and SC nodes.
Normal ranges of ABGs? (doesnt req mechanical ventilation)
PaO2 of (50-60)
PaCo2 (40-50)
pH = 7.35-7.50
What causes a pleural effusion?
1. Increased fluid into the plerual space/drainage
2. Increased production of fluid by cells into the pleural space
3. Decreased drainage of fluid from the pleural space
In patients with COPD, which vaccinations are required?
Influenza vaccination annually
Pneumococcus polysaccaride vaccination of 5-6 years

postoperative cholestasis can develop after a prolonged surgery characterized by hypotension, extensive blood loss in tissues, and massive blood replacement.

T or F

Alveolar filling diseases causing restrictive lung disease?
-idiopathy hemosiderosis
-alveolar proteinosis
How might one diagnose air in stomach by auscultation?
ET tube may not have been placed correcly by ventialtion – check bilateral breath sounds and CXR. 3-5 cm above carina
Clinical features of COR PULMONALE
decreased exercise tolerance
cyanosis/digital clubbing
signs of RVHF; hepatomegaly, edema, JVD
parasternal life at P2 (seen in p HTN)
polycythemia vera present if COPD cause of COR pulmonale
Underlying cause of clubbing in patients?
#1 cause is chronic hypoxia
Diff diagnosis: LUNG cancer, CF,ILD, empyema, sarcoid, mesothelioma, heart dz, bacterial endocarditis, cirrhosis, IBD, primary biliary cirrhosisORDER CHEST XRAY IF THINK LUNG DISEASE +/-

Causes of COR pulmonale:

1. Right sided counterpart to LV heart dz due to systemic HTN – RVH with eventual RVF from pulm HTN 2/2 pulm disease

2. Doesnt include pulm HTN du to left sided HD like MS of LVF

Causes: 2dary to COPD; recurrent PE, ILD, asthma, CF, sleep apnea, penumoconiosis

Noncaseating granulomas involving the lungs at hilar (LAD). Eyes, skin, heart, MS, CNS also involved.

#1 cause of death = H.D.
#1 population affected:

1. AA females <40YO
-85% change of acute (noncronic) infection
Classic criteria of ARDS:
1. hypoxemia that is refractory to oxygen therapy ==> ratio of PaO2/FiO2 </= 200
2. bilateral diffuse pulmonary infiltrates on CXR
3. No evidence of CHF: PCWP </= 18 mm Hg
Fever night sweats wt loss hemoptysis
B SYMPTOMS – associated with TB and HIV
Centrilobar emphysema v. panlobar emphysema
-centrilobar is the most common
-destruction at respiratory bronchioles (proximal) with little distal change.
-upper lungs-alpha1antitrypsin deficiency
-proximal and distal acini
-goes for bases of lungs

What is the I:E ratio?

amount of time alloted to I in comparison to Expire in 1 breath.

duration of each breath preset by RR. This increases the time spenin in INHALATION and decreases the time spend in EXPIRATION.

Want 1:2 for (I:E)

Mixed capillary (at site of A–>V) and prevapillary causes of PULMONARY HTN:
Lung dz of the parenchyma or of the pulmonary vessels
-includes obstructive – COPD, asthma, CB
-includes restrictive lung disease ILD
Malignant mesothelioma
2/2 abesteos exposure
-dyspnea, weight loss, cough, bloody effusoin on thoracentesis

MODALITIES for Asthma:

1. Rescue inhalants for ACUTE ATTACKS
2. Longer acting with nighttime asthma and exercise induced asthma
3. Decreased airway hyperresponsivity, decreased annual number of exacerbations

Albuterol – ST B2 agonist
Salmeterol LT B2 agonist
Inhaled corticosteroids
-inc risk core throat/candidiasis (thrush)
-increased risk of hoarseness
Diagnosis of lung CANCER
1. CXR =
2. CT scan =
3. Cytoloic sputum exam =
4. Fiberoptic bronchoscope =
5. Transsthoracic needle biopsy =
6. Mediastinoscopy =
1. Most important study for diagnosis but NOT for screening. If greater than 2 years without change in the lesion; then BENIGN
2. Staging lung CA; LOCAL v. DISTAL met
3. CYTO = centra tumor diagnosis (80 %) not peripheral more likely to be detected early.
4. Fiberopti goes 2/2 branches of the tree – good dz of the central CA IF VISIBLE, diagnostic jumps to 95% of causes.
5. TNB = highly accurate, good for peripheral lesions as well – invasice, selected pts only.
6. MED = direct visualization of medistinum

What are the subtypes of the 75% of Lung CA that are 2/2 NSCLC?


How does this compare to that of SCLC?

1. SQCC (30% of all LUNG CA) — Central location — Cavitation on CXR
2. Adeno (25% of all LUNG CA) — Peripheral location — Pleural involvement (20%) without smoking, may have pulmonary fibrosis
3. Large cell (5-10% of all LUNG CA) — peripheralSCLC — (20-25% all LUNG CA) — narrow bronchi (associated with LE syndrome) 50-75% mets

Clinical features of mediastinal masses
1. Due to compression or invasion of neighboring structures
2. Cough
3. Chest pain
4. Post obstructive pneumonia
5. Dysphagia
6. SVC
7. Compressed nerves (recurrent laryngeal CN X)
-horners SCG
-diaphragmatic paralysis (C3-c5)
AC Ventilation
assisted controlled ventilation
-guarantees a backup minute ventilation that has been present
-delivers breath when patient intitiates breath
-if the patient doesnt initiate breath, ventillation takes control and delierates a predetermined breathe.
-delivers the same predetermined TV
Primary PULMONARY Htn (PPH?)
1. Pulmonary HTN in absense of heart dz or LUNG dz
2. Diagnosis of exclusion
3. INcreased PA pressure leads to thickening of pulmonary arteriolar walls thus worsense pulm HTN, increases wall thickening
4. #1 in middle aged women
5. Poor prognosis (2-3 years)
Evaluation of hemoptysis
1. CXR
-look if TB, penumonia, granuloma, opacities
-if normal, then increased risk of PE2. FIBEROPTIVE BRONCHOSCOPY
-perform CXR, if normal, then do this to r/o MALIG
-look for small tumor

3. CT of chest

For lung CA, what lab tests should be ordered/imaging to confirm diagnosis of NSCLC v. SCLC?

CXR, CT scan, TISSUE biopsy

Tissue biopsy is what determines that between NSCLC and SCLC

DI-restrictive lung diseases
AMIODARONE (K+ channel blocker)
When should a pateint be taken off the ventilator
1. Check if the patient has an adequate respiratory drive
2. Intact cough
3. PaO2 > 79 mmHg PaCo2 < 45 4. O2 saturdation > 90% with PEEP of < 0.5cm H2O; FiO2 < 40-50% 5. TV > 5mL/kg
6. RR < 30 breaths/minute
7. VC = 10-15
8. NegI pressure <-20cm
Recuurent pneumonia in the same lobe location should be a red flag for?
LUNG CA – get CT of the chest
How does elastase result in a change in alveolar wall destruction in emphysema?
excessive elastase will be produced in cases with alpha1antitrypsin or a deficiency of antiprotease activity in lung.
-macrophages and pmns digest human lung
how might pulmonary HTN be characterized?
PAPressure > 25 mm Hg at rest
PAPressure > 30 mm Hg exercise
1. To determine the underlying mechanism of hypoxeima
-PaCO2 level
-A-a gradiant
-Response to supplemental O22 A-a gradiant is normal if HYPOVENTILATION or low inspired O2 is the only mechanism

3. If V/Q mismatch/shunting presenting then both PaCO2 and A-a gradient elevated

4. Supplemental O2 differs between two mechanisms

What is the number 1 parameter used to decipher ARDS from CHF?
PCWP – if low (< 18mmHg) then ARDS PCWP – if hi (> 18) cardiogenic PEdema
How to diagnosis primary pulmonary htn
1. Cardiac cathederization
2. CX shows enlarged central pulmonary arteries, increased RV with CLEAR LUNG FIELDS!
3. PFT shows restrictive pattern
Treatment of aspirations and aspirations pneumonia

CAB – airway breathing circulation = SUPPLEMENTAL o2

Penicillin G – to cover gram +
CLindamycin – to cover the anaerobes

If foul smelling sputum think ANAEROBIC COVERAGE NEEDED! go for the good antibiotics for anaerobes (that includes bacteroidies, clostridium, pepto)

How is airway obstruction diagnosed?


Normal –> elevated TLC, elevated RV, elevated FRC
Decreased FEV1
Decreased vital capacity

Clinical features of aspirations pneumonia

~40% develop symptoms 2-3 days post organisms areobic –> anaerobic (primary klebsiella)

-acute repiratory distress
-SOB, cough fever, tachypnia, hypoxemia, frothy sputum

causes = decreased level of consciousness, aspirations by alcohol, vomiting, ileus

HOW is the diagnosis of ASTHMA made?

1. PFT required = obstructive pattern with elevated TLC and RV and elevated FRV however will have lower TV low FEV1 and low FEV1/FVC ratio

2. SPIROMETRY = get before and after albuterol (B2 agonist) if increased FEV1 or FVC by 12%, then confirms the diagnosis.

3. PFR = peak flow rate: (450-650 in males; 250-500 in females); mild >300; moderate = 100-300; severe = <100

4. Bronchovocation test if no PFT

Goodpastures syndrome

Autoimmune (HLA DR2) antigbm type II hs to the alpha3-chain of collagen type 4 (IgG-AB)

1. Hemoptysis *cough up blood
2. SOB
3. Hematuria
4. Burning urination – renal failure and protein in urine

Diagnosis by: TISSUE BIOPSY

What is minute ventilation?

(RR x Vt) = measures ventilation. To decrease PaCO2 in patient, decrease the RR or TV.

Want patients baseline < 45 mmHg (PaCO2)
-initial TV of 8-10 mL/kg is appropriate in most cases (lwoer TV recommneded in patients with ARDS and COPD)
-10-12 breaths /minappropriate

What is ILD – classifications?
Intersitital lung disease (RESTRICTIVE LUNG PATTERN)
-inflammatory lung disease involving the alveolar wall (resulting in widespread fibroelastic proliferations, collagen deposition leading to irreversible firbosis/imparied O2 exchange/change in lung struccture-environmental lung dz
-ILD with granulomas (sarcoid)
-Alveolar filling disease (ARDS)
-HS lung disease

Treatment of an acute exacerbation on hospital admission (asthma)?
PEV < 60% of predicted – req systemic steroids 1st – inhaled B2 agonists -via nebulizer/MDI (metered dose inhalter) -occurs in min 2nd – corticosteroids -administer IV intiailly then orally when clinical improvement seen -then inhaled 3rd – theophylline and IV magnesium -keep O2 saturation >90%
Workup of PE:
Tests providing basis for treatment of PE with anticoag
1. Intraluminal filling defects in pulm atery on helical CT
2. DVT diagnosed on US and clinical suspician
3. Positive pulmonary angiogram (proves PE)Rule OUT PE:
1. Low probability V/Q scan or normal helical scan and low clinical suspician
2. Negative pulmonary angiogram
3. Negative D-dimer

Increased intrathoracic pressure causing pulmonary HTN?

Increased blood viscosity causing pulmonary arterial pressure of > 25?

1. Mechanical ventilation with PEEP, COPD, causes pulmonary HTN (>25 mmHg at rest)

<50 YO, non smoker, <2.0cm nodule, no growth in > 2 years, circular, regular, central laminated with Ca2+

>50YO, prior smoker, >3.0 steady growth, nodule grossly irregular, stippled or eccentric pattern of calcification


ILD with restirctive pattern and honeycoming or ground glass on CXR. Cause is unknown and definitive diasnosis requires a lung biopsy

-presents with gradual SOB, nonproductive cough, dry cough and as survivial of 3-7 years

Treatment: no effective treatment available – majority of patients >70% do not improve with O2, corticosteroids, lung transplant

When does a patient require mechanical ventialtion?
significant respiratory distress (increases RR)
-impaireddec level of consciousness; cannot protect airway
-metabolic acidosis (doesnt adequately compensate with hyperventilation thus hypoV) and decreased pH
-respiratory muscle fatigue
-PaO2 < 70 mmHg or hypercapnia PaCo2 > 50; respiratory acidosis (pH<7.2) with hypercapnia
Diagnosis of PULMONARY HTN

ECG: RVH, RA-deviation, right atrial abnormality (myxoma)

ECHO: dilated pulmonary artery; dilitation/hypertrophy of RA/RV; abnormal movement of IV septum; right heart catheterization shows increased PA pressure

WHen should O2 therapy in patient with COPD be considered?
If PaO2 is 55mmHg or O2 saturaation is < 88%
If PaO2 55-59 mmHg + Polycythemia vera or COR Pulmonale (RCHF)
“All causes of wheezes”?

#1 is asthma but not ALL wheezes are asthma, but all that have asthma do wheeze.

1. CHF – edema in airways and mucosa
2. COPD – inflammation causes narrowing
3. Cardiomyopathyies – pericardial dz, edema near bronchi
4. Lung CA due to obstruction of AIRWAYS

Treatment of PE:
1. Supplemetnal O2 for hypoxia
2. Acute anticoag therapy of UFMH or LMWH
-start immediately if suspect
-give one bolus with IV infusion 5-10 days to maintain apTT 1.5-2.5x
3. Oral warfarin LT – start hep on day 1 and continue 3-6 months
4. Streptokinase/tPA
local invasion symptoms of lung CA v. metastatic disease sites?
Local invasion:
1. SVC syndrome -obstructed SVC by mesdiastinal tumor = seen in SCLC facrial features = seen in SCLC facial fullness, JVD, ARM edema.
2. Phrenic nerve palsy
3. Recurrent laryneal nerve palse
4. Horner’s syndrome (PTOSIS, MIOSIS, ANHIDROS)
5. Pancoast tumor – SUPERIOR SULCUS TUMOR
6. MALIGNANT pleural effusionMestastsis: BRAIN BONE LIVER ADRENALS

ILD associated with granulomas
1. Sarcoidosis -along with other organs
2. Histocytosis x – langerhands cells CD1 esterase
3. Wegeners granulomas (sinus infection/hemoptosis plus hematuria)
4. Churg-strauss syndrome (IgE)
CPAP – continuous posistive airways pressure
positive pressure (0-20 cm H20) delivered continuously by ventilator but doesnt change volume of breaths delivered
-the patient breaths on own.
-set PEEP and pressure support
What is the diagnosis of a pleural effusion?
1. CXR – PA and LA view – blunted costophrenic angle – ~250 mL of fluid must accumulate to detect effusion on CXR. Determine if free flowing or loculated.
2. CT scan more reliable than CXR
3. THORACENTESIS – useful if unknown etiology
-75% diagnosis of patients; >10mm think of LLdecub
-therapeutic – drainage for relief
-pneumothorax – complication in 10-15% patients
-send fluid for: CHEMISTRY (protein, glucose); CYTOLOGY; CBC and CULTURE
Necrotizing granulomatous vasculitis that affects:
1. lungs/hemoptysis
2. kidneys (+/- hematuria – RPGN)
3. Upper airway/lower resp
4. cANCA
5. perforated nasal septum
How is COPD monitored?
1. Serial FEV1
2. Pulse Ox
3. Exercise intoleranceVC = IRV + TV + ERV

TLC = IRV + TV + ERV + RV = VC + RV

If a 36 yo patients comes to office with cc of progressive fatigue with a PMH of infiltrative TB and a blood culture indicating two populations of RBC (hypochromic and normochromic) – what is the next best step in this patients management if already on the “RIPE” regimen and a lab value status indicating (CBC) microcytic anemia with elevated serum iron levels and decreased TIBC?

Addition of pyridoxine – why?

Because the patient has a probably SIDEROBLASTIC ANEMIA. his condition results from defective heme synthesis that is most commonly 2/2 imparitment in the early steps of heme synethesis. Because the patient is on the TB regimented treatments, and ISONIZED comparitively can act as a antagnosit to pyridoxine, pateints should be expected to have an acquired sideroblastic anemia.

This will result in two groups of RBc on microscopy (one group in which manifests as microcytic hypochromic anemia that simulates iron deficiency anemia, and another group that are normochromic – hence the dimorphic population of cells). The decreased TIBC and elevated iron helps to differenciate sideroblstic anemia from that of iron-def anemia

What complications, then, are associated with mechanical ventilation?
1. Anxiety/agigtation/discomfort
-must sedate, use benzos or morphine, use propofol
2. Difficulty with tracheal secretions
3. Nosocominal pneumonia (if intub > 72 hr)
3. Extubation
5. barotrauma (high PEEP/O2 toxicitiy if FiO2 > 0.6) for greater than 2-3 days.
6. Hypotension 2/2 increased thoracic pressure by PEEP (increased intrathoracic pressure that decreases venous return and increased SVR – and ultimately cor pulmonale


Treatment with steroids

HOw might PPH be treated for?
1. Pulmonary vasodilators like (PROSTCYCLINS – EPOPROSTENOL)
2. CCB decreased PVR
3. Vasodilator trial = O, IV adenosine, ORAL CCB
4. Anticoag with warfarin 2/2 venous statis and prevention of PE
5. Lung transplantation

Cardio: CHF, JVD, EDEMA, Hepatomegaly, P. Edema, Tachypnea, Tachycardia, volume overload.

ARDS: sepsis, increase RR, increased HR, doesnt respond to supplemental O2; cannot ventilate bc high peak airway pressures 2/2 stiff lungs.

Although the effects of both CARDIOGENIC PULMONARY (FLASH) EDEMA and ARDS are the same, how does the causality differ?

Increaed alveolar capillary permeability causes ARDS; thus the interstitial edema, SOB, increased HR and RR, hypoxemia with shunting that doesnt respond to O2.

In cardiogenic pulmonary edema – congestive hydrostatic forces cause the increased interstitial fluid.

-SOB (most often NOT releived by albuterol)
-Increased sputum production and cough that is (NOT relieved by theophylline)
-Increased respiratory failure +/- ventilation (O2 therapy for HYPOXIA)

What is INR?

What increases the value?

“therapeutic range”?

International ratio that reports the PROTHROMBIN TIME (PT) by that of the extrinsic pathway affected by warfarin (wafarin thus increases the INR at clotting factors 2, 7, 9, 10 and protein C and S)

Therapeutic = 2-3

What are some causes of hypersenitivity pneumonitis and differentiates it from other causes?
Acute: flu-like with fever, chills, cough, SOB – CXR infiltrate
Chronic: Restictive lung diseaseExtrinsic allergic alveolitis:
1. Farmers lung, modly hay
2. Birds breeders lung
3. Air conditionals lung
4. Bagassosis (sugar cane)
5. Msuchroom workers lung
6. Spores of thermophilic actinomycetes

Diagnosis of IgG and IgA in serum with ILD symptoms

Post capillary causes of pulmonary HTN (> 25 mm Hg)

primary due to L side of heart that will increase pressures on the PULMONARY VEINS like that of MITRIAL stensis (will be a diastolic murmur with OS).

ex: Mitrial stneosis (backs up blood into lungs and icnreases pressure of pulmonary capillary); LV dysfunction (LVH can cause); ATRIAL MYXOMA primary lipoma located in the R atriaum that is most liekly to cause a mid diastolic murmur in patients with no other underlying etiology and CAN result in a thrombus formation that can undergo embolic stroke.; CONSTRICTIVE PERICARDITIS

Mediastinal masses
1. Metastatic cancer (#1 lung) most common cause of mediastinal mass in older patients
2. Anterior = thyroid, thymoma, lymphoma
3. Middle = lung, lymphoma, aneurysms, cysts
4. Posterior = neurogenic tumor, esophageal tumor
Chronic treatment of ASTHMA
1. Mild intermittent
2 . Moder persistent
3. Sev persistent
1. Mild intermittent – 2x/week == NONE (chronically)
2. Moderate persistent – daily —DAILY INHALED corticosteroid
3. SEVERE continuous —daily inhaled corticosteroids, LT B2 agonist
Ventilation versus oxygenation?

Both are unrelated to one another – o2 saturdation can be 100% with increased PaCO2 and be in ventilary failure

ventilation monitored by PACO2
-to decreased paCO2, must INCREASE or INCREASE TV
-minute ventilation = RR x VT
-to decrease paCO2, want to increase ventilation and thus increase RR and VT

oxygenation monitored by O2 saturation
PaO2 – to decrease PaO2 in the ventilated patient one must either decreased FIo2 or decreased PEEP

CLINCIAL features of a tension pneumothorax?
1. Hypotension – cardiac filling decreased due to compression of great veins
2. JVD
3. Mediastinal deviation away from side of lesion
4. Decreased breath sounds over collapsed lung
5. Hyperresonance
-chronic ILD with ABNORMAL PERFORATION OF the langerhan cells of bone marrow that can migrate
-90% smokers
-localized to bone or lung (eosinophilic granuloma or 2dary types – HAND-SULLER CHRISTIAN OR LETTERER-SIWE disease)
Treatment of tension pneumothorax


2-3rd intercostal space in the midclavicular line – then chest tube it

What is the FEF50% for normal , obstructed, restricted lung?
Forced expiratory flow (FEF50%)
-normal = 3.2
-obstructed = 0.5
-restricted = 1.9
Prognosis of patients with PE diagnosis?
1. recurrence common (clinically silent)
-can lead to chroni PULM HTN and CHRONIC COR PULMONALE2. PULM HTN (2/3) pts
-30% death d/t recurrent PE left undiagnosed

Paraneoplastic syndromes associated with
– PTHrP-hormone with elevated Ca2 decreased phos and elevated parathyroid hormone)
-hypertrophic pulmonary osteoarthropathy2. SCLC –
-Lambert eaton syndrome at NMJ;
-SIADH from ectopic tissue;
-ACTH secretion from ectopic tissue (carcinoid?) increased cortisol and increased cushings

3 Adenocarcinoma – hypertrophic pulmonary osteoarthropahty

75% NSCLC 25% SCLC
-SQUAA (30)
-Adenocarcinoma (35%)
-Large cell LC (5-10%)
Increased P2 on auscultation on/at 2nd parasternal border L side with a subtle lift of sternum

Rare condition due to excess accumulation of surfactant-like protein and phospholipids in alveoli


Dry cough, SOB, rales, HYPOXIA

Diagnositc: LUNG BIOPSY
CXR: ground glass appearance with bilateral alveolar infiltrations that resumble a bat shape

Exudative effusion treatment
Treat underlying disease
-bacterial inf/tb
-viral infectoin
What are the requirements to use NPPV?

1. Neurologically intact – aware, cooperative, protect airway

If doesnt improve, BIPAP should be d/c and conventional therapy for endotrachial intubation and mechanical ventilation.

Gold standard to diagnose PE:

Decision to rule criteria (DUKES!)

Pulmonary angiography – definitive diagnosis of exclude PE but is invasive

Symptoms and signs of DVT = 3 pts
ALT dx less likely thank PE = 3 pts
HR > 100 bpm = 1.5 pts
Immobilization > 3days/surgery past 4 weeks = 1.5 pts
Previous DVT = 1.5 pts
Hemoptysis = 1.0
Malignancy = 1.0

APICAL tumor of the lung involving C8 and T1-T2 nerve roots (radiating) pain down arm: Most common in SQUA CC with CENTRAL cavitation

(+) Association with HORNERS 60% of the time

Pleural effusion
Symptoms/pearls:1. In increased pleural fluid amylase, think:
2. If milky, opalescent fluid, think:
3. If purulent fluid/pH < 7.2 think:
4. If bloody effusion think:
5. If exudative + lymphocyte think:
6. If pH < 7.2 think:

1. Esophageal rupture, pancreatitis, malignancy
2. Chylothorax
3. Empyema – pus in the pleura
4. Malignant if bloody
What is the first treatment for spontanous pneumothorax? Why?
Supplemental O2
-hastens the resorption of air in the pleural space
Hypercapnia –> ___ ____
can lead to SOB, VASODILATION OF CEREBRAL VESSELS with increased intracranial pressure and papilledema and coma
respiratory acidosis
pH<7.35-7.45 PCO2 > 35 mmHg

Granulomatous vasculitis in patients with asthema, increased pulmonary infiltrates and RLD; increased RASH and increased eosinophilia


Churg strauss syndrome
When a pateint is ventilator dependent for 2 or more weeks, a tracheostomy is usually performed to prevent softening of tracheal cartilage

Interstitial pulmonary inflammation that occurs in patients with prio treatment to breast, lung, lymphoma, thymoma, CANCER

1. Acutely forms 1-6 mo post treatment or chronically 1-2 years later with alveolar thickening and pulmonary fibrosis leding t a dever, couh, chest fullness, pleruitis chest pain and hemoptysis

2. CT SCAN – DIFUSE INFILTRATES WITH GROUND GLASS densities with pleural/pericardial effusion
SOB on exertion + syncope + fatigue + chest pain on exertion
What causes bronchiectasis? How can this be treated

Cause: permanent dilitation of the bronchioles and destruction of the bronchial walls with damaged cilia.

#1 – CYSTIC FIBROSIS most common AR in causcasions (~50%) for delta-F508 CFTR gene mutation

#2 – infection, humoral immunodeficiency or airway obstruction

Hypoxemic respiratory failure and oxygenation

Hypercarbic respiratory failure and oxygenation

1. Lowest concentration of oxygen that provides sufficient O2 to avoid O2 toxicity (free radical)

2. High concentrations of O2 causes CO2 retention especially in patients with COPD because pt doesnt ventilate off of CO2 – thus hyPOventilation.

What are the classic types of COPD?

List the four risk factors:

1. Chronic Bronchitis – productive and chronic cough of sputum for at least 3months/year
2. Emphysema – permanent enlargement of air spaces due to surfactant destruction of alveolar walls at terminal bronchiRisk factors:
1. Tobacco use (90%) COPD
2. alpha-antitrypsin
3. second hand smoke
4. chronic athsma

Which lung is most common to develop aspirations penumonia 2/2 anatomy?
Lower segment of right upper lobe
upper segment of right lower lobeBecause the RM bronchus follows straight path

Which paraneoplastic syndromes are associated with SCLC (20-25%) of ALL lung CA?

1. SIADH – 10% – ectopic tissue which increased ADH; this causes increased H2O retention that will bind and increase AQP2R while likewise increases that of sodium out. Thus, will have hypoatremia bc body trying to unload with hypervolemia and decrease RAAS

2. ECTOPIC ACTH: SCLC, increased cortisol, increased cushings
3. Lambert-eaton syndrome

Peripheral pulmonary infiltrates with a fever and elevated eosinophils without changes in IgG and IgA
What is the treatment of SPONTANEOUS pneumothorax?
1. PRIMARY –> If small and patients is asymptomatic then
-OBSERVE – resolves in 10 days
-small CHEST TUBE (one way valve)2. PRIMARY –> if LARGE/symptomatic (cough, SOB, sudden and UNILATERAL CP
-chest tube placement/insertion


Causes of acute repiratory failure 2/2 shunts? (ittle or no ventilation in perfused areas due to collapsed or fluid filled alveoli – pneumonia – the venous shunts to the arterial circumation without getting oxygenatued and thus results in that of ARF 2/2 decreased oxygenation)
1. Atelectasis (collapsed)
2. Fluid build up in alveoli
-pneumonia/pulmonary edema
3. Drect RIGHT to LEFT shunt d/t congenital abnormalitydoesnt respond to supplemental O2

What are the clinical features of pulmonary embolism

increased HR, RR, SOB

1. DYSPNEA (72%)
3. COUGH (27%)
4. Hemoptysis (13%)

1. Tachypnea (RR) *70%) – hypercarbic ventilatory failure
2. Rales (51%)
3. Tachycardia (30%) increased HR
4. S4 (24%)

1. Passive = resistance to pumonary venous drainage. Not actively in pulmonary best – further down. Mitrial stensosis, LVF, ATRIAL myomxa (most common cause of a mid diastolic heart murmur)
2. Hyperkinetic = L–> R cardiac shunts that include VSD, ASD, PDA
3. Obstructive = resistance to flow through P. arteries = PE, PA setnosis
4. Obliterative = resistance due to fibrosis PPH (primary pulmonary HTN, CVD, crest)
5. Vasoconstrictive – hypoxia induced (COPD)
What are the risk factors for LUNG CA?
1. Cigarette smoking > 85% of cases
-adenocarcinoma lower associated lung CA to smoking.
2. Passive smoking (2nd hnd)
3. Asbestos: ship building, construction, cars, smoking and asbestos increase risk
4. RADON – found in basements
5. COPD – independent risk factor once smoking considered
What are the clinical features of pulmonary HTN?

Symptoms: SOB on exertion, fatigue, chest pain (exertional), syncope (exertional) with severe disease)

Signs: loud pulmonic component of P2 and lift of the sternum (RV dilitation); when RVfailure occurs = JVD, peripheral edema, ascites

-lung lavage or GSCMF – increase the granulocytes by stimulatied neulasta or filgrastin.
Hypocarbia is common is asthmatics under respiratory distress, why?

Have increased respiratory rate thus should cause PaCO2 to decrease (breathing off the CO2)

Increased PaCO2 is a sign of respiratory muscle fatigue or severe airway obstruction thus INTUBATION may be required

CXR: egg shell calcifications
-localized and nodular peribronchial firbosis of the UPPER LOBES that can be acute (rapid onset + death) or chronic (symptoms yrs post exp)
-#1 symptom = exertional dyspnea
Diagnosis of acute respiratory failure:
1. ABG
2. CXR or CT scan
3. CBC and metabolic panel
4. If cardiogenic P. edema, get enzymes
When are DDIMERs elevated?
DIC (SEPSIS – 2dary)
What are the constitutional symptoms of LUNG CA – both SCLC and NSCLC?
1. Anorexia, weight loss, weakness
2. Indicates advanced stage is cachexia
3. SOB, hemoptysis, cough, wheeze
4. Recurrent pneumonia
Decreased tactile frematis; decreased breath sounds over effusion, dullness to percussion:
pleural effusion
empyema causes:

differs from a parapneumoni effusion becase it is a “complicated” effusion in which contains infection and pus within the pleural space. Number one cuse is 2/2 that of bacterial infectoin like S. pneumonia.

Diagnosis: CXR and CT scan of the chest
Treatment: Thorcentesis wth AB therapy; repeat drainage req bc difficult to eradicate; if persistant than a rib retraction may be required.

What systems are interrupted/dysfun if repirations become decreased and HYPOXIA ensues *HYPOXEMIA?
1. CNS – brain = drug OD; stroke; trauma
3. Upper airway = obstruction 2/2 to a number of causes like stenosis, paralysis
4. Thorax/pleura = mechanical restriction due to kypho or flial chest
5. CV system = CHF, valvular dz, PE, anemia
6. Lower airway and alveoli = asthma, COPD, pneumonia
Letterer-Siwe disease?
langerhan cells that proliferate into many tissues
What are the side effects of PEEP?
1. Barotrauma = pneumothorax
2. Decreased CO d/t decreased VR in setting of hypovolemia = lowers venous return because increased intrathoracic pressure. Increased SVR due to decreased VR. Can cause COR PULMONALE.
CRYPTOGENIC ORGANIZING PNEUMONITIS (COP) Differs from the other types of restrictive lung diseases in that it?
-inflammatory lung dz; similar CXR to infectious pneumonia (locular or diffuse) – due to viral, medicational, or CTDz that is uaully idiopathic
-AB effective
-spontanous recovery or corticosteroids is mainstay
-relapse common post corticosteroids

Obstructive lung disease:

Peak flow (expire)

decreased FEV1
decreased FEV1/FVS ratio
decreased PEV
increased RV
increased TLC
decreased VC


Dx and Rx

BRONCHIECTASIS – cough, SOB, BLOOD (hemoptysis) and persistent recurrent pneumonias

Dx: High reoslution CT scan; PFT of obstructive pattern (elevated TLC and RV and FRV and decreased TV and FEV1 low and FEV1/FVC low; then order a CXR

1. Antibiotics if acute exacerbation
2. Bronchial hygiene (hydration/chest percussion, inhaled bronchodilators)

ARDS characteristics = patients at risk for?



Berylliosis as a pneumoconiosis?
Acute rapis onset early death
Chronic: >15 years exposure-upper lung diffuse pneumonitis
-similar to sarcoidosis (granulomas, skin leisons, hypercalcemia)

dx: beryllium lymphocyte proliferation TEST
rx: glucocorticoid

If anticoagulation is contraindicated in patient with PE (cannot use LMWH, WARFARIN or thrombolytics) what is indicated?

Inferior vena cava filter (greenfield filter placement)

indications – if documented DVT/PE then complication with current anticoag; failure of adequate anti-coag by recurrent DVT/PE; high risk pts with death

If pleural fluid glucose < 60, r/o ____ ____. What else can decrease the glucose in plerual effusion?

Rheumatic Arthritis

TB, Esophageal rupture, malignancy, lupus

SCLC treatment?
1. Chemotherapy #1 for both: LIMITED and EXTENSIVE
2. Radiation therapy useful in limited stage disease (thus lung and superclavicular nodes) and not extensive – inclusive of external chest (BRAIN, BONE, ADRENAL, LIVER)
3. Surgery not good
Causes of tension pneumothorax?
Air trapped within the pleural space such that tissues surrounding pleural cavity act as one way valves allowing air to enter pleura, but not allowing escape.
-accumulation of air under (+) pressure collapses ipsilateral lung and moves mediastinum away from side of pneumothorax.*Mechanical (barotrauma) ventilation

When is a chest x ray ordered in asthmatics
only in SEVERE ASTHMA with PEV < 100 to excluse conditions like:
1. Pneumonia
2. Pneumothorax
3. Foriegn body
Treatment of SARCOID?

Most spontanously resolve in 2 years and do not require meds

Corticosteroids are the treatment of choice 2nd line is MTX

Sources of PE to the lung:
#1 DVT
1. Fat emboli if longbone frature
2. Amnion fluid embolism (post delivery)
3. Air emboli (trauma to thorax or an indwelling V/A line)
4. Septic emboli (bacterial endocarditis – IV drug use)
5. Schistosomiasis
What causes increased CO2 production resulting in hypercapnia?
PaCO2 > 60 mmHg and hypercapnic RF?
(hypercarbia – increased PaCO2 yeilding respiratory FAILURE)
treatment of COPD?
1. SMOKING CESSATION (by age 35, decreasing FEV1 by 25-30mL/year; therefore decrease the rate of decline of FEV1 if quites but doesnt result in complete reversal.
-prolongs survivial
-symptoms get better within one year of cessation2. B2 agonists inhaled )albuterol – SA; salmeterol – LA
3. Anticholinergic inhaled (ipratropium) – i pray I can breathe
4. Corticosteroid (budesonide/fluticonizone)

If patient develops:

1. Dyspnea
2. Petechiae
3. Mental status change

Think ___ ___ as cause of ___ ___

fat emboli
pulmonary embolism

Restrictive lung disease


FEV1 = normal to slightly elevated
FEV1/FVC normal to high
PEV is normal
RV is low, normal or HI
TLC low

Hemorrhagic pneumonitis + glomerulonephritis + hemoptisis and increased IgG

Goodpastures syndrome

1. Plasmaphoresis
2. Cyclophosphamide
3. Corticosteroids

How is a transudative effusion treated?

1. LDHp is not created than 2/3 the serum value. LDHp/LDHs is not greater than 0.5 and PROTEINp/proteinS is not greater than 0.6

-diuretics (LOOPS), with salt restriction
-therapeutic thoracentesis only if CXR is lat > 10,, and massive enough to cause dyspnea; chance of pneumothorax is 10-15% thus want to dec RISK

What is NPPV and when is it indicated in patients?
noninvasive + pressure ventilation
-set with inspiratory and expiratory pressures
-delivery by mask
-admin to pts in attempt to avoid intubation and mechanical ventilation
Predilectation for the lower lobes, inhalation of the asbestos fibers can diffusely insult the lung with restrictive pattern – thus process takes >10-20 years post exposure
Asbestosis (ILD of the lOWER LOBES)
-dyspnea, cough, fatigue, CTD, rales at the bases
DIfferential diagnosis of
1. Anterior mediastinal masses v. MIDDLE mediastinal v. POSTERIOR mediastinal
Anterior: thyroid, teratogenic, thymoma, lymphoma
Middle: Lung CA, lymphoma, aneurysm, cysts, morgagi hernia
Posteiror: neurogenic, esophageal mets, enteric cysts, bochadalaks hernia
Helical spiral Ct scan of the CHEST?
1. >90% sesitivitiy/speificity
2. Visualizes small clots that are < 2mm
3. Replaced V/Q scan as the test of choice
IF EXUDATIVE effusions suspected – what must be performed?
Thoracentesis and do test on the PLEURAL fluid:
1. Diff cell count
2. glucose
3. pH
4. amylase
5. TG
6. Microbiology
7. Cytology

What are the three characteristics of ASTHMA:


Extrinsic v. intrinsic asthma?

1. Airway inflammation
2. Hyperresponsitivity
3. Airway obstructionExtrinsic (most)
-atopic production of IgG to enfironeent with eczema or HAY fever
-asthmatic at young age

-unrelated to environment

Two types of pneumothorax
1. Traumatic
-transthoracic needle aspiration to diagnose NSCLC to SCLC
-thoracentesis to dx a P effusion
-central line placement2. Spontaneous pneumothorax
-primary (simple) without underlying lung disease
-spontaneous rupture of subpleural blebs at the apex of the lungs
(paraacinar emphy)
-tall young lean males
-2/2 to lung disease

Two major types of RESPIRATORY FAILURE
1. HYPOXEMIC RF = < 50 mmHg PaO2
-low PaO2 with a PaCO2 low or normal
-PaO2 < 50mmHg/PaCO2 > 60
-present when O2 sat < 90% despite FIO2 > 0.6
-include disease processes of lung itself (ARDS, pneumo, pelmonary edema)2. HYPERCARBIC RF =
-decreased minut ventilation
-increased phsioloic dead space leads to increased CO2 retention
-caused by BOPD, asthma, CF, bronchitis
-CNS depression (thus diaphragmatic paralysis) cannot ventilate 2/2 accessory muscles being unable to maintain movement

Pt with 2 days SOB, RSided CP, and progressive back pain that has limited her mobility. PMH of breast CA. Had adjuvant therapy with masectomy 6 mo prior and currently on tamoxifen and MVitamin. Temp 100.4, BP 100/60, pules 110, RR 18. Lung examiantion shows decreased breathe sounds in the right base. Chest XR shows infiltrate oscuring the right heart border and sight sidered pleural effusion.

Pleural fluid:
pH = 5.75
nucleated cells = 8050
glucose = 38
protein = 3.9
RBC = 1500
LDH = 620

Serum chemistries show LDH = 310 U/L and protein concentration of 6.1

Most likely ddx?

Can be HF, penumonia, DI-lupus, PE, hypoalbuminemia

What to do? Pt has Right mIDDLE LOBE infiltrate and RS pleural effusion concerning for pneumonia with complicated parapneumonic effsion. Frist step is to differentiate wither the effusion is an exudate or transduate. MUST USE “Lights Criteria” in which one of the following must be present for exudate
1. Pleural Fluid protein/serum protein ratio > 0.5
2. Pleurl fluid LDH/serum LDH ratio > 0.6
3. Pleural fluid LDH > 2/3 of the upper limit of normal for serum LDH

This pt has a PF protein/S protein ratio of (3.9/6.1) which is > 0.5
This pt has a PF LDH/S LDH ratio of (620/310) which is >0.6
And thus she by having at least ONE of three lights criteria fits that of an EXUDATE.

What to do? Pt has exudative effusion – is it complicated or uncomplicated? Complicated fluid has a positive gram stain, postivive culture, pH <7.2 and glucose level <60 and requires chest tube drainage because it is unlikely to resolve spontaneously (HENCE AN EMPYEMA – which is frank pus in pleural space).

This pt has nucleated cells, and low flucose, and a low pH. She fits criteria for a complicated exudative effusion. AND as such she requires BOTH AB therapy AND a chest tube to drain effusion.

Transudative effusion v. EXUDATIVE effusion – CRITERIA?

Transudative: increased Pcapillary pressure in the viseral or parenteral pleura (CHF) or decreased plasma oncotic pressure (hypoalbuminemia 2/2 nephrotic syndrome for example) which will pull nothing into vessel. Ex include CHF, cirrhosis, PE, nephrotic syndrome, peritoneal dialysis, hypoalbuminemia, atelectasis (collapsed lung)

Exudative: increased permeability of pleural surface or decrased lymphatic flow from pleural surface 2/2 damaged pleural membranes/vasculature. Examples includ bacterial pneumonia, malignancy, TB, PE, viral infection, PE, CVD.

USE LIGHTS CRITERIA to dx that of exudative:
-must have one of any three to be diagnosed with a transudative versus an exudative:

1. Pleural LDH/Serum LDH > 0.6
2. Pleural protein/Serum protein > 0.5
3. Pleural LDH > 2/3 upper limit of serum LDH

What tissue biopsy technique performed to dx ILD?

Fiberoptic bronchscopy – only limited amount (transbronchial biopsy)

Open lung biopsy or video assisted thorascopic lung biopsy

What are the three major causes of JAUNDICE:
1. Hemolysis of RBC
2. Liver DZ
3. Biliary obstruction
Treatment of acalculous cholecystitis
Emergent cholecystectomy is the treatment of choice – patients who are too ill for surgery, perform percutaneous drainage of he GB with cholecystostomy
What are the complications of acute pancreatitis?
Complications of pancreatitis (ACUTE):
1. Pancreatic necrosis – can be sterile or infected
a. sterile heals on own
b. infected has high mortlatlity rate 2/2 multiple organ failure in 50% of causes; surgical debridement and antibodics indicated
2. Pancreatic pseudocyst
a. encapsulated fluid collection that appears 2-3 weeks after an acute attack – unlieke a true cyst, it lacks an epitheliel lining.
b. complications of untreated pseudocysts include rupture, infection, gastric outlet obstruction, fistula, hemorrhage into cyst, and pancreatic ascites. It may impinge on adjacent abdominal organs (duodenum, stomach, transverse colon) if large enough; or if located at the head of the pancreas, can cause comepression of the CBD
c. diagnosis by CT
d. IF cysts < 5cm then observe, if > 5cm then drain
Clostridium difficile presents with which hypervirulent features?
Severe ileus
marked leukocytosis (15k-50k)
severe metaboli acidosis with elevated LACTATE levels
Increased need for colectomy
barium swallow
Cirrhosis of the liver v. Hepatitis of the liver

Cirrhoses – chronic liver dz characterised by fibrosis, disruption of the liver architecture and widespread nodules in the liver (the fibrous tissue replaces damaged or dead hepatocytes)

Hepatitis – inflammation of the liver hepatocytes.

Coagulopathy occurs 2/2 synthesis of clotting factors being decreased:
1. Prolonged PT; PTT may be prolonged with severe disease
2. Vitamin K is ineffective because it cannot be used by diseased liver
3. Treatment of coag is FFP
Prognosis of carcinoma of the GB
90% die of advanced disease within 1 year of dx 2/2 underdetection

Adenocarcinoma of the esophagus is one of two types of esophageal CA that affects what population?

Risk factors?

Most common in white males
most common in distal 1/3 of esophagus @ GE junctionRF: GERD and Barretts esophagus are main risk facors; alcohol and tobacco may not be as important as in SCC

IF a PEPTIC ULCER is uncomplicated, then a _____ _____ or ______ is not needed initially. Initiate empiric therapy. If you suspect any complications of PUD, order confirmatory testss
barium swallow, endoscopy
Patients with UC may have ______ ____ at first with eventual progression to bloody diarrhea
nonbloody diarrhea
Murphys sign v. BOAS sign

Murphy’s sign: RUQ pain, inspiratory arrest during deep palpation of RUQ, not present in many causes) – fever and leukocytosis – cholecystitis

BOAS sign – right should pain 2/2 that of gall stone – cholelithiasis

What is the most common location for liver abscesses (both pyogenic and amebic)?
Right lobe of the liver
What is the diagnosis of jaundice?
Serum levels of unconjugated v. conjugated BR.
-if unconjugated, then there must have been an issue prior to hepatic uptake and thus check CBC, reticulocyte count, haptoglobin, and LDH (with peripheral smear) to r/o hemolytic anemia
-if conjugated hyperbilirubinemia, then there must have been an issue after the bilirubin-albumin complex formed and after hepatic uptake either within or after the hepatic ducts. LFTS may points to cause
-get US/CT to assess biliary tract for obstruction or anatomic changes
-additional tests ERCP if conj with obstruction 2/2 US/CT
-liver biopsy is the last resort and indicated in some cases to determine cause of HCC injury
Clinical features of SBO?
Cramping abdominal pain (if continuous and severe then expect strangulanous activity.
-n/v may be feculent
-obstipation (LACK OF STOOL and FLATUS)
-abdominal distention
Radiation therapy is indicated in patients with ____ cancer but NOT indicated in patients with >>>>
Can use for patients with rectal cancer
Cannot use for patients with colon CA
Treatment of hemochromatosis? Diagnosis?
1. Marked elevation in serum iron and serum ferritin
2. Elevation of iron saturation (transferritin sat)
3. Decreased TIBC
4. Liver biopsy (determines hepatic iron concentration)
5. Genetic testing for chromosomal abnormalityTREATMENT: perform phlebotomies to removes excessive serum iron
-treat any complications (CHF. DM. hypothyroidism, arthritis) and consider liver transplantation if late stage hemacrhomatosos

Inflammatory bowel disease (IBD)
1. Regional enteriritis (CROHNS DZ)
2. Ulcerative enteritis

Diseases of the appendix:

Acute appendicitis:

Lumen of the appendix is obstructed by:
1. Hyperplasia of lymphoid tissues (60%) of cases
2. Fecalith (35% of cases)
3. Foreign body
4. PARASITE/CARCINOID TUMOR (other rare causes)
Treatment of zenkers diverticulum
surgical: cricopharyngeal myotomy

Skin and soft tissue infections (SSTI’s) are the most common of all infections

What are the categories?

Superficial uncomplicated infections
Necrotizing infections
Infections associated with bites and animal contact
surgical site infections
infections of the immunocompromised host

Most patients with acute pancreatitis have mild to moderate disease, but to up 25% have severe disease

What are the causes of acute pancreatitis:

1. Alcohol abuse (40%)
2. gallstones (40%) – galllstone passes into the bile duct and blocks the ampulla of vater
3. post ERCP – pancreatitis occurs in up to 10% of patients undergoing ERCP
4. VIral infections (mumps or COXSACKIEBVIRUS)
5. Drugs (sulfonamides), HCTZ, ferusemide, estrogens, HIV medications, and many other drugs have been implicated
6. Post operative complications (HIGH MORTALITY RATE)
7. Scoprion bites
8. Pncreas divisum
9. Pacnreatic CA
10. HyperTG hyperCa
11. uremia
12. blunt abdominal trauma (most common cause of pancreatitis in children)
What are the clinical features of pseudomembranous colitis?
1. Profuse watery diarrhea
2. Crampy abdominal pain
3. Toxic megacolon with risk of perforation
Choledocholithiasis clinical presentation:
ASymptomatic for years
-RUQ pain/epigastric pain and jaundice
Autosomal recessive – Polyps plus cerebellar medulloblastoma or glioblastoma multiforme?
Albumin as a liver function test:
Albumin is decreased in chronic liver disease, nephrotic syndrome, malnutrition and inflammatory states *burns/sepsis/trauma
Clinical features of PANCREATIC CA

Very nonspecific – thus by the time dx is made, often too late and incurable.

1. Abdominal pain
2. Painless jaundice bc @ head of pancreas
3. Weight loss
4. Onset of glucose intolerance but the GM is mild
5. Depression/weakness/fatigue
6. Migratory thrombophelbitis – develops in 10% of cases
7. Courvoisier’s sign (palpable GB) present in 30% of patients involved head of pancreas – presents without pain

1. PSC major RF
2. UC
3. CHoleochal cysts
4. Clonorchis sinensis infestation (Hong kong)
Treatment for patients with achalasia
1. Adaptive measures: chew food to consistency of pea soup b4 swallowing; sleep with trunk elevated, avoid eating before sleeping
2. Medical therapy
a. antimuscarinics (DICYCLOMINE) usually unsatisfactory
b. sublingual nitroglycerine – long acting nitrates, CCB
3. injection of outlimun toxin into the LES during endoscopy
-blocks cholinergic activity in the LES
-can be effective in up to 65% of cases; however, repeat procedure needs to be performed every 2 hrs
Tests to order in patients with GI bleeding and hematochezia:
first rule out anorectal cause (hemorrhoids). Colonoscopy is the intial test bc colon cancer is the main concern in patients > 50YO
Acute infectious diarrhea – top cases are what organisms?
1. Salmonella (14.6 cases)
2. Campylobacter (12.7 cases)
3. Shigella (4.7 cases)
4. E. Coli O157H7 (1.1)
5. Crptosporidia (3.0 cases)
What is alreay present (symptomatically) in a MW syndrome
Hematemesis is always present – it varies from steaks of blood in vomitus to massive bright red blood.
As many as 25% of patients with bleeding AV malformations have aortic stenosis however, no ____ and _____ relationship has been noted.
cause and effect (AVM and AVS)
Clinical features of esophageal cancer:
-dysphagia (MOST COMMON – to solids only then to liquids!)
-weight loss (second most common symptom)
-odynophasia (pain with swallowing)-late finding that suggests extraesophageal involvement (mediastinal invasion)
-hematemesis, hoarseness of voice, recurrent laryngeal nerve involvement
-aspiration pneumonia, respiratory symptoms due to involvement of traceobronchial tree
-chest pain
If ALT and AST levels are mildly elevated (low hundreds), think of what diagnosis?
Chronic viral hepatitis or acute alcoholic hepatitis (AST < 500) and (ALT < 300)
ORGANS effected by Wilsons dz v. Hemochromatosis

Kidney, liver, cornea = wilsons

liver (primary), pancreas, heart, joints, skin, thyroid, gonads, hypothalamus = hemo

Pigmented stones are the second type of GB stones that occur 2/2?


BROWN stones are usually found in BILE ducts and are associated with a BILIARY tract infection

bright red blood per rectum
-represents lower GI source (LEFT COLON OR RECTUM)
-consider diverticulosis, arteriovenous malformations, hemorrhoids, and colon CA
What is a bleeding scan?
radionucleotide scanning that reveals bleeding even with a low rate of blood loss. It does not localize the lesion; it only identifies continued bleeding. Role is controversial but it may help determine where arteriography is needed
Clinical features of cirrhosis?
-asymptomatic in early dz
-portal HTN, varices, ASCITES, hepatic encephalopathy, hepatorenal syndrome, spontaneous bacterial peritonitis, hyperestrinism
How do signs and symptoms change in relation to the effected side of colon (right v. left)
Right sided colon tumors:
-obstruction is unusual because of the larger luminal diameter (the cecum has the largest luminal diameter of any part of the colon that often allows for tumor growth to go undetected.
-common finding is occult blood in stool , iron deficiency anemia and MELENA (BLACK STOOL)
-change in bowel habits is uncommon
-triad of anemia, weakness, RLQ mass (occasionally) is present
Metastasis of GASTRIC carcinoma
1. Krukenberg’s tumor: metastasis to ovary
2. Blumer’s shelf: metastasis to rectum
3. Sister Mary Josephs node: met to periunbilival lymph node
4. Virchows node – metastasis to the supraclavicular fossa nodes
5. Irish’s node (metastasis to the left axillary adenompathy
Acute uncomplicated UTI prevention of precurrences
Some supportive evdience
-cranberry juice (200-750 mL/d) or cranverryo concentrate tablets (12-20% reduction)
-topical estrogen creams
-avoid exposure to vaginal spermicidesNo supportive evidence
-postcoital voiding
-“enhanced” urinary hygiene
-oral estrogen replacement

Toxic megacolon, growth retardation, narcotic abuse all can result from Crohns. T or F
RUQ ultrasound has high sensitivity AND specificity when accounting or stones that are > ___mm.
Gastric lymphoma
A type of NHL that arises in the stomach
Celiac sprue
Hypersensitivity to gluten
-weight loss, abdominal distention, bloating diarrhea
-biopsy in prximal small bowel reveals flattenng of villi which causes malabsorption
-strict adherence to gluten free diet
What are the majority of cases regarding PUD related to?
1. Helicobactor pylori infection
2. NSAIDS-inhibit prostaglandin production which leads to impaired mucosal defenses.
3. Acid hypersecretory states like ZE syndrome (excessive production of gastrin)
Considerations with acute bacterial sinusitis that recurs?
1. Inadequate course of therapy
2. Concurrrent allergic rhinitis
3. Anatomic abnormalities that block ostia
4. undiagnosed immundeficiency states
-cystic fibrosis
-common variable immunodeficiency
-immotile cilia syndrome (karteganer’s)
The level of either _____ or _______ in acute pancreatitis does not reliably predict the severity of disease.
What are the clinical feature of budd-chiari syndrome:
Hepatomegaly, ascites, abdominal pain RUQ; jaundice, variceal bleeding


Ascending cholangitis and be 2/2 ______ obstruction in the ampulla of Vater, leading to infection of the biliary tract.

The higher the AST-ALT ratio the greater the likelihood that —— is contributing to the abnormal LFTs
What patients should not be treated if acute infections diarrhea is clinically present?
Pts with mild disease without systemic toxicity or dehydration
pts with spontaneously remitting sxs
pts with suspected shiga toxin-producing e. coli infection (O157H7) –> bloody diarrhea in an afebrile pt with a h/o eating raw hamburger or seed sprouts or visiting a petting zoo
Paraesophageal hernias tend to enlarge with time, and the entire stomach may ultimately move into the _____. Type 3 hernias (combination of type 1 and 3) are treated as type _____ surgically.
type 2
Complication of diverticulosis versus diverticulitis

Diverticulosis: painless rectal bleeding and diverticulitis

Diverticulitis: includes bowel obstruction, abscess and fistulas

How are CIRRHOTIC patients managed LONGTERM?
1. Periodic lab values 3-4 months (CBC, CMP, RFTs, LFTs, coagulation tests)
2. Perform an endoscopy to determine the presense of varices
3. If hepatocellular carcinoma is suspected then perform a CT guided biopsy for diagnosis
Treatment of pancreatic CA
1. Whipples procedure is the only hope for cure; only a minority of tumors resectable. Pronosis post resection with 5 year survival rate of 10% – grim.
2. If the tumor is unresectable and biliary obstruction is present , perform PTC or ERCP with stent placement across the obstruction for palliation.
What exacerbates GILBERTS syndrome?
fasting (crash diets); fever, alcohol, and infection. Asymptomatic in most cases, but occasionally jaundice is seen.
Clinical geatures of HCC
-abdominal pain
-weiht loss, anorexia, fatigue
-signs and symptoms of CLD; portal HTN, ascites, jaundice, splenomegaly
-paraneoplastic syndromes:
F. hypoglycemia
80% of episodes of upper GI bleeding stop spontaneously and only need supportive therapy – T OR F?
The development of a palpable mass in the epigastrium four weeks after the onset of acute pancreatitis is HIGHLY suggestive of a ______ _______ formation
Pancreatic pseudocyst formation

inflammation of the gastric mucosa 2/2 NSAIDS/ASA, H. pylori, alcohol, heavy cigarette use, smoking, caffeinel extreme physiologic stress (eg shock, sepsis, burns). It can either be asymptomatic or cause epigastric pain. The relationship between eating and pain is NOT consistent.

IF LOW PAIN or MODERATE and not worrisome, empiric therapy + acid suppress is good treatment with the stopping of NSAIDs

Ulcerative colitis:

CHRONIC INFLAMMATORY DISEASE of colon or rectal mucosa that occurs at any age but usually young adulthood.

-distribution os UC involves to rectum in all caes and can involve the colon paritally or entirely
a. rectum along (10%)
b. rectum and left colon (40%)
c. rectum, left colon, right colon *30%)
d. pancolitis

unpredictable course and variable

Acalculous cholecystitis

Acute cholecystitis without stones that obstruct the cystic duct (up to 10% of patients with acute cholecystitis)

-idiopathic in patienst with underlying illness associated to dehydration ischemia burns trauma and a postoperative state

-signs and symptoms are the same as for acute cholecystits

1. fistula between colon and other segments of intestine (enteroenteral), bladder, and vagina and skin.
-anorectal dz in 30% pateints – fissues, abscesses, perianal fistulas
-SBO 20-30%
What are the signs of appendiceal rupture 2/2 untreated acute appendicitis?

Complications -20% of cases

RF: delay in treatment (>24 hours) and extremes of age
-signs of appendiceal rupture (high fever, tachycardia, marked leukocytosis, peritoneal signs, toxic appearance)

Percent of women per year diagnosed with acute uncomplicated UTI (cysitis)?
HNPPCRC – without adenomatous polyposis
Lynch I v. Lynch II
Lynch syndrome I: site specific CRC – early onset CRC without multiple polyposis
Lynch syndrome II: cancer family syndrome – all features of lunch 1 plus increased number and early occurrence of other cancers (female genital tract, skin, stomach, pancrea, brain, breast, biliary tract).
Causes of hepatic encephalopathy:
1. Toxic metabolites
2. occurs in 50% of all cirrhosis cases
3. Hypokalemia and alkalosis (2/2 diuretics), dedating drugs (narcotics, sleeping meds), GI bleeding, systemic infection, and hypovolemia
4. Clinical features: confusion, asterixis, rigidity and fetor hepaticus
Rectal cancer versus CRC
20-30% of all CRC are rectal
1. Hematochezia is the most common symptom
2. Tenemus
3. Rectal mass, feelin of incomplete evacuation of stool due to mass
What indicates a non-neoplastic polyp?
A benign lesions with no malignant potential
-hyperplastic (metaplastic polyp) most common (90%); generally remain small and asymptomatic
-no specific therapy required but difficult to distinguish from neoplastic polyps
-juvenile polyps are highly vascular and common (if younger than 10) so remove
-inflammatory polyps (pseudopolyps) are associated with UC
What is the treatment of patients with suspected ascending cholangitis?
1. Blood cultures
2. IV fluids
3. Empiric antibiotics with good anaerobe and gram – coverage –
4. Decompress the CBD when patient becomes hemodynaicmally stable.
Signs of intestinal infarction:
hypotension, tachypnea, lactic acidosis, fever and AMS
What is the prognosis of acute pancreatitis?

RANSON’S CRITERIA is used to determine the prognosis and mortality rates:

*pts with more than 3 or 4 Ranson’s criteria should be monitored in ICU

1. (GALAW) Admission criteria:
Glucose >200;
LDH >350;
2. Initial 48 hours criteria (C HOBBS)
Ca2+ < 8 mg/dL Decrease in Hematocrit (>10%)
PaO2 < 60 mm Hg BUN increase >8mg/dL
Base deficit > 4 mg/dL
Fluid sequestration > 6L
3. Mortality
<3 criteria – 1% 3-4 criteria – 15% 5-6 criteria – 40% >7 criteria – 100%

#1 cause of PANCREATIC CA?
Arteriography is used for which reason in GI BLEEDING?
-mostly used in pts with lower GI bleeding
-should be performed during active bleeding
-potentially therapeutic (embolization or intra-arterial vasopressin infusion)

Pateint with a history of AORTIC GRAFT SURGERY who has a small bleed of GI involving the duodenum before massive, fatal hemorrhage hours to weeks later.

Performing an endoscopy or surgery during this small window of opportunity to prevent death is quinticential to survivial.


CA-P duration of therapy
1. ID society:
– s pneumona treat until afebrile for >72 hr
– s aureus< GNRS, anaerobes, atpicals, > 2 weeks
normal LES pressure
SCHATZKIS RING (Distal esophageal web)
circumferential ring in the lower esophagus that is always accompanied by a sliding hiatial hernia.
What are the clinical symptoms of primary biliary cirrhosis of the intrahepatic bile ducts?
RUQ discomfort
Xanthomata and xanthelasmata
Portal HTN with resultant sequelae
Treatment for ESOPHAGEAL CA

Palliation is the goal in most patients becase the disease is usually advanced at presentation HOWEVER PERFORMATION OF AN ESOPHAGECTOMY MAY BE CURATIVE IF STAGE 0,1,2A.


Complications of hemachromatosis:


#Cardiomyopathy – CHF, arrhythmias

#DM – due to iron deposition in the pancreas

#Arthritis-most common sites are the 2nd and 3rd metacarpelphysial joints HIPs and KNEES

#Hypogonadism – loss of labido, mensus, impotence


#hyperpigmentation of skin

1. Liver disease with acute hepatitis, cirrhosis or fulminant hepatic failure
2. KAYSER-FLEISCHER RINGS (yellow rings in the cornea representative of cu2+ accumulation and deposition in cornea…do not interfere with vision.
3. CNS findings:
-extrapyramidal signs= parkinsonian symptoms with resting tremor, rigitity, radykinesia, chorea, drooling, incoordination due to copper depostition in BG
-psychiatric distrubances – depression, neuroses, peraonlity changes, psychosis
4. Renal involvment
-aminoaciduria, neprhocalcinosis

SR: moderate dysphagia may be present; 2/2 alkali, acids, bleach, detergents (suicide attempts). Stricture formation indicates inc risk for esophageal cancer

Treatment: esophagectomy i full thickness necrosis has occurred. Pt should avoid vomiting, gastric lavage and all orgal intake which cnan compound the original injury. Give the pt steroids and AB its well

PVS: Anemia, oral mucosa, upper GI esophageal webbing causing dysphagia

Major differential points of SSTI’s (skin and soft tissue infections)
Community v. Hospital acquired
-community: s aureus >>> group A streptococci and GBS
-hospital: s aureus, GNRs, enterococciErythema only v. pus &/or open wound
-erythema only: strept
-pus/open wound: s aureus

acute appendicitis
What is a flexible sigmoidoscopy?
Can be used to reach the area where approximately 50-70% of polyps and CA occur
Can be diagnostic in about 2/3 of all CRCs
How is hepatic functional reserve assessed?
Child’s classification
-estimates hepatic reserve in liver failure; it is used to measure disease severity and is a predictor of morbidity and mortality.
-childs class C is the most severe disease and childs class A is the least severe disease.
Chronic gastritis
-autoimmune gastritis lads to chornic atrophic gastritis with serum antipareital and anti-intrinsic factor antiboide (possible dvelopment of pernicious anemia)
-most pts are asymptomatic and never develop complications – manifests as epigastric pain similar to PUDcomplications: gastritis, carcinoma, mucosa-associated lymphoid tissue lymphoma (MALT)

Acute UTI uncomplicated diagnosis:
Consistent symptoms + positive dipstick (U/A) = UTI (culture NOT NEEDED)
Pathophysiology of SBO
Dehydration is a key event in SBO
-intesntinal distention causes reflex vomiting, increased intesinal secretion proimal to point of obstruction and decreased absorption. This leads to hypochloremia, hypokalemia and metabolic alkalosis
Third most common cancer in the United States (in men and women)
Reynolds pentad is associated with ____ _ and is a highly toxic state that requires emergency treatment and can be rapidly fatal
acute cholangitis
Obstructive jaundice
Acute pancreatitis
Biliary colic
biliary cirrhosis
Diagnosis of HCC
Liver biopsy – required for definitive diagnosis
-lab tests (hepatitis B and C serology, LFTs, coagulation tests
-imaging studies: US, CT scan (chest abdomen pelvis; MRI/MRA if surgery is an options because they provide more detail about anatomy.
-tumor marker elevation of AFP is useful as a screening tool. AFP level may be elevated in 40-70% of patients with HCC and is also helpful in monitoring response to therapy.
What is the general characteristic of diverticulosis?

1. Increased intraluminal pressure-inner layer of colon bulges through focal area of weakness in colon wall (usually an area of blood vessel penetration)

2. LOW FIBER diets: contipation cause sintraluminal pressures to increase with a positive family history increases the risk

3. Most common location is the sigmoid colon however diverticula may occur anywhere in the colon.

Hemorrhagic pancreatitis is another complication of acute pancreatitis:
Cullen’s sign (periumbilical bleeding)
Grays sign (flank ecchymoses)
Fox’s sign (inguinal ecchymoses)CT scan with TV contrast is the study of choice

Melena or hematochezia
Alkaline phosphatase (ALK-P) is elevated in which clinical scenarios?
1. ALK-P is elevated when obstruction to bile flow(cholestasis); in any part or biliary tree. If normal, unlikely biliary obstruction
2. IF EXCESSIVELY high (10 fold) think of extrahepatic hiliary tree obstruction or intrhepatic cholestass (PBC or DI-cirrhosis)
3. If level are elevated, measure the GGT (gamma-glutamyl transferase) level to make sure the elevation is HEPATIC origin (rather than bone or intestinal). If GGT is also elevated, then strongly suggests hepatic origin. If GGT level is normal but ALP elevated – think bone or pregnancy issue
What are the clinical features of achalasia:
1. Dysphagia (odynophgia less common) – both solids and liquids
2. Regurgitation
3. Chest pain
4. Recurrent pulmonary complications secondary to aspiration, which may cause lung abscess, bronchiectasis, hemoptysis
What is the LAB TEST that diagnosis for GI bleeding?
-stool guiac for occult blood
-Hgb/hct level (may not be decreased in acute bleeds)
-A hgb level >7-8 acceptable in young health patients without active bleeds
-A hgb level in most elderly patients should have hgb level ?10 g/dL
-low MCV is suggestive of iron deficiency anemia and chronic blood loss
-coag profile (plt ct, PT, PTT, INR)
-LFTs, renal function
-the BUN-creatinine ratio is elevated with upper GI bleeding. This is suggestive of upper GI bleeding if patient has no renal insufficiency
What is the TREATMENT of PBC?
1. Cholestyramine for the pruritis
2. Vitamin D, Calcium, Bisphosphonates for osteoporosis
3. Ursodeoxycholic acid (hydrophilic bile acid) has been shown to slow progression
4. Liver transplantation is only curative therapy.AUTOIMMUNE AB: (+) antimitochondrial antibodies

What medication should be avoided in patients with mesenteric ischemia?
Vasopressors because it worsens the ischemia.

Treatment of GALLSTONES

symptomatic v. asymptomatic

SYmptomatic-elective cholecustectomy for patients with recurrent bouts of biliary colic

asymptomatic – no treatment

Dark urine and pale stools signal a diagnosis of?
NASH histologically is identical to patients with ____ liver disease, but these patients do not usually have a history of substance abuse.
Treatment of SBP:
spontaneous bacterial peritonitis
1. Broad spec therapy then give specific once identify bacteria.
-clinical improvement should be seen within 24-48 hours. Repreat paraventesis in 2-3 days to document a decrease in ascitis fluid PMN < 250
What risks can exacerbate PUD?
1. Smoking
2. Alcohol and coffee
3. Emotional stress and type A personality
Empirical treatment for CA-MRSA:
TSX, clinda, mino
Signs of acute liver failure:
1. Jaundice
2. Elevated LFTs
3. Coagulopathy
4. Hypoglycemia(liver stones glycogen)
5. Hepatice encephalopathy 2/2 ammonia intoxication
In acute pancreatitis:
1. Serum amylase:
2. Serum lipase:
3. LFTs:
4. Hyperglycemia/hypoxemia/leukocytosis:
5. Order the following for assessment of prognosis:
“ransons criteria”
1. Amylase = most common tests but many conditions cause hyperamylasemia and its absense doesnt rule out acute pancreatitis. If levels are >5x NL then highly specific for acute pancreas.
2. Lipase = more specific for pancreatitis than amylase
3. LFTs – to identify cause (gallstone pancreatitis)
4. Glucose, [email protected]+. hct, BUN, ABG, LDH, WBC count
Treatment for PUD: Medical
1. d/c nsaids/asa
2. rstrict -OH use but not foods
3. Stop smoking/dec emotional stress
4. Avoid eating before bedtime and dec coffee intakeACID RESTRICTION!
1. H2 blockers, PPIs, antacids

ERATICATE H. PYLORI with tripple therapy regimen


Surgical: Rarely needed – required for ocmplication of PUD(bleeding performation gastric outlet obstruction

Barium enema are good for?
Evaluates the entire colon, completmentary to fleximble signmoidocopy – disadvantage is that any abnormal finding needs to be evaluated by colonoscopy
Complications of UC
1. IDA
2. Hemorrhage
3. Lytes and h20
4. Structures, benign, malignant usally malignant
5. Colon ca- increas risk
6. Cholangiocarcinoa (half of all biles duct CA are associated with UC)
7. Sclerosing cholngitis
8. Toxic mega
9. MR
Diagnosis of crohns
-diarrhea (nonbloody)
-malabsorption and weight loss
-abdominal pain RLQ n/v
-fever malaise
-extraintestinal manifestiations in 15% – uveitis, arthritis, anklosing SpA, erythema nodosum, pyoderma gangrenosum, aphthough oral ulcers cholelithiasis and neprholithiasis
If a patient with GERD also has a diatal hernia, the hernia often wrosens the symptoms of GERD – T or F
Types of varices 2/2 liver disease:
1. Esophageal
2. Gastric
3. Hemorrhoids
4. Caput medusae (distention of abdominal wall veins)
In cholelthiasis, biliary colic can lead to acute ________.
In choledocholithiasis, onset of symptoms leads to _____ and/or ______ which are life threatening causes.

Acute cholecystitis (obstruction of the GB leading to inflammation – not due to infection).

Acute pancreatitis or CHOLANGITIS

The distortion of the liver anatomy in CIRRHOSIS causes which two major events:

1. Decreased blood flow through the liver and thus causing PORTAL HTN (therefore associated ascites, esophageal varices, splenomegaly, peripheral edema, variscosity of veins “back stream” in circulation, hemorrhoids)

2. Hepatocellular failure that leads to impairment of biochemical functions such as decreased albumin synthesis and decreased clotting factor synthesis (thus can no longer carry Ca2+ or protein and will have increased bleeding 2/2 decreased coag.

Complications with CHRONIC pancreatitis:
1. Narcotic addiction – most common complication
2. DM/impaired glucose tolerance
3. Malapsorption/steatorrhea
4. Pseudocyst formation
5. Pancreatic ductal dilitation
6. CBD obstruction (2/2 to fibrosed portion in head of gland)
7. VItamin B12 malabsorption
8. Effusions (pleural, pericardial, peritoneal)
9. Pancreatic carcinoma (increased risk)
If prolonged PT –
advanced liver disease
Porcelain gallbladder is defined as:
intramural calcification of the gallbladder wall
-prophylactic cholecystectomy is recommended bc 50% becomes malignant
SCC is most commonly seen in which patients regarding esophageal CA?
black males
most commonly located in upper thoacic and mid thoacic esophagus
1/3 in distal 10 cm of esophagusRF: alcohol and tobacco use, nitrosamines (diet), achlasia, PV syndrome, caustic ingestion, nasopharyngeal carcinoma

A lower GI bleed or positive occult blood test in stool in patients > 40YO is ___ ___ until proven otherwise
colon cancer
COmplication of cholecystitis: (inflammation of the GB)
1. Gangrenous cholecystitis
2. Perforation of GB
3. Emphysematous cholecystitis
4. CHolecystenteric fistula with gallstone ileus
5. Empyema of the GB
How should JAUNDICE be evaluated?
Initial step:
–> Hx, PE, LABS: ALT, AST, Bilirubin, ALKPHOS, ALBUMIN, PTIf normal LFTs (ALT, AST, ALKPHOS, albumin, PT)
–>conjugated hyperbilirubinemia
-DJ syndrome/rotors syndrome
–>unconjugated hyperbilirubinemia
-see test for differential; hemolysis and gilberts syndrome most common

If abnormal LFTS (intrahepatic issue)
–>suspected intrahepatic disease based on LFT
-viral seriology/AMA/ANA/SMA/cerruloplasmin/Fe-TIBC/AAT
-STOP drugs
-consider liver bx
-consider CT scan to r/o structureal dz
-medical management v. observation
-ducts will be normal
–>suspected extrahepatic obstruction
-noninvasive imaging (US/CT)
a. Normal ducts
b. Normal ducts but suspecte extrahepatic cholestasis
c. Dilated ducts
i. Direct duct visulaization – ERCP or PTC
–> if seen, then relieve obstruction
(surgically, endoscopicallly, percutaneously)

Hundreds of adenomatous polyps in the clon, the colon is always involved and the duodenum is involved in 90% of cases . Polyps may also form in the stomach, jejunum and ileum. This is an autosomal dominant d/o
Metabolic activity post SBO?
Hypovolemia, tachycardia, hypotension, teachypnea, AMS, oliguira
What is the hormone that relaxes the sphictor of Oddi and contracts the gallbladder:
Treatment of epiphrenic diverticulum (distal 1/3)
AR disorder with increased skin pigmentation, DM, cirrosis and arthralgia in late stages
Clinical features of cholelithiasis?
1. MAJORITY ARE ASYMPTOMATIC – if found incidentally – dont touch it no need to remove
2. Biliary colic is due to temporary obstruction of the cystic duct by a gallstone.
3. Pain is 2/2 the gallbladder contractng AGAINST the obstruction
4. RUQ or epigastrium and mild-severe pain
5. BOAS SIGN – riht subscapular pain of biliary colic
Most common causes of ACUTE pancreatitis:
Sulfasalazine is metabolized by bacteria to 5-ASA and sulfapyridine. 5ASA is the _____ _______ of the drug
effective moality
Pseudomembranous colitis

-Antibiotic associated colitis because many patients do not have grossly visible pseudomembranes

a. AB rx kills organisms that normally inhibit the growth of Cdiff.
b. Overgrowth of C. diff and toxin production
c. almost all antibiotics have been associated but the most common include;
i. Clindamycin
ii. Ampicillin
iii. Cephalosporins

Symptoms usually begin during first week of antibiotic therapy but can continue 6 weeks after stopping AB.

HOW does CRC spread?

Direct extension – circumferencially and then through the bowel wall to invade other abdominal organs.

-portal circulation to the liver, liver is the most common site of distant spread
-lumbar/vertebral veins to lungs
-lymphatic (regionally)
-transperitoneal and intraluminal

Decreased liver syntheic function will cause a decrease in serum albumin concentration and an increase in INR (why?) Hypoalbuminemia can contribute to edemain end stage liver disease.
because the liver produces albumin and clotting factors. If clotting factors are low, then PT and PTT times will take longer and the INR will be hypercoaguable because there are minimal being produced
Diagnos gastric CA
Stage gastric CA
Endoscopy with multiple biopsies
Abdominal CT
Multiple hamartomas that may be scattered through the GI tract that cause pigmented spots around the lips, oral mucosa, face, genitalia and palmar surfaces. These are very low malignant potential. Intussesception or GI bleeding may occur.
Peutz Jeghers
Prognosis of PANCREATIC CA?
Dismal – diet within months of diagnosis
Diagnosis of ACHALASIA

Dx: barium swallow (“birds beak”) beak-like narrowing of distal esophagus and a alrge, dilated esophgus proximal to the narrowing

dx: UPPER GI endoscopy to r/o secondary causes of achalasia (gastric carcinoma) and retention esophagitis or esophageal CANCER

dx: manometry to confirm the dz; reveals failure of LES relaxation and aperistalsis of esophageal body

When is discharge appropriate for CA-P?
When VS are stable for 24hr (temp <100; RR<24; HR<100, SBP >90, sat 90%)
-able to take ATB po
-able to maintain hydration and nutrition
-MS is normal or at baseline
-no other active clinical or psychosocial issues requireing ongoing hositalization
Treatment of MW syndrome/tear
upper endoscopy is diagnostic, most causes stop bleeding without any treatment but if treatment is required it is surgical (overing the tear) or angiographic embolization if bleeding continues, but this is raraely necessary. Acid suppression is used to promote healing.
Clinical features of PSC:
1. Begin insidiously
2. Chronic cholestasis include jaundive, pruritis; all patients eventually present with chronic obstructive jaundice.
3. Other symptoms include: fatigue, malaise, weight loss
SQAA of the esophagus
20% survivial rate at 1 year
5% survival rate at 5 years
Acute versus Chronic Mesenteric Ischemia


1. Results from a compromised blood supply, usually to the superior mesenteric vessels
2. Four types of acute mesenteric ischemia:
a. Arterial emboli (50% of cases) – cardiac origin (afibb, MI, valvular)
b. Arterial thrombi (25% of cases) – CAD, PVD, STROKE (atherosclerotic)
c. Nonocclusive mesenteric ischemic – splanchnic vasocontriction 2/2 CO dec
d. Venous thrombus – many predisposing factors – eg infection, hypercoag states, OCP, portal HTN, malig, pacreatitis

3. Mortality rate for all types is about 60-70% – if bowel infarct occurred, rate >90%


1. Caused by atherosclerotic occlusive disease of main mesenteric vessels (celiac artery, superior and inferior mesenteric articles)
-abdominal angina, dull pain, typically postprandial (when there is increased demand for spanchnic blood flow); analogous to anginal pain of CAD
-weight loss 2/2 abdominal angina
-mesenteric arteriography confirms the diagnosis
-surgical revascularization is definitive treatment and leads to pain relief in 90% of cases

Which aminotransferase is more specific for liver damage?
How is wilsons disease dx? How is it treated?
Dx: Hepatic dz w/ elevated ALT>AST with impaired syn of clotthing factors
-decreased serum ceruloplasmin levels although ranges within normal dont exclude dx
-liver biopsy (elevated Cu2+)
-if dx, then warn first degree relativesRx: chelating agents – penicillamine that removes nad detoxifies the excess Cu2+ deposits.
-ZINC – prevent uptake of Cu2+
=liver transplantation if unresponsive to chelation + zinc
-montior Cu2+ levels, urinary copper excretion, ceruloplasmin and liver function: phsycial examination for isgns of liver or nerologic disease – psychological health

Treatment for DES?
-nitrates and CCB which decreases contractions but not curative
In patients with GI bleeding, always ask if taking >>>>, >>>>, >>>> po, prn.
NSAIDS, ASA, anticoags

What is the most common causes of cirrhosis?

What is the primary method of diagnosis?

1. Alcoholic liver disease
2. Hepatitis CDx by liver biopsy (gold standard)

Nasogastric tube and diagnosis of GI bleeding>
Initial procedure for determining whether GI bleeding is an upper or lower GI source
-use the NG tube to empty the stomach to prevent aspiration
-false negative findings are possible if upper GI bleeding is intermittent or from lesion in the duodenum
-evaluation of aspirate
-bile but no blood –> UPPER GI BLEED UNLIKELY; source probable distal to lig of trietz
-BRIGHT red blood or “coffee” grounds appearance – upper GI bleeding
-nonbloody aspirate (clear gastric fluid) – upper GI bleeding unlikely but cannot be ruled out definitively (source may possibly be in the duodenum)
Complications associated with diverticulosis?
1. Painless rectal bleeding (up to 40% of patients)
-bleeding is usually clinically insignificant and stops spontaneously. No further treatment is necessary in these patients.
-if bleeding beomes severe (5%) a colonoscopy may be performed to locate the site of bleeding. If doesnt stop, segmental colectomy may be required
PATIENTS with colonic distention that exceeds that of 10cm increases the risk of bowel ruptures leading to either peritonitis and even death – treatment?
Decompress immediately.
Complications of cholelithiasis?
1. Cholecystitis
2. Choledocholithiasis with assoicated symptoms
3. Gallstone ileus
4. Malignancy
Gastric lymphoma

NHL in stomach with features similar to those of adenocarcinoma of the stomach however includes bleeding, obstruction and perforation.

-EGD is standard diagnosis – same as adenocarcinoma of stomach.
-treatment depends upon the stage of the disease and complications

Complication of diverticulitis:
1. Abscess formation: drined either percutaneously under CT guidance or sugically
2. Colovesicular fistula (50% of fistulsa secondary to diverticulitis)
3. 50% close spontaneously
4. Obstruction-due to chronic inflammation and thickening of bowel wall
5. Free COLONIC PERFORATION – uncommon but catacstrophic and leads to peritonitis
Treatment for SBO
1. If incomplete – nonoperative management
2. IV fluids establish urine output; add K+ to correct hypokalemia
3. NG tube to empty stomach (gastric decompresion)
4. AB
5. Surgery is indicated for complete obstruction, for patial obstruction that s persistent and or associated with constant pain or if strnagulation is suspected. Perform an exploratory laparomty with lysis of adhesions and resection of necrotic bowel.
Clinical features associated with esophageal perforation?
-PAIN (severe/retrosternal/chest/shoulder pain),
-hamman’s sign (“mediastinal crunch”) produced by the heart beating against airfilled tissues, pneumothorax or pleural effusion

Antibiotics for acute bacterial sinusitis that is uncomplicated?

If complicated (severe sinusitis)

Trial of symptomatic rx for 7days, if no better than treat with amox, doxy or TSX for 10days

consider CT scanning at baseline
treatment with azithro, FQs, or amox/clav for 10-14d – if no better after 3 days then change treatment

Gray turners sign, cullens sign, foxs sign =

Incidence of CRC at 20 years with UC is?

At 30 years?

CRC + UC at 20 years – 5-10%
CRC + UC at 30 years -12-20%
How is budd-chiari diagnosed?
hepatic venography, serum ascites albumin gradient > 1.1 g/dL
Adults respiratory distress syndrome is a secondary complication to acute pancreatitis in what way?
LIFE THREATENING with high mortality rate
IF ALT and AST levels are moderately elevated (Low hundreds) think of?
acute viral hepatitis
Acute infectious diarrhea options for empirical therapy
Ciprofloxacin 500 mg bid x 1-5d
Levofloxacin 500 mg daily x 1-5d
Erythromycin or azithromycin should be added in the immunocompromised host with increased risk for possible FQ resistant campylobactor infection

What type of hernia (esophageal) accounts for 90% of cases. Both the gastroesophageal juntion and portion of the stomach herniates into the thorax through the esophageal hiatus (so that the GE junction is above the diaphragm)

This is also the most common and benign finding that is assocated with GERD

Complication of liver failure (AC, 9H)

What are the common comorbitidies associated with NASH?
1. Obesity
2. Hyperlipidemia
3. DM (some patients have none of these)
4. Usually asymptomatic and a benign course (but cirrhosis develops in 10% to 15%)
5. Typically discovered on routine laboratory tests (mild elevation in ALT and AST)
6. Treatment is not clearly established
Hepatic abscess is the most serious complication of acute cholangitis with a HIGH _____ _____
mortality rate
Diseases of the esophagus: Two types of esophageal cancer?
SCC and Adenocarcinoma
Increased capillary permeability is the mechanism by which _____ ascites forms.
What is the treatment regimen for H PYLORI
Triple therapy: PPI + 2 AB –> take 2x daily –> more exp than bismuth-based
Quadruple therapy: PPI + BISMUTH + 2 AB –> dalf the time as triple therapy (1-week program opposed t 2 weeks for triple) –> expensive of PPI-If H. pylori test positive then begin eradication therapy with triple or quad therapy. BEGIN ACID SUPPRESSION WITH ANTACIDES OR A PPI

-if ACTIVE NSAID induecd ulcer – stop NSAID USE. Also begin with either PPI or misoprostol. Continue 4-8 weeks depending on severity – treat the H. Pylori infection

Pathology of UC
1. Uinterupted involvement of the rectum and the colon without skip lesions
-inflammation is not transmural like CROHNS – here it is only mucosal and submucosa
Treatment of two possible causes of liver cysts:
1. Polycystic kidney disease: no treatment necessary
2. Hyadatid cysts: surgical resection without spilling + mebendazole
Treatment of acute cholecystitis?

Conservative meausres: (1) hydration with IV fluids (2) NPO (3) IV antibiotics (4) analgesics

Surgery: cholecystectomy is indicated in most patients with symptomatic gallstones. Early cholecystectomy is preferred (first 24-48 hours)

Focal nodular hyperplasia
benign liver tumor without malignant potential that occurs in women of childbearing years with NO assciaation with oral contraceptives
-usually asymptomatic. Hepatomeg present
Treatment of CRC
1. Surgical resection of tumor containing bowel as well as redection of regional lymphatics
2. CEA level should be obtained before surgery
3. Adjuvant therapy:
-Dukes C colon ca: postoperative chemo (5FU and leucovorin) but no radiation
-Dukes B2/C rectal: both chemo (5FU) and radiation therapy postoperatively
4. F/u is important and caries among physicians
-stool guiac test
-annual CT scan of abdomen/pelvis/CXR for up to 5 years
-colonoscopy 1 year then every 3 years
-CEA levels are checked periodically (3-6 mo)
i. Postop CEA <2-3 good prognosis
ii. Subsquent increase in CEA is marker for recurrance
iii. often, second look operations are based on HIGH CEA levels post resectioniv. VERY HIGH ELEVATIONS OF CEA suggest liver involvment

Crohns disease has a chroni, indolent course characterized by unpredictable flares and remissions. The effectiveness of medical treatment will ____ with advaning disease and complications eventually develop requiring surgery.
Clinical symptoms of appendicitis:
1. abdominal pain – starts in epigastrium, moves toward umbilicus, then to RLQ with distention of the appendix – the parietal peritoneam may become irritated leading to sharp pain
2. anorexia always present
3. nausea, vomiting (typically following pain)
Zenker’s Diverticula v. Traction Diverticula v. Epiphrenic diverticula

Zenkers – most common type; found in upper 1/3 of the esophagus: failure of the cricopharyngeal muscle to relax during swallowing leads to increased intraluminal pressure. This causes outpouching of mucosa through an area of weakness in the pharyngral constrictors.

CLINICALLY: dysphagia, regurgitation, halitosis (BAD BREATH), weight loss, chronic cough

Traction diverticula: located in the midpoint of the esophagus near tracheal bifurcation. Due to traction from continguous medistinal inflammation and adenopathy (pulmonary tuberculosis). Tb causes hilar node scaring which causes retraction of the esophagus…it is usually asym and causes no treatment

Epiphrenic diverticula: found in the lower third of the esophagus. It is usually associated with spastic esophageal dysmotility or achalasia. Symptoms of dysphasia are more often realted to the udnerlying motility disorder unless the diverticulum is very large.

Acites is defined as the accumulation of fluid into the peritoneal cavity 2/2 portal HTN (increased hydrostatic pressure) and ________ (reduced oncotic pressure)


Ascited = portal HTN (increased hydrostatic pressure) and hypoalbuminemia (reduced oncotic pressure). Thus will also have abdominal distenstion, shifting dullness and fluid wave.

Abdominal ultrasound can detect >30mL fluid
Diagnostic = paracentesis to determine whether ascites 2/2 portal HTN or another cause. Looks at cell count, ascites albumin, gram stain, culture to r/o SBP (spontaneous bacterial pneumonitis)

-meausre the serum ascites albumen gradient. If >1.1g/DL, portal HTN likely. If <1.1 then portal HTN is unlikely and other cause.

1. Bed rest; low sodium diet; diuretics (furosemide and spironolactone)
2. Perform paracentesis if tense ascites, SOB or earlysatiety.
3. Peritoneovencous shunt or TIPS to reduce HTN

When should a CULTURE be drawn on a skin and soft tissue infection:
Systemic symptoms/signs
sepsis syndrome
abscess or draining pus
necrotizing infection

Carcinoid tumor v. Carcinoid syndrome
Carcinoid tumors originate from neuroendocrine cells and secrete serotonin
-the most common site for these tumors is the appendix, but they can be found in a variety of locations (small bowel, rectum, bronchus, kidney, pancreas)syndrome results in 10% or patients with c. tumors.
-excess serotonin secretion can lead to carcinoid syndrome which is manifested by cutaneous flushing, diarrhea, sweating, wheezing, abdominal pain, heart valve dysfunctoin

-risk factors for mets increase with size of tumor – rare with appendiceal tumors however ilieal tumors have greatest likelihood for malignancy – surgival resection is tretament of choice.

Adenomatough polyps differ from inherited polyposis syndromes in what way?
Benign lesions that have significant malignant potential that are precursors of adenocarcinoma
INFECTIOn of the biliary tract 2/2 to obstruction which leads to biliary stasis and bacterial overgrowth.
RIsk factors for CRC
1. Over 50yo
2. Adenomatous polyps (premalignant lesions but most do not become CA)
-villous adenomas have higher malignant potential than tubular ademona
-the larger the size the greater the number of polyps the higher the risk of malignancy
3. Personal history or prior CRC
4. IBD
5. Family Hx
6. Dietary factors
7. Major polyposis syndromes
How is spontaneous bacterial peritonitis diagnosed?
Estalished by paracentesis and examination of ascitic fluid for WBCs *especially PMNs) gram stain with culture and sensitivies.
=WBC >500
=PMN >250
=+ ascites culture – culture neg CBP is common
What is diagnostic for CHRONIC PANCREATITIS?
1. Steatorrhea
2. DM
3. Pancreatic calcification of plain films or CT


It can be difficult to distinguish the CHEST pain of DES from cardiac chest pain – thus what work up must be done?

Cardiac catheterizaton to r/o ischemic causes of chest pain, before an esophageal cause is investigated

-then perform upper GI barium swallow

Pancreatic cancer – what are the general characteristics?

Elderly (75% > 60YO); rare before 40YO; common to AA

Location: Pancreatic head (75%); pancreatic body (20%); pancreatic tail (5-10%)

When should a patient be hospitalized for CA-pnemonia?

CAP The CURB-65 score

1. Confusion (1 point)
2. BUN >19 (1 point)
3. RR >/= 30 (1 point)
4. SBP <90 or DBP </= 60 (1 point) 5. Age >/= 65 (1 point)

CURB score: 0-1 low risk, outpt rx; 2 short inpatient stay or closely monitored supervised outpt treatment; 3-5 severe pneumonia, inpt managment

What are the key features of the plummer vinson syndrome?


-also KIOLONYCHIA (spoon shaped fingernails)
-10% develop SCC of the oral cavity, hypopharynx or esophagus

What imaging studies can be performed in patients with acute pancreatitis that will lead to its diagnosis?
1. Abdominal radiograph – has a limited role in dx of acute pancreatitis; instead rules out that of other diagnosis such as intestinal perforation (free air)l presense of calcification suggests CHRONIC, not acute PANCREATITIS.
2. Abdominal ultrasound – helps identify the cause of pancreatitis (gallstone) and useful for pancreatic abscesses or pseudocysts
3. CT scan of the abdomen – most accurate test for dx of acute pancreatitis and for identifying complications of the disease
4. ERCP – severe gallstone pancreatitis with biliary obstruction; identidy uncommon causes of acute pancreatitis if the disease is recurrent
Etiology of biliary cirrhosis – this disease occurs in response to chornic biliary obstruction from the following:
1. Long-standing mechanical obstruction
2. Sclerosing cholangitis
3. Cystic fibrosis
4. Biliary atresia
Diverticulitis recurs in about –% of pateints treated medically, usually within the first 5 years. Lower GI bleeding is RARE in diverticulitis but common in diverticulosis.
aquired motor d/o of the esophageal smooth muscle in which the lower esophageal sphinctor fails to completely relax with swallowing and abnormal peristalsis of esophgeal body replaces normal peristalsis of the esophageal body
How might colonic volvulus be diagnosed? What are the two types?

Colonic volvulus can most commonely be in the sigmoid colon 75% or the cecum 25%.

-cecal volvulus most commonly occurs in younger population. Cecal due to lack of right colonic fixation to retroperitoneam.

1. Plain abdominal film: sigmoid looks like an omega loop; cecal looks like coffee bean.
2. Sigmoidoscopy preferred diagnosetic and therapeutic test for sigmoid volvulus (NOT SECAL!); leads to successful treatment in many cases.

What is the prognosis of HCC?
If it is unresectable then the prognosis is less than 1 year
-if it is RESECTABLE then 25% of patients can live > 5 years
What is cholelithiasis? What are the three types of GB stones?

stones in the gallbladder

1. Cholesterol stones
2. Pigmented stones
3. Mixed stones (cholesterol and pigment) – most common

“Coffee grounds” emesis
suggests upper GI bleeding as well as lower rate of bleeding (enough time for vomitus to tranform into “coffee ground”
nonfibrolamella carcinoma of the liver:

(most common HCC) – usually associated with hepatitis B or C and cirrhosis. Unresectable with very short survival time (months)

Fibrolamellar – usually not associated with hepa B and C; is resectable; relatively llonger survival timel seen most commonly in adolescenets and young adults.

Treatment options for acute uncomplicated UTI
1. TMP-SMX 1 DS po bid x3day
-success rate 94%
-first line unless local resistance >15-20%2. FQ (NOT moxi) x 3d
-success >94%
use when rx with TSX is contrandicated

3. Nitrofurantoin (***can instigate G6PD/exacerbate it!) 100mg po bid x 7d
4. Fosfomycin 3 gm po x 1 dose

Symptoms of acute cholecystitis:
-Pain is always present and is located in RUQ or epigastrium; it may radiate to the right schould or scapula (BOAS SIGN)
Closed loop versus open loop obstruction in SBO
Closed loop, the lumen is occlused at two poitns by an adheive band or hernia ring. This can compromise blood supple requiring emergent surgery
For diverticulosis – test of choice?
For diverticulitis – test of choice?
1. Barium enema
2. CT scan (barium enema is contraindicated 2/2 to acute bleeding)

Cystic dilitations of biliary tree involving either the extrahepatice or intrhepatic duct or both; more common in women (4:1)

-EPIGASTRIC PAIN, jaundice, fever, and RUQ mass
-complications: CHOLANGIOCARCINOMA (MOST FEARED); HEPATIC ABSCESS< RECURRENT cholangitis/pacreatitis, rupture, biliary obstruction, cirrhosis, and portal HTN

-US is the best noninvasive tests, and ERCP is definitieve diagnosis

Treatment is surgery: complete resection of the CYST with a biliary-enteris anastomosis to restore continuity of biliary system with bowels

How might PUD be diagnosed?

Endoscopy is the most accurate. Essnetial in diagnosis of gastric ulcers because a BIOPSY is req to rule out melignancy of duodenal ulcers do not require biopsy bc dec likelihood.

-preferred when severe or acute bleeding is present (can perform electrocautery of bleeding ulcers) – biopsy can also be taken for H. pylori test if gastric also.

Diagnosis of acute cholangitis versus other biliary tract issues?
1. RUQ US is the initial study
2. Lab: hyperbilirubinemia, leukocytosis, mild elevation in ALT/AST
3. Cholangiography (PTC or ERCP) – definitive test but not perfrmed during the acute phase of illness. Once resolved, then proceed with PTC or ERCP.PTC before ERCP when the duct system is dilated (per US) and use ERCP when the duct system is normal

Cholelithiasis v. Choledocholithiasis

Clinical features

Cholelithiasis (A) and Choledocholithiasis (B)

I. Abnormality (A) – gallstone in gallbladder
(B) – stone in the COMMON BILE DUCT
II. Features (A) – asymptomatic + biliary colic if obstructed stone 2/2 contracting GB
(B) – asymptomatic + RUQ pain/jaundice/eipgastric pain
III. Diagnostic (A) – US or CT
(B) – ERCP is the test of choice for RUQ US not sensitive
IV. Treatment (A) – resection if symptomatic (GB)
(B) – removal of stone via ERCP and spincterotomy

What are the clinical features of diverticulosis?
-Asymptomatic and dsicovered incidentally on barium enema or colonoscopy done for another reason.
-Vague LLQ discomfort, bloating, constipation/diarrhea may be present
-only 10-20% become symptomatic (develop complications)

Pancreatic necrosis is a complication of ACUTE pancreatitis. What are the two main types of necrosis:


1. Sterile pancreatic necrosis and infected pancreatic necrosis differ by a CT GUIDED PERCUTANEOUS ASPIRATION WITH A GRAM STAIN/CULTURE OF ASPIRATE
LFT Pearls:
1. Cholestatis LFTS:
2. Hepatocellular necrosis/inflammation
1. markedly elevated ALK-P and GGT; slightly elevated AST and ALT
2. normal or slightly elevated ALK-P and markedly elevated ALT and AST
How does cholangiocarcinoma differ from carcinoma of the gallbladder?
This is a tumor of the intrahepatic or extrahepatic bile ducts: most adenocarcinomas
-7th decade diagnosis
-located in three regions: (1) proxmial 1/3 of CBD, (2) distal extrahepatic, (3) intrahepatic)
-most likely to be resected is distal and least likely is intrahepatic.
When might an upper GI bleed result in hematochezia?
If the bleeding is very briskand doesnt remain in colon to turn into melena
-this indicated heavy bleeding and patient often has some degree of hemodynamic instability
-an upper GI leed source is present in 5% of patients with hematochezia
What is the “best” rx for C. diff acute diarrhea in 2011?
Traditional treatment
-d/c the offending ATB (if possible)
-avoid narcotics and anti-motility agents
-oral metronidazole >>> oral vancNew recommendations
-treatment based on dz classification: mild, moderate, severe, severe complicated
-increase role for po vanc

Treatment of esophageal hiatal herniation

1. Sliding: medically with antacids, small meals, and elevation of head post meals; 15% requires a nissens fundoplication

2. Paraesophageal: treatd with elevtice surgery due to risk of above complications

Treatment of hepatic encephalopathy?

Lactulose prevents absorption of amonia. Metabolism of lactulose by bacteria in colon favors the formation of NH4+ which is poorly absorbed from GI tract, thereby promoting excretion of ammonia.

-NEOMYCIN (AB) kills the bowel flora, so decreases the ammonia production by intestinal bacteria

-DIET: limit protein to 30-40 mg/day

Characteristics of jaundice:
1. Yellow coloration of skin, sclera, mucous membranes, sclerae due to over production or dec clearence of bilirubin
2. Clinical jaundice usually becomes evident when total bilirubin is > 2mg/dL
3. Conjugated v. unconjugated bilirubin
a. Conjugated (direct) –
loosely bound to albumin and therefore water soluble
when in excess, excreted in urine and is dark (only dark if conj br)
b. Unconjugated (indirect) –
tightly bound to albumin and therefore not water soluble
cannot be excreted in the urine even if blood levels are high
toxic, unbound form can cross BBB and cause neurologic deficits
Depending upon clinical setting/features
-risk of CA-MRSA: TSX, clinda or minocycline
-Cat bite: augmentin
-DM foot ulcer: cipro/clinda
-noncholera vibrio: doxy
-erysipelas: PCN or amoxicillinIf hospitalized (IV)
-MRSA: Vanc (or linezolid or dapto)
-Cat bite: Unasyn
-DM infectoin: ERTAPENAM

% of patients with HCC in patients with diagnosed CIRRHOSIS
Laboratory testing (NOT IMAGING OR BIOPSY) for PUD?
REQUIRED to diagnose H. pylori
1. Biopsy by endoscopy: histologic ecal of endoscopic biopsy is gold standard.
2. UREASE detectoin via urea breathe test is the most convenient test (Sensitivity and Specificity > 95%)
3. Serology – presense of AB to H. pyloris doesnt indicate a CURRENT infection bc AB to H pylori can remain levated for mo-yrs post eradication of infection.
Diagnosis of UC (perform these studies)
1. Stool cultures for cdiff, oca, parasites to rule out infection
Diagnosis of SBO

1. Barium ENEMA – to rule out colonic obstruction if plain film do not distinguish small from large bowel obstruction; barium enema identifies sites of obstruction

2. Upper GI series with small bowel follow-through if above are not diagnosed

Crohns disease
1. chornic TRANSMURAL inflammatory dz that affects any parrt of GI mouth to ANUS ubt most commonly involves small bowel at terminal ileum
2. three major patterns: *1-40% have disease at ileum and cecum. *2-30% of patients have disease confined to small intestine. *3 25% patients have disease at colon ONLY
Acute appendicitis with obstruction leads to _____ of fluid and mucus, which promotoes ________ growth leading to inflammation. Distention of the appendix can compromise ______ supply resulting in ischemia and necrosis if untreated. Necrosis results in perforation and peritonitis.
Diagnosis of pseudomembranous colitis
C. diff toxins in stool is diagnostic but results take at least 24 hours (95%) sensitivity
-flexible sigmoidoscopy is most rapid test and is diagnostic but not frequently done
-abdominal radiograph to r/o toxic megacolon and perforation
Diagnosis of choledocholithiasis:
Order CMP with LFTS:
1. Labs: total and direct bilirubin levels are elevated and ALK-P
2. RUQ ultrasound usually intial study but will perform ERCP as the gold standard
3. PTC is an alternative to ERCP
Treatment of colonic volvulus

Sigmoid volvulus: nonoperative reduction (decompression) is successful in 70% of cases. The recurrent rate is HIGH so elective sigmoid colon resection is recommended

Cecal volvulus: emergent surgery

What are the clinical features of CHRONIC pancreatitis?
1. Epigastric pain
2. Recurrent abdominal pain
3. May be aggravated bya a drinking episode or by eating
4. Radiates to the back (in 50% of cases)
5. WEIGHT lOSS 2/2 malabsorption, alcohol abuse, DM; steatorrhea 2/2 to malabsorption
Cholestasis referes to obstruction of ____ _ from ANY cause. If LFTs reveal cholestasis (markedly elevated ALKPHOS), then obtain?
bile flow
abdominal or RUQ ultrasound
Forceful dilation and what other surgical methods can treat but NOT CURE achalasia?
Forceful dilatation – mechanical, pneumatic, or hydrostatis
a. pneumatic balloon dilatation is most effective
b. Lowers basal LES tone by distrupting the muscular ring
c. Can be effective but there is a 5% risk of performationSurgical
a. “HELLER MYOTOMY” – circular muscle layer of LES is incised
b. usually reserved for patients who do not respond to dilation therapy

Clinical features of cholangiocarcinoma

Obstructive jauntice and associated symptoms – dark urine, clay colored stool, pruritis


Which esophageal cancer is the most common in the USA?
Used to be SCC > 90% cases but not the incidence of adenocarcinoma has increased dramatically in the US
Tests to order in patients with GI bleeding and MELENA

UPPER ENDOSCOPY intitial test bc the most likely bleeding site is in the upper GI tract.

ORDER COLONOSCOPY if no bleeding site is identified from the endoscopy

Acute infectious diarrhea (stool cultures: indications)
-acutely ill patients with fever and fecal WBCs
-diasease in very young and very old
-common source outbreaks
-food handlers
-persistent diarrhea after foreign travel
Carcinoma of the CB
Most are adenocarcinomas and occur in the elderly
-associated with gallstones in most cases but include cholescystemeric fisutla and porceliain gallbladder
-clinical features are nonspecific and suggest extrahepatic bile duct obstruction: jaundice: biliary colic: weight loss: anorexia: and RUQ mass
-difficult to remove with surgery: cholecystecotmy versus radical cholecystectomy with wedge resection of the liver and lymph node dissection – depending on depth of underlying condition
-pronosis is POOR bc disease underdetected until it is advanced.
What are the two etiologies of a LIVER ABSCESS?
1. Pyogenic liver abscess: most common cause is biliary tract obstruction – obstruction of bile flow allows baterial proliferation. Other causes include GI infection (diverticulitis, appendicitis) with spread by the portal veonous system and penetating liver trauma (GUNSHOT WOUND, SURGERY)
-causative organisms: E. coli, klebsiella, proteus, eneterococcus, anaerobes
-features: fever, malaise, anorexia, weight loss, nausea, comiting, RUQ pain, jaundice.
diagnosis by US or CT scan: elevated LFTs
-treatment: FATAL if untreated *treatment with IVAB and percutaneous drainage of the abscess. which reduces the mortality to about 5-20%. Surgical drainage is sometimes considered2. Amebic liver abscess: most common in men (9:1); homosexual. Fecal oral contact transmission. Caused by intestinal amebiasis (e. histolytica) – the amebae reach the liver via the hepatic portal vein.
-clinical features: fever, RUQ pain, n/v, hepatosplenomegay, diarrhea
-seriological testing (immunoglobulin G enzyme immunoassay) will estbolish diagnosis. Elevated LFTs; E. histolytica stool antigen test *detects protozoe in the stool). Imagine studies (US/CT) identifies the abscess but it is difficult to distinguish from a pyogenic abscess.
-IV metronidazole is effective treatment in most cases. Therapeutic aspiration of the abscesss (IMAGE_GUIDED percutaneous aspiratoin causses. Therapeutic aspiration of the abscess may be necessary if the abscess is larger (HIGH RISK OF RUPTURE) or if there is no response to medical therapy

RUQ tenderness, rebound tenderness in RUQ
-murphys sign is pathogmonic (inspiratory arrest during deep palpation of the RUQ; not present in many cases)
-hypoactive bowel sounds
-lowgrade fever with leukocytosis
What is cholestasis?

Blocking of bile either intrahepatically or extrahepatically with increased conjugated bilirubin levels.

symptoms: jaundice, gray stools, darkened urine, bile salt deposition in skin causing pruritis, elevated serum alkphos, elevated serum cholesterol (impaired excretion), skin xanthomas (local accumulation of cholesterol), malbsorption of fats and fat soluble vitamins.

Treatment for acute primary biliary cholangitis: (PSC)
1. No curative treatment other than liver transplantation
2. When dominant stricture causes cholestasis, ERCP with stent placement for biliary drainage and bile duct dilatation may relieve symptoms
3. use cholestyramine for symptomatic relive to decrease pruritis
What is the treatmet for colonic polyps?
Complete removal of the polyp
Diagnosis regarding esophageal CA
Barium swallow – useful for dysphagia
-UPPER endoscopy with biiopsy and brush cytology is required for deinitive diagnosis. It confirms the diagnosis in 95% if cases
-TEE US to determine the depth of penetratoin of the tumor *most reliable to test staging of local CA
-full metastatic workup (CT scan of chest/abdomen, CXR, bone scan)
Primary hemochromatosis verus secondary hemachromatosis?

Primary – early diasnogsis and treatment before development of complications (primary cirrhosis ut also heart dz and diabetes) imrpoves survival.

Secondary – iron overload 2/2 multiple blood transfusions or in CHRONIC HEMOLYTIC ANEMIA!

Best diagnostic test for esophageal diverticulum
Barium swallow
Screening for CRC
Fecal occult blood testing annually (poor sensitivity/specificity)
Colonoscopy every 10 years(over the age of 50 OR 10 years prior to the diagnosisof CRC in family member)

CHRONS: involves transmural wall from mucosa to serosa; discontinous with skips
UC: mucosa and submucosaCD: termianl ileum most commmon but can involved any part of GI
UC: colon and rectum – starts at rectum nd goes up

CD: fistula and abscesses
UC: SC and colorectal CA

black 2/2 hemolysis
brown 2/2 biliary tract infection
What is acute pancreatitis:
inflammation fo the pancreas resulting from prematurely activated pancreatic digestive enzymes that invoke pacreatic tissue autodigestion
A non-alcoholic patient has an asymptomatic elevation of serum transaminases (ALT/AST) and increased serum iron and feritin levels, and a family history of non-alcoholic liver cirrhosis. This diagnosis is strongly suggestive of?
Childs classification system to assess severity of LIVER DISEASE
1. Ascites: NONE
2. Bilirubin: <2.0 3. Nutrtional status: excellent 4. albumin: > 3.5Class B:
1. Ascites: controlled
2. Bilirubin: 2-2.5
3. Nutritional status: good
4. Encephalopathy: minimal
5. Albumin: 3-3.5

1. Ascites: uncontrolled
2. Bilirubin: >3
3. Nutritional status: poor
4. Encephalopathy: severe
5. Albumin: <3

Left sided colonic tumors and symptoms:
1. Smaller luminal diameter, signs of obstruction are more common – change in bowel habits more common – alternating constipation/diarrhea narrowing of stools (“pencil stools”)
2. Hematochezia more common
What are the clinical features of gastric cancer
abdominal pai and unexplained weight loss are most common symptoms; reduced appetitie, anorexia, dyspepsia, early satiety, nausea and vomiting, anemia, melena, guiac positive stool

Peritoneal fluid (third space) can develop due to many causes – one of which being portal HTN, trauma, pancreatitis and malignancy.

How might one distinguish a diagnosis amongst the above as the causitive agent of the abdominal distention?

1. distinguish exudative from transudative fluid accumulation
-use SAAG which (serum ascites albumin gradient) is calculated bysubtracting the ascites albumin concentration from the serum albumin concentration.
-A difference of 1.1 g/dL or greater is 95% accurate in diagnosing a transudative process consistent with portal hypertension.
Where are most polyps found?
rectosigmoid region and most patients are assymptomatic
-#1 symptoms is rectal bleeding
1. Medical
a. Sulfasalazine (useful if colon involved bc is a 5-ASA *mesalamine) as tha active compound released in colon that is more useful in uS than in Crohns, 5-ASA compounds bock PGE release and serve to decrease inflammation
-there are preparations of 5ASA that are more useful in distal small bowel disease.
b. Metronidazole
c. corticosteroids *prenisone for exacerbations and if no repsonse to metronidazome)
d. immunosuppressants AZA 6MP) with steroid if patients doesnt responseto above agents
e. BA sequetrants (cholestyramine or colestipol) pts with severe ileal disease who cannot absorb bile acids
Mallory Weiss syndrome

MUCOSAL tear at the GE jundtion as a result of forceful vomiting or restching. It usually occurs after repeated episodes of vomiting but it may occur after one episode

-most commonly associated with binge drinking in alcoholics but any isorder that causes vomiting can induce the musocal tear

Angiodysplasia of the colon (arteriovenous malformations, vascular ectasia)
refers to?
-tortous, dilated veins in submuscosa of the colon (usually proximal) wall
-a common cause of lower GI bleeding in patients over age 60YO
-bleeding usually low grade but 15% of patients may have massive hemorrhage if veins rupture
-diagnosed by colonoscopy (preferred over angiography)
-in 90% of patients, bleeding stops spontaneously
-treated by colonoscopic coagulation of the lesion.
-if bleeding persists, a right hemicolectomy should be considered
ALT and AST usually have a similar increase, however in alcoholics, we expect an elevation in which enzyme?
elevation is AST>>>>ALT
Esophageal manometry is diagnostic –
simultaneous, multiphasic, repetitive contraction that occur after a swallow; spinhicter response is normal

HCC is likely in a patient with cirrhosis who has a palpable liver mass and elevated AFP:

T or F

HOw long might it take a pancreatic abscess to form in acute pancreatitis?
Although RARE< will occur 4-6 weeks post acute pancreatitis
-black tarry lquid foul smelling stool
-caused by depradation of hgb by bacteria in teh colon; presense of melena indicates that blood has remained in the GI tract for several horus
-the further the bleeding site fom retum, the more likely melena will occur
-note that dark stools can also result from BISMUTH, IRON, SPINACH, CHARCOAL, LICORICE
-melena sugests upper GI bleeding (esophagus, stomach, duodenum) – occasionally the jejunum or ielum is source but usualy if caused but colonic lesions – but if so then the ASCENDING COLON is the most common colonic location
In patients with CIRRHOSIS (fibrosis of liver tissue), the ALT/ASTs are ____ or ______ or meatstatic liver disease because the number of ealthy functioning hepatocytes are markedly decreased.
normal to low

PBC can occur secondary to PSC

T or F

Colonoscopy identifies the site of LOWER GI BLEED IN ___% of cases and can also be therapeutic
Diagnostic test of choice for diverticulosis (LLQ, painless rectal bleeding, constip/diarrhea) and bloating)
Barium enema is the test of choice
-abdominal xrays are usually normal and are not diagnostic for diverticulosis
Pain in acute cholecystitis is 2/2 gallbladder wall inflammation whereas pain in biliary colic is 2/2?
contraction of the gallbladder against the obstructed cystic duct. ALso the pain of acute cholecytitis persists for several days whereas the pain of biliary colic lasts only a few hours.
Treatment for gastric CA

Surgical resection with wide (>5cm) margins (total or subtotal gastructomy) with extended lymph node dissection

-chemotherpay may be appropriate in some causes

What is hemobilia?

When blood fraining into the duodenum via the common bild duct. Soundce of bleeding can be anywhere along the biliary tract, the liver, or the ampullary region.


Diagnostic: Arteriogram is diagnostic – upper GI endoscopy shows blood coming our of the ampulla of vater

Treatment: resuscitation (+/- transfusoin) If bleeding is severe, surgery is necessary (options include ligation of hepatic arteries or arteriogram with emnolization of vessel).

Paralytic ILEUS
peristalsis is decresd or absent without mechanical obstruction
-resolves with time or when the cause is adddresed medically – surgery is not usually needed.CAuses: medications (narcotics, anticholinerguc effects) post operative state, spnal cord injury, shock, metabolic disorders (espcially hypokalemia) and eritonitis
-abdominal plain filmss show a unifrom distribution of gas in small bowel, colon and rectum
-failure to pass contrast medium byuond fized point is diagnostic.

RX: FLUIDS – NPO, correcton of electrolytes; NG suction if necessary and placeebt if long tube if ileus persists postoperatively

What is the DEFINITIVE DIAGNOSTIC STUDY to diagnose esophageal perforation?

CONTRAST ESOPHAGRAM = soluble gastrografin swallow preferred

-then a CXR shows air in the mediastinum
-if stable and perforation is small, medical management is appropriate (IV FLUIDS< NPO, AB, H2 blockers)
-if patient is ILL and perforation is large (or communication into the cavity, surgery should be performed within 24 hours of presentation = success rate is higher)

Indication for sinus aspiration 2/2 bacterial sinusitis (acute)
-associated with intracranial complications (empyema, meningitis, brain abscess)
-sinusitis in the immuncompromised host
-sinusitis that fails to respond to a “readonable course” of “appropriate” ATB reaction
The diagnosis of acute pancreatitis is normally made by:
1. Clinical presentation.
2. Lab studeies are supportive (amylase/lipase)
3. and CT scan is confirmatory
Causes of BUDD-CHIARI syndrome
Hypercoaguable state
myeloproliferative d/o (polycythemia vera)
chronic inflammatory diseases, infection
-CONDITON is idiopathy in 40% of cases

Presentation of a young, non-obese and on-blacnk patient with HTN should rasie suspician for ______ _______. FUrther, lab values with severe HTN, and elevated HR with serum chemistry levels revealing normal glucose, and normal serum creatinine, elevated sodium and low potassium, and a CT scan with a 2cm mass on left adrenal gland should be indicative of?

What would plasma renin be? what would serum aldosterone be? What would serum bicarbonate be?

-secondary HTN
-primary hyperaldosteronism causes HTN, hypernatremia, hypokalemia, and metabolic alkalosis-excess aldosterone promotes distal tubular reabsorptin of sodum which results in volume expansion and secretion of poassium and ydroge ions. he mass on pt CT likelt to be adrenal adenoma. Likewise, Conn’s syndrome should have aldosterone levels and renin levels checked. Aldosterone release is regulated by renin and therefore while aldosterone levels are increased, renin levels will be decreased 2/2 feedback inhibition. Muscle weakness and exercise intolerance are the result of hypokalemia
-the HIGH levels of serum bicarb are what will be present 2/2 the effect of aldosterone on intercalated B cells. decreased K+ causes deposition of intersitial cells and uptake of H+ ions which further increases the serum pH

Acute gastritis is best assessed by which method?
UPPER GI Endoscopy is the best test for evaluating a pt with epigastric pain. It can diagnose PUD, gastritis, esophagitis and can r/o CA of esophagus and stomach and H. pylori with BIOPSY
When should therapy be considered in acute infectious diarrhea?

Treatment for febrile, CA-diarrhea should be considered for the pt with:

1. sig systemic tox and dehydration esp in ver young and very old (>70)
2. bloody diarrhea or dysentery
3. fecal WBCs or lactoferrin
4. immunocompromising conidtions
5. suspected complicating bacteremia

What are the clinical findings in patients with hepatic encephalopathy?

Decreased mental function, confusion, poor concentration, stupor, coma

Asterixis (hand flapping tremor)

Rigidity and hyperreflexia

Fetor hepaticus (MUSTY ODOR OF BREATH)

Paraesophageal hiatal hernia accounts for <5% of cases. Describe dx
The stomach herniates into thorax through the esophgeal hiatus but the GE junction doesnt, it remains below the diaphragm. THis uncommon hearnia can become strangled and should be repaired surgically
What is hepatorenal syndrome?

progressive renal failur in advanced liver disease, 2/2 enal hypoperfusion resulting from vasoconstriction of the renal vessels that is precipitates by infection or diuretics.

-functional renal failure where the kidneys are normal in terms of morphology and no specific causes of renal dysfunction are eventend. The condition doesnt responde to volume expansion and thus asotemia, oliguria, hypoantrmia, hypotension and lo urine sodium results.

Treatment is by liver transplantation ONLY

Boas sign v. Murphys sign v. Chargot’s triad
Boas sign – cholelithisis – gallstone – right should/scapular pain
Murphy’s sign – RUQ pain/tenderness on inspiration and palpation
Chargots triad – RUQ pain, jaundice, fever (seen in 70% of patients with this disease)
Diagnosis of PANCREATIC CA:

ERCP most sensitive test to distinguis CA of head of pancreas from tumors of the ampulla and lymphomas.

CT scan is the perferred test for diagnosis and assessment of DISEASE SPREAD
tumor markers: CA19-9 (83 sensitivity nd 82 specificity) CEA (sensitivity of 56% and specificity 75%)

Risk factors associated with HCC
Cirrhosis-especially in associated alcohol or hepB/C; forms in 10% or cirrhostic pts
Carcinogens (aflatoxin, vinyl chloride, thorotrast)
AAT deficiency
Hemocrhomatosis, Wilsons dz
hepatic adenoma (10% risk of malignant transformation
cigarette smoking
Most common cause of LOWER GI BLEED IN PATIENTS < 60YO? Most COMMON cause of LOWER GI BLEED in PATIENTS > 60YO?
Angiodysplasia if >60YO
Diverticulosis if <60YO
What is the treatment for GI bleeding:
1. If the patient is hemodynamically unstable, resuscitation is always TOP priority
-remember CABs – once the patient is stabilized , obtain a diagnosis
A. supplemental O2
B. place two large bore IV lines. Give IV fluids or blood if pateint is volume dep
C. draw blood for hgb, hct, PT, pTT, plt, INR; monitor hgb Q4Q8
D. Continue to monitor until 24 hours of stable hgb
E. type and crossmatch adequate blood (PRBCs). Transfuse as the clinical condition demands *shock, patients with cardiopulmonary DZ2. Treatment depends on the CAUSE/SOURCE
i. EGD with coag of bleeding vessel. If bleeding cont, repeast endoscopic therapy or proceed with ligation therapy
i. colonoscopy – polyp excision, injection, laser, cautery
ii. arteriogrphic vasoconstrictor infusion
iii. surgical resection of involved area – last resort

3. Indications for surgery
-hemodynamically unstable patients who have not responded to IV fluid, transfusion, endoscopic intervention or correction of coags
-severe initial bleed or recurrence of bleed post treatment
-continued bleeding for more than 24 hours
-visible vessel at base of ulcer (30-50%) chance of rebleed
-ongoing transfusion requirement (5U within first 4-6 hours)

Portal HTN as a complication of cirrhosis (severe liver disease)
-bleeding/hematemesis, melen, hematochezia) 2/2 esophagogastric varices is the most life-threaning complication of portal HTN.
-diagnose based upon clincial presense of about. paracentesis can help dx
-use transjugular intrahepatic portal-systemic shunt (TIPS) to lower portal pressure
Surgical intervention in CROHNS
1. reseve for complication of crohns dz. Sedmental resection of involved bowel. Recurence rate after surgery byyt up to 50%
2. Indications: SBO, fistula, diabling disase, performation of abscess…
Gallstone enters the bowel lumen via cholecystenteric fistula and gets stuck in the terminal ileum and causes obstruction at the ileocecal valve – causes obstruction and accounts for 1-2 % of bowel obstructions
Large bowel obstruction:
1. Causes: volvulus, adhesions, hernias, COLON CANCER (#1)
2. LBO v. SBO: LBO has less fluid and lyte loss
Hepatocellular adenoma

benign liver tumor seen in females 15-40YO 2/2 OCP use, anaboli steroid use with RUQ pain or fullness.

diagnose with CT scan, US

Treatment: d/c OCP; surgically remove tumors >5cm that do not regress s/p OCP d/c

What is the peak incidence of appendicitis?
Peaks in the teens and mid-20s – prognosis worse in infants and elderly 2/2 higher rates of perforation
IDSA/SHEA Tretment recommendations for C. Diff Acute Diarrhea (CDAD)
-(WBC<15k, crt WNL/unchanged) -drugs: metronidazole 500 po 10-14d Severe uncomplicated -(WBC >/= 15K or inc serum creat; >50% baseline preCDAD
-drugs: Vancomycin 125mg po or via NGT qid 10-14daySevere complicated
-(WBC>above criteria with dec BP or shock, megacolon, perforation or severe colitis on CT)
-if NO ILEUS: Vancomycin 500mg po qid + metronidazole 500-750mg IV Q8hr
-if ILEUD: Vancomycin 500 mg via NGT or po + Metronidazole 500-750 IV Q8 + Vanc enema

First recurrance: same as initial episode
Second or further: PO vanc taper or pulse

Esophageal Diverticula

Most esophagel diverticula are caused by an underling motility disorder of the esophagus:

1. Zenkers diverticulum
2. Traction diverticulum
3. EPiphrenic diverticula

Special associations during skin and soft tissue infections
1. Recurrent boils
2. DM
3. Neutropenia
4. Bite wounds (human, cat, dog, eikenella, pasturella multiocida, capnocytophaga)
5. Water exposure
7. S aureus, GBS, others
8. P aeruginosa, GNRs
9. Vibrios, Aeromonas, M,marinum
Diagnosis of appendicitis:
acute appendicitis is a clinical diagnosis
-lab: leukocytosis
-imaging: CT scan (lowers false postivie rate significantly)

Polyposis PLUS osteomas, dental abnormalities, benighn soft tissue tumors, desomis tumors, sebaceous cysts. The risk of CRC is ____% by approximately age 40.



Gardners syndrome

Treatment for acute pancreatitis?
Bowel rest (go NPO) – goal to REST THE PANCREAS
-IV FLUIDS – may have severe intravascular volume depletion
-Pain control – be cautious with narcotic
-Nasogastric tube if severe nausea/vomiting or ileus present; routine use is controversal
Risk factors regarding pancreatic cancer:
2. Chronic pancreatitis increases risk
3. DM
4. Heavy alcohol use
5. Exposure to chemicals-benzidine and b-naphthlyamine
How does DES (diffuse esophageal spasm) differ from achalasia?

DES – nonperistaltic sponaneous contraction of the esophageal body – several segments of the esophagus contract simultaneously and prevent appropriate advancement of food bolus

ACHALASIA – spincter function is normal (normal LES pressure)

GI bleeding
1. Upper GI bleeding v. Lower GI bleeding
UPPER GI bleeding: source of bleeding above the ligament of trietz
LOWER GI BLEED: source of bleeding below the ligament of trietz
Initial empirical therapy for CA-P

Outpatient: if healthy without recent ATB: treat with macrolide or doxy; if recent ATB then use FQ or macrolide+amox

Comoribitidies – no recent ATB : adv macrolide or FQ; recent ATB treatment FQ or Adv macrolife + b-lactam

Inpatient: 3rd gen ceph + FQ or macrolide; at risk for pseudomonas then used antipseudomonal B lactam +AMG+FQ or macrolide or antipsydomonary b-lactam + cipro


1. Chronic/progressive/ cholestatic LD/characterised by destruction of intrahepatic bile ducts with PORTAL inflammation and scarring – INTRAHEPATIC DUCT SPECIFIC

2. SLOWLY progressive dz with variable course can progress to cirrhosis and End stage liver dz

3. THIS IS AUTOIMMUNE WITH ANTI-MITOCHONDIAL AB, CARDIOLOPIN – and is often associated with other autoimmune disorders.

4. It is most common in middle-aged women

biliary cirrhosis, often abbreviated PBC, is an autoimmune disease of the liver[1] marked by the slow progressive destruction of the small bile ducts (bile canaliculi) within the liver. When these ducts are damaged, bile builds up in the liver (cholestasis) and over time damages the tissue. This can lead to scarring, fibrosis and cirrhosis. It was previously thought to be a rare disease, but more recent studies have shown that it may affect up to 1 in 3-4,000 people; the sex ratio is at least 9:1

Two main types of LIVER CYSTS:
1. Polycystic liver cysts
2. Hyatid liver cysts
An autosomal RECESSIVE disease that is 2/2 copper metabolism. This normal excess usually excreted by the liver however whene the patients liver has a deficiency in ++++++++, copper will accumulated in the liver cells (hepatocytes). What happens to the hepatocytes?
Wilsons disease
-as the hepatocytes die 2/2 to Cu2+ accumulation; the copper leaks into plasma and accumulates in various organs (kidneys, cornea, brain0
-most occurs during childhood/adolescence (5YO)
-diagnosis within 5-35YO
If there is not hemolysis, isolated hyperbilirubinemia (unconjugated) may indicate _______ syndome which is assymptomatic and requires no rx.
Treatment of HCC
1. Liver resectoin (in the 10% of patients who have resectable tumors)
2. Liver transplantation if diagnosis is made early
Bleeding from small bowel::
Bleeding from the colon::
-hematochezia, melena
-occult blood, hematochezia
Staging for CRC using Dukes’ staging

Performed cia CT scan of abdomen and CXR

Stage A – stage I limited to muscularis mucosa
Stage B – stage II that goes past mm without node involvement
B1 – into submucosa/muscularis propria
B2 – through entire bowel wall
B3 – through bowel wall into adjacent structures
Stage C – positive regional lymph nodes
Stage D – stage IV goes to distant metastasis

What imaging can be done for upper GI bleeds:
Upper endoscopy
NG tube
Anoscopy or proctosignmoidoscopy
Bleeding scan
Exploratory laparatomy – last resory
GI bleeding is a complication associated with PUD:

bleeding may be slow (anemic symptoms) or rapid and severe (leading to shock)

Resuscitation: daignose site of bleed via endoscopy and test: performatm surgery for acute bleeds that require transfusion of >6U

-most common cause of upper GI bleeding is 2/2

CAuses of acute uncomplicated UTI in women/males
75-90% of cases E. coli
5-15% is S. saprophyticusProbability of cystitis >90% in woman with dysuria and frequency w/o vaginal d/c

What is the treatment for acute mesenteric ischemia?
Supportive: IV fluids, broad-spec antibiotics
-direct intr-arterial infusion of papaverine (vasodilator) into the superior mesenteric system during arteriography is the therapy of choice for all arterial causes of acute mesenteric ischemia
-direct intra-arterial infusions of thrombolytics or embolectomy inficated in pations with embolic acute mesenteric ischemia
-heparin anticoagulation is the treatment of choice for venous thrombosis
-surgery (resection if nonviable bowel) may be needed in all types of acute mesenteric ischemia if signs of peritonitiis develops
Signs of biliary tract obstruction
INC alk-phos and inc GGT
elevated conjugated BR
elevated jaundice
dark urine
pale stool
Proximal v. distal SBO
Distal obstruction causes distention of proximal bowel segments, making the diagnosis easier on plain radiograph
Treatment of diverticulitis:
1. If initial episode of diverticulitis (fever, LLQ pain, leukocytosis)
a. Use of IV antibiotics, bowel rest (NPO), IV fluids.
b. Mild episodes can be treated outpatient basis if patient is reliable and has few or no comorbiditie.
c. IF persists > 3-4 days then require surgery2. If second or subsequent episodes of diverticulitis:
a. surgery is recommended (resectionof involved segment) once acute inflammation resolves

3. Low-residue diet (eg: no nuts, seeds)

What are the causes of CONJUGATED hyperbilirubinemia?

-Urine positive for bilirubin

1. Decreased intrahepatic excretion of bilirubin
-hepatocellulr disease (viral, or alcoholic hepatitis, cirrhosis)
-inherited disorders (DUBIN-JOHNSON syndrome, Rotor’s syndrome)
-drug-induced (OCP)

2. Extrahepatic biliary obstruction
-carcinoma of head of pacreas
-periampullary tumor
-extrahepatic biliary atresis

How does hyperestrinism result in patients with CIRRHOSIS of the lIVER?
1. SPinder angiomas-dilated cutaneous arteriold with central red spot and reddish extensions that radiate ourward like a spiders web.
2. Palmer erythema
3. Gynecomastria
3. Testicular atrophy

Bowel duct stricture is 2/2 an _______ injury (like that of biliary surgery or cholecystectomy, liver transplantation); other causes include recurring choldocholithiasis, chornic pancreatitis, and PSC.



EPIGASTRIC PAIN that is aching/gnawing in nature with NOCTURNAL SYMPTOMS and the EFFECT OF FOOD ON SYMPTOMS is present.

+/- Upper GI bleeding

Acute bacterial sinusitis
most common health problem in the US
-develops subsequent to viral rhinosinusitis in 0.5-2% of all cases
-should be suspected in pts with symptoms of virl rhinosinusitis that persis for more than 10d or worsen after 5-7
Hypo or hypercalcemia results from acute pancreatitis?
HYPOcalcification is due to fat saponification: fat necrosis binds to calcium
Charcots triad (fever, jaundice, RUQ pain) + septic shock + AMS (CNS depression – coma-disorientation)
WHat is choledocholithiasis?
Gallstones that are found in the CBD
-primary v. secondary causes;
primary-originate in the CBD (usually will be pigmented)
secondary – originate in the GB and then pass into the CBD (usually cholesterol/mixed) – 95% of all cases
What is CEA?
Tumor marker for pancreatic cancer, not useful for screenin; useful for baseline and recurrence surveillence
How might one determine whether or not a polyp is malignant?
1. Size (the larger the polyp, the greater the malignant potential)
2. Histologic type
3. Atypia of cells
4. Shape (sessile-flat, more likely to be malignant) versus pedunculated (on a stalk)
PSEUDOCYSTS may be present at sites distant to the ______ but are still 2/2 acute pancreatitis.
What causes the elevation in ALT or AST levels in asymptomatic patients (ABCDEFGHI)
Autoimmune hepatitis
Hepatitis B
Hepatitis C
Drugs or toxins
Fatty liver (TG)
Growths (tumors)
Hemodynamic disorders (CHF)
Iron (hemachromatosis), copper (wilsons), AAT deficiency
Diagnosis of PBCirrhosis:
1. Laboratory findings – cholestatic LFTs (elevated ALKphos)
-positive antimitochondrial antibodies (AMAs) found i n90% to 95% of patients
-this is hallmark of the disease (specificity) of 98%; if serum is positive for AMAs, perform liver biopsy to confirm diagnosis
-elevated cholesterol, HDL
-elevated immunoglobulin M2. Liver biopsy – percutaneous or laparacopic to confirm ddx

2. Abdominal US or CT scan to rule out biliary obstruction

What are the clinical features of Esophageal Hiatal Hernias?
asymptomatic, incidentally found
-heartburn, chest pain, dysphagia
What is NASH?
Non-alcoholic steatohepatitis (NASH)
Treatment of cirrhosis of the liver:
1. Treatment of underlying cause (alcohol, interferons for hepC/B)
2. Once cirrhosis develops aim to treat via managment the complicatoin. Most serious complication is the esophageal varices that are actively bleeding and hepatic encephalopathy
3. Liver transplant is the only hope for a cure. Abstinence from alcohol for more than 6 months is requiredbefore a patient is eligile for transplantation
Primary sclerosing cholangitis (PSC)
-general characteristics include:
1. Chronic/idiopathhic/progressive intrehepatic or extrahepatic duct disease
2. Thickened bile duct walls ad narrowing of their lumens; leads to cirrhosis, portal hypertension and liver failure.Strong associates with UC (less with that of Crohns) – UC is present in 50-70% of patients with PSC; often the UC dominates the clinical picture. The course of PSC is unaffected by a colectomy done for UC

BARRETTS esophagus
is a complication of longstanding acid reflux disease in which thre is columnar metaplasia of the squamous epithelium. Patients with Barretts esophagus are at increased risk of developing adenocarcinoma of the esophagus.
Why might a serum gastrin level be used in the dx of PUD?
If potential for ZE syndrome as a diagosis
Diagnosis for UC
1. Stool culture for cdiff ova parasits
2. fecal leukocytosis
-WBCs can appear in UC ischemic colitis or infectious disease
How is acute cholecystitis diagnosed?
RUQ ultrasound is the test of choice
a. HIGH sensitivity and specificity
b. Findings include thickened gallblasdder wall, pericholecystic fluid, distended gallbladder and presnse of stone(s).CT Scan is as accurate as ultrasound but is more sensitive in identifying complicatons of acute cholecystitis (performation, abscess, pancreatitis)

RADIONUCLEOTIDE scan (HIDA-hepatoiminodiacetic acid)
-used when US is inconclusive-its sensitivity and specificity paralel that of ultrasound. If HIDA scan is normalthen acute cholecystitis can be ruled out
-positive HIDA scan means the gallbladder is not visualized
-if GB not visualized 4 hours after injection, diagnosis of acute cholecystitis is confirmed

What is Budd-chiari syndrome?

Liver disease caused by the occlusion of the hepatic venous OUTLFLOW which leads to hepatic congestions and microvascular ischemia.

-variable vourse – indoent, gradual development of portal HT and progressive deterioration of Liver FUNC

-can lead to acute liver failure, which can be fatal without immediate therapy

Causes of SBO?
1. Adhesions from prior abdominal surgery
2. Incaercerated hernias
3. Malignancy, intussusception, Crohns disease, carcinomatosis and superior mesenteric artery syndrome (compression of third part of duodenum)
Pathology of Crohns
terminal ileum is hallmark location but other sites of GT tract may also be seen
-skip lesions
-luminal strictures
-noncaseating granulomas
-transmural thicknening and infalmation *full thickness wasll involvement)
Mesenteric: fat creeping” onto antimesenteric border of small bowel

What is the biliary dyskinesia?


Motor dysfunction of the sphincter of Oddi which leads to recurrent episodes of biliary colic without any evidence of gallstones on diagnostic studies such as ultrasound, CT scan, ERCP

Dx: made by HIDA scan – once the gallbladder is filled with labeled radionuclide; give CCK IV then determine the ejection fraction of the GB. If low then dyskinesia likely

Treatment: laparoscopic cholecystectomy and endoscopic spincterotomy

An underlying motility d/o is the cause of both proximal (ZENKERS) and distal (EPIPHRENIC) diverticula. Surgical treatment is aimed at correcting the motility d/o via ______.

A ______ is of 2ndary inportance in both cases



Esophageal/gastric varices are a complication of cirrhosis. What are the clinical findings? How is it diagnosed and how is it treated?
1. Massive hematemesis, melena, exacerbation of hepatic encephalopathy; esophageal >90% and gastric >10%.
2. Diagnosis emergeent upper GI endoscopy once patient is stabilitys if patient presents with hematemesis.
3. Initial treatment: FLUIDS to maintain BP and get hemodynamically stable
4. 2/2: administer BB as LT therapy to prevent rebleeding.
What is the risk of CRC in patients with FAP?
100% by age 30 or 40 thus requires prophylactice colectomy for treatment

EPIGASTRIC abdominal pain that radiates to the back in 50% of patients that is often steady, dull, and severe that gets WORSE WHEN SUPINE and POSTPRANDIALLY.


Acute pancreatitis
What are the complications of severe pseudomembranous colitis?
Toxic megacolon
Colonic perforation
Anasarca, electrolyte disturbances
Treatment of choledocholithiasis
ERCP with sphincteromtomy and stone extracton with stent placement (successful in 90%) of patients with it.
-laparoscoptic choledocholithiotomy in select cases
Diagnosis of chronic pancreatitis:

CT scan is the initial study of choice – shows calcifications not seen on plain film. Mild to moderate cases may not be detectable, so a normal CT scan doesnt rule out chronic pancreatitis.

Abdominal radiographs: pacreatic calcification = 99% specific but only found in 30% of cases

ERCP is the GOLD STANDARD but not done routinely because of its invasiveness

Lab studies not helpful because serum amylase and lipase levels arent elevated in CHRONIC pancreatitis

Prothrombin time as a LFT describes?

THe liver synthesizes clotting factors I, II, V, VII, IX, X, XII, XIII, the function of which is reflected by PT

PT is not prolonged until most of the liver’s synthetic capacity is lost which corresponds to advanced liver disease.

diagnosis of cholangiocarcinoma
1. PTC/ERCP for diagnosis and assesssment of resectability
2. IF patient has an unresectable tumor (more likely the case with proximal than distal bile duct tumors) – stent placement is an option during PTC or ERCP to relieve the obstruction
Performance of surveillance _______ in patients with known achalasia has been shown to detect the tumor at an early stage.
Acute Infectious Diarrhea is defined as:
increased frquency of defecation (>/= stools/day) lasting <14days
-accounts for 900k hospitalizations and 6k deaths annually
Tests to order in patients with GI bleeding and OCCULT BLOOD
colonoscopy is the initial test in most cases (colon CA is the main concern) Order and upper endoscop if no bleeding site identified from the colonoscopy
What are the causes of unconjugated hyperbilirubinemia?

(Urine negative for bilirubin)

1. Excess production of BR – hemolytic anemias
2. reduced heaptic uptake of BR or impaired conjugation
-GILBERTS syndrome
-drugs (sulfas, penicillin, rifampin, radiocontrast agents
-criggler najjar syndrome types I/II
-physiologic jaundice of newborn (immature conjugating system)
-diffuse liver dz (cirrhosis/hepatits)

Staging esophageal cancer that have invaded the muscularis propria and has positive regional nodes:


Stage 1: tumor invades lamina propria or submucosa; nodes negative
Stage 2a: tumor invades muscularis proprai or adventitia; nodes negative
Stage 2B: tumor invases up to muc propria with positive regional nodes
Stage 3: tumor invades adventitia (positive reional nodes) or tumor invades adjacent structures (positive or negative nodes)
Satge 4: distant mets

Clinical features of acute mesenteric ischemia versus chronic mesenteric ischemia
Acute: severe abdominal pain disproportionate to the physical findings. Pain is due to ischemia or possibly infarction of intestines analogous to MI in CAD. Abdomen may appear benign even when there is severe schemia. This can lead t a delay in dx. Acutesness and the severity of pain vary depending on the type of acute mesenteris ischemia
-anorexia, vomiting
-GI bleeding (mild)
-peritonitis, sepsis, shock may be present in adv diseaseChronic: results in weight loss, abdominal angina postprandially.

Autosomal recessive disease of iron absorption-
-escessive iron absorption in the intestine leads to ncreased assumulation of inro (as ferritin and HEMOSIDERIN) in varous organs. Over years, fibrosis isn involved organs will occur seoncdary to OH free radials generated by excess iron
Most sensitive and specific test for CRC
Hemochromatosis v. Hemosiderosis?

Hemochromatosis: common AR disease in US homozygous for C282Y on chromosome 6. Causes increase intestinal iron absorptino with elevated accumulation of iron in the liver, pancreas, heart adrenals tests pituitary kidneys joints and skin. Disease onset is after age 50 with nonspecific symptoms in early stages. Later signs include arthropathy, hepatomegatly, skin pigmentation and cardiac enlargement, DM and impotention. Patients WILL DEVELOP HEPATIC AND PACNREATIC INDUFFICIENCY with possibly CIRRHOSIS and HCC, CHF, and hypogonadism.

Lab findings will be elevated LFTs with elevated plasma iron and increase 50% sat of TIBC and elevated ferritin.

Hemosiderosis is the deposition of excessive iron in the tissues. This is caused by a variety of inherited metabolis disorders or by environmental exposures to iron containing substances and is therefore NOT considered to be a distinct disease entitiy.

What percent of patients with biliary coloic develop acute cholecystitis in 2 years?
Treatment of UC:
medical: corticosteroids for acute exacerbaton
-SULFASALAZINE is he mainstay of treatment – it is effective
-immunosuppressivessurgical – curative (UNLIKE CROHNS disease) involves total colestomy

Factors increasing mortality of GI bleeding
>65YO, severity of initial bleed
extensive comorbid illnesses
onset or recurrency of bleeding while hospitalize for another condition
need for emergency surgery
transfusion requiresments
diagnosis (esophageal varices have a 30% mortality rate)
endoscopic stigmata of recent hemorrhage
Causes of cirrhosis?
1. Alcoholic liver disease (most common cause)
-range of conditions from fatty liver (reversible due to acute ingestions) to cirrhosis (irreversible).
-15-20% of heavy drinkings develop alcoholic cirrhosis2. Chronic hepatitis B and C infections

3. Drug toxicity: acetaminophen toxicity, MTX

4. AI hepatitis

5. Primary biliary cirrhosis (PBC); secondary biliary cirrhosis

6. Hereditary metabolic diseases (Hemachromatosis, Wilson’s disease (deposition of iron or copper)

7. Hepatic congestion 2/2 RHF or constrictive pericarditis


9. Hepato veno-occlusive disease can occur after bone marrow transplantation

“pencil stools” are highly indicative of?
Left sides tumors in regards to CRC
Diagnosis of gastric CA

Endoscopy with multiple biopsies is the most accurate!

-barium upper GI series less accurate but can completment upper endoscopy biopsy findings
-abdominal CT scan to stage and detect mets

if a patient presents with peritoneal fluid excess with exertional dyspnea. What is likely the cause of the patients distended abdomen and edema if a paracentesis shows an albumen level of 2.5 and a blood study shows an albumin of 3.8?

SAAG – serum albumen ascites gradient

serum albumin – ascites albumin = 1.3 therefore because it is greater than 1.1, we can denote his cause to portal HTN

SBO (small bowel obstruction): Three points to differentiate between:
1. Partial v. complete obstruction
2. Closed loop v. open loop obstruction
3. Proximal v/ distal loop obstruction
Treatment for BUDD-CHIARI syndrome
1. Medical therapy is uaually unsatisfoatory (anticoag, thrombolytics, diuretics)
2. Surgery is eventually necessary in most cases (balloon angioplasty with stent placement in IVC, portocaval shunts)
3. LIVERTRANSPLANT if cirrhosis is present!
ALT is primarily found in the ____
AST is primarily found in the ____
AST – more nonspecific: kidney, heart, brain, skeletal muscle
What diagnosis does an upper GI barium swallow show (“corkscrew esophagus”) – in 50% which represents multiple simultaneous contractions?

Pacnreatic ascites/pleural effusion is the MOST COMMON CAUSE OF INFLAMMATION of the PERITONEAL SURFACE.


IF AST and ALT are severely elevated (>10,000) extensive hepatic necrosis has occured. This includes:
1. Ischemia
2. Shock liver (prolonged hypotension or circulatory collapse)
3. Acetominophen toxicity
4. Severe viral hepatitis
What are the risk factors for acquisition of clostridium difficile?
Hospitalization or residence in a chronic care facility
-AB exposure – nearly all AB implicated however the big three (CLINDA, CEPHS, FQ)
-Advanced age (esp >65)
Infection ascites fluid that occurs in up to 20% of patients hospitalized for ascites
1. occurs in patients with ascites caused by chronic liver disease with HIGH mortality rate 20-30%
2. high recurrence rate (70%)
3. E. Coli, Klebsiella, Streptococus penumoniae
4. CLinical features: abdominal pain, fever, vomiting, rebound tenderness. SBP can lead to SEPSIS****REBOUND TENDERNESS! = SBP!

47YO DM female presents with onset of tremors. Undergone both pancreatic and renal transplantation 2/2 ESRD and DM. Takes medications including that of immunosuppressants. BP 152/90 and pulse and RR WNL. Examination shows gum hypertrophy and labs show an increased BUN and inc CREATININE. Which immunosuppressant is likely to be responsible for the presentation of patient?

(Tacrolimbus, cyclosporine, AZA, Mycophenolate)


most commonly used and acts by inhibiting the trancription of IL-2 and severeal other cytokines (mainly the THELPER LYMPHOCYTES

-glucose inteleratnce
-malignancy of SQCC of skin and lymphoproliferative D/O
-gingival hyperplasia and hirsuitism

RIght scapular pain 2/2 biliary colic

Signs, symptoms, radiographic evidence of large bowel obstruction are present but no mechanical obstruction.

-causes: surgery, trauma, serious medical illness (sepsis, malignancy) and medications (narcotics, psychotrpoic drugs, anticholinergics)

-diagnosis: not confirmed until mechanical obstruction of colon is exluded

-treatment: stop offending agent (narcotic) or supportive measures (IV fluids/electrolyte repletion)

-decompression with gentle enemas or NG suctions may be helpful
-colonoscopic decompression is usually successful
-surgical decompression with cecostomy or colostomy is LAST result

What is the treatment for diverticulosis?
1. High fiber foods (bran) increase the stool bulk
2. Psyllium *if the patient cannot tolerate bran)
Gilbert’s syndrome

Occurs in 7% of population-autosomal dominant condition in which there is decreased activity of hepatic uridine diphosphate flucuronyl transferase activity (UDP transferase);



Term used to describe esophageal perforation:


Boerhaave’s syndrome
Manifestations of strangulated bowel in SBO includdes fever, severe and continuous pain, hematemesis, schock, gas in bowel wall or PV, adbominal free air, peritoneal signs and _____. Will check _____ _____ to see if gut ischemia present
acidosis, lactice acid increased
Clinical indicators of Acute bacterial sinusitis
“double sickening”
unilateral pain
pain above or below the eyes on leaning forward
maxillary toothache
purulent rhinorrhea by hx
poor response to decongestants0-1 = no treatment
2-3 = XR
4+ = ATB treatment

What are the signs associated with acute pancreatitis?
1. Low grade fever, tachycardia, hypotension, leukocytosis
2. Epigastric tenderness, abdomial distention
3. Decreased or absent bowel sounds indicate patial ileus
4. The following signs are seen with hemorrhagic pancreatitis as blood tracks along fascial planes:
-Grey turners sign (flank ecchymoses)
-Cullen’s sign (periumbilical ecchymoses)
-Fox’s sign (ecchymosis of inguinal ligament
Increased glomerular filtration pressure will increase glomerular _____ rate and decrease the serum ______ concentration. This will NOT cause ascites
Acid suppression therapy for pts with PUD includes:
H2 blockers; ranitidine; famotidine; cimetidine; PPI; esmoprezole; omeprazole; lansoprazole; pantoprazole, rabeprazole
Clinical features of UC
1. Hematochezia
2. Abdominal pain
3. Bowel movement
What is the recurrence rate post surgical resection of CRC within 3 years?
Diagnosis of crohns

endoscopy (sigmoidoscopy or colonoscopy) with BIOPSY – typical findings are apthous ulcers, cobblestone appearance, pseudopolyps, patchy skip lesions

barium enema

upper GI with SBfollow through

Familial juvenile polyposis coli
RARE = in childhood; only small risk of CRC
-more than 10 and up to hundred of juvenile colon polyps.
CLinical signs of appendicitis:
1. Mcburneys point (tenderness)
2. Rebound tenderness, guarding, diminished bowel sounds
3. Low-grade fever
4. Rovsings sign: deep palpation is LLQ causes referred pain in RLQ
5. Psoas sign: RLQ pain when right thigh is extended as patient lies on the L side
6. Obturator sign: pain in RLQ when flexed right thigh is internally rotated when pt is supine.
Treatment of bleeding esophageal VARICES:
-initial endoscopic treatment of choice; effective control of ACTIVE BLEEDING
-lower rate of rebleeding than scleotherapy2. ENDOSCOPIC SCLEROTHERAPY:
-sclerosing substance is injected into varices during endoscopy
-this controls acute bleeding in 80-90% of cases with 50% haveing rebleeds

3. IV vasopressin
-alternative to octraotide but LESS POPULAR due to risk of complication.
-vasoconstriction of mesenteric vessels reduces portal pressure
-NG is admin to prevent side effects of vasopressin (coronary vasoconstrict/MI, decreased CO/HTN)

3. IV octreotide
-now replacing vasopressin as firstline therapy; causes splanchnic vasoconstriction and reduces portal pressure
-fewer side effects

Esophageal hiatal hernia has two main types:
Two main types:
1. Sliding
2. Paraesophageal hiatus
Rectal CA v. Colon CA
Rectal CA has a higher recurrence rate and a lower 5 year survival rate than colon CA
Three types of adenomatous polyps:
1. Tubular
2. Tubulovillous
3. Villous*tubular is the most common type in up to 60-80% of cases
*tubulovillous has an intermediate risk of malignancy
*villous is the GREATEST risk of becoming malignant

What accounts for 60% of all cases of ascending cholangitis?
Inflammatory bowel disease v. CRC
Both UC and Crohns increase risk, but UC>>> than crohns
Tests to order in patients with GI bleeding with HEMATEMESIS:
Two types of liver cysts and causes:
1. Polycystic liver cysts: AD usualy associated with ADPKD. Results in renal failure and is the main determinant of the prognosis whereas the liver cysts RARELY lead to hepatic fibrosis and liver failure.
-usually asymptomatic; some patients have absominal pain and upper abdominal masses
-treatment: unneccessary2. Hyadatid liver cysts: caused by infection from the tapeworm ECHINOCOCCUS GRANULOSUS or ECHINOCOCCUS MULTIOCULARIS. Cysts most commonly occur in the RL of the liver.
-small cysts are asymptomatic; larger cysts may cause RUQ pain and RUPTURE into the peritoneal cavity, causing fatal anaphylactic shock.
-treatment: SURGICAL resection (caustion to avoid spilling contents of the cysts into the peritoneal cavity). Mebendazole is given after surgery

How might HIDA diagnose that of acute cholecystitis? When is it superior to an US?
HIDA – radionuclide scan – hepatoiminodiacetic acid) is used to diagnose inflammation of the GB when US is inconclusive. If the scan is normal, then acute cholecystitis can be ruled out. If the test is positive then the GB cannot be visualized 4 hours after injection, diagnosis of acute cholecystitis is confirmed
HIGH fat and LO FIBER diets increase the risk of?
Cavernosis hemangiomas

Vascular tumor that are small, asymptomatic and most commony type of BENIGN liver tumor.

size increases 2/2 pregnancy or OCP use

complications: rupture with hemorrhage, obstructive jaundice, coagulopathy, CHF seondary to a large AV shunt and gastric outlet obstruction

Dx with US or CT with IV contrast – no biopsy indicated

Absolute criteria for achalasia:
Aperistalsis of esophagus
Incomplete relaxation of the LES
1. Prevalence
2. Setting
3. Transmission
4. Strain
1. emergence is nationwide
2. both children and adults in variety of settings affected –> contact sports (wrestling, football and fencing), correctional facilities, native american communities, MSM
3. Transmission is person to person or by fomites
4. Strains causing MRSA (community) appear distinct –> unique resistance cassette (SCC mec IV) & broader susceptibility
Cholesterol stones are one of three major types of GB stones that are _____ – _____ in coloration and are associated with the following:
1. obestity
2. DM
3. HLD
4. multiple pregnancies
5. Crohns dz
6. Native american ancestry
7. Cirrhosis
8. Cystic fibrosis
Treatment of appendicitis:
APPENDECTOMY – usually laparoscopic. Up to 20% of patients who are dx with acute appendicitis are found to have a normal appendix during surgary. Because illness is potentially life threatening, acceptable risk even during pregnancy.
RISK FACTORS of gastric CA:
1. atrophic gastritis
2. adenomatoush gastric polps
3. H pylori infecction -3-6x inc
4. Postantrectomy – many causes post billroth II anastomosis (15-20yrs post surgery)
6. Menetriers disease
7. High intake preseved foods
8. Blood type A
Management of uncomplicated UTI (acute)
1-2 recurrences per year
-intermittent self treatment (educable, typical sxs)
-TSX, TMP, FQ x 3 days>2 recurrences/yr associated with coitus
-postoital prophylaxis
-TSX, NTF, or FQ after intercourse

>2 recurrentces without coitus
-continuous prophylaxis (95% reduction)
-TSX, TMP, NTF, F! qhs x 6 mo

What is the treatment for chronic pancreatitis?

Nonoperative management: narcotic analgesics for pain; bowel rest (NPO); pancreatic enzymes inhibit CCK release and thus decrease pancreatic secretions after meals; H2 blockers inhibit gastric acid secretion, preventing degradation of the pacnreatic enzyme supplements by gastric acid; INSULIN may be necessary if SEVERE pancreatitis; alcohol abstinence; small volume low fat meals – may improve abdominal pain.

Surgical managment on chronic pancreatitis: main goal is relief of incapacitating abdominal pain.
1. pancreaticojejunostomy (Pancreatic duct drainage procedure to decompress the dilated pancreatic duct – most common)
2. Pancreatic resection (distal pancreatectomy, Whipples procedure)

CA-penumonia diagnosis:
Typical symptoms: cough, SOB, sputum, pleuritic chest pain
Infiltrate on CXR is gold standard for dx
Transmural tear throught the esophagus via the GEJ v. Muscosal

Boerhaave’s syndrome

MW syndrome

1. IV AB and IV fluids
-close monitoring of hemodynamics, BP and urine OUTPUT is important
-most patients respont rapidly. Once patient stabilized – ERCP or PTC performed for evaluation of underlying condition.2. Decompress the CBD via PTC (catheder drain); ERCP (spincterectomy or laparotomy) – (T tube insertion) once the patient is stabilized, or emergently if the condition doesnt respond to the antibiotics.

Treatment for C diff colitis:
d/c offending agent
-metronidazole is the drug of choice (cannot be used if infant/preg)
-oral vanc used if patient resistance to met or cannot tolerate it
-redarless of choice of AB, recurrence may occur within 2-8 weeks after stopping the AB
What is diverticulosis?
pouches in the colon wall that should be distinguished from diverticulitis, which refers to inflammations or infections of the diverticula and is a complication of diverticulosis.

GGT is often used to confirm that the elevated ALK-P is of hepatic origin

T or F

vomiting blood; suggest uper GI bleeding
What are the clinical features of CRC?
Abdominal pain is that most common feature – where CRC is the most common cause of large bowel obstruction in adults
-weight loss
-blood in stool
-colonic perforation is the most life threatening

Hepatocellular CA accounts for > 80% of primary liver CA and although rare in US, accounts for most deaths 2/2 cancers world wide. Highest in Africa and asia.

What are the two pathologic types?

nonfibrolamellar carcinoma

fibrolamellar carcinoma

Most common type of tumor within the intra/extra hepatic bile ducts
-tumors in proximal third of the CBD – involve the junction of the right and left hepatic ducts with very POOR prognosisbecausethey are unresectable.
Occult blood in the stool
source of bleeding can be anywhere along the GI

Obstruction of the cystic duct (not infection) induceing acute inflammation of the gallbldder wall

-chronic forms when recurent bouts of acute cholecystitis
-10 percent of patients with gallstones develop acute cholecystitis

Partial v. complete obstruction
Partial: with partial obstruction, patients are able to pass gas or have bowel mvmts as opposed to complete obstruction however patients with complete obstruction may occasionally be able to pass gas or stool because they may have residual stool or gas in the colon

Diverticulitis can occur in 15-25% of all patients with diverticulosis however this is not always a precedent of diverticulitis.

Pathophysiology of diverticulitis?
Diagnostic examinations?

1. Occurs when the feces become impacted in the diverticulum, leading to erosion and microperforation

2. Clinical features; fever, LLQ pain, leukocytosis (elevated WBC); alteration in bowel habits, vomiting, sometimes a painful mass on rectal exam if inflammation is near the rectum.

Diagnostic tests for diverticulitis:
1. CT scan of abdomen and pelvis with ORAL and IV contrast is the test of choice
-reveals a swollen, edematous bowel wall or an abscess.
2. Abdominal radiographs help in excluding other potential causes of LLQ pain that can rule out obstruction or ileus.
3. Barium enema and colonoscopy are contraindicated in ACUTE DIVERTICULITIS due to the risk of perforation

What is the metabolism of BILIRUBIN
-80% of BR is derived from hemoglobin (RBC breakdown). The rest comes from myoglobin breakdown and liver enzymes
-hemoglobin is coverted to BR in the spleen. This unconjugated BR circulates in plasma, bound to albumin. This BI-albumin complex is not water soluble; therefore it is not excreted in the urine.
-in the liver, it dissciates from albumin and the BR is conjugated and excreted into the intestine, where bacteria act on it to produce urobilinogen and urobilin
-therefore, unconjugated hyperbilirubinemia results when there is a defect BEFORE hepatic uptake. Conjugated hyperbilirubinemia results when there is a defect AFTER hepatic uptake
Treatment for cholangiocarcinoma:
1. most patients do not have resectable tumors at diagnosis
2. survival rate low despite aggressive therapy and stenting or biliary drainage
Duodenal ulcer differs from gastric ulcer in what ways?
1. Duodenal: by an increase in offensive factors (higher rates of basal and stimulated gastric acid secretion). H. pylori in 70-90% of patients. LOW MALIGNANCY; majority are located within 1-2cm distal to pylorus usually on posterior wall. Age is YOUNGER (<40). BLOOD TYPE O. Risk factors includes NSAID use. Other – eating usually relieves pain and NOCTURNAL pain is more common than in gastric ulcers. 2. Gastric ulcers – caused by decrease in defensive factors (gastric acid level is normal) low unless ulcer is pyloric or prepyloric. H. pylori infection in 60-70%. HIGH LEVEL MALIGNANCY – must undergo biopsy to rule out malignancy). Location: Type I: most common – 70% on lesser curvature Type II: gastric and duodenal ulcer Type III: Prepyloric (within 2 cm of pyloris) Type IV: near esophagogastric juntion Age distribution occurs in older patients (>40). BLOOD TYPE A. RIsk factors smoking. Eating does not usually relieve pain. Complication rates are higher than those of duodenal ulcers. There is a higher recurrence rate with medical therapy alone.
Empiric treatment for cat bite?
plummers disease
toxic thyroid adenoma
hashimotos (transient)
differ radioiodide scan in graves vs plummers disease vs thyroid nodules vs thyroiditis
diffuse uptake in graves
patchy uptake in plummers
absence of uptake in “cold thyroid nodule”
decreased uptake in thyroiditis because cells are damaged and annot trap iodide.
rare causes of hyperthyroidism
postpartum thyroiditis
iodine induced hyperthyroidism
excessive doses of levothyroxine
Hyperthyroidism in elderly
classic symptoms of hyperthyroidism (nervousness, insomina, hyperactivity) may be absent. The only manifestation may be weight loss, weakness, and or atrial fibrillation –> consider hyperthyroidism before assuming that an elderly pt with unexplained weight loss has depression or occult malignancy.
what are the clinical features of hyperthyroidism (name 5)
weight loss
heat intolerance
muscle weakness
what are three symptoms that are specific to GRAVEs disease
pretibial myxedema
thryoid bruit
pt comes in with signs of hyperthyroid and a tender thyroid – dx?
subacute thyroiditis
pt comes in with signs of hyperthyroid and a nontender thyroid – dx?
pt comes in with signs of hyperthyroid and a bumpy, irregular and asymmetric thyroid – dx?
plummers disease
pt comes in with signs of hyperthyroid and a single nodule – dx
toxic adenoma
hot thyroid nodule
cardiovascular effects of hyperthyroid
atrial fibrillation
premature ventricular contractions
sinus tachycardia
what is the initial test of choice for a pt who is hyperthyroid?
SERUM TSH – should be low –> if TSH is normal to high then hyperthyroidism is low as a differential. After ordering TSH follow up with levels of T4 (t3 is typically not necessary)
free thyroxine index (FTI)
proportional to free T4 concentration!
(as T4 decreases, radioactive T3 should increase and vice versa)
–> normal values are 4 to 11.
what is tx for hyperthyroidism
-Methimazole and PTU – a/e agranulocytosis (order leukocyte count)
-B blockers – mgmt of sx
-sodium ipodate or iopanoic acid – lowers t3 and t4 lvls, this is a second line agent.
-radioiodine 131 – *MC therapy in us for gravers*
-surgery – subtotal thyroidectomy – only indicated for persistent, recurrent episodes, refractory to pharm therapy, or if concomitant large goiter is present (common in TMNG)
pregnant women with graves
PTU and BB
nonpregnant with graves
methimazole and BB
treatment of thyroid storm
cooling blankets
IVF + glucose
Hypothyroid myxedema coma
depressed state of consciousness
profound hypothermia
resp depression
may develop after years of hypothyroid
precipitating factors = trauma, infection, cold exposure, narcotics
*tx with IV thyroxine and hydrocortisone*
follicular carcinoma of thyroid
-avidly absorbs iodine
-poor prognosis – even though its a “carcinoma” travels hematogenously – thus mets to brain, lung, bone, liver
-tumor extension through the tumor capsule – thus distinguishing follicular from a benign adenoma –> *must obtain a tissue biopsy* FNA will NOT r/o
-slow growing but more malignant
-one variant is hurthle cell carcinoma –> radioiodine resistant (differ from follicular) and will have *characteristic cells with abundant cytoplasm and oval nuclei with a prominent nucleoli*
medullary carcinoma of thyroid arises from what cells?
parafollicular C cells –> thus can stain for calcitonin.
-amyloid present –> apple green bifrigence
-associated with MEN IIa
treatment for papillary ca
lobectomy with isthmusectomy
what are indications for total thyroidectomy
papillary ca >3cm
tumor is bilateral
follicular carcinoma
medullary carcinoma
tumor is advanced
distant mets
tx for anaplastic ca
surgery may be indicated for palliative
whats the first test for suspected pituitary adenoma?
tx for pituitary adenoma
transsphenoidal surgery is indicated for pituitary adenomas *EXCEPT FOR PROLACTINOMAS* which are MC
what are causes for hyperprolactinemia?
h2 blockers
psychiatric meds
renal failure
suprasellar lesions that compress the hypothalamus
how can suprasellar lesions that compress the hypothalamus cause hyperprolactinemia?
hypothalamus release prolactin inhibiting factor – my decreasing the release of that factor then prolactin release becomes upregulated from pituitary.
clinical features of hyperprolactin in men
decrease libido
galactorrhea or gynecomastia
visual defects (bitemporal hemianopsia)
whats reason for clinical features of hyperprolactin in men
Prolactin inhibits GnRH –> thus high levels decrease GnRH and thereby decrease LH and FSH – remember that LH is a potent stimulator of testosterone production @ leydig cells in testes.
clinical features of hyperprolactin in women
irregular periods
vaginal dryness
decrease libido
inc risk of osteoporosis
postmenopausal –> look for visual defects (bitemporal hemianopsia)
Dx hyperprolactinemia
order levels of prolactin
pregnancy test and TSH level (as these are causes for hyperprolactinemia)
tx hyperprolactinemia
Drugs: bromocriptine or cabergoline (dopamine agonist)
only consider surgery if refractory to med therapy
whats the most common cause of death in pts with acromegaly?
cardiovascular disease –> high output cardiac heart failure
clinical features of acromegaly
coarse facial features
broadening of skeletal structure
increased height
elevated glucose level
hypertrophic cardiomyopathy
enlarged jaw
arthralgia due to joint tissue overgrowth
what are some parasellar manifestations and complaints of pts with acromegaly
visual defects (bitemporal hemianopsia)
sleep apnea
lateral growth = cavernous sinus compression and as such (OTOMCAT- abducens effected first)
inferior growth = sphenoid sinus compression
diagnose acromegaly
glucose tolerance test
IGF1 (somatomedin C)
can you assess levels of GH in acromegaly as a diagnostic marker?
NO – reason being that GH levels constantly fluctuate and cannot be used as a diagnostic marker
what is tx of choice for acromegaly?
transsphenoidal resection of pituitary adenoma
what are some meds that can be used to treat acromegaly
octreotide – will help suppress GH
what are clinical features of reduced GH
heart failure
decreased size
increased LDL
what are clinical features of reduced ACTH
adrenal insufficiency
what are clinical features of reduced Prolactin
inability to breastfeed
what are clinical features of reduced FSH and LH
decreased libido
loss of secondary sex characteristics
what are clinical features of reduced TSH
what are clinical features of reduced ADH
diabetes insipidus
what are clinical features of reduced MSH
decreased skin pigmentation and hair pigmentation
whats the ddx for polyuria and polydipsia
diabetes mellitus
diabetes insipidus
diuretic use
what are causes of central diabetes insipidus
Idiopathic is MC
head trauma
hans-schuller christian disease (triad of exopthalamos, lytic bone lesions, diabetes insipidus d/t pit stalk infiltration)
eosinophillic granuloma
what is tx for nephrogenic DI?
decrease sodium in diet and thiazide diuretics –> decrease sodium results in increased sodium absorbed at PCT and as such water follows – thereby preventing increased water loss
SIADH – what electrolyte will be low in serum?
sodium –> hyponatremia for 2 reasons
increase VOLUME leads to hyponatremic hypervolemia – however no edema seen due to ANP – this increases naturesis and in doing so further decreases sodium absorption @ PCT – thus increase sodium loss.
what are 6 causes of SIADH
1. CNS disorders (stroke, head trauma, infection)
2. Malignancy (lung cancer, bladder cancer) lymphoma, leukemia
3. ventilation with positive pressure (CPAP, PRVC, BIPAP)
4. Pneumonia
5. Drugs (SSRI, vincristine, morphine, desmopressin)
6. Postoperative state (as a result of anesthetia)
in a pt with hyponatremia whats the risk if sodium is corrected too quickly?
cerebral pontine myelinolysis – do not correct faster than 0.5mEq/L per hour
clinical features of hypoparathyroidism
cardiac arrhythmias
rickets and osteomalacia
tetany –> hyperactive deep tendon reflexes
chvostek sign
trousseaus sign
grand mal seizures
basal ganglia calcifications
dx hypoPTH
low serum calcium
low urine cAMP
low PTH
high serum phosphate
complication of treating hypoPTH
kidney stones
what are clinical features of hyperPTH
stones, bones, groans, and psychiatric overtones
stones = nephrocalcinosis, nephrolithiasis
bones = osteitis fibrosa cystica (brown tumors) –> pathologic fractures
groans = muscle pain and weakness, pancreatitis, PUD, gout, *constipation*
psychiatric overtones = depression, sleep disturbance
dx hyperPTH
NORMAL PTH levels – in hypercalcemia the PTH lvl should be drastically reduced
calcium levels increased
urine cAMP is elevated
chloride/phosphorous level of >33 is diagnostic of what disease?
hyperparathyroidism – the chloride is high 2/2 renal bicarb wasting which is a direct effect of PTH and phosphate dumping is increased with PTH.
subperiosteal bone resorption of 2 and 3rd phalanges indicative of what disease?
what are indications for surgery in hyperPTH
age <50 marked dec in bone mass nephrolithiasis very high serum calcium urine calcium >400mg in 24 hours
water deprivation test
evaluation of hypertension with hyperkalemia
secondary adrenal insufficiency d/t hypopituitarism – while rare – will present with?
signs of panhypopituitarism, glucocorticoid insufficiency, BUT NOT mineralcorticoid deficiency as aldosterone from zona glomerulosa is ACTH independent, therefore look for weakness, fatigue, loss of appetite, *eosinophilia*, postural hypotension, loss of libido, bradycardia, anemia, decrease deep tendon reflexes, hypoglycemia.
what is the most common treatment in the US for graves disease?
radioiodine ablative therapy
congenital adrenal hyperplasia – whats the most common enzymatic def
21 hydroxylase def
next is 11 hydroxylase def
how will women present with 21 hydroxylase def?
ambiguous genitalia with normal uterus and ovaries.
21 hydroxylase clinical features
lack of mineralcorticoid
lack of cortisol
hypoglycemia, hyponatremia, hyperkalemia
emesis, dehydration, hypotension, and shock
what test is used to detect 21 hydroxylase def
elevated levels of 17 hydroxyprogesterone
tx of 21 hydroxylase def
cortisol and mineralcorticoid administration –> this will decrease levels of ACTH thus decrease shunting of pathway (to greater sex hormone levels)
what MHC class is associated with diabetes type I
HLA (MHC) class 2 –> HLA DQ/DR on chromosome 6
what diabetes has a greater degree of genetic concordance?
what is the greatest risk factor for the development of DM2
how does obesity lead to DM2?
obesity is associated with increased plasma free levels of free fatty acids, which make muscle more insulin resistant, reducing glucose uptake. Therefore, obesity exacerbates insulin resistance. *look for lipid profile of hyperTAG with HDL depletion.*
how to diagnose diabetes
-fasting glucose lvl >126 (2 occassions)
-random blood glucose >200 with symptoms
-elevated insulin following oral glucose tolerance test
-HbA1c >6.5%
dawn phenomenon and somogyi effect
both result in elevated glucose in the morning, however both mechanisms are a bit different. The dawn phenomenon is due to elevated levels of growth hormone overnight that result in elevated glucose in the AM, whereas the somogyi effect is a counter regulatory mechanism for hypoglycemia overnight. To differentiate either as a cause – take blood glucose level at 3 am, if pt is hyperglycemic then the cause is the dawn phenomenon, and insulin dose should be elevated prior to bed to combat the elevated GH and its effect. If at 3 am the pt is hypoglycemic then its the somogyi effect and the insulin level should be decreased at night prior to bed.
recommendations for diabetic pt
hba1c every 3 months <7.0 1x yr microalbuminuria screen (if positive start ACEi or ARB) 1x yr opthamologist screen check feet and BP every visit if LDL >100 start statin
daily aspirin >30 yrs
pneumoccocal vaccine
diabetes drugs a/e
1. sulfonyurea –> hypoglycemia *weight gain*
2. metformin –> diarrhea, nausea, abdominal pain, lactic acidosis, metallic taste
3. acarbose –> diarrhea, nausea, abdominal pain
4. Thiazolidinediones –> hepatotoxicity (must monitor LFT)
what is insulin sliding scale?
predetermined scale that looks at the patients glucose level and wherever the value falls designates an arbitrary amount of insulin units to that level. For example if pt has a glucose level of 150-200 then 2 units should be given… 201-250 req 4 units… 251 – 300 req 6 units and so on. (inc by intervals of 50)
what is the definition of microalbuminuria
levels are 30-300mg/day of albumin in urine
what is treatment for diabetic gastroparesis?
what is the screening test for diabetic nephropathy?
microalbuminuria –> this is bc proteinuria will only be detected @ >300mg/day.
Once diabetic nephropathy has progressed to stage of proteinuria or early renal failure, glycemic control does not influence its course. What are recommendations?
ACEi and dietary restriction are recommended.
what will fundoscopic examination show in a pt with diabetes
venous diltation
what is the leading cause of vision loss in pts with diabetes
edema of the macula
key features of proliferative retinopathy
complications = 1. vitreal hemorrhage 2. retinal detachment–> which can both lead to blindness –> *tx is laser photocoagulation*
what is the best management to reduce microvascular complications in a diabetic pt?
TIGHT GLUCOSE CONTROL – however no evidence for reducing macrovascular complications which are leading cause of death
what are macrovascular complications
stroke, MI/CHF (CAD)
MC cause of death = CAD
CN complications in diabetic pt
secondary to nerve infarction
most often involves CN III but may also involve VI and IV
*diabetic third nerve palsy* = eye pain, diplopia, ptosis, inability to adduct the eye; *PUPILS ARE SPARED*
mononeuropathies in diabetic pt
diabetic *lubosacral plexopathy* = severe deep pain in thigh; atrophy and weakness in thigh and hip muscles; recovery takes weeks to months
diabetic pt are at risk for what sort of infections?
polymicrobial foot ulcers
what is tx for *painful* diabetic neuropathy
what are precipitating factors of DKA?
trauma (trauma, MI, stroke, recent surgery, sepsis, GI bleed)
poor insulin administration
what is the differential diagnosis of DKA
alcoholic ketoacidosis (pt may be *euglycemic*)
hyperosmolar hyperglycemic nonketotic syndrome (MORE DANGEROUS)
intoxication (methanol, ethanol, isopropyl alcohol, paraldehyde)
what are two requirements to dx DKA
how are sodium levels changed in pt with elevated glucose?
serum sodium decreases by 1.6 for every 100 increase in glucose level bc of osmotic shift –> Total body sodium is normal thus generally does NOT require treatment
tx of DKA
give IVF, give insulin and then START potassium soon after –> CLOSELY monitor potassium levels bc insulin will quickly shift potassium into the cells thus resulting in hypokalemia –> pt must have potassium of 4 before giving insulin. *PT MUST NOT BE HYPOKALEMIC BEFORE GIVING INSULIN* for pt can develop *FATAL* arrhythmia associated with hypokalemia.
main differentiating factors between DKA and HHNS
no ketoacidosis in HHNS – d/t presence of small amounts of insulin
hyperglycemia >900 in HHNS compared to DKA >450
NORMAL pH in HHNS vs DKA acidosis <7.3 hyperosmolarity in HHNS >320
higher mortality in HHNS
clinical features of HHNS
thirst, polyuria
signs of EXTREME volume depletion = seizures 2/2 hyperosmolarity
lethargy and confusion
diagnosis of HHNS
elevated glucose >900
elevated serum osmolarity
prerenal azotemia is COMMON
normal pH
tx of HHNS
FLUID resuscitation with NS – then switch to 1/2NS once pt stabilizes.
@250 glucose add D5
like in DKA rapid lowering of blood glucose can lead to *cerebral edema*
clinical features of hypoglycemia
sympathetic activation –> diaphoresis, palpitations, tremors, high blood pressure, anxiety
neuroglycopenic symptoms – headache, visual disturbances, confusion, seizures
how to diagnose insulinoma
72 hour fast –> insulin levels SHOULD be low, however if normal or elevated consider INSULINOMA
food relieves symptoms
what is whipples triad?
blood glucose <50
glucose administration RELIEVES symptoms
how to differ btwn insulinoma and sulfonyurea overdose?
both will have elevated insulin and c-peptide – difference is level of *proinsulin* –> in insulinoma its increased whereas in sulfonyurea drugs its normal
tx of insulinoma
surgical resection
glucagonoma clinical features
necrotizing migratory erythema (below waist)
*low amino acid levels and high glucagon levels*
treatment is surgical resection
somatostatinoma clinical features
early metastasis
poor diagnosis
CLASSIC TRIAD *gallstones, diabetes, steatorrhea*
*treatment is surgical resection*
VIPoma clinical features
watery diarrhea leading to dehydration, *hypokalemia*, acidosis
*treatment is surgical resection*
treatment for ZES
high dose PPI
surgical resection
treatment for VIPoma
before going to surgery pt MUST NOT BE dehydrated.. common question will ask what first step in management is – pt must be stable before surgery thus correct fluid balance.
Clinical features of touretts and two types of tics:
1. Motor tics (multiple) – jerking, shrugging, grimace, blinking
2. phonics (at least 1 kind) – grunting, sniffing, clearing throat, copralacia, repetition of words
Most common intracranial neoplasma in adults are brain mets from?
Treatment of SAH
1. Surgical
2. Medical
1. Consult neurosurgery. Berry aneurysm treat surgically
2. Therapy dec risk of rebleeds and vasospasms
-bed rest and quiet
-stool softeners to decreased straining (will otherwise inc ICP and inc rebleed risk)
-IV fluids for hydration
-control HTN

Myasthenia gracis is liminted (often) to _____ in elderly

Age of M v. F?

EOM (extraocular muscles)
peaks- in females at 20-30YO
peaks-in males 50-70F>M

Huntingtons chorea characteristics

autodomal dominant chromosome 4; CAG trinucelotide repeat:

1. Chorea
2. Crazy
3. CAG repeat
4. Cuarenta (40YO)
5. Chromosome 4

-progressively worsens by generation
-mutation on chrom 4 expanded repeat CAG 0 loss of GABAergic in striatum (dec negative feedback and thus lack of inhibition

Abrupt onset of ASCENDING paralysis and weakness in all 4 limbs progressing to repiratory/facial/bulbar muscles
1. Symmetric
2. weakness mild-severe
3. weaknesss distal to central
4. Painful extremities but NO sensory loss
GB syndrome (starts low and GOES HIGH)
Lacunar infarct causing dysarthria and clumsy hand
What is a TIA?

neurological deficit that lasts from a few minutes to NO more than 24 hours (~30 min = normal)

-doesnt cause permanent infarction

Autopsy of AD lesions show:
Enlarged ventricles
Cerebral atrophy-quantity of senile plaque (age specific) focal collections of dilated neuritic processes surrounding amyloid core (b- protein amyloid)

-quantity of neurofibrillary tangles *agespecific
-neurofilaments in cytoplasm of neurons – neuronal degeneration

Neurocutaneous syndromes

NF type I = AD; care au lait spots, neurofibromas, CNS tumors, glioma and meningiomas with MR, short height, macrocephalus

NF type II = AD/chromosome 22, bilateral acoustic schwannomas/multiple meningiomas/cafeaulait spots

Tuberosclerosis (TS) = AD/cog impairment, epilepsy, skin lesions, angifibromas, retinal hamatomas, renal angiomylipo, rhabdomyolipioma of heart

Sturge-weber syndrome = aquired; capillary angiomatosis of PIA mater. Facial vascular NEVI (port urine stain)

VHL disease

Generalized treatment of seizures
standard antiepileptic drug used to provide control in 70% of patients
-if partial (simple/complex) or grand mal use phenytoin/carb
-if absense = ethosuxamide/valproic acidIf persists – increase dose of first antiepitleptic until signs of toxicity appears then add the second

Continue 2 years as controlled then TAPER down

Differential diagnosis of ring-enhancing brain lesion
1. Metastatic cancer
2. Brain abscess
3. Glioblastoma multiforme
4. Lymphoma
5. Toxoplasmosis

Bilateral fixed, dilated pupil caused by: ____ ___

Unilateral fixed; dilated pupils caused by:

Pinpoint pupils caused by:

Severe anoxia

Herniation with CN3 compression

narcotics, ICH

Treatment for MG?
What drugs exacerbate them?
Treatment: pyridostigmine/edrophonium – ACHEi
-thymectomy – symptom benefit and complete remission +/- thymoma
-immunosuppressed = corticosteroids/aza/cyclosporins

AB- aminoglycosides (GNAT); tetrcyclines; BB; antiarrhythmics, quinidine, procainamide, lidocaine

forgetfulness v. dementia

Some degree of memory loss is accepted as a normal part of aging. May be difficult to distinguish this condition from TRUE dementia

Benign forgetfullness doesnt adversly affect ADL but can be a risk factr for progressive dementia such as AD

What infections can cause dementia?
HIV infections (AIDS related dementia)
cryptococcal injection of CNS
Creutzfeldt-jakob disease (spongiform)
PML from that of lysosomal d/o
Levodopa (portion of SINEMET) has what action:
aspect of sinemet that shows an “on-off” phenomenon over daily coarse leading to fluctuation of symptoms
-dose dependent response

Risk factors for alziemers dementia


Family history (especiall for early onset AD)

Down syndrome

Etiology: chromosome 14, 19, 21 linked to AD

When are patients screened with carotid duplex?
1. Carotid bruit
2. PVD
3. Coronary artery dz-measures degree of stenosis if present

Diagnosis of MS
1. Fatigue – most common complaint
2. Motor symptoms – weakness, spasticity (UMN) involved
3. Visual disturbances – optic neuritis (loss of mononuclear vision) pain of eye mvmt, central scotoma, decreased pupillary light reflex
-internuclear ophthalmoplegia – lesion to MLF adduction defect and horizontal nystagmus of abduction.
4. cerebellar inovlvement-ataxia, intention trmor, dysarthia
5. bladder control – decreased with neuropathic pain
If ACA infarction =
contralateral lower extremity of body and face
If the patient presents to ED with findings suggestive of an acute stroke, order:
1. Non contrast (CT scan) of brain
3. CBC, platelets
5. Electrolytes
6. Glucose
7. Bilateral carotid US
8. Echocardiogram
Duchenne’s myotonic dystrophy
XLR (males)
-dystrophen gene mutaiton: proteins in muscle cells that die and increase fat
-no inflammationFeatures = weaknes of muscles – symmetric and starts in childhood
-primary pelvic girdle – GOWERS
-enlarged calfs due to pseudohypertrophy

Dx: serum creatinine PK increases; DNA testing > muscle biopsy

Two major categories of hemorrhagic stroke?
ICH – intracranial into parenchyma
SAH – bleeding into CSF; outside brain parenchyma
Which medications cause parkonsonian like side effects
HIGH potency neuroleptics or antipsychotics
-chlopromazine, haloperidol (haldol), perphenazine
What is a lacunar stroke?
Small vessel thrombotic disease
-20% of all strokes affecting:
1. Basal ganglia causing parkinsonian symptoms
2. Thalamus-gateway to brain
3. Internal capsule-pathway from thalamus to the cortex and cortex to the SC thus can affect motor OUTput
4. Brainstem
Symptoms of TIA from carotids
1. Temporary loss of speech
2. Paralysis of contralateral extremity
3. Clumsiness of limb
4. Amarosis fugax (ex of TIA): Transient curtain like loss of sight, of ipsilateral eye d/t microemboli to the retina

What is the third most common cause of death in the USA?

Most common type?

-ischemic stroke (85%) of cases
-hemorrhagic is 15% of cases
-severe depression may cause dec in cognitive function that is difficult to distinguish clinically from AD but is responsive to antidepressant therapy
How might GB be treated?
1. Carefully monitor pulmonary function
-mechanical ventilation may be necessasry
2. Administer IV immunoglobulin if patient significant weakness. Plasmaphoresis can decrease disease
3. Do not administer steroids – harmful

Treatment of ISCHEMIC stroke =


1. Acute: airway protection, O2, IV fluids
-choose broad efficacy and safety treatment
-choose tPA (thrombolytics) if administered within 3 hrs of the onset of an acute ischemic stroke
-do not admin tPA if unknown time, >3 hr passed or patients has HTN, bleeding d/o, anticoagulated, or recent trauma/surgery
-must keep BP < =185/110 mm Hg
How do ischemic strokes appear on CT? How do hemorrhagic strokes appear?
Ischemic – appears dark and takes 24-48hr to se infarct
Hemorrhagic – appears white
Both ___ and ___ are not administered to patients with acute stroke
Heparin f/u with warfarin

what symptom has a better prognosis in patients dx with parkinsons?

List one surgical intervention

tremor with bradykinesia

DBS if pts do not respons to treatment like SINEMET or those dx <40

Presense of UMN and LMN signs, no sensory involvement. Starts at 50-70 years old with a prognosis of 80% within a 5 year period
ALS or Lou Gehrigs disease – only 10% familial but the remainder is sporatic
Thrombotic stroke (causing ischemia)?
Atherosclerotic lesions in lage arteries of the neck (CAD) or in medium sized arteries in the brain – especially MCA
Guillain-barre syndrome

Inflammatory demyelinating polyneuropathy that primarily affects motor nerves

Preceded by a virl/mycoplasmal infection of the upper GI = campylobacter jejuni, CMV, hepatits, HIV

Hodgkins, SLE, post surgically, HIV

Variants of MS
1. Clinically silent
2. Secondary progressive
3. Relapsing remitting
4. Primary progressive
Parkinson’s disease
-clinical features:
1. Substantia nigra (loss of DAminergic containing herons-nerve cells that are located in the pigmented substantia and locus ceruleus of midbrain)
2. 50 YO
3. Pill-rolling tremor at rest, gets worse with stress, goes away with intention; bradykinesia, slowness of mvmt, cogwheel rigidity; poor postural reflexes, shuffling steps; expresionless faces
Key neuronal finding in brains of patints with parkinson’s disease?
Lewy bodies (hyaline inclusion body)
Causes of hemorrhagic stroke
#1 HTN (sudden elevation in BP)
-50% of all hemorrhagic strokes
-ruptures vessels within the brain parenchyma
-chronic HTN causing degeneration of small arteries leading to microaneursm which can rupture easily#2 AGE

Two most important indcations for ordering an MRI to rule out an intracranial mass?
1. New onset of seizures
2. New and persistent/progressive headache
When is an ECG ordered in patients with stroke (+/-)?
to rule out acute MI as cause of embolic strokes by AFIBB or an MI
2 extraparenchymal brain tumors
1. Meningiomas (capable of resection)
a. high recurrance rate
b. benign but can cause significant compression of tissue
c. 40-50YO F>M; attach to dura; extrapyramidal
2. Schwannomas
a. Benign tumors with no malignant potential
b. almost always unilateral if bilateral this is pathopneumonic for neurofibromatosis type II
Hemisection of the SC = diagnosis
Contralateral loss of pain
Ipsilateral loss of moto (LMN at site) UMN becomes slow
Ipsilateral loss of sensationex: Stab woulds
-movement at level would have HYPOreflext ipsilateral and hyper reflexia would be seen

What is the definitive test for identifying stenosis of the head and neck?
#1 senosis of head and neck
#2 aneurysms (looks at carotids, VB arteries, COW, ACA, MCA, PCA
What is the diagnosis of GB syndrome:
1. CSF analysis – elevated protein and cell count
2. Electrodiagnostic studies – decreased motor nerve conduction velocity
3. CLinical findings – ascening motor weakness with normal sensation preceeding infection of c. jejuni, CMV, HIV, hepatitis
3rd and 4th most common cause of death in the USA
1. Stroke = #3
2. AD
-prevalence increases with age (10-15%) of individuls >65YO
-15-30% of individuals >80 YO
treatment used to:
adverse effects:
Ldopa + carbidopa that ameliorates all symptoms of parkinson’s disease
-most effectiveCauses:
1. Dyskinesis (involuntary mvmt post 5-7 year use of Rx) – thus want to delay therapy for as late as possible
2. N/V, anorexia, HTN

Demyelination of CNS with multifocal zones of demyelination involving the white matter of the brain and SC without gray matter involvement
Multiple sclerosis
-common to women
-more likely at high latitudes and less at the equater
-involves pyramidal, cerebellar, MLF, optic nerve, posterior columns

Diagnosis of huntingtons and treatment:

What other disorder affects young patients with movement disorder?

MRI of head and caudate nuclei
DNA testing to confirm diagnosis – genetic counseling impNo curative treatment – DA blockers help with psychosis and chorea with anxiolytic and SSRI.


Stepwise deterioration of symptoms and neuro abnormalities are compatible with prior strokes and neuroimaging showing evidence of prior infarcts =
multi-infarct dementia

What is the most common cause of death after severe head injury?

What is normal ICP?

Increased ICP #1 cause of death
-normal 5-15 mmH20
-ICP > 20mmH2O is not good
-ICP is determined by volume of brain, volume of blood, volume of CSF
Diffuse axonal injury
Global damage to entire brain during impact
-may cause coma in patient
-CT scan doesnt show increased ICP but does show puntuate hemorrhages in the involved tracts
When should an LP not be performed in a patients with HIGH clinical suspicion of SAH?

IF CT scan reveals it, then look at the site of bleeding via cerebral angiogram

If papilledma is present, this indicates elevated ICP; thus this would lead to herniation and hemorrhaving if performed LP thus always perform opthalmologic exam

LE myasthenic syndrome
-autoAB against the presynaptic Ca2+ channels on NMJ.
-proximal muscle weakness and HYPOREFLEXIA
-symptoms improves with muscle stimulation
PEAK age (40-50)
-malignant and nonresectable glioma
-more indolent progression than fibrillary astrocytomas
-survival = 10-15 years post presentation
Drugs and toxins causing dementia
Aniline dyes
Metals (lead)
Chronic alcoholism
Childhood in onset, has ataxia, decreased sense of virbration, decreased proprioception, nystagms plus teleangiectasia
-increased cancer risk!
Dementia with Lewy Bodies
Both AD and parkinsons disease but progression may be more rapid than AD. Visual hallucinations predominate that include extrapyramidal features of functioning mental status
-treatment is similar to that for AD with neuroleptic selegiline can slow progression of dz.
Petit mal seizures are characterized by sudden _____ of mental activity. An episode is very short, but may occur _____ times per day. THere fore no associated signs of complex automatisms. This is confirmed by what type of test?
EEG study
How might MS be diagnosed?
1. MRI – test of choice (most sensitive) and first diagnostic in the majority of cases abnormal in 90%.
2. CSF and LP analysis – although no labs are specific for MS (+) oligonal bands and IgG in 90%.
3. Evoked potentials suggest demyelination of ceratin areas by measuring the speed of nerve conduction within brain. Newly remyelinated nerves will conduct sensory impulses more slowly
How is delirium diagnosed?
1. Mental status examination, MMSE
2. Laboratory (chem panel, B12, thiamine)
3. LP (perform in any febrile deliruis patient unless contrindiation like cerebral edema – perform fundoscopy)
Epidural hematoma v. Subdural hematoma

EDH = rapid surgical decompression

SDH- surgical evaluation if acute; not always if chronic

Vertebrobasilar TIA symptoms:
1 Decrease perfusion to posterior fossa
2 Dizziness, DB vision, vertigo, numbness of ipsilateral face and contralateral limbs, dysarthria, horseness dysphasia, projetive vomiting, headaches, drop attacks.
Assessing the initial steps of COMA
1. ABCs – vitals
2. Stabilize cervial spine and asses the patients for signs of underlying causes of trauma
2. Assess level of consciousness using glascow coma scaleRapid motor examination
Brainstem reflexes – round, symmetric, reactive (intact midbrain) whereas if assympetric (uncal herniation)

lab tests – CBC, Calcium, Bun/cr, ABG, CT/MRI

What is progressive supranuclear palsy

#1 = middle aged and elderly males (>50YO)

Degenerative condition involving the bstem, BG, cerebellum leading to bradykinesia, limb rigidity, cognitive decline, follows progressive course

NO resting tremor but postitive for opthalmplegia

Clinical features of a thrombotic stroke v. embolic stroke

Thrombotic = rapid/stepwise; awakens from sleep with neuro defects

embolic = rapid, mazimal defects initially

Good TCA for parkinsons disease
Horners syndrome
clinical feature
Site: pregang = central lesions/postgang = distal to SCG
features = anhydrosis, ptosis, MIOSIScauses: idiopathic, pancoast tumor *UPPER LOBE); ICA dissection, brainstem stroke, neck trauma

Diagnosis of alzeimers dementia
-clinical diagnosis of exclusion
-CT scan or MRI showing diffuse cortical atrophy with enlargment of ventricles strengthens the DxACE inhibitors have decreased levesl of ACh. Avoid anticholinergic treatment use DONEPOIL( > tacrine)

Clinical approach to dementia
1. Patient Hx
-ask patients and their family members about the nature of onset specfic eficits, physical symptoms, cormorbid conditions2. PE
-focus on through neurologic examinatino
-gait aalysis shed light on movement disorders with mass lesions and non pressure hydrocephalus.

3. LABS and imaging
-get CBC with DIFF to look at electrolyes, liver enzymes (asterixis abnormal gait hepatic encephalopathy) and diff to r/o infection. Get chem panel, thyroid, B12 for posterior column deficit folate, VDRL (for syphilis), HIV screen *viral load(, CT scan to look for SAH/ICH

What is the first imaging study that should be ordered if stroke is expected:
CT scan
1. Ischemic stroke (85%)
2. Hemorrhagic stroke (15%)-identifies 95% of all SAH and all bleeds > 1cm; identifies abscess, tumor; subdural v. epidural hematoma
60 YO white male with worsening confusion and memory loss for three weeks. Muscle twitching and gait problems present but no fever headache or GU problems. Doesnt drink or smoke – normal pulse, pressure and temp. Poor grooming and disorientation noted. Nystagment and postivie extensor plantar response bilaterally on physical exam. Crit is 40%, WBC are 6k, platelets are 160k. Noncontract head CT = normal. EEG shows periodic sharp waves. Most likely dx:
Creutzfeldt Jakob syndrome – why?
1. Fatal neurodegenerative dz caused by PRIONS
2. Suspect in elderly patient with RAPIDLY progressive:
PERIODIC HIGH VOLTAGE COMPLEXES ON EEG.3. These are the top diagnostic clues. EEG pattern of periodic bi or tiphagic sharp wave complexes is typical for CJ syndrome. Majority is sporatic and not genetically inherited (80%)

CLinical characteristics of huntingtons

chorea; face/head/neck/tongue/trunk/extremities

change in behavior – irritable/change in personality antisoail behavior, depression, OCD

decreased mentation-progressive dementia < 50YO (~90%)

GAIT-unsteady and irregular

What happens if cerebral perfusion pressure is compromised due to increased ICP?
1. Loss of autoregulation thus asodilation is evident in cerebrum
2. Vasogenic edema occurs as fluid is lost into extravascular space
3. Systemic BP becoes sole determinant of cerebral blood flow
Shy-drager syndrome is =
Parkinsonian symptoms + autonomic insufficiency
Mimics coma because patients paralyzed although spares muscles required for respiration, blinking, vertical eye movement
-patients fully aware of surround and can feel pain
-caused by?
“Locked in syndrome” – infarctions/hemorrhage of ventral pons
Hypertension, bradycardia, and respiratory irregularity
CUSHINGS TRIAD – due to elevated ICP causing a low HR which causes peripheral vasocontriction and hence the HYPERTENSION.
CNS tumors capable of resection:

1. Meningiomas/pituitary adenomas/schwannomas

The most common primary CNS tumor (GLIOMAs – astrocytomas and oligodendrocytes) CANNOT be resected

What are the predisposing factors of lacunar strokes?
#1 HTN in 80-90%
#2 DM Type II
#3 Narrowing of lumen due to thickened vessel walls

Intraparenchymal brain tumor related to immunosupression and encountered especially in recipients of transplants organs and in patients with AIDS

-survival rates

Primary lymphomas survival < 2 years
How is tourettes syndrome treated?

if symptoms affecting patiets QOL then patient education is important

1. Clonidine – CNS a2 agrenergic acting centrally to decrease CNS by negative feedback
2. Pimozide – antipsychotic drug like chlorpromazine (HIGH POTENCY – causes tarditive dyskinesia)
3. Haloperidol

What is status epilepticus?
Prolonged sustained periods of unconsciousness with persistant convulsive activity.
-Medical emergency = 20%
D/T poor anticonvulsive activity, alcohol withdrawal and intracranial infection/neoplasmsTreatment: ABC, IV DIAZEPAM, IV PHENYTOIN, 50mg DEX. If resistance – phenobarbitol

Symptomatic therapy for MS:
1. BACLOFEN for muscle spasms
2. CARBAMAZEPINE/GABAPENTIN for neuropathic pain
Prognosis of GB syndrome

signs of recovery within 1-3 weeks after onset. If >6weeks, chronic replapsing course more likely and prognosis is less favorable

5% die from respiratory failure, pnemonia, arhythmias

Treatment of acutely altered mental status
-Intact brainstem
-Intact cerebrl cortexTreatment underlying cause; then haloperidol
Arousal dependent upon = agitation/psychotic
Cognition dependent upon = delirium behavior

Primary CNS tumors in adults:
Most common: GLIOMAS (~50%); MENINGIOMAS (~25%)
Treatment of syringomyelia
Diagnosis with MRI
-surgical syringosubarachnoid shunt
Sign of basilar skull fracture
1. Raccoon eyes – periorbital ecchymoses
2. Battle signs – post auricular eccymosis
3. Hemotypanium
4. CSF rhinorrhea/otorrhea
When should ASA be administered to stroke patients with an acute stroke
within 24 hrs onset
-no admin if thrombotic therapy, inc risk of ICH
How is ICH diagnosed?
CT Scan is 95% ICH
-ischemic -dark
-hemorrhagic -lightcoagulation panel and platelets to evaluate bleeding diathesis

EMG and NERVE conduction studies?
EMG measures contractile properties of skeletal muscle
-LMN lesions fibrillations/fasciulations at rest
-myopathy – no electrical activity at rest, decreased amplitude with muscle contractionNC studies = demyelination will slow nerve conduction velocity (MS/GB); repetitive stimulation causes fatigue (MG)

Treatment of strokes is ______. Once stroke has occurred, goal is to?

Prophylactic – prevent future strokes

1. control risk factors (HTN/HM/SMOKING/HYPERCHOL/OBESITY)
2. ASA
3. Surgery (carotid endarterectomy in patients with CAS)

Major complication in patients POST SAH?
#1 Vasospasm in 50% of patients
#2 rereupture of same vessel (30%)
#3 hydrocephalus; elevated ICP, use mannitol
#4 seizures (blood irritatnt to it)
#5 SIADH = hypovolemia with hyponatremia
Pure motor lacunar infarct:
internal capsule
Meningial carcinomatosis
Cancer that metastasizes to meninges via the bloodstream
-may cause focal deficits depends on the involved locations
-CSF = malignant cells, inc protein, inc lymph, dec glucoseRx: intrathecal chemotherapy

Interferon therapy for MS:
1. Recombinant interferon B-1a, recombinant interferon B-1b, GLATIRAMER acetate have shwon a reduction in relapse rates 37%, 33%, 29%
2. Interferons can cause flulike symptoms
3. Interferon therapy started early in course of disease before disability becomes irreversible
Pupillary findings of patients with ICH?
Causes of seizures
1. What are the 4 M’s and 4 I’s?
Metabolic – decreased Na2+, H2O intoxication, hypo.hyperglycemia, thyroid storm (thyrotoxicosis where elevated T3/T4 must be treated with either PTU or radioactive iodide therapy).
Mass lesions – brain mets, primary tumors
Missing drugs – noncomplicance/acute withdrawal from alcohol, benzo and barbs
Miscellaneous – pseudoseizureIntoxication – cocaine/lithium/lidocaine/theophylline
Infection – septic shock
Ischemia – stroke/TIA
Increased ICP – d/t trauma

Partial seizures: Is consciousness impaired?
IF N – then simple partial and treat with phenytoin and carbamazepine
IF Y – then complex partial and treat with phenytoin and carbamazepine
NPH is suspected in any patient (normal pressure hydrocephalus) with


CT will show ventricular enlargement

What are the secondary insults associated with head trauma?
1. hypotension (<90/60)
2. hypoxia (<60mmHg) 3. Hypercapnia (>50 mmHg)
4. Increased ICP
5. Intracranial mass effect – epidural hematoma, SD hematoma
6. anemia = blood loss in trauma

coup = injury at the site of injury

contracoup = injury at the site oppositeto point of impact

1. Most common primary CNS neoplasm (80%)
2. Exclusive in the cerebral hemisphere
3. Features:
-tumors infiltrate brain with indistinct boundary
-tend to spread along WM tracts and may cross the corpus callosum into opposite hemisphere
-poor prognosis
-glioblastoma multiforme is worst prognosis
What anticholinergics are used to treat the resting tremers associated with parkinsons
What are 2 implications associated with head trauma
1. Irreversible damage
2. Secondary insults
Which arteries are responsible for lacunar strokes?
Small branches off of the MCA that make up the COW and the basilar and verteral arteries. Once occluded, small infarcts result. These heal and form “lacunes”
Most common site of SAH?
Junction of the A communicating artery with ACA
Junction of the P communicating artery with ICA
Bifurcation of the MCA
Most important regulator of cerebral vessel dilation/contriction:
Increased PaCO2 because it results in vasodilation and subsequently causes cerebral vasodilation
Which is most sensitive for ischemic strokes (MRI or CT)?
MRI > CT because identifies all infarcts early in comp to CT however not preferred in ED because taes long time to perform and not good in unstable patients
COMA – general characteristics
Decreased level of consciousness to extent that patients unresponsive to stimuli:
1. Structural brain resins causing come = bilateral
2. Global brain dysfunction
3. Conversion d/o and maligering difficult to diagnose from COMA

In symptomatic pateints, what is the benefit of patients to endarterectomy of carotid?

Recommendation if asymptomatic?

> 70% if carotid stenosis

If asymptomatic, dec atherosclerotic risk factors and use of ASA are recommended, prevents embolic strokes with ASA and prevents lacunar strokes with HTN.

Hereditary causes of muscle weakness?
1. Mitochondial d/o – maternal inheritance (RED RAGGED FIBERS)
2. Glycogen storage d/o like mcardles dz or glycogenphosphorylase deficiency
3. DMD, Beckers MD, myotonic MD (CTG trinucleotide repeat)
Pure sensory infarct of lacunar arteries
TOP causes of SAH
1. Saccular aneurysm rupture (ADPKD1/ADPKD2)
2. Trauma
3. AV malformation
Treatment for head trauma
1. ABC
2. Lower ICP
-reverse trendelenburg position, if spine cleared, elevate head of bed.
-intubate (+) hyperventilation is effective in decreased ICP. Hyperventilation causes decreased PaCO2 and decreases vasodilation
-maintain PaCO2 level at 30-35
3. Mannitol
SAH characteristics
Mortality ratio is HIGH (40-50%) @ 30 days
-saccular aneurysms occur at bifurcations of arteries at the COW
Normal cerebral perfusion pressure?
-how does pupil size indicate increased ICP?In the ICU, what is the goal of managment?

>50 mmHg
-bilateral fixed and dilated pupils suggest diffusely increased ICP-keep the mean arterial pressure > 80 and ICP <20. Ensures a cerebral perfusion pressure of at least 60 mmHg

Medical emergency that can occur in patients with MG?

MG crisis is a 15% likelihood where the disaphragm and intercostals fatigue in respiratory failure

Treatment : PEEP with mechanical ventilation

Ataxia: gait instability, loss of balance, impaired limb coordination
1. Alcohol intox (anterior vermis of cerebellum)
2. Vitamin B12/thiamin B deficiency
3. Cerebellar infarct
4. Demyelinating disease (MS, GB, AIDS, tertiary syphilis)
5. Inherited causes
-freidrichs ataxia (frataxin gene – GAA trinucleotide repeat)
-ataxia telangiectasia
How might brain herniation be treated by
-neuro consult
-lower ICP
Causes of an acute confusional state (delirium)
P – postoperative state (compounded with treatment for pain)
D – dehydration and malnutrition
I – infection (sepsis, meningitis, encephalitis, UTI
M – meds/drug intoxs (TCAs, cortisteroidsm anticholinergic)
M – metals (heavy metal exposure)
W – withdrawal states form OH + benzos
I – inflammatory fevel
T – trauma burns
How are CNS neoplasms diagnosed?
MRI without GADOLINUM = #1
BRAIN BIOPSY = only definitive way to diagnose a brain tumor and determine the specific type
Ataxia, nystagmus, dec vibration sense and proprioception (GAA)
Friedreichs ataxia
-autosomal recessive inheritance by youdn adulthood
Average time of death from onset of A.D.
5-10 years
1. Stage (early) = mild forgetflness; imparied ability to learn new; decreased erformance at work, decreased concentration; change in humor/change in personality
2. Intermediate = memory decline; denial may be present; visual disturbance of condition; getting lost in familiar place and difficult following direction
3. Later assistance needed with ADL; paranoid delusions and hallucination
4. Advanced disease – complete debilition and dependent of others (bowel and bladder)
What is VHL disease
-cavernosis hemagiomas of brain and brain stem
-renal angioma
-cysts in organs
-increases the risk of RCC
Diagnosis of patient with primary seizure
1. EEG with neuroconsult
2. Anticonvulsant agent
3. Risk of recurrence if normal EEG
– Low 15% year 1
4. If abnormal – then risk is 41% in first year
General seizures: Are they convulsive?
If Y – TONIC CLONIC or MYOCLONIC then treat with phenytoin and carbamazepine
If N – then absense and treat with ethosuxamide and VALPROIC acid
What are the risk factors regarding ischemic stroke (cerebral infarction)?
Most important:
1. Age
2. hypertensionothers:
1. Smoking
2. DM
3. Hyperlipidemia
4. Atrial fib
5. CAD
6. Family hx
7. TIA history
8. Carotid bruits

IF MCA is occluded, what symptoms would be expected?
Contralateral hemisensory hemiparesis of body
Asphasia if dominant hemisphere (BROCAS)
Apraxia, contralateral body neglect and confusion if nondominant hemi involved
Types of dementia
1. AD — 66% of all cases of dementia
2. Vascular dementia = multi-infarct dementia; BINSWANGER DISEASE
3. Space occurping lesions = brain tumor, chronic SDH
4. NPH – triad of dementia, gait distubrance, incontinence (wacky, wobbly, wet)
5. Dementia with lewy body
6. Pick’s disease = identical to AD but had pick bodies
Tourette’s syndrome
Obsessive compulsive disorder
onset < 21YO
autosomal dominant inheritance pattern
not all have “TICS”
not all experience involuntary swearing
Most important risk factor for dementia
preservation of consciousness with deterioration of intellectual function
What treatment should be used to dec risk of rerupture of SAH for vasospasms?
CCB – nifedipine

Treatment of coma if:

Narcotic OD
Alcoholic coma
Identify and treat herniation

Supplemental O2
Thiamine b4 glucose
lower ICP if ICH
Treatment used to decrease ICP in patients with increased ICH/SAH risk?
Treatment used to decrease BP in patients with iCH/SAH?
Decrease ICP = mannitol (osmotic agent) – only if inc ICP
Decrease BP = nitroprusside if BPsys>160-180 or BPdys>105
Hemorrhagic stroke (ICH/SAH) clinical findings
1. Abrupt in onset of focal neuro deficit that worsens (30-90 min)
2. Altered level of consciousness, stupor, coma
3. Headache, vomiting
4. Signs of increased ICP
Origins of embolic stroke
1. Heart (most common) – embolism of mural thrombus, atrial fibb
2. Internal carotid artery (ICA)
3. Aorta
4. Paradoxical = embolit that arises from blood clots in perhpheral vein that passes from RH to LH by ASD, VSD, PFO or pulmonary AV fistula and GOES to brain
Treatment of parkinson’s disease
-no cure for parkinsons
-delay disease progression
-use symptomatic treatment#1 = carbidopa-levodopa (SINEMET)

What are the classes of ischemic strokes (85%)
1. Transient ischemic attack (TIA)
2. Reversible ischemic neurologic deficit is the same as TIA except the duration of symptoms lasts longer than 24 hours but resolves in < 2 weeks
3. Evolving stroke (worsening)
4. Completed stroke (maximal deficit has occured)
What is the cerebral perfusion pressure?

Mean arterial pressure minus ICP

CPP = MAP – ICP want to be <60

How is MG diagnosed?
1. AChR antibody test is the test of choice
-20% AB (-)
2. EMG decreases response to stimulation of motor nerves
3. CT scan of thorax to r/o thymoma (10-15% of MG patiets; thymus histologically abnormal in 75% of patients)
4. Edrophonium (tensilon test) – achE treatment causes elevation in smptoms
Most common brain mets:
GI TRACT(prostate CA, non-melanoma and esophageal CA will never met)

Treatment of ICH/SAH
1. ICU admission
2. ABC airway management
3. BP reduction – inc BP and inc ICP and can INC bleeding.
4. Hypotension can also lower blood flow so must slowly decrease BP
-use nitroprusside
How is MS treated?
1. Short term therapy
2. Longterm therapy

ST: (1) high dose IV corticosteroids can shorten an acute attack; these do not change course of MS. (2) Theraprutic plasma exchange (TPE) for steroid refractory acute demyelinating attacks at 42%

-interferon therapy
-nonspecific immunosuppressive therapy like cyclophosphamide should be reserved for rapidly progressive disease

4 causes of ischemic stroke:
1. Embolic stroke
2. Thrombic stroke
3. Lacunar stroke
4. Nonvascular causes (decreases CO, anoxia – global ischemia and infarct)
First line agent for AD
Donepozil (newer AChEi than tacrine)
-advantages over tacrine include
-1 per day dosing with better and decreased side effects
-tacrine 4x/day another AChEi
-vitamin E
-may slow dz progression
What is the diagnosis if patient history is unclear of seizure d/o
1. CBC, electrolytes, blood glucose, LFT, RTF and serum Ca2+ and UA
2. CTs of the head
3. MRI with then without GAD
4. LP and cultures
Poliovirus = myelitis
Ant horn cells and MN of the SC and BStem
-LMN involvment (HYPOREFLEXIA)
-asymmetric muscle weakness
-absent DTR, flaccid m and normal sensation
-+/- bulbar involvement (IX/X)
Abnormal pupillary light reflex- structural intracranial lesions like ____ or _____; drugs including (____,______) and anoxia can result in change.

hemorrhage, mass

morphine; atropine-like agents

Types of seizures
Partial v. general
Risk factors for CVA in young patients?
Sickle cell anemia
Hypercoaguability states (protein C/S deficiency, increases clotting)
Antiphospholipid AB syndrome
vasocontrictive drug use (cocaine, amphetamines-methamphedamine, ephedrine)
polycythemia vera (myeloproliferative dz)
What is binswangers disease?
vascular dementia with insidious onset due to diffuse subcortical white matter degeneration, mst commonly seen in patients with londstaning HTN and atherosclerosis
How is SAH diagnosed?
1. CT scan noncontrast – identifies hemorrhagic strokes
2. Lumbar puncture if CT scan unremarkable or (-) with high suspician. LP is diagnostic; if (+) for blood, then hallmark for SAH. If xanthochromia (yellow) in CSF – also diagnostic
3. Cerebral angiogram once diagnosed to detect site of bleeding of the SAH
What is “subclavian steal” syndrome?
Treatment is by surgical bypass
1. Stenosis of subclavian before the vertebral artery
-dec cerebral blood flow (stolen) from basilar system
-causes symptoms of vertebral basiliar arterial insufficiency
-claudication of upper arm BP in Larm
Medical emergency involved with GB?
Rapidly progressive respiratory failure can occur within horus
-if suspect GB syndrome
-immediately admit patient to the hospital for monitoring
Cranial nerves affected by schwannoma
1. Start @ CN VIII, CNV and CNVII
-hearing loss is usually the first symptoms
-other symptoms may include tinnitis, loss of balance, nystagmus, and motor and sensory deficits involving the face
Ecclampsia v. pre-eclampsia and the treatment?

Ecclampsia = HTN in pregnancy with seizures

Treatment = MAGNESIUM infusion

Two main causes of carotid bruits
1. Murmur referred from the heart
2. Turbulence in the ICA (serious stroke risk)
Treatment of RA?
1. Principles of treatment
-goals of treatment are to prevent or halt joint destruction and to come as close to clinical remission as possible while avoiding the toxicity of nti-RA medication
-treatment must be individualized to the patient.
-a treatment regimen that works for one patient may not work for another.2. Exercise helps to maintain range of motion and muscle strength

3. SYmptomatic treatment
-NSAIDs are the drugs of choice for control of pain. They play an important role in controlling inflammatoin and should be part of most treatment regimens
-corticosteroids low dose) – use these if nSAIDS do not provide adequate relief.
-short term treatment may be appropriate
-avoid long term high dose steroids – these can be detrimental
-longterm, low dose corticosteroids may actually alter the course of the disease (have been shown to diminish radiographic progression) – more sudies are needed before this can be considered a disease-modifying drug.

Temporal arteritis

General characteristics:

aka: “Giant Cell arteritis”
-vasculitis of unknown cause; typical patients is >50 YO and twice as common in women as in men
-temporal arteries are most frequently affected but it may involve other arteries such as the aorta or carotids
-associated with increased risk of aortic aneurysm and aortic dissection
Diagnosis of reactive arthritis
Synovial fluid for analysis – this r/o infection and crystals
How is the diagnosis of wegeners made?
chest radiograph is abnormal (nodules or infiltrates)
-laboratory findings: high ESR, anemia (normochromic/normocytic)
-hematuria: positive CANCA in 90% patients both sensitive and specific.
-Thrombocytopenia may be presentCONFIRMATION of dx: LUNG BIOPSY

Clinical features of takayasu’s arteritis
-Consitutional symptoms: fever, night sweats, malaise, arthralgias, fatigue
-Pain and tenderness over involved vessels
-Absent pulses in carotid, radial or ulnar arteries, aortic regurgitation may be present
-Signs and symptoms of ischemia eventaully develop in areas suppled by involved vessels.**TREATMENT: Steroids; treat HTN with antiHTN meds; surgery or angioplasty if recannulation of vessel is required. Can use bypass

How is RA diagnosed?

High titers RF are asociated with more severe disease and are generally nonspeific. RF is eventaully presnt in 80% of patients with RA (may be ansent early in the diese) but it is also present in up to 3% of the healthy population.

1. ELevated ESR, CRP
3. Normocytic normochormic anemia (anemia of chronic disease)

-loss of juxtaarticular bonemass (periarticular osteoporosis) near the giner joints
-narrowing of the joint space (due to thinning of the articular cartilages) is uauly seen late in teh diases
-bone EROSIONS at the margins of the joint

Features that are unique to dermatomyositis?
1. Helicotropic rase (butterly) around eyes, bridge of nose, cheeks
2. Gottron’s papules – papular, erythematous, scaly lesions over the knuckles (MCP, PIP, DIP)
3. V sign – rash on the face, neck, anterior chest
4. Shawl sign – rash on shoulders and uper back, elbows, and knees
5. Periungual erytema with telangiectases
6. Subcutaneous calcifications in chidlren can be extremely painful
General characteristics of ANK SPONDYLITIS
-strong association with HLA B27
-3x > males than in females
-look for pos famil hx of ank spondylitis, inflammatory bowel dz, psoriasis
-bilateral sacrolitis is a prereq for mkaing the diagnosis.
-onset in teenage years or early 20s
-characterized by fusion of the lumbar spine that ascendings to the cervical area.
CLincal features of Polymyalgia rheumatica
Hip and shoulder muscle pain (proximal)
-often starts abruptly
-stiffness in regions after period of inactivity is the most prominent symptoms
-pain occurs on moveemnt; muscle strength is normal
-profound morning stiffness is commonConsitutional sypmtoms are present malaise, fever, depression, weight loss, fatigue

Joint swelling
-up to 20% of patients have synovitis in knees, wrist, hand joints (can be confused often with RA)
-synovitis and tenosynovitis around the shoulder may lead to rotator cuff tendonitis or adhesive capsulitis

Signs and symptoms of temporal arteritis (if present)

Diagnosis of Temporal Arteritis
ESR elevation (but can be normal)
-biopsy of temporal artery has sensitivity 90%
What is the recommended treatment for acute gout?
1. bed rest
3. Colchicine – an alt for patients who cannot take NSAIDs or did not respond to NSAIDS; do not useif renal insufficiency or cytopenia
4. Corticosteroids (7-10d course)AVOID ASA AND ACETOMINOPHEN

What is the treatment for SLE?
avoid sun exposure because ti can exacerbate cutaneous rashes
NSAIDS – for less severe symptoms
local or systemic corticosteroids if for acute exacerbations
cytotoxic agents like cyclophosphamide for active glomerulonephritis
monitor the following and treat appropriately (renal dz and HTN)
Sjogrens syndrome has an increased risk of __________ ____. What is the most common cause of death?
non-hodgkins lymphoma
Gout v. Avascular necrosis

Gout: uric acid deposition in joints. Pain. Great toes, ankles, wrist, elbow effected. Lumby bumby appearance on plain film; punched out lesions with overhangiing rim of corticol bone “rat bite”

Avacasular necrosis: 2/2 bone destruction with lack of blood supply. It is a complication of steroid use, trauma, lupus, SCD, number of oter processes. Affects the proximal and distal femur most often. Pain is the msot common symptom

Vasculitis can be classified into size of vessels:
Large vessel: takayasu;s, TA
Medium vessel: PAN, Kawasakis, Wegeners, Churg Strauss, MPA
Small: HSP, HS vasculitis, Behcets syndrome*blood vessels are inflammed and vascular necrosis results. Findings depend upon the size of the vessel involved and THEREFORE the location of involvement will indicate the organ of ischemia.

Amyloidosis is probable to cause a nephrotic like picture in patients with which clinical predispositions?

1. Rheumatoid
2. Enlarged kidneys
3. Hepatomegaly


-renal amyloid deposits that show apple-green birefringence under polarized light after staining with Congo red
How does Baker’s cyst present? What does it consist of?
Result of excessive fluid production by an inflamed synovium as occurs in cases of rheumatoid arthritis, osteoarthritis and cartilage tears. The excess fluid accumulates in the popliteal bursa which expands, creating a tender mass in the popliteal fossa. Bake cysts bursa and release contents into calf resulting in a “DVT” appearance.
What are the variants of RA?
1. Feltys syndrome: anemia, neutropenia, splenomegaly, and RA
2. Juvenile RA: begins before 18 years of age. Extra-articular manifestatins may predominat (Stills disese) or arthritis may predominate
10% of patients with polymyalgia rheumatica also have ___ ___ whereas up to 40-50% of patients with ____ ____ have coexisiting polymyalgia rheumatica.
Temporal arterities
Temporal arteritiesThus half of patients with TA have PR, but <10% pts with PR have TA

AA female, photodistriuted skin rash, artralgias. Low range proteinuria and abnormal urinary sediment. Biopsy findings are consistent with focal proliferative glomerulonephritis. COMPLETE CBC shows:

dec erythrocyte
dec platelet
dec leukocyte

Hematological findings?

pancytopenia 2/2 SLE. Formation of autoAB against blood cells form a type II hypersensitivity reaction

Sjogrens syndrome is an autoimmune disease most commonly seen in women. _________ infiltrate and destroy the lacrimal and salivary glands. This is a multisystem disease (involves the —-,—-,—,—,—

WHat is primary v. secondary sjogrens?

-skin, liver, lungs, thyroid, vesselsPrimary sjogrens syndrome: dry eyes, dry mouth, lymphocytic infiltration of the minor salivary glands (on histology); patients do not have another rheumatologic disease.

Secondary sjogrens syndrome: dry eyes and dry mouth along with a connective tissue disease (RA, systemic sclerosis, SLE, polymyositis)

Prognosis for SLE?
Most patients do not acheive normal life expectancy.
-with proper treatment, severe organ damage can be prevented and symptoms controlled in many cases
-the most common causes of death are oppourtunistic infections and renal failure
-fatigue, malaise, fever, weight loss
-butterfly rash, photosensitivity, discoid lesions *erythematous eevated patch); raynauds,
-joint pain, athritis (inflammatory AND symmetric but NON erosive like RA)
-pericarditis, endocarditis (libb man sacks NBSE), myocarditis
-pleuritis, pleural effusion, penomitis leading to fibrosis, pulm HTN (rare)
-hemolytic anemia with anemia or retics of chronic dz, leymphopenia, trombocytopenia
-proteinuria > 0.5 g/day with nephrotic syndrome; cellular casts; GN (may have hematuria); azotemia, pyuria, uremia, HTN
-immunologic; impaired immune response due to many factors including autoAB to lymphocytes abrnomal T cll function and immunosuppressive meds
What is the pathogenesis of GOUT?

1. Increased UA production –> hypoxanthine-PP synthetase deficiency (lesch nyhan); phosphoribosyl pyrophosphate synthetase overactivity; increased turnover assoicated with a number of conditions, including cancer chemotherapy, chronic hemolysis, and hematologic malignancies.

2. Decreased excretion of UA (accts for 90%)
-renal dz; NSAIDSs/diuretics; acidosis

Treatment of temp arteritis once diagnosed
1. HiD prenisone early to prevent blindness
2. Start rx immedicately, dont wait for biopsy results
3. If dz confirmed, continue rx for 4 weeks the taper gradually. Maintain therapy for 2-3 years. Relapse is likely if stop prednisone early.
4. F/u with ESR levels to monitor effectiveness of treatment
5. Visual loss in one eye may be temporary or permanent.
6. Even is untreated the disease is self limiting in most patients but the vision can be a permanent issue
What is GOUT?

Inflammatory monoarticular arthriti caused by crystallization of monodosium urate in the joints. Hyperuricemia is a hallmark of the dz but it can present without indication of gout.

90% of men over 30YO most likely to be diagnosed. Women are not affected until post menopause

Polymyalgia Rheumatica

Major association:

autoimmune process (likely) with a genetic link (HLADR4) most common in elderly patients – rarely before age 50 but usually dominant in 70YOF.
-cause is unknown
-self limited disease (1-2) years!***
Diagnosis of FMS
1. Diagnostic criteria: widespread pain including AXIAL pain for >3 months, pain in at least 11/18 tender points
2. Before confirming FMS dx, must r/o myofascial syndromes, rheumtoid, PR, SLE, AS, chronic fatigue syndrome, lyme disease, hyPOthyroidism, polymyositis
Diagnosis of PAN
-bipose of involved tissue or mesenteric angiography
-high ESR
-pANCA pos
-test for fecal occult blood
Wegeners granulomatosis (granulomas with polyangiitis) clinical features?
upper respiratory symptoms (sinusitis) purulent or bloody nasal discharge
-oral ulcers may be painful
-pulmonary symptoms (cough, hemoptysis, dyspnea)
-renal involvement (GN – may have rapidly progressive renal failure)
-eye dz *conjunctivitis/scleritis)
-MSK arthralgias, myalgias
-tracheal stenosis
When should uricouric agents be admin to patients with GOUT?
1. Uricosuric drugs (probenecid, sulfinpyrazone) if the 24hr ua level is < 800 mg/day then this indicates an undersecretion or URATE. THese durgs increase renal excretion of UA and should be used only in pt with normal renal function. 2. Allopurinol – is a xanthine oxidase inhibitor that decreases UA synthesis – if the 24hr uric acid is >800 m/day this indicates overproduction. Never give this for acute gout; it maks it worse. Use once-daily dosing. IT is well tolerated
Associated findings with dermatomyositis?
1. Vasculities of the GI tract kidneys lungs and eyes (more common in children)
-increased risk of malignancy in oler adults (lung, breast, ovary, GI tract, and myeloproliferative disorder)
-once dermatomyositis is diagnosed make an effort to uncover an OCCULT MALIGNANCY. Dermatomyositis is associated with malignancy and will remit once tumor removed.
What is the treatment for Sjogrens syndrome?
1. Pilocarpine (enhances secretions)
2. Artificial tears for dry eyes
3. Good oral hygiene
4. NSAIDS, steroids for arthralgias, arthritis
5. Patients with secondary Sjogrens syndrome- therapy for connective tissue disease
HLA associations with rheumatic diseases: RA
Prognosis of CHURG STRAUSS
poor with a 5 year survival of 25% (death is usually due to cardiac or pulmonary complications) with treatment (steroids), the 5 year prognosis improves to 50%
Normal synovial fluid analysis:
Clear fluid
<200 WBC
<25% PMNs
What cervial spine involvement is associated with RA?
Cervical spine involvement is common at C1-C2 subluxation and instabiliy, but it is less common in the lower cervical spine.
-instability of the cervial spine is a potentially life-threatening complication of RA. Most patients do not have neurologic involvement, but if they do, it can be progressive and fatal if not treated surgically.
-this is seen in 30-40% of patients
-all patients with RA should have cervical spine radiographs before udnergoing any surgery (due to risk of neurologic injury during intubation)
what does the term “undifferentiated” spondyloarthropathy used to indicate?
when a pt has features of reactive arthritis but there is no evidence of previous infection (in the FI or GU tract) and the classic findings of reiter’s syndrome are absent
What is the most common finding (usually present at diagnosis) of lupus? What are the types?
Lupus nephritis
1. Type 1 – 5 % – minimal lesions, renal failure is rare
2. Type 2 – 20 % – mesangials lupus GN – rarely renal failure
3. Type 3 – 25 % – focal proliferative GN -renal failure is uncommon
4. Type 4 – 40 % – diffuse proliferation GN – renal failure is common
5. Type 5 – 10% – membranous GN – renal filures is uncommon
HLA associations with rheumatic diseases: HLA DR2 and DR3
Precipitation of an acute gouty attack
decreased in temp
excessive alcohol intake
Takayasu’s arteritis
General characteristics
1. Most common to young asian females
2. Vasculitis of aortic arc and its major branches – potentially leading to stnsosis or nrrowing of the vessels
3. Diagnosed via ateriogram
Buergers Disease (aka Thromboangiitis Obliterans)
Occurs mostly in young men who smoke cigarettes
-acute inflammation of small and medium sized arteries and veins, affecting arms, and the legs
-can lead to gangrene
-clinical features include ischemic claudication: cold, cyanotic, painful distal extremities, parethesias of distal extremities and ulceration of the digits.
-smoking cessation is mandatory to reduce progression
What organisms are most commonly associated with REACTIVE arthritis?
Salmonella, Shigella, Campylobactor, Chlamydia, Yersinia
What is the diagnostic criteria for POLYMYOSITIS?
If two of first four –> possible polymyositis
If three of first four–>probably polymyositis
If all four –> definite polymyostis
-symmetric and proximal muscle weakness
-elevation in serum CPHOS
-EMG findings of myopathy
-BIOPSY evidence of myositis
-caracteristic rash of dermatomyositis
What is BEHCETs syndrome?
An autoimmune, multisystem vasculitis disease, cause is unknown
-clinical features: recurrent oral and genital ulcerations that are usually painful, arthritis in the nees and ankles, eye involvement (evwitis, optic neuritis, iritis, conjunctivitis), CNS involvement (meningoencephalitis, intracranial HTN, fever and weight loss
-Diagnosis: made by biopsy of involved tissue – no labs are helpful
-Treatment – steroids
In RA, changes in the joint are usually more extensive than in OA because the entire synovium is involved in RA. Notes that ______ is a characteritic of OA and NOT that of RA.
Prophylaxis for gout?

1. Wait until pt has two acute gouty attacks before starting therapy. Two attacks per year sometimes used as a rough guidline. This is because the second attack may take years to occur if at all, so the risk to benefit ratio for prophylactic medications (allopurinol) is not favorable after one gouty attack.

2. When given prophylaxis, add either colchcine or NSAID for 3-6 mo. The colchicine or nSAID can be d/c and the pt can remain on the uricouric agent or allopurinaol indefininely.

3. The choise of whether to use uricosuric drugs or allopurinaol depends on how much UA is exceted in the urine in a 24 hour period.

What is the diagnosis of Sjogrens?
ANAs are pressent in 95% of the cases –> 50-75% of patients with seondary disease
-Ro (SS-A) present in 55% of patients, and La (SS-B) Abs present in 40% of patients.
-nonspecific findings: increased erythrocyte sedimentation rate (ESR), normocytic, normochromic anemia, leukopenia (normal ESR 10-20)Patietns with antibodies to Ro (SSA) are at increaed risk of having a child with neonatal SLE (with congenital heart block).

Which cardiac abnormalities are involved with RA?
Pericarditis, pericardial effusions, conduction abnormalities, and valvular incompetence
General characteristis:
1. Population
2. Age:
3. Key to dx:
1. Adult women 80-90% of cases
2. Chronic nonprogressive course with waxing and waning in severity; many patients improve with time
3. Key to dx: multiple TRIGGER points (points that are tener to palpation)
-eighteen characteristic locatoins have been identified, including OCCIPUT, NECK, SHOULDER, RIBS, ELBOWS, BUTTOCKS, KNEES
4. Etiology is unknown however somatization is still NOT a proven cause
What the clinical features of FMS?
-stiffnes, body aches (MSK); fatigue
-pain is constant and aching, and is aggreavates by weather changes, stress, sleep deprivation, and cold temperatures. Worst in the morning
-sleep patterns disrupted and sleep is unrefreshing
-anxiety and depression common
What are the clinical features of Sjogrens?
dry eyes –> burning, redness, blurred vision
dry mouth
arthralgias, arthritis, fatigue
many extraglandular manifestations (more common in primary disease) such as chronic arthritis, interstitial nephritis, and vasculitis
Pathophys of PAN
PMN invasion of all layers and fribinoid necrosis plus resulting intimal proliferation leading to reduced luminal area which results in ischemia, infarction and aneuryms
What is the treatment for poly/dermatomyositis?
Corticosteroids intially
-taper slowly p to 2 years-immunosuppressive agensts for patients who do not respond to steroids (MTX, cyclophosphamide, chloambucil),
-physical therapy

Common laboratory markers in which disease: ANAs
SLe, Scleoderma, SS, Polymyo
-highly sensitive for SLE but not for the others
Course of SLE
chornic disease characterized by exacerbations and remissions
-malar rash
-joint pain
-most common initial findings with more advanced disease – renal, pulmonary, CV, and nervous system are affected.
What surgical procedures can be done on patients diagnosed with RA?
1. Synovectomy (arthoscopic) decreases joint pain and swelling but des not prevent xray progression and does not imporve joint ROM
2. Joint replacement surgery for severe pai unresponsive to conservative management
Septic arthritis synovial fluid analysis
Turbid and purulent
>50,000 WBC
>70% PMNs
synovial fluid culture positive for most cases of bacterial arthritis except gonococcal (only 25% are positive)
Diffuse versus limited scleroderma:

1. Diffuse: widespread skin involvement; rapid onset of symptoms (skin and other comlications occurs rapidly after osnet of Raynauds phenomenon); significant visceral involvement (fibrosis of internal organs – lungs – heart – gi – kidneys); associated with ANAs but absense of anticentromere antibody; poorer pronosis – 10 year survivl is 40%-65%; peripheral edema, polyarthritis, faitgue andweakness, carpel tunnel syndrome, renal failure can occur, but now rare; interstitial lung disease more common

2. Limited. Skin involvement limited to distal extremities and face and neck – sparing of the trunk; delayed onset, skin involvement occurs slowly after the osnet of raeynauds phenomemon. Threfore the patient ahs a long history of rayneuds phenomenon before other symptoms begin.; visceral involvement occurs LATE (pulmonary HTN rater than fibrosis, ischemi vascular disease; minimal contiustional symptoms); Anticentromere antibody is found in most patients; better prognosis than diffuse form; normal life span is expected in most cases, unless severe pulmonary HTN develops. Crest syndrome is a variant (CREST – calcinosis of the digits, raynauds phenomenon, esophageal motilitty dysfuntion, sclerodactyly of the fingers, telangientases (over the digits and under the nails).

What are the consitutional symptoms can be prominent in RA?
1. Morning stiffness (present in all patients) – improves as the day progresses
2. Low grade fever, weight loss
3. Fatigue can be prominent because this is a systemic disease.
What is the clinical course of SLE?
1. chronic disease charactertized by exacerbations and remissions
2. malar rash, joint pain, and fatigue are the most common intiial findings with more advances disease, renal, pulmonary, CV and nervous systems are affected.
When should one suspect takayasu’s arteritis?
In a young women with:
1. Decreased peripheral pulses
2. Discrepancy of BP (arms) versus (legs)
3. Arterial bruits
Polyarteritis Nodosa (PAN)
1. VAsculitis of medium sized vessels
2. Involves the nervous system and GI – NOTHING TO DO WITH PULMONARY
3. Can be associated with HBV, HIV, and drug reactions
What are the four stages of gout?
1. Asymptomatic hypruricemia
2. Acute gouty arthritis
3. Intercritical gout
4. Chronic tophaceous gout
What are the four classes of rheumatoid arthritis?
1. Patient has an acute attack, which subsides, and never has an attack again (10%)
2. Undulating course, periods of exacerbations and remission (20%)
3. Patient has periods of exacerbations and “remissions” but “remissions” are really improvements, as patients are symptomatic at all times to some extent (65%)
4. Severe, progressive course (5%)
Most common joints affected in PSEUDOGOUT?
THe knees and wrists
-classically MONOARTICULAR but can be poly
What are te clinical features of ank spondylitis?
Low back pain and stiffness (2/2 sacroilitis) limited motion in lumbar spine
-neck pain
-limited motion of cervical spin – occurs later in course of disease
-ethesitis (INFLAMMATION OF THE TENDINOUS INSERTIONS INTO BONE (achilles tendon and surprspinatus tendon most common)
-with spinal involvement, the spine becoes brittle and prone to fracture with minimal truama.
-chest pain and diminised chest expansions
-shoulder and hip pain (most common)
-constitutional syptoms (fatigue, fever, malaise)
-Extra articular involvment (ACUTE ANTERIOR UVEITIS OR IRIDOCYCLITIS is the most commone other features that can occur can be cardiac, renal , pulm
-loss of normal posture as disease progresses
Treatment for acromegaly, carcinomid syndrome and VIPoma
Features of raynauds?
-vasospams and thinked vessels
-leads to digital ischemia
-cold temperatures and stress bring about color changes of fingers, blancing first then cyanotic, then red. (WHITE BLUE RED)cutaneous fibrosis
-tightening of the skin face and extrmeities (sclerodactyly)
-lead to cutaneous contractures, disability and disfigurement

GI involvement
-occurs in most patients (both diffuse and limited)
-findings include dysphagia/reflux from esophageal immobility with delayed GI empting, abdominal distention, and pseudoobstruction. Prolonged acid reflux may eventaully lead to esopageal strictures

Wegeners granulomatosis:
Vasculitis predominantly involving the kidneys and upper and lower respiratory tracts *sometimes other organs
What is antiphospholipid antibody syndrome?
A hypercoaguable state that can be idiopathic or associated with SLE (or other CVD)
-findings include venous thrombosis – PE is a risk
-recurrent arterial thrombosis
-recurrent fetal loss (abortions)
-livedo reticularisLaboratory findings: presense of lupus anticoagulant, anticardiolipin antibody, or bot. Prolonged PTT or PT is not corrected by additing normal plasma

-treatment is long term anticoagulation with an INR 2.5-3.5 (lupus anticoag is the anti-thrombin AB)

What are the clinical findings associated with NEONATAL LUPUS?
skin lesions
cardac abnormalities (AV BLOCK) – transposition of the great vessels
valvular septal defects
What are rheumatoid nodules?
subcutaneous nodules ocer the extensor surfaces (elbows sacrum occiput) that can also occur in visceral structures (eg lungs, pleura, pericardium)
What conditions is ANA elevated?
Polymyositis and dermatomyositis
Drug induced lupus
Common laboratory markers in which disease: ESR

conditions: infection (acute/chornic); malignancy, rhumatiologic diseases, miscellaneous (tissue necrosis, pregnancy)

comments: low sensitivity, and specificity. Major uses: diagnose/rule out inflammatory process and monitor course of inflammatory conditions

Diagnosis of Polymyalgia Rheumatica
clinical diagnosis
-ESR usually elevated and aids in diagnosis
-almost always >50, frequently >100
-Correlates with disease activity
Pathophys of inflammation in GOUT
PMNs play the role in the acute inflammation
-develops when the UA crystals collect in the synovial fluid as the extrecellular fluid becomes saturdated with uric acid.
-IgGs coat monosodium urate crystals, which are phagocytied by PMNs, leading to the release of inflammatory mediateors and proteolytic enzymes from the PMNs which then result in inflammation
Clinical finidings associated with NEONATAL LUPUS
skin lesions, AV BLOCK, transposition of the great vessels
-valvular and septal defects
Clinical findings of PAN:
1. Early symptoms are fever, weakness, weight loss myalgias and arthralgias, and abdominal pain (bowel ANGINA)
2. Other findings are HTN, mononeuritis muliplex and livedo reticularis
Common laboratory markers in which disease: RF
RA (70%) of patients
Healthy population 3%-neither sensitive OR specific for RA

What disease modifying drugs are associated with RA?
General principles:
1. Can reduce morbidity and mortality (by nearly 30%) – by lmiting complications, slowing progression of disease, and preserving joint function
-should be initiated early (at the time of diagnosis)
-they have a slow onset of actoin (6 weeks or loner for effect to be seen),
-they have a slow onset of action (6 weeks or longer for effect to be seen), so begin treating RA while weaiting for the disease-modifying therapy to take effect. Once the effect is evident, gradually taper and discontinue NSAIDS an corticosteroids and cotinue the disease-modifying program2. First-line agents
-MTX: most popular treatment right now – first line therapy
–initial improvement is seen in 4-6 weeks
– 80% of treated patients will experience moderate to excellent symptomatic benefit from treatment although remission is rare
–MTX highly associate with interstitial pulmonary fibrosis

-this is an alternative first line agent, but usually not as effect as MTX
-requres eye examinations every 6 mo 2/2 retinopathy (although quite rare)

Sulfasalazine – alternative first line agent, but less effective than MTX

Second line agents include: gold compounds, penicillamine, aza, and cyclosporine

Treatment and management of FMS
1. Advise pt to stay active and productive
2. Meds generally ineffevtice. SSRIs and TCAs are beneficial but avoid narcotics
3. Cognitive behavioral therapy, exercise, consider psychiatric eval
Classifications of idiopathic inflammatory myopathies:
1. Polymyositis
2. Dermatomyositis
3. Childhood onset dermatomyositis – subcutatneous calcifications
4. Myositis associated with CVD
5. Myositis associated with malignancy
6. Inclusion body myositis – “oddball” for the following reasons: affects male more than female patients, absense of autoantibodies, distal muscle involvement nd relatively low creatine kinae; poor prognosis
Treatment of GOUT?
Avoid seondary causes of hyperuricemia
-medications that increase uric acid levels (thiazide and loop diuretics)
-reduce alcool intake
-reduce dietary purine intakeComplications of gout
-nephrolithiasis – risk is small less than 1% per year
-degenerative arthritis occurs in <15% of patients.
-incidence is decreasing due to effective tretment of hyperuricemia and conseqeunt prevention of tophaceous gout

CLINICAL features of reactive arthritis?
Look for evidence of prior GI or GU infection 1-4 weeks prior
-asymetric arthritis – new joints may be involved sequetially over days. Joints are painful with effusions and lack of mobility.
-fatigue, malaise, weight loss and fever are common
-joint pain may persist or recur over a long-term period
What is usually the first symptom of SLE?
joint pain (MSK)
Cure for systemic sclerosis?
no effective cure
-treatsymptomatically with NSAIDS for MSK pain, H2 blockers or PPI for esophageal reflux
-raynauds phenomenon- avoid cold and smoking – keep hands warml if severes use CCB
-treat pulmonary and renal comlications if present
How is Churg Strauss syndrome dx?
-associated with P-ANCA
How does the “daily” activity of someone with ANK SPONDYLYTIS PROGRESS?
worse in the morning but gets drastically better withe exercise, hot showers, and worsens with inactivity
What is inclusion body myositis?
Most common in males (elderly)
-insidious onset of slowly progressive proximal and distal weakness that often leads to delay in its diagnosis
-early weakness and atrophy of the quads, forearsm and tibialis anterior muscles. Involvement is assymmetrical. Facial wekaness can occur in 1/3 of patients and dysphagis in one-half of patients.
-patients can also have loss of DTR although nerves are not involved in the poly or demato
-extramusclelar manifestations are rare
-diagnosis is bya slight elevation in CK levels
-poor response to therapy
Complications of ANK SPONDYLITIS
1. Cauda equina syndrome (this is medical emergency)
2. Osteoporosis
3. Spondylodiscitis
4. Restrictive lung disease
5. Spine fracture with spinal cord injury
Common laboratory markers in which disease: CRP

conditions (inflammatory states and infection. Miscellaneous condisitons (MI, vasculitis, trauma, malignancy, pancreatitis)

comments: primarily used for infection – much more sensitive and specific than that of ESR. If markedly elevated (>15, normal is 0-10) then expect a bacterial infection.

How is gout diagnosed?

joint aspiration and synovial fluid analysis (under a polarizing microscope) is the only way to make a definitive diagnosis – needle shaped and negatively birefringent urate cyrstals will appear in synovial fluid

-serum uric acid is not helpful in fiagnosis because it can be normal even during an acute gouty attack.
-radiographs reveal PUNCHOUT erosions with an overhanging rim of cortical bone

What pulmonary involvements are associated with RA?
pleural effusions; interstitial fibrosis may occur
Churg Strauss Syndrome
-Vasculitis involving many organ systems (pulmonary, renal, cardiac, GI, skin, neuro)
-clinical features include constitutional symptoms; prominent respiratory tract findings like (asthma, dyspnea) and skin lesions (subcutaneous nodules, palpable purpura).
Noninflammatory arthritis synovial fluid analysis:
Clear, yellow opssible red if traumatic
-WBC < 2000
-PMNs <25%
RBCs for trauma
RA v. Osteoporosis

Rheumatoid arthritis: most common cause of polyarticular inflammatory arthritis. Typically affects the hands, wrists, feet and ankles. Xrays of patients with long-standing poorly controlled disease will reveal periarticular osteoporosis, joint errosions and joint space narrowing.

Bone demineralization is hallmark for osteo. Disease predisposes patients to pathologic fractures of the hip and vertebrae but doesnt cause joint destruction itself.

Treatment of Polymyalgia Rheumatica
CORTICOSTEROIDs – will respond within 7 days
-no curative but effective for suppression of inflmammation until disease resolves itself.
-post 4-6weeks, begin to taper slowly
-60-70% of patients can stop corticosteroids within 2 years. A few patients have symptoms for up to 10 years**self limited – on suppressive and supportive therapy for symptomatic therapy – no cure

What hematological symptoms can occur with RA?
1. Anemia of chronic disease: mild, normocytic, normochromic anemia
2. thrombocytosis
Prognosis and treatment of PAN
poor prognosis
-improved to a limited extent with treatmentRx:
1. Start with roids
2. If PAN is severe, add cyclophosphamide

Major cause of death in patients with WEGENERS?
renal disease
Common laboratory markers in which disease: P-ANCA
Polyarteritis nodosa
-70-80% sensitive for microscopin PAN – not specific – also present in PBC likely associated with ULCERATIVE COLITIS
What is a mixed connective tissue disorder (MCTD)?
overlap syndrome with clinical features similar to those of SLE, RA, systemic sclerosis and polymyositis. Findings consistent with each of these disases do not necessarrily occur simultaneously. It usually takes some time for a pattern to be identified and a dianosis of MCTD to be made.
Treatment for reactive arthritis?
NSAIDs are first line therapy
-if there is no resoonse then try sulfasalazine and immunosuppreive agents such as AZAthioprine
-antibiotic use is controversial and not given
HLA associations with rheumatic diseases: HLA DR3
What is the course of ank spondylitis?
1, slow progression but he course is highly variable
What is the cause of myopathies?
Dermatomyositis v. POlymyositis and inclusion body myositis
-dermato is humoral immune mechanism
-poly is cell-mediated
The degree involvement in patients with systemic scleroderma predicts the diagnosis: diffuse v. limited
Diffuse: worse prognosis
Which symptoms/clinical features make RA unlikely?
1. Joint distribution is not symmetric OR
2. DIP is involved OR
3. Constitutional symptoms (espeically morning stiffness) are absent
Key to diagnosing TEMPORAL ARTERITIS?
Age > 50YO
New headache
tender/palpable temporal artery
HIGH ESR *ESR 10-20, CRP 0-10
Jaw claudication
Common laboratory markers in which disease: C-ANCA
Wegeners granulomatosis (Polyangiitis with granulomas disease)
=sensitive and specific
=may vary with disease activity
Prognosis and treatment of WEGENERS?
Poor – most die within 1 year post diagnosis
-combination of cyclophosphamide and corticosteroids can induce remissions in many patients but a relapse may occur AT ANY TIME
-consider renal transplantation if the patient has end stage renal disease (ESRD)
What is feltys syndrome?
Triad of RA, neotropenia and splenomegaly:
-also anemia, thrombocytopenia and LAD
-associated with high titers RF and etra articular disease
-increases susceptibility to infection
-usually occurs fairly late in disease process

Psoriatic Arthritis

General characteristics:

Develops in fewer than 10% of patients with psoriasis
-gradual in onset
-patients usually have skin disease for months to years before the arthritis develops
-usuall asymmetric and poly articular
-upper extremties most often involved; small joints are more common than larger jointsInitial treatment: NSAIDS but persistant arthritis may req drugs similar to that of RA

What is the differential for raynauds?
Primary – no other disorder exists
Vasculitis (Buergers)
Certain meds (BB, nicotine, BLEOMYCIN)
DIsorders that disrupt blood flow or vessels such as thromboangiitis obliterans
Clinical features of RA?

1. symmetrical inflammatory polyarthritis –> symmetrical joint swelling is the msot common sign. THis can involve every joine in the body EXCEPT the DIP joints

2. pain on motion of joints/tenderness in joints

3. joints commonly inolved include joints of the hands (PIP, MCP) and wrists, kneees, ankles, elbows, hips, and shoulders

4. characteristics hands deformities
-ulnar deviation of the MCP joints
-boutonniere deformities of the pIP joints (PIP flexed, DIP hyperextended)
-swan-neck contractures of the fingers (MCP flexed, PIP, hyperextended, DIP flexed)

HLA associations with rheumatic diseases: HLA b27
Ank spondylitis, Reiters syndrome, psoriatic arthritis
Clinical features of temporal arteritis
1. constitutional symptoms
2. headaches
3. Visual impairment (25%-50%) 2/2 opthalmic atery, optic neuritis, amaurosis fugax, can lead to blindess in up to 50% of patients if not treated
4. Jaw pain with chewing
5. Tenderness to palpation over the temp artery without temp pulse
6. Palpable nodules
7. 40-50% patients also have PR
If temporal arteritis is suspected…begin which treatments empirically?
How is systemic scleorissi diagnosed?
almost all have elecated ANA – high sensitivity but low specificity
-anticentromere antibody
-anti-topoisomerase i – antischleoderma 70 AB is very specific for the diffuse form
-barium swallow (esophageal dysmotility and pulmonary function test) are used to detect complications
Treatment for Ank Spondylitis
-indomethacin for symptomatic relief
-physical therapy (maintaining good posture, extension exercises)
-surgery may be necessary in some patoietns with severe spinal deformity
-pts with ank sponylitis who sustain even minor trauma and who complain of neck or back pain should be strictly immobilized to prevent spinal cord injury until thorough imaing studies are obtained
1. Ankylosing Spondylitis
2. Reactive Arthritis
3. Psoriatic Arthritis
4. IBD associated
What is reactive arthritis?
A CLINICAL DX. It is an asymmetric inflammatory oligoarthritis of lower extremities (less common to upper) in which is preceded by an infectious etiology that is remote from the site of arthtritis (1-4 weeks prior) – most commonly 2/2 enteric and or UG infections like the clap.
-occurs most commonly in HLAb27
-REITERS syndrome is an example of reactive arthritis but most patients do not have theh classic findings of reiters (cant see cant pee cant climb a tree) so NOW we use REACTIVE ARTHRITIS
Epidemiology of SLE
women, child bearing age acct 90% cases
-AA pateints more frequency than caucasion
-mild in elderly, severe in children.
Pseudogout – general characteristics?

Calcium pyrophosphate crystals deposit in joints, leading to inflammation

Risk factors:
1. Deposition increases with age and with OA of the joints. THerefore pseudogout is common in elderly patients with degenerative joint dz – other conditions that may increase crystal deposition include hemochromatosis, hyper parathyroidism, hypothyroidism and Bartters syndrome

How is Ank Spondylitis diagnosed?
imagig studyies of lumbar spine and pelvis 9plain film, MRI, CT) reveal sacroiliitis 0 sclerotic changes in the sacroiliac area. Eventually, the vertebral columns use, producing “bamboo spine”
-elevated ESR in up to 76=5% of patients (due to inflammation) nonspecific
-HLAB27 is NOT necessary for diagnosis
What antibodies are common to the diagnosis of MCTD?
1. Increases ANA
2. Increased RF
3. Increased anti-RNP AB is a key lab finding
How might polymyositis/dermatomyositis be diagnosed?
1. Labs:
-SK level is significantly elevatd. CK levels correspond to the degree of muscle necrosis, so on can monitor disease severity
-LDH, aldolase, AST, ALT elevated
-ANA in over 50%
-antisynthetase antibodies (antijo1) abrupt onset of fever, cracked hands, raynauds interstitial lung disease, arthritis, doesnt response well to therapy
-Anti-signal recognition particle (cardiac manifestiation – worst prognosis)
-anti-mi-2 antibodes – better prognosis
-EMG – abnormal 90%2. Biopsy
-shows inflammation and muscle fiber fibrosis in all three
-dermatomyositis – perivascular and perimysial
-polymyositis and inclusion body myositis – endomysial

Common laboratory markers in which disease: Lupus anticoagulant
antiphospholipid antibody syndrome
What features are found in both poly and dermatomyositis?
1. Symmetric proximal msucle weakness
-earlier and more severe muscle weakness n the neck flexors, should girdle, and pelvic girdle muscles.2. Myalgia in 33% of patients
3. Dysphagia in up to 30% of patients (involvement of esophageal muscles)

What is RA?
chronic inflammatory autoimmune disease involving the synovium of joints. THe inflamed synovium can cause damage to both cartilage and bone. It is a systemic disease tat has many extra-articular manifestations
-it is a systemic disease that has many extra-articular manifestations
-the usualy age of onset is 20-40 years; it is more common in women than in men (3:1)
-disease severity is variable – some patients hae moderate restrictions and are capable of performing activites of daily living, whereas others are confined to a wheelchair or bed. Etiology is uncertain. It may be caused by an infection or a series of infections (most likely viral), but genetic predisposition is necessary.
Classic triad of REITERS syndrome?
1. Arthritis
2. Urethritis
3. Ocular inflammation (conjunctivitis) or (anterior uveitis)*these symptoms do not always occur together

Inflammatory arthritis (RA, gout, pseudogoat, Reiters syndrome)
cloudy yellow
->5000 WBC
-50-70% PMNs
-positively birefringent crystals with pseudogout, negatively birefringent with gout
young man, firm mass in testicle, painless, preseumed to have testicular cancer until proven otherwise: true or false
Postrenal failure: ARF characteristics
least common cause of ARF
-obstruction of UTI with intat kidney causes increased tubular pressure
-urine produced doesnt get excreted leading to decreased GFR
-blood supply and renal parenchyma intact
-function restored if obstruction relieved b4 damage to kidney
What should a patient do if stone is passed at home?
recover the stone passed – good for analysis and helpful in both treatment and prevention of recurrence
treatment of UtO? what factors (duration, location, cause, duration of obstruction).

if lower: urethral cath for acute onset of obstruction or dilitation with internal urethrotomy if cause is a stricture

if upper: nephrostomy tube drainage = acute…ureteral stent (cytoscope) if there is a ureteral obstruction

When is a renal biopsy indicated?
Only if suspician of acute GN or allergic interstitial nephritis
FSGS as a primary GN
25% causes nephrotic syndrome
-edema, hypoalbuminemia, hyperlipidemia, proteinuria
-HTN, hematuria comon
-variable prog
*do not admin steroids; renal insufficiency 5-10 yrs; progressiverx; cytotoxic agents; immunosuppressants

CLinical features of ADPKD:
1. ARF
2. Berry aneurysm with intracranial hemorrhaging
3. Down syndrome association – marfanoid hapbitus
-HTN > 50% causes
-PALBABLE KIDNEY on abdominal exam
-CVA complication on PE
penile cancer
incidence peaks in mAles in 70 years
-circumcision is protective and is rare in pts who are
-hsv-2 and hpv 18 infection is risk enhancing
-exophytic mass on penistretment is local excision

2 major methods of dialyzing patients
1. Hemodialysis – hospitals/dialysis centers
2. Peritoneal dialysis – CAPD (chronic ambulatory)

Stones that pass spontenous, stones that do not pass spontaneously

Reccurence rate nephrolithiasis

If > 1cm –> will not pass
IF < 0.5 cm then will usually passUP TO 50% with recurrences in 10 years of having first stone

Classification of urinary obstruction
1. Acute v. chronic
-sudden onset v. progressive RF/uremia and recurrent inf/bladder calculi
2. Lower v. upper obstruction
-below the ureterovesicular junction = affects urination
-above the ureterovesicular juntion = renal colic and affects concentration
3. Complete verrsus partial obbstruction
4. unilateral v. bilarterall obstrruction
Hereditary nephritis (______) SYNDROME
-xlinked/AD/variable penetrance
-hematuria, pyuria, proteinuria
-hearing los without deafness
-renal failureNo treatment

CRF diagnosis
UA = examine sediment
measure cr clearance to estimated GRF
CBC (anemia/thrombocytopenia)
electrolytes serum
renal US = evaluates the size to r/o cysts
-small kidneys = CR insufficiency w/ little chance to survive
-preseve of normal kidney without excessive CRF
-renal biopsy
How might RENAL ARTERY STENOSIS be diagnosed?
#1 GOLD STANDARD – renal arteriogram (do not use in patients with renal failure 2/2 contrast toxicity#2 MRA = magentic dye that doesnt cause nephrotoxicity so CAN be used in pts with CRF

#3 Captopril renal scintigram (SCAN); good but non-invasive in pts with good renal function

germ cell nongerminoma testicular tumors:

-embryonic carincoma



-yolk sac tumor

emb- high mlig potential, hemorrhage, necrosis common, mets to lungs and abdominal lymph

chorio is the most aggressive ig mets that have occured by the time of diagnosis

teratoma rarely mets

yolk sac tumor is rare in men but common to boys

Causes of ATN
1. Ischemic ARF
-2/2 severe dec in RBF as in shock, hemorrhagic, sepsis, DIC HF
-ischemia results in death of tubular cells2. Nephrotoxic ARF
-injury 2/2 to substances that direcly injure renal parenchyma and result in cell death
-antibiotics; radiocontrast agents, NSAIDS

What CRF-endocrine related disorder results in necrotic vascular skin lesions called “CALCIPHYLAXIS”
Hyperphosphatemia secondary to CRF = precipitation of PO43- and Ca2+ leads to vascular compostitions
What are specific measurements for patients with nephrolithiasis?
1. Mild – moderate pain
-high fluid intake, oral analgesics while waiting for stone to pass spontaneously
2. Severe pain with vomiting
-IV fluids, pain control
-KUB and IVP to find set of obstruction
-if not passed in 3 days – urology consult
3. Ongoing obstruction
-surgery necessary
-extracorporeal shockwave lithotripsy
-percutaneous nepholithotomy
signs of early prostate cancer
signs of later prostate cancer
late signs of prostate cancer

asymptomatic ; peripheral and goes central; obstructive symp occurs later bc cancer starts outer and goes inner

symptoms due to obstruction occurs; metastasized to bone and lymph nodes possible with difficulty voiding and increased urinary frequency

bone pain from mets with weight loss, affects the vertebral bodies pelvis and long bones however increases osteoblastic activity

1. GN caused by immunemediated mechanisms
2. Metabolic hemodynamic disturbances
MVP heart abnormality seen in which congenital renal dz?

Pruritis is commonly seen in patients with CRF – what is the treatment?

What is the only CURE to CRF?

Pruritis – capsacician cream, cholestyramine, UV liegh


causes of hyperoxaluria

severe steaorrhea of any cause can lead to calcium oxlate strones due to increased absorption of oxalate

small bowel disease/crohns disease
pyridoxine deficiency

What is orthostatic proteinuria?

patient is standing; has proteinuria, when recombinant, none.

Self limiting/benign

HIV nephropathies 2/2 GN
1. Proteinemia, edema, hematuria
2. Histopatho – looks like FSGS
3, Improves with prednison, ACEi, retroviral
UA findings of renal failure:
1. Prerenal
2. Renal
3. Postrenal
1. Prerenal
Cause: renal artery stenosis
Urine sediment: benign, hyaline
Protein: negative
Blood: negative2. Intrarenal
Cause: (1-ATN)(2-AGN)(3-AIN)
Urine sediment: (1-muddy brown renal casts, granular)(2-dymorphic RBC with cases, WBC and casts, fatty casts)(3-RBC,WBC,EOSINO, WBC+CASTS)
Protein: (1-trace)(2-4+ protein)(3- 1+)
Blood: (1-negative)(2-3+)(3-2+)

3. Postrenal
Cause: BPH
Urine sediment: Benign +/- RBC
Protein: negative
Blood: negative

Medullary sponge kidney v. Simple renal cyst kidney
MSK: cystic dilitation of collecting ducts
-hematuria, UTI, nephrolithisis
-associated with hyper-pth and parathyroid adenoma
-dx by intravenous pyogram
no Rc necessary – prevent stone formation and treat UTISimple cyst
-very common (50% > 50YO); incidence increases with age;
-may be single, may be multiple
-asymptomatic, discovered incidentally
DO NOT treat

Why might there be a delay recovery of epithelial cell function relative to GFR in pts with ATN?
2/2 tubular cell damage with prolonged osmotic diuresis due to retained solutes during the oligo phase
Imaging of nephrolithiasis
1. Plain radiograph of kidney, ureter, bladder (KUB)
-initial imaging detecting stones that are ca-ox/caphos/struvite/uric acid but NOT able to note cysteine stones2. CT scan without contrast (spiral) – most sensitive and detects all stones

3. IVP – degree/extent of UTO – decides whether or not pt should have surgery

4. Renal ultrasonography – hydronephrosis/ureter obstruction

Limitations/complications with dialysis
1. Doesnt replicate kidney synthetic function of EPO and VITAMIN DComplications
1. Hemodialysis
-hypotension often causing MI and fatigue
-hypo-osmo of ECF compared with BRAIN = n/v/headache
2. First use syndrome
3. Anticoagulation
4. Infection

Pathophysiology of CRF:
1. Plasma cr vaires inversely with GRF
2. Cr clearance is most common clinical measure of GFR
3. Inc plasma cr indicates disease progression; dec plasma Cr indicates recovery of renal function
4. > Africa americans than caucasians
What is azotemia?
Progosis of ARF:
Elevated BUN and Cr
-increase BUN = catabolic drugs (steroids); GI/soft tissue bleeding, dietary protein
-increase creatinine = increased muscle breakdown and various drugs (baseline or level varies proportionally with muscle mass)
Membranous GN
Nephrotic syndrom: proteinuria, hypoalbuminemia, hyperlipidemia
-thickened glomerularocapillary walls; primary dz idiopathic, secondary disease d/t infection (HCV/HBV/syphilis, malaria)
-drugs – gold, captopril, penicilamide)
-neoplasms or lupus can result in DNRx: remission (40%)/RF(33%) steroid therapy

How might fanconis syndrome be treated for?
-ALkali/salt supplement
HydrationWHY? bc the proximal tubulae cannot administer glucose or resorb it (AA, Sodium, potassium, phosphorus, UA, HCO3-)

Struvite strones
radiodense and visible on KUB
rectangular prismsRecurrent UTIs = urease + organisms (proteus, enterobacter, serratia, klebsiella)

Facilitates by an ALKALINE URINE (which is seen in patients with RTA 1 and 2) and urea splitting bacteria that convert urea into ammonia

Ammonia thus combines with excess mg2+ and phos 2+ and forms struvite staghorn stone

WBC Casts are indicative of a ______ ________ inflammation due to a type of ________
renal parenchymal (inflammation) due to a type of INFECTION
Proteinuria is decribed as the urinary excretion of >____mg/protein/24hr.
4 major classifications:

>150 mg protein24hours

1. Glomerular
2. Tubular
3. Overflow proteinuria
4. UTI, Fever, CHF, prenancy, orthostatic proteinuria

How are uric acid stones diagnosed if not picked up on XRAY?
elevated release of pruines
-see on CT, US, IVP for detection
-will treat with allopurinol for prohylaxis TLS and will treat with rasciabine to break apart the already formed urate if leukemic pt undergoing chemo
causes of lower tract obstruction
Bph, prostate cancer
urethral stricture, stone
neurogenic bladder (ms) or DM
bladder ca
secondary glomerular disorders
Diabetic nephropathy
HTN nephropathy
Good pastures
sc nephropathy
HIV nephropathy
GN in endocarditis
Fluid and electrolyte disorders in patients with CRF
-volume overload
-hyperkalemia – decreased urinary secretioin
-hypermagensiemia – 2/2 urinary dec secretion
-metabolic acidosis (loss of renal mass, dec ammonia production and kidneys cannot exeed H+)
What treatment (anti-htn meds) are contraindicated in patients with RENAL ARTERY STENOSIS?
ACEi because will dilate the efferent arteriole and further decrease GFR and increase RBF – the GFR is already below normal 2/2 RAS so wouldnt want to exacerbate
Clinical features of CRF:
1. CV
2. GI
3. Neurologic
4. Hematologic
5. Endocrine
6. FLuid/electrolytes
1. CV: HTN, secondary to sodium retntion; dec GFR, increased RAAS, increased BP
2. CHF = volume overload; HTN; anemia; pericarditis = uremic
3. GI = due to uremia (n/v) loss of apetitie
4. NEURO = lethargy, comnlence, confusion, peripheral neuropathy, uremic seizures (asterixis, hyperflexia0; restless leg, Hypocalcemia
5. Heatologic = normocytic, normochromic anemia (dec EPO)
6. Endo = Ca2+/PO4- distubance
7. Volume overload: hyperkalemia; elevated mag; elevated phos; decreased pH
Advantages v. disadvantages of hemodialysis

Advantages: more efficient than peritoneal dialysis; high flow rates and efficient dialyzers short period of time required for dialyisisl QUICK to initiate than peritoneal use of temp vascular access in emergency

Disadvantages: less similar to function of natural kidney; increased hypotension to rapid change in volume; hypo oSmo 2/2 rapid removal of solute; regular vascular access

Intrinsic renal failure (ARF)

Kidney tissue is damaged such that glomerular filtration and tubular function are significantly impaired and tubular function are significantly impaited and cannot concentrate urine efficiently

Causes: ATN, GN (good pastures, wegeners, post GN), Vascular Dz(renal artery occlusion -TTP/HUS), Intersitial Dz (allergic intersisital nephritis)

Sickle cell nephropathy
sickling of RBC in microvasculature leads to renal infarction in the papilla
-recurrent papillary infarct leads to papillary necrosis and renal failure and UTI

Prostate cancer:


95% adenocarcinomas

rf include that of:
AA race
high fat diet
positive family history
exposure to herbicides or pesticides in certain occupations including farming and chemical industries

Clnical features of glomerulonephropathies

impairment of selective filtration of blood – increased excretion plasma proteins and blood cells

as disease >>, GFR dec –> renal failure

Proteinuria and hematuria

Which disease commonly associates with
-intracranial berry aneurysm
-abormal heart dz (MVP)
-cysts in other locations in body (liver, pancraease, brain)
-renal failure ain 50-60YO patienst
What is overflow proteinuria?
increased production of small proteins that overwhemlms tubules ability to reabsorbs them. BJ protein in MM good ex.
if a patirnt has an acute obstuction, next step?
emergent dx test: renal US, excretory urogram
immediate intervention
Post-streptococcal GN = #1 cause of ____ ______
NEPHRITIC syndrome
1. occurs 10-14 post streptococcal infection by GASPopulation: children 2-6YO
-hematuria, edema, HTN, proteinuria; dec complement; elevated ATO
-self limited (wks to MO) – good Px
can become RPGN in adults

Treatment: antiHTN, loops for edema; noAB

What is the most common cause of secondary HTN?
Renal artery stenosis
-decreases blood flow to the JGA thus the RAAS becomes activated and vasocontricts the effecrent arteriole and releases aldosterone for H2o resorption, etc.
Whenever a patient presents with elevated Cr levels, what is the first thing to do when diagnosing or patients with CRF or ARF?
Determine the baseline creatinine (cr)
-determines if ARF, CRF, Chronic RF/imposed ARF (“acute on chronic”
Frequency and access in CAPD versus that of HDialysis?

Diasylate fluid drained/replaced each HR in acute peritoneal, but 1x 4-8 hours in CAPD

Access CAPD: diasylate infused into peritoneal fluid by catheter. If acute PD, temp catheder used

Atheroembolic disease of the RENAL arteries

Cholesterol crystals dislodge from plaques in large arteries and embolize in the renal vasculature (cholesterol emboli syndrome is similar)

-can occur in retina, brain, skin

when might a cystourethirography be indicated for use?


CT scan?

lower tract obstruction

evaluate urethra and or bladder

cause of obstruction

Prognosis of ARF?

>80% of patients in whom ARF develops never completely.

Older patients have decreased recovery = #1 cause of death – infection

Minimal change disease
1. Nephrotic = edema, proteinuria, hyopalbuminemia, hyperlipid
2. most common to children
3. most common to NHL and Hodgkin association
4. No histological changes on light microscopy – fusion of foot processes on EM
4. Excellent prog with treatment of steroids 4-8 weeks relapses common
When is a renal US useful?
1. Kidney size ,function –> r/o UT obstruction (ex: postrenal failure)
-bilateral hydronephrosis
-hydroureter; BPH2. Order for pts with ARF unless obvious that patient doesnt have postrenal failure

ADPKD = Renal cystic disease
Autoimmune DOM condition
-variable course, EDRS commonly develops in 50% of patients by age 50-60s but remainder have normal lifespan

risk factors for testicular cancer?


– surgical correction doesnt eliminate riskklinefelters sydrome
– xyy

painless mass or lump; firmness of testicle beacuse of lack of pain that goes unnoticed until advanced

Hyaline casts are seen in ____ ______
Pre-renal failure
How might amyloidosis occur in patients on dialysis?
Hemodialysis – associated amyloidosis of B2 macroglobulin in BONES and JOINTs
What is the renal failure index if >1% or if <1%?
Urine sodium
-Ucreatinine/Pcreatinine x 100 = RF index
-Values <1% = prerenal failure -Values >1% = ATN (intrinsic)
What are uric acid stones?
account for 10% of all renal stones and cause:
1. hyperuricemi, secondary gout/chemotherapy via TLS for lymphoma and leukemias
-release of pruine from dying cells is what causes the elevated uric acid
-flat [ ] plates; stones (not seen onXRAY)
What is renal failure

rapid decline in renal function with an increase serum creatinine level (inc 50% or absolute 0.5-1.0 mg/dL)

urine output can be (oligouric, anuric, nonoligouric) – severe arf occurs without a decrease in urine output

Characteristics of UT obstructions
Leads to renal insufficiency and hydronephrosis (dilation of UT = pelvis and calysis)
More common in males 2/2 BPH and prostat CA
UTO doesnt cause ARF unless obstruction is bilateral OR prior damage occurs

Nephrotic v. Nephritic


-patho: abnormal GN permeability
-causes: many conditions; MGN = #1; then DM, HTN, SLE, RX, FSGS/MCD
-labs: Proteinuria <3.5 g hypoalbumin/hyperlipid
clinical: edema, hypercoag, hyperlipidemia, hypoalbuminemia, inc infection riskNephritic:
-patho: inflammation of glomeruli due to any cause of GN
-post streptococcal GN #1
-hematuria, HTN, ARF (azotemia, oligouria); proteinuria

how might renal cc be diagmosed versus rx.
renal us to detect the mass v cyst
abdominal ct to determine shape and stagetreatment
– radical nephrectomy excision of kidney and adrenals influding gerotas fascia with excison of nodsl tissue at renal hilum for stage

Prognostic factors to consider in ARF
1. Severity – magnitude of inc cr; oligouria;excretion of sodium; req of dialysis; duration of renal failure; abnormalities on UA
2. Health of patient – age, presense, severity, reversibility of disease
3. Clinical circumstances – cause of RF; # failed organs
What are the CLINICAL FEATURES of someone with renal artery stenosis (will result in AKI prerenal)
1. HTN – will be sudden in onset with a pt lacking a significant family hx. Severe HTN (may become malignant and refractory medical therapy)2. DECREASED renal function. Will have a BUN:Cr <20:1 will have a FENa of <1% and will have low urine sodium

3. ABDOMINAL BRUIT = RUQ if right kidney; LUQ if left kidney or epigastrium

Which calcium/phosphorus disturbances occur in pts with CRF?

Pts with CRF are unable to readily clear phosphorus therefore becomes hyperphosphatemia; which results in dec renal production of 1,25D3. Thus HYPOcalcemia causing 2ndary hyperpTH, increased PTH

Hypocalcemia, hyPERphosphatemia, but longstanding secondary hyperPTH and calcium based phosphate binders cause = HYPERCALCEMIA

secondary type PTH = renal osteodystrophy (bonepain/bonefractures)

Hyperphosphatemia = Ca2+, increase phos to precipitate, increased vascular calcification causing skin resins.

How is the patients blood retrieved (on hemodialysis)
1- central catheder placed in th subclavian vein for temp access
2 – AV fistula – #1 form of permanent dialysis artery and vein to forearm; requires CV surgery to connect the RADIAL ARTERY and VEIN to one antoher in forearm – 6 weeks to mature and heal – audible bruit over the fistula = PATENT, so this is a good thing.
3 – implantable graft
Nephrosclerosis due to HTn is the SECOND most common cause of ESRD, what is the first most COMMON cause of ESRD?
HTN 2/2 DM = most common
HTN 2/2 nephrosclerosis = 2nd msot common
RPGN is a clinical syndrome that includes any type of GN in which a rapid (acute) deterioration occurs over _____ to _____ Outcome:
ESRD and RF = outcome

transitional cell carcinoma accts for ____% od bkadder cancers

squamous cell carcinoma accts for ____%

adenocarcinoma accts for _____%

What clinical assocations are seen with folks with ADpkD
#1 intracerebral berry aneurysm in 5-20% of cases
#2 Diverticula (colon
#3 Infection of hte renal cysts; bleeding into cysts
#4cysts on other organs (liver, spleen, pancreas, brain)
#5renal failure (late)
#6 kidney stones
#7 heart abnormality
Glomerular diseases
two broad categories:
1. Intrinsic patholgy (primary)
2. 2/2 DIT systemic disease-present with nephrotic syndrome or nephritic syndrome
-duration varies (days to weeks) – acute GM disease and years if CHRONIC

Treatments of ARF generally:
1. Avoid rx: decreases RBF like NSAIDS; nephrotixic: aminoglycosides, radiocontrast agents
2. adjust doses of medicibes depending upon renal fcn
3. Correct fluid balance – if dehydrated = IV fluids; if overload = loops or dialysis monitor by day weight
4. Correct electrolyte imbalance
5. Optimize cardiac output BP 120 to 14/80 to 90
6. order dialysis if uremia, hyperK
Asymptomatic proteinuria
1. Transient
2. Persistent

Transient: excellent prognosis (without further eval)

Permanent: req workup to r/o renal disease

Most common sites of nephrolithiasis
development of stones within the urinary tract
1. Ureterovesicular junction = #1
2. Calyx of kidney
3. Ureteropelvis junction
4. Intersection of ureter and liac vessels
How might a urine chemistry distinguish between different forms of ARF?
1. Urine Na+ depends upon sodium intake
2. FENa: collect urine and plasma electrolytes simultaneously (Usodium/Psodium)/(Ucrt/Pcrt) x 100If <1% then prerenal
If 2-3% = intrinsic or ATN – FENa useful if oligouria present

What are two major associateition with hyperparathyroid and parathyroid adenoma/
Medullary spondge kidney
Urinalysis of nephrotic syndrome can reveal?
1. Proteinuria with dipstick
2. RBC casts if GN; WBC casts if peylonephrotis and interstitial nephritis; fatty casts sugest nephrotic syndrome due to lipiduria
3. If UA confirms protein, perform 24 hr urine collection (alb and Cr) to establish presense of proteinuria
prostatic cancer treatment
if localized to prostate then
– radical prostatectomy or watchful waiting in older males who are asymptomaticif locally invasive then
– radiatino therapy plus androgen deprivation
– no cure just decreases spread

if met
– then decrease testosterone
– perform orciectomy and anti-androgen therapy
– LRH agonist —– LEUPROLIDE

What is the GFR of:

2. Moderate CRF
3. Severe CRF

1. 70-120 mL/min
2. 30-70 mL/min
3. <30mL/min
4. <10mL/min
Advantages CAPD v. Disadvantages CAPD
-dialysis done independently
-mimics physiology of normal kidney
-high glucose can cause hyperglycemia and hyper TG
-increased abdominal girth

When might a renal vein thrombosis be seen?
1. Nephrotic syndrome
2. Invasian of the RV by that of RCC
3. Trauma
4. Pregnancy/oral contraceptive
5. extrinsic compressions (retroperioneal fibrosis, AORTIC abominal aneurism, LAD, dyhydration
diagnosis v treatment of bladder cancer
-ua/uc to rule ut infection
-urine cytology that detects malignant cells
-cystoscopy biopsy – definitive
-cxr/ct scan to stagestages
0-superficial limited to mucosa in situ
a-transurethrll resection of bladder tumor
b-muscle invasion
c-extends periumb fat
d- mets

Fanconi’s syndrome

Hereditary/aquired proximal tubule dysfcuntion leading to defective transport of GLUCOSE/AA/sodium?K/PHOS/UA/HCO3-.

Leads ultimately to glucosuria, phosphaturia (RICKETS) with imapried ffrowth, osteomalacia (osteoprorosis), proteinuria, polyuria. RTA (HCO3-); elevated Ca2+ urinae, decreased K+ serum

Treatment of
1. Asymptomatic transient proteinuria
2. Asymptomatic persistant proteinuria3. Symptomatic proteinuria

1. Asymp + transient = no further workup
2. Asymp + transient = check BP; UA; LDL/HDL3. Testings:
-treatment disease = DM, MM, SLE, MCD
-ACEi = decrease albumin loss and prog]]ress of nephrotiosis. Essential if CRF with DM and HTn and should be admin b4 fixed albuinuria present

4. Diuretics, dec protein
5. Vaccine – pneumococcal, influenze

Hartnup syndrome
AR inheritance of defective amino acid transporter
=doesnt reabsorp that of tryptophan and other neutral AA – resulting in nicotinamide deficiency = pellagra, glossitis, diarrhea, dermatitis, ataxia, death
=administer supplemental nicatinamide to symptomatic patients
RBC cases are indicative of a _______ disease
glomerular (nephritis)
Complications associated with peritoneal dialysis?
peritonitis = cloudy fluid fever, abdomenal pain
abdominal/inguinal herniation
hyperglycemia = DM pts especially
protein malnutrition

Forms of reversible ARF on restoration of blood flow – but if reperfusion dont occur or hypoperfusion persists – then ischemia results and leads to _____.

Pre-renal failure v. ATN?

Acute tubular necrosis (ATN)

Pre-renal failure:
1. Urine osmo: >500
2. Urine Na+: <20
3. FENa: <1% 4. Urine sediment: scant ATN 1. Urine osmo >350
2. Urine Na+ > 40
3. FENa >1%
4. Urine sediment: full browish pigment graular casts with epitherlial casts

What are struvite stones and what are they made up of?
Mg-Phos-Ammonia stones in which can become “staghorn”
-seen on XRAY
-rare but can occur
Risk factors fo RCC
cigarette smoking like that for pancreatic CA
phenacetin analgesics in high doses
chronic dialysis ife multicytic kidney disease
heavy metals including mercury and cadmium
Differentiation between CRF and ARF
Chronic – hx of kidney dz, HTN, abonormal UA, edema
-small kidney on US
-irreversible damage
-hyperK, acidemia, phosphatemia, anemia
-UA broadcasts >2-3 WBCAcute
-normal function returns
-hyperkalemia, acid, hyperphos, anemia

Why might HYPERLIPIDEMIA be seen in patients with increased hepatic synthesis of albumin 2/2 nephrotic syndrome (hypoalbuminemia)
increased hepatic LDL/VLDL because increased albumin
RTA type I
-inability to secrete H+ at distal tuble; thus new HCO3- cannot be produced
-inability to acidify the urine = metabolic acidosis
-urine pH >6 (normal is 4.7) therefore if urine pH is > 4.7 then assume urine “alkalosis”
-inc ion excretion of (sodium, ca, K, sulfate, phosphate)
-dec ECF, hyPOkalemia; renal stones/neprhocalcinosis 2/2 elevated calcium phosphorus imbalance
Azotemia v. Uremia

azotemia: increased BUN

uremia: signs and symptoms assciated with accumulation of nitrogenous wasts due to impaired renal function. Occurs when BUN > 60mg/dL

Alternative to traditional hemodialysis
continuous AV hemodialysis (CAVHD)
continuous venovenous hemodialysis (CVVHD)used in hemodynamically unstable patients like ICU patients with ARF
-low flow rate of blood and diasylate enable dialysing dialysis to occur while dec rapid shift in volume and osmolarity.
-require highly efficient dialyzers to be effective

Pathophysiology of ARF
Dec clearance of metabolits (BUN, Cr, Uremic toxins)renal parenchyma is undamaged, tubular function (there the concentrating ability) is preserved. Thus, the kidney responds appropriately – conserves as much sodium and water

In rare cases, ++++++++ can cause malignant HTN
bladder cancer chracteristics

bladder carcinoma is the most common type of tumor in the GU with 90% being transitional cc

occurs from kidney to bladder but 90% in bladder

route of spread is local to tissues

recurs post removal

Causes of atraumatic cases of hematuria?
25% infections (cystitis, urethritis, prostatitis)
20% kidney stones, bladder malig/RCC; glomerular DZ IgA nephropathy; trauma = foley cath, blunt trauma; strenuous exercise (marathon) fever; systemic disease (SLE, RF, HSP, WG, HUS, GPS)bleeding d/o, rx, ADPKD, BPH

Type I RTA v. Type II RTA
Type 1: distal
-hypok, hyperchloremic
-metabolic acidosis
-nephrolithiasis (ca2+ and phos binding)
-Rx: HCO3-Type 2: proximal
-hypok, hyperclor
-ma w/out ag
-no nephrocalcinosis/lithiasis
-dont treat w/ bicarb bc is not being absorbed proximally
-urine alkalosis
-Rx: Sodium restrictiong will inc Na+ resorption and HCO3- in urine

Fatty cases in urine indicative of a ______ syndrome
Glomerular proteinuria v. Tubular Proteinuria
-increased glomerular permeability to proteins – becoming nephrotic
-seen in GN
-more severe protein loss-small proteins filtered at glomerulus then reabdorbed by tubules appear in urine d/t abnormal tubules (ATN)
-less severe = DIT: sickle cell, UT obstruction, interstitial nephro

What are the complications in early phase of ARF?
1. ECF volume expansion –> pulmonary edema
-treatment with that of FUROSEMIDE2. Metabolic = hyperkalemic: dec K+ excret and movement of K+ from ICF–>ECF due to tissue destruction & acidosis. 2. Acidosis = inc anion gap d/t H+; if <16 – use sodium bicarb. 3. Hypocalcemia – dec vitamin. 4. Hyponatremia 5. Hyperphosphatemia. 6. Hyperuricemia

Risk factors involved with nephrolithiasis?
1low fluid intake = #1 risk factor
2. family history
3. GOUT/CROHNS/hyperPTH/TypeIRTA(distal)
4. Medications: loops, acetazolamide, antacids, chemotheraputic treatment that cause cell to be brown (uric acd stones)
5. Males (3x more likely)
6. UTI (especially with urease-producing bactrim)
PSA asy is refined due to
1. age adjusted psa because will increase with age
2. PSA velocity is the analysis of the rate of increase in levels overtime
3. free v. bound serum PSA
-psa produced by prostate cancer is plasma protein bound
-psa produced by normal cells = free PSA
4. PSA density = correlation of psa levels with prostate volume
Causes of nephrotic syndrome
1. Primary glomerulonephritis disease (50-70%)
a. Membranous GN most common
b. FSGS (25%) – HIV
c. Membranoproliferative CN (15%)
d. Minimal change disease (75%) children
2. Systemic diseases: DM; CVD; SLE; RA arthritis; HSP; PAN; Wegeners
3. Amyloidosis.cryoglobulinemia
4. Medications: Captopril (ACEi), heroin, metal, NSAIDS, penicillamide
5. Infection = b, v, protozoal
6. Malignant, HTN
Chronic interstitial nephritis
slowly progressive IN leading to fibrosis ESRD over the years
-renal papillary necrosis can be present
-no signs of hypersensitivity like AIN
-causes = prolonged UTO reflux nephropathy, heavy analgesics use, ?lead/camin”; arterioar nephroschlerosis with HTN.

chronic renal failure differs from RF in which ways?

2 most common causes?

1. Irreversible
2. Progressive loss of GFR happening months – years1. DM (30%)
2. HTN (25%)
3. Chronic GN (15%)
4. Interstitial nephritis
6. Obstructive
7. Delay in ARF rx

Process of peritoneal dialysis
1. Peritoneam = dialysis membrane
2. Infuse diasylate into peritoneal cavity and fluids/solute from peritoneal capillaries diffuse into fluid diasylate and is then drained from abdomen
3. Hyperosmolar (HIGH GLUCOSE) solution used and water is removed from blood by osmosis
Pre-renal failure
#1 cause of ARF = potentially reversible
etiology-dec systemic arterial blood volume or renal perfusion
-hypovolemia = dehydration, excessive diuretic use, por fluid intake, vomiting, diarrhea, burns, hemorrhage
-peripheral vasodilation = sepsis, excessive antiHTN meds
-renal arterial obstruction
-hepatorenal syndrome
Renal vein thrombosis clinically presents with
decreased renal perfusoin –>ESRD
flank pain
1. renal venography visualizing occluding thombosis
2. IVP
3. Anticoagulation therapy to prevent PE

Postrenal rx in ARF
bladder catheder inserted to decompress the urinar tract. Get urology consult

testicular cancer


men 20-35 yo
high cure ratetypes

1. germ cell tumor – 95% all testicular ca – 20-40 yo; cure > 95%
-seminoma -35% slow growth and radiosensitive
-nonseminoma -65% mixed cell ; choriocarcinoma; teratoma; yolk sac
2. nongerm cell tumor 5%
-leydig cell tumor
-sertoli cell tumor

Tests used to determine etioogy of nephrotic syndrome?
Creatinine clearance = best test of renal function
Serum BUN/Cr
CBC – detects anemia d/t renal fail
Serum albumin level
renal US – obstruction, mass, cystic dz
IVP – chronic pyelonephritis
ANA- lupus; antigbm; hepatitis serology; antistrepto AB titers, complement levels
serum and urine electrophoresis (myeloma)
Diagnosis of ARF is usually made by finding elevated ____ and ______ but is asymptomatic
Type 4 RTA

1. any condition of hypoaldosteronism or inc renal resistance to aldosterone such that doesnt allow intercalated A or B cell of collecting duct to fcn, therefore no secretion of H+ from urine.

If interstitial renal dz, DIABETIC nephropathy decreases sodim absorption with dec H+/K+ secretion at distal tubule. Therefore will be HYPERKALEMIA (retention of K+) and urine acidosis

3 tests for POSTRENAL failure
1. Physical examination – palpation of the bladder
2. Ultrasound – look for obstruction, hydronephrosis
3. Catheder – look for bleeding
Diagnosis of ARF
1. Blood tests
a. increased BUN/increased CR levels
b. electrolytes (K+, Ca2+, PO4 3-), albumin levels, CBC with diff2. UA
a. dipstick (+) for protein (3+ and 4+) suggests intrinsic renal failure due to glomerular insult
b. Microscopic examination of urine sediment is very helpful

3. Urine chemistry
4. Urine culture
5. Renal US
6. CT Scan
7. Renal biopsy

What is “first use syndrome”
chest pain
back pain
anaphylais post new dialysis machine
Lab findings of acute renal failure –> PRE-RENAL
1. Oligouria – always found in prerenal ARF (This is to preserve volume)
2. Elevated BUN to serum creat ratio = >20:1 ratio – hence the kidney can reabsorb urea.
3. Elevated urine osmolality *>500mOsm/kg water because the kidney can reabsorb H20
4. Decreased urine sodium (<20mEq/L with fractional excretion of sodium <1%) beacuse sodium is avidly resorbed (FENa <1%) 5. Elevated urine/plasma Cr ratio (>40:1) filtrate is reabsorbed
nonseminoma disease treatment for testicular tumor
orchiectomy and retroperitoneal lymph node dissection
Of the 4 types of renal stones, which is most common?
Calcium stones (80-85%) = calcium oxalate and calcium phosphate
-biconcave ovals
-radiodence (seen on KUB!)
Acute renal failure can be divided into:
I. Pre-renal (40-80%)
-causes: volume loss/sequestration, decreased cardiac output, hypotension
II. Post-renal (10-30%)
-causes intrarenal: crystals/proteins
-causes extrarenal: pelvis/ureter/bladder/urethra
III. Renal (5-15%)
-glomerulonephritis/vascular disorder/interstitial disorder/ATN
What are the clinical features of RCC

gross hematuria is the most common sxs in 70 % of pts

adominal or flank pain in 50% of pts

adominal or flank mass in 40% of pts

wt loss plus fever

paraneoplastic syndromes (epo, pth like with elevatd calcium, renin (2 htn), cortisol (2 cushings)

Nitrates in urine v. leukocytes esterase
nitrites = bacteria in urine
leukocye esterase = WBC in urine
What is renal papillary necrosis?

analgesic nephropathy (pathology to the nephron); DM nephropathy; SCD, UTO, UTI, alcoholism, renal transplant rejection

Dx: excretory urogram will show changes in both the papilla and medulla
treatment: sloughed, necrotic papilla causing urethral obstruction; treat cause and STOP offending agent

Process of hemodialysis:

How frequent?

-blood pumped to articial dialyzer outside of body through dialyzer, typically consisting of fine capillary netweoks of the semipermeable membranes. The diasylate flows on OUTSIDE of networks and fluid/solute flows on/across the membrane and re-enters circulation.

Frequency: most hemodialysis pateints require 3-5 hours of dialysis 3 days per week.

what is orthostatic proteinuria?
occurs most often in <30 yo patients
-3-5% teens affected
– dx by UA microsopy, urine protein, 24 hr collection with inc protein excretion in the upright position but normal when supine (< 50 mg/8 hr)ex: LRV entrapment or nutcracker syndrome occurs by the entrapment if the left renal vein by the aorta and sma may be the cause

treament is benigh

Hypertensive nephrosclerosis defined:

-systemic HTN with increases capillary hydrostatis pressure in the flomeruli leading to benign/malignant sclerosis

1. Benign nephrosclerosis: thickening of the glomerular afferent arterioles; develops in pts with longstanding HTN
-mild-moderate increase in creatinine levels with microscopic hematuria; protein + in urine
2. Malignany nephrosclerosis: longstnding benign HTN/undiagnosed pt will because malignant.
-dec renal function and accelerated HTN 2/2 diffuse intrarenal vascular injury
-increased in AA
-elevated BP: papilladmia, cardiac decomp; CNS changes
-renal (inc CR, proteinuria, hematuria, RBC/WBC casts, nephrotic syndrome

Dialyzable substances
ethylene glycol
magnesium-containing laxatives
3 types of ARF
1. Prerenal = decrease in RBF (60-70%) of cases
2. Renal = damage to renal parenchyma (25-40%) cases
3. Postrenal = UT obstruction (5-10%) cases
Which meds in patients with decreased perfusion causes precipitate prerenal failure?
risk factors for bladder cancer
cigarette smoking
industrial carinigens anx aniline dye or azo dye
radiation, biologic agents, coffee sweeteners
lt use of cyclophosphamide causes hemorrhagic cystitis
diagnosis of hematuria
1/ urine dipstick
2/ UA – look at sediment (RBC casts – interstitial/tubular/GN); pyuria (send urine culture) (+) blood, but no RBC think hemoglobinuria/myoglobinuria
3/ UA specimen = CYTOLOGY to detect CA
4/ 24 hour urine = treatment for Cr and protein to look at RF
5/ Blood tests
6/ IVP, CTScan, US if above doesnt dz
7/ renal biopsy last dx test
RTA type II

Defect in the ability to reabsorb HCO3- at the proximal tubule, inc in HCO3- excretion of bicarbonate in the urine and metabolic acidosis. Losses of K+ and Na+ in urine

1. Hypokalemia
2. Hyperchloremic non-anion gap metabolic acidosis

2 most common mortal complication of early ARF:
1. Hyperkalemia cardiac arrest
2. Pulmonary edema
diagnosis of testicular cancer
1. PE – palpable testicular mass
2. Ultrasound- intial test for localizing tumor
3. Markers-
-bHCG always elevated in choriocarcinoma and may be elevated in other nonseminomatous germ cell tumors like embry or teratoma or yolk sac
-AFP increasd in embryonal tumors 80% – never seen in chorio or semino4. ct scan cxr for staging

Outcome of patients with sickle cell nephropathy
Nephrotic syndrome can develop which leads to renal failure
ESRD (50%)
Ischemis injury occurs, increases risk of dehydration (imparing urine concentration)
Sickling crisisTreatment: ACEi is best

how are the electrolytes abnormalities treated in patients with CRF?
1. hyperphosphatemia – with ca2+ citrate (calcium citrate) = phos binder
2. pteitns with CRD treatent with :T pra; ca;cium and vitamin D to allow decreated seoncary hyper PTH and uremic osteodystrophy
3. acidosis – treatment underlying cause (RF) and administer bicarbonate
Treatment if history of renal stones:

HCTZ – if hypercalcemia or hypocalcuria

Allopurinal – if uric acid stones

either way – DRINK MORE WATER!

stages of prostate cancer
1. nonpalpable and confined to prostate
2. palpable nodule but confined to prostate
3. extends beyond capsule but no mets
4. mets
Diagnosis of nephrotic syndrome
1. UA – dipstick and read colors
a. albumin – detects concentration of > 30 mg/dL or higher
b. graded 0; trace; 1+ (15-30 mg/dL) through 4+ (>500 mg/dL)
c. more sensitive to albumin than Ig; thus can be false (-) if urine protein is globulin (light chains) in MM2. Urinalysis
3. Microalbuminuria

Clinical features of AIN:
Causes ARF
-rash, fever, eosinophilia
-pyuria, hematuriaDx: if pt knownto have offending agents and has the following:
RASH, fever, AR insufficiency + eosinophils – think AIN

High post residual volume can result post overflow incontinence 2/2?
autonomic neuropathy of detrouser m of bladder
How can RAS be treated?
1. REVASCULARIZATION with percutaneous renal angioplasta as the inital treatment in the majortiy of patients (PRTA)
– the > success in pts from FM dysplasia than atherosclerotic patients2. Surgery is PTRA doesnt work (BYPASS)
3. Conservative treatment therapy (ACEi, CCB) alone if PRTA and surgery are contraindicated

Absolute indications for dialysis “AEIOU”
1. Acidosis – significant, intractible, metabolic acidosis
2. Electrolytes – severe persistance hyper K
3. Intoxications – methanol, ethlyne glycol, lithium, ASA
4. Overload – hypervolemia not managed by other means (furosemide)
5. Uremia – clinical presentation, not lab values, uremic pericarditis = absolute
Diagnosis of kidney stones (nephrolithiasis)
1. UA – microscopic/gross hematuria
2. reveals associated UTI if pyria/bacteria is present
3. examine the urinary sediment for crystals – CA2+/ammonia+mg+phos/struvite stones, cystine, UA stones)
4. Determineurinary pH = alkaline urine indicates urease + bacteria (struvite) that can lead to infection OR can indicate possible renal tubular acidosis
5. ACIDIC urine is USUALLY indicative of renal stones
6. Urine culture
7. 24hr urine
8. serum chemistries
painless hematuria and dysuria frequency
bladder cancer
What is an IVP?
Intravenous pyelogram used to diagnose pyelonephritis
Treatment of CRF
1. Diet – low proteiin (0.7-0.8 g/kg) – use low salt diet (HTN, CRF, OLIGO) – restrict K+ and phos/mag
2. ACEi = dilates efferent arteriole so ^RBF and ^GFR and dec rate of ESRD
3. BP control = strict control to dec rate of prog ACEi are preferred agents
4. Glycemic control = prevents worsening if DM
5. Correct electrolytes
6. Anemia – rx EPO
7. Pulmonary edema = dialysis
What makes type IV RTA different from type I and II?
Type IV: hyperkalemia/acidic urine
Type I/II: hypokalemia/alkalosis of urineBUT both still results in metabolic acidosis with non anion gap

Prerenal treatment
1. underlying disorder
2. give NS to maintain euvolemia and restore BP but not to pts with edema/ascites
3. stopping antiHTN treatment – eliminate offenders ACEi/NSAIDS
4. If UNSTABLE = use swan-ganz monitoring for assessment of intravascular volume
treatment for testicular cancer

1. removed surgically to confirm diagnosis by inguinal approach because a scrotal incision may lead to tumor seeding of the scrotum

2. post orchiectomy, peorm a ct scan of chest abdomen and oelvis for staging
3. bHCG and AFP measurement post orchiectomy and for comparison
4. further trestment is dependent upon histology

Postrenal obstruction, if untreated, can lead to?
Acute tubular necrosis
Treatment of nephrolithiasis
1. Analgesics: morphine IV, parenteral NSAIDS (ketorlac)
2. Vigorous rehydration: beneficial in ALL forms of stones
3. Antibiotics = it + pyuria
4. Outpt management for most pts; hos admission if pain is not controlled; anuria; renal colic + UTI and or fever; strone > 1cm and unlikely to pass spontaneously
RCC characteristics
twice as comon in males than in females
– sporatic with less than two percent 2/2 autosomeal dominant VHL syndrome
– cause is unknown
– area of mets = lungs liver brain bone
Key features of nephrotic syndrome
1. Proteinuria (>3.5g/24hrs –> 2+)
2. Hypoalbuminemia (hepatic albumen syn cannot kep up with the protein loss renally) – leads to decreased plasma oncotic pressure leading to edema
3. Edema (pedal edema, periorbital, anasarca, ascites, effusion). dec albumin, increased aldosterone
4. Hyperlipidemia
Renal tubular acidosis

RTA disorder of renal tubules leading to nonanion gap hypercloremic metabolic acidosis:

-decreased H+ excreted in urine leading to acidemia and urine alkalosis with MeTABOLIC acidosis

Types: 1, 2, 4

testicular torsion v. epididymis
testicular torsion is a surgical emergency (<6hr)
-immediate detorsion and orchieoplexy to scrotum req
-twisting of spermatic cord leading to arterial occlusion and venous outflow obstruction
-adolescent male pts
-acute pain swelling and elevated testicleepididimydis
-infection to epididymis
-in children and elderl 2/2 e. coli
– young males 2/2 chlamydia or gonococcus
– swollen, tender, dysuria, fever, scrotal pain
-r/o TT and awdmin AB therapy

Monitoring a pt with ARF:
1. Daily weights
2. Intake
3. Output
4. BP
5. Watch for infection
A> Causes of hypercalciuria, hyperoxaluria
B> Causes of hypercalciuria
1. increased interstitial absorptin of calcium
2. dec renal reabsorption of calcium, leading to increased renal excretion of Ca2+
3. increase bone reabsorption of Ca2+
4. Primary hyperparaTH
5. Sarcoidosis
6. Malignancy (MM)
7. Vitamin D excess
classical triad of rcc
flank pain
abdominal mass< 10%

What is hematuria and how might “gross hematuria” be an emergency?
> 3 erythrocytes/HPF on UA
-microscopic more commonly glomeruluar in origin
-gross is more commonly associated with nonglomerular origin
-gross hematuria is common in presention of pts with BLADDER cancer (80%) and RCC in up to 40% of cases
most common findings in patients with ARF?
Weight gain
(2/2 H2O and sodium balance)
Causes of type II RTA?
wilsons dz
lead tox
nephrotic syndrome
When is a renal arteriography ordered?
evaluate for renal artery occlusion – only perform if speific therapy makes difference
most testicular cancers are ____ whereas extratesticular tumors within the scrotum are benign
Courses/phases of ATN
1. Onset
2. Oligouric phase(azotemia, uremia (10-14days); urine output <400 -500mL/day 3. Diuretic phase (urine output >500mL/day) – high urine output 2/2 fluid overload (retained salt, water, other solutes that were retained during oligouric phase)
4. recovery phase – recovery from acute tubular function
How might CRF alter the sexal reproduction function of pateints?
Hypothalamic-pituitary disturbances and gonadal response to sex hormones
1. In men = dec testosterone (gynecomastia)
2. in women = amenorrhea, infertility and elevated PROLACTIN

Rx for obstructed stone:

1. Extracorporeal shock wave LITHOTRIPSY


Most common method is the shock wave lithotripsy
-breaks apart stone; once fragmented will pass spontaneously (best if 5mm-2cm in diameter)If lithotripsy fails, use percutaneous nephrolithotomy if stones > 2cm

diagnosis of prostate cancer
DRE = carcinoma hard, nodular, irregular
-normal feels like thenar eminence
-cancer feels like a knuckle; once palpable its 60-70% likely to have mets somewhere else
-if abnormal then a TRUS is req regardless of PSAPSA = not cancer specific but can be increased with massage and needle biopsy, bph, prostatistis and age

TRUS with biopsy = repeat for definite diagnosis; indicated with psa > 10ng/dL; PSA velocity > 75 / year~ with abnormal dre

Why might patients with nephrotic syndrome have increased coaguabiltiy?
Because hepatic synthesis of clotting factors is upregulated 2/2 increased albumin production and 2/2 loss of anticoags in urine.
-increased risk of thromboembolism (DT, Rvein thrombus) PE.
_________ ______ may manifest itself as low back pain in an elderly man with prostate cancer
vertebral mets
Acute interstitial nephritis v Chronic interstitial nephritis

AIN-rapid deterioration in renal funtion and is associated with interstiail eosinophils or lymphocytes

CIN – IN has indolence coure and assoicateions with tubulointerstitial fibrosis and atrophy

Intrinsic rx of renal failure
Once ATN develops:
1. supportive therapy
2. eliminate cause/offending agent
3. if oligouric, trial of loops can help blood flow
life threatening complications in CRF?
1/ hyperkalemia – get ECG; K+ levels can still be increased without a change on ECG
2/ Pulmonary edema secondary to volume overload – look for weight gain3/infections (pneumonia, sepsis, UTI)

What is the diagnosis of/for colicky flank pain that radiates into groin that has a positive UA for blood (hematuria)
Those with nephrotic syndrome should be tested with/for microalbuminemia. Why?
-albumin excretion 30-300 mg/dayIf + perform radioimmunoassay
-most sensitive and specific test
-early sign of DM nephropathy

gold std to diagnise ureteral specific obstuction?
IV urogram
– not in preegnant women
-not in allergic patients to dye
-not in RF pts
Type II RTA Treatment
sodium restriction, inc Na+ reabsorption which inc HCO3- reabsorption in the proximal tubule
Causes of Postrenal FAILURE (ARF)
1. Urethral obstruction 2/2 enlarged prostate – BPH
2. Obstructed solitary kidney
3. Nephrolithiasis
4. Obstructing neoplasm (bladder cervix, prostate)
5. Retroperitoneal fibrosis
6. Ureteral obstruction uncommon cause because must be bilateral to cause renal failure
Glomerulonephritis in endocarditis as a secondary GN disease

1. Immune complex mediated as if that of RF

Treatment of rheumatic fever
Rx infection

seminoma treatment?
inguinal orchiectomy and radiation
Lab findings of inter/intrinsic renal failure (ARF)
Bun:Cr serum
-,20:1 because both BUN and Cr levels still elevated but less urea is reabsorbed
->40mEq with FENa > 2-3% because sodium poorly reabsorbed with decreased urine osmolarity <350 H20; renal absorptino impaired
Urine osmolarity (<350) Crur:Crpl = 20:1 –> filtrate cannot be reabsorbed thus excreted
Crur; Crpl
Studies to differentiate prerenal v. intrinsic ARF
Pre-renal Intrinsic
1. UA – hyaline abnormal
2. BUN:Cr (>20:1) <20:1
3. FENa <1% >2-3%
4. Urine Osmo > 500 mOSM 250-300 mOsm
5. urine sodium <20 >40
Hematuria + pyuria in pt with nephrolithiasis:
renal stone + infection

Urinarlysis collection:

1. three steps
a. Visual
b. Dipstick
c. Microscopic

clean catch, midsteam sample aftercleaning urethral meatus (usually adequate for UA and UC)

1. Color, clarity
2. Dipstick reactions
-pH = avg ~6 (4.5-8.0)
-specific gravity = proportional to urine osMo *~1.002 –> 1.035)
-increases with volume dec/dec when volume inc
-Protein = >150 mg/day (proteinuria); >3.5g/day (nephrotic); 50-150 mg/day ( (trace); 1+ = 150-500/day; 2+ 0.5-1.5g /day
a. proteinuria: >150 mg/day
b. nephrotic: >3.5 g/day
c. trace protein: 50-150 mg/day
d. 1+: 150-500 mg/day
e. 2+: .5-1.5g/day
-Glucose – excesive = DM
-Blood = hematuria
-Nitrites = bacteria in urine
-Ketones = DKA, starvation
3. Microscopic eval of sediment
-casts, cells, bacteria, WBC, RBC,
8. Leukocyte esterase = WBC in urine

“Analgesic nephropathy pearls”

FOrm of toxic injury to the kidney 2/2 excessive OTC use of pheactein, acetominphen, NSAIDS, ASA

Results in either: Intersitial nephritis (inflammation of interstitium of nephrons) OR renal papillary necrosis

ULtimately leads to either: ARF or CRF

What is IgA nephropathy aka (____ Dz)
Most common cause of GN is IgA
-“Bergers disease”
-asymptomatic recurrent hematuria with mild proteinuria common
-gross hemaruia post infection/exercise common
-renal function is normalmedangial deposition IgA with C3 on EMNo treatment, steroid therapy can work, good Px with RF

how can we rule out testicular torison from epididymis

toirsion is acute

torsion has no fever

Pre-renal failure (ARF)
Serum BUN/Cr >20:1
Urine mOsm/kg H20 inc >500
Dec urine Na+ <20mEq/L (reabsorbed)
FENa+ <1% Urine/plasma Cr >40:1

Nonemergent indication for = dialysis


1. Cr and Bun levels are no indications for dialysis
2. Symptoms of uremia:
-lethargy/decreased mental status/encephalopathy
Most common cause of death in patients with ARF?
Infection – 75%
Cardiorespiratory complications
Cystinuria resulting in hexagon-shaped crystals are poorly visualized?
cystine stones
upper tract obstruction causes
-kidney stones
-blood clots
-sloughed papilla
-crystal deposition
-retroperitoneal fibrosis

RTA type I leads to:
Metabolic acidosis without anion gap
urine alkalosis 2/2 decreased H+ excretion
increased susceptibiility to renal stones
—->nephrolithiasis (70-80% kidney stones)Causes: congenital/MM/nephroTOX/AI = SLE, SS/medullary sponge kidney, analgesicnephro

Treatment: administer bicarb for metabolic acidosis – prevents stones too
administer phosphate salts

MPGN as a 2ndary GN disorder
due to HCV (also HBV, syphilis and lupus)
-associated with cryoglobulin
-poor prognosis)
-RF > 50%no treatment

Suspect renovascular HTn in which 4 situations:
1. Malignant HTN >220/120 and sudde
2. No prior family hx of HTN and sudden in onset
3. Worsening and sudden
4. The HTN is not responding to standard antihistamines
which hormonally active tumor is associated with precosious puberty in children but gynecomastia in adult males
rare 5% non germ cell tumor : Leydig cell tumor
-usually benign
-if malignant then poor prognosis
What is the different between CRF and CHRONIC RENAL INSUFFICIENCY

CR insufficiency = when a patients renal function is irreverisble compromises but not failed.

Usually patients have a serum Cr 1.5-3.0 mg/dL

Preventative measures v. pharmaceutical measured for nephrolithiasis

1. Dietary – high fluid intake (2L/day) – limit animal protein intake if pt has hyperuricouria (UA stone) and limit Ca2 intake if pt has Ca2+ stones

2. pharmacologic – thiazides (HCTZ) diuretics decrease Ca2+ in urine and decrease the recurrence rates especially in pts with hypercalcuria. ALLOPURINOL is best used and effective in patients with UA stones and prevents elevated UA in urine. Good for pts on chemo

Diagnostic approach in ARF
1. Hx/physical exam
2. duration of renal failure; baseline Cr level provides this information
3. 2nd task to determine whther ARF 2/2 prerenal intra; psotrenal causes
-signs of volume depletion and CHF suggests prerenal
-allergic rxns (rash) suggests AIN and intrinsic etiology
-suprapubic mass, BPH, bladder dysfunction suggests post-renal
4. Med review

When might these be performed:

1. prostate specific antigen PSA which normal is less than four
2. digitsl rectal examination DRE
3. transurethral ultrasonography TRUS

1. if psa greater than 10ng/mL then TRUS indicated regardless of DRE
2. if abnormal DRE, TRUS with biopsy indicated regardless of psa levels
3. if psa < 4 ng/mL and DrE is negative than perform an annual follow up
4. if psa = 4.1 ng/mL and or < 10 ng/dL and DRE negative then controvery as what to do next
Tubulointerstitial diseases: AIN – acute interstitial nephritis
Inflammation of interstitium (that which surrounds GM and tubulues)
-10-15% ARF
-causes = allergic treatment to: penicillin, NSAIDS, diuretics, anticoags, phenytoin, sulfas
-infections = GAS, legionella
-CVD = sarcoidosis
Possible presentaiton of GN disease

1. Isolated hematuria
2. Isolated proteinuria
3. nephritic syndrome (hematuria, HTN, azotemia)
4. neprhotic syndrome (proteinuria, edema, hypoalbumin, hyperlipidemia, hypercoag)Dx: UA (hematuria and proteinuria)
blood test (RFT)
needle biopsy

How is AKPKD diangnosed? Treatment
Ultrasound is confirmatory- – multiple custs appear on the kidney
#2 CT scan//MRITreatment:
1. No curative therapy available
2. drain cysts if symptomatic
3. treat infection with AB
control HTN

Analgesic nephropathy is the most common form of DI-chronic renal failure. Both _____ _______ and ______ _____ nephritis are the most common pathologies that are seen with analgesic nephropathy. Patients with chronic analgesic abuse are likely to also develop:
Papillary necrosis
Tubluointerstitial nephritisAnalgesics include: ASA, naproxen that is seen after ingestion of 2-3 k of the index drug. Will have polyuria and setile pyuria )WBC casts seen)

will also develop: premature aging, atherosclerotic vascular disease, and urinary tract cancer

What is dialysis?

Artificial mechanism by whcih fluid and toxic solutes are removed from cicultaion when kidneys cannot do so sufficiently

process: blood interfaces with an articifial colution resembling human plasma (diasylate). Diffusion of fluids and solutes go across semipermeable membrane

clinical features of nephrolithiasis
renal colic
sudden pain that gradually worsens and becomes severe (patient cannot sit still)
n/v are common
ut obstuction has what clinical features?
renal colic pain = common if acute obstruction … (kidney stone, papilla) clot
recurrent UTi
Good pastures syndrome as a 2ndary disorder causing GN:
1. Triad for proliferative GN (crescenteric)
c. IgG AntiGBM AB2. Fever, malsia, RPGN, hemoptysis, cough, SOB

3. Lung DZ b4 renal (days – weeks)

What are the primary causes of renal artery stenosis?
1. Atherosclerosis
-usually elderly males
-(1/3) will occur bilaterally
-smoking and inc cholesterol predisposing factors2. Fibromuscular dysplasia
-seen in younger females especially
-will be BILATERAL 50% of the time

What is the treatment of hypokalemia?
Treat underlying cause
-d/c any meds that aggravate hypokalemia
-oral KCl (Klorcon) safest method of replacement-test always post admin
-10 mEq of Kcl inc K+ levels by 0.1 mEq / L
-slow acting/fast acting
-IV Kcl can be admin if severe hypK (< 2.5)
-admin slowly to avoid hyperK
Add 1% lidocaine to bag – POTASSIUM BURNS!
Hormone maintaining sodium homeostatis? H20 homeostasis?
What is the treatment for hypercalcemia?
Increase urinary secretion
-IV fluids (normal saline)
-diuretics (ferosemide) – inhibits ca2+ resorption LOOSE CALCIUMInhibit bone resorption in patients with osteoclastic disease
-bisphosphonates (pamidronate)

Administer glucocorticoids if vitamin D mechanism (intoxications, granulomatous d/o) + multiple myeloma

HTN plus hypokalemia =
No HTN with hypokalemia =

1. excessive aldosterone activity (bind to aldo R and inc sodium resorption which results in water retention and increase HTN

2. GI or renal loss of K+ likely

Kcl IV infusion pearls to replenish if patient is severely hypokalemic?
1. Max infusion rate of 10 mEq/hr in peripheral IV line
2. Max infusion rate of 20 mEq/hr in central IV line
3. May add 1% lidocaine to bag to decrease the pain; potassium burns by IV


Normal values:
Locations in body:
Potassium secretion

-3.5-5.0 mEq/L
-most of the potassium (98%) intracellular
hypo = elevated pH, alkalosis, insulin administratino (becuase if alkalotic then cells will push OUT H+ to decrease pH and thus decrease serum K+)
-hyper = dec pH, acidosis, cell lysis, increased serum k+ (both force K+ out of cells into the ECF)
-K+ secretion: most occurs through kidneys (80%); remainder by GI. Aldosterone role in K+ secretion

What causes an elevation in serum K+ > 5.0meq/L

A. Increased TOTAL BODY K+ due to:

1. RF
2. Addisons disease (inc primary secretion of cortisol
3. K+ sparing diuretics (spironolactone and epleronone)
4. Hyporeninemic, hypoaldosteronism
5. ACEi
6. Iatrogenic OD – exercise cause with KCl in patients with ARF
7. Blood transfusion
What is the interpretation of urine potassium in hypokalemia?
Low with GI loss (<20mEq) High with renal losses (>20mEq/L)
Most dangerous complication of hypokalemia?
-flattened t wave +/- inversion
-U-wave appears
Increased PTH, Increased urinary cAMP, increased Ca2+
Primary hyperparathyroidism with secondary hypercalcemia
Three reasons for oligourina
1. Low blood flow to kidney (assess heart – CHF)
2. Kidney problem (ARF)
3. Postrenal obstruction
-Placement of foley catheder
Patients with sepsis, fever, burns, open wounds, have high insensible losses and due to _____ _______ demand
HIGH METABOLIC demans. Increase in insensible losses (>600-900mL)/day due to
Normal output due to:
1. Urine =
2. Feces =
3. Insensible losses =
1. Urine 800-1500 mL/day
2. Stool 250 mL/day
3. Insensible losses 600-900 mL/day by sweat, hyperventilation and trachiostomies
Patients with liver failure, nephrotic syndrome, any condition causing hypoalbuminemia tends to ______-________ fluid out of the vasculature and may be totoal body hypervolemic but intravascularly depleted
Third space
For each degree of atmostpheric temp > 37 degrees C – bodys water loss increases by ___ mL/day
100 mL/day
Any disorder that decreases Co2 clearance (adequeate ventilation) can lead to?
Respiratory acidosis
If change in anion gap is ? than the change in HCO3-, then:
Metabolic alkalosis and high AG acidodid
-when AG increases, the acid must be bufferent by HCO3-, so HCO3- will dec. If HCO3- doesnt decrease, then you started at a high HCO3- (THUS must have been alkalosis meta)
With metabolic acidosis
-PaCO2 =With metabolic alkalosis
-PaCO2 =

Failure of respiratory compensation indicates an additional primary respiratory AB disorder

PaCO2 decreases
PaCO2 increases
most common cause of hypophosphatemia?
alcohol abuse
What is the normal body fluid compartment for men? for women?
Men TBW = 60% body wt
Women TBW = 50% body wt
Metabolic acidosis
1. characteristics

dec pH (<735) with a bicarb (<22 mm Hg)

goal to idenify cause

When pH is elevated (alkalotic), calcium bound to albumin will ____. Thus serum or total calcium will be ____ but ionized calcium will be low.
increased ca2+ with albumin, decreased ionized ca2+, resembles signs of hypocalcemia
#1 way to distinguish b/t metabolic acidosis with volume contraction v. volume expansion
Cl- concentration by UA – contraction if LO urine CL and expansion if elevated urine CL
Pathophysiology of metabolic acidosis
1. fixed acid (lactate) is added, H+ from fixed acid is buffernd by bicarbonate system
2. CO2 formed and removed by lungs – HCO3- levels decreased in ECF therefore kidneys reabsorb more HCO3- *new- to maintain pH

Causes of proximal RTA:

Causes of distal RTA:

Proximal RTA – decreased bicarbonate resorption = MM, cystinosis, Wilsons disease
-carbonic anhydrase inhibitors or acetozolamideDistal RTA – make HCO3- = SLE, Sjogrens, AMP B

Plasma phosphate concentration:


<2.5 >5
What is winters formula?

1.5(measured HCO3-) + 8 (+/-) 2

If PaCO2 doesnt fall within acceptable range: another prim AB d/o
If PaCO2 falls in predicted range: simple metabolic acidosis with appropriate 2ary hypercapnea.
If actual PaCO2 is higher than measured/calculated PaCO2: sign of impending respiratory failure to compensate
If PaCO2 is lower than calculated: then metabolic acidosis with primary respiratory alkalosis

Treatment if low phos?
If mild – >1mg/DL admin oral supplement
-neutra phos capsules
-K+ phos tablets
-MILKIf severe or NPO = parenteral supplement

Hypocalcemia causes:
1. Hypoparathyroidism (due to surgical disturance on parotid gland with damage to nearby PTH)
2. Acute pancreatitis – deposition of Ca2+ deposits that lowers serum Ca2+ levels
3. Renal insufficiency – mainly due to decreased products of 1,25-dihydroxy vitaD
4. Hyperphosphatemia – PO4 precipitates with Ca2+ resulting in Ca2+ Po04 deposition
Bicarbonate level obtained in a serum chemistry panel v that in an ABG?
serum chem panel (venous CO2) is amesured value and more reliable
-abg level of HCO3- is calculated
Clinical features and diagnosis of metabolic alkalosis
1. asymptomatic
2. pts medical therapy/history (vomiting, gastric drain)
3. Diagnosis:
-pH inc
-HCO3- inc
-hypoK is common
-PaCO2 is HI as compensatory mechanism due to hypoventilation
-PaCO2 exceeds 50-55 mmHg is rare, if higher indicates resp acidosis
-urine cl (SS v. SR)Treatment: NS and Klorcon (K+) if saline sensitive; address cause or give spironolactone if vol expanded (urine cl > 20 or saline R)

Three situations that can arise from met acidosis
1. A change in ANION GAP is equal to change in HCO3- = simple MA
-addition of acid causes anion gap to increase proportionally
2. the change in anion gap is less than change in HCO3-
-normal AG acidosis plus high AG acidodid (if after addtion of acid, the HCO3- is < calculated preidction, then started with decreased HCO30) 3, a change in AG > change in HCO3- then MA with HI AG
Clinical features of metabolic acidosis
1. Hyperventilation to breathe off excess CO2 produced from buffered HCO3- + H+ yielding H20 and CO2
-deep rhythmic breathing
-Kussmaul’s respirations
-compensatory response to m. acidosis2. Decreased cardiac output and decreased tissue perfusion
-acidosis decreases tissue responsivity to NE, E, DA leading to decreased perfusion, lactic acidosis, cardiac output, hypotension, tissue perfusion

Hypophosphatemia causes:

1. decreased intestional absorption due to *alcohol abuse*, vitamin D deficiency, *DKA*,malabsorption of phos; excessive use of phosphate binding antacids, hyperalimentation (TPN) and/or starvation

2. elevated renal excretion (excess PTH hormone) states if itamin D def or primary hyperparathroid)

4. Inc renal excretion with HYPERGLYCEMIA – *DKA*
5. Respiratory alkalosis, seteroids, hyperthermia, *DKA*, hungry bones syndrome

Treatment for metabolic acidosis
1. Sodium bicarb (esp for normal AG)
-takes HCO3- 24 hours to get to brain
-hyperventilation will continue until reaches brain – thus PaCO2 gets/stays low while HCO3- increases – danger combo –> [H+] = 24 (PaCO2/HCO3)2. Mechanican ventilation may be required if patient fatigued from prolonged hyperventilation especially in DKA

Hyperphosphatemia (> 5mg/DL)
1. Renal insufficiency
2. bisphosphonates; hypoPTH, VitD intox or tumor calcinosis
3. rhabdo, cell lysis/acidosis (releases P04 into ECF)1. met calcification
2. hypocalcemia can lead to neuro change

1. Phosphate binding antactids with AI-oh or carbonate; hemodialysis

Other causes of hypocalcemia?
-vitamin D deficiency
-malabsorption – SB syndome
-blood transfusions with citrated blood (ca2+ binds to citrate)
-osteoblastic metastasis
-hypoalbuminemia by IONIZED is normal so hypoalb is clinically irrelevant
Causes of MAcidosis
1. Increased AG
2. Normal AG

AG: Methanol, urea, DKA, paraldehyde, iron/isonizid, lactiv acidosis (los tissue perfusoin, shock state, excessive energy loss), ethanol/ethlyene glycol, salisylic acid

2. hyperchloremic metabolic acidosis – dec HCO3 associated with inc Cl- so that AG = normal. Renal loss of HCO3 – protimal tubular acidosis, DTA OR

-hypercholremic MA – RTA I or RTA IV
-GI loss of HCO3 (diarrhea, pancreatic fisutla, SBO, uterosignmoidostomy

The USPSTP does not have a formal recommentation for prostate cancer in patients less than 75 years of age, as there is no evidence demonstrating that screening improves mortality.

Therefore – when should a physciain discuss possible PSA screening?

If > 75 or if case/case basis
Metabolic alkalosis characteristics

increase blood pH and plasma HCO3-

uncomplicated Malkalosis typically transient because kidneys can normally excrete excess HCO3-

2 events of metabolic alk
1. Loss of H+ via gastric drainage/vomit or increased HCO3- due to ECF volume contraction
2. Mechanism that maintains m. alkalosis due to kidneys inability to excrete

54 YO M with abdominal distention. SOB, Hodgkin lymphoma dz. Alcohol use. Normal temp, BP 120/76, pulse 80/min RR 20. JVD of 7; dullness to percussion and decreased breath sounds in RL base. Abdomen distened with flui wave. Hepatomegaly present. Extremities have 2+ lower edema.

Labs: serum cr = normal (0.8); Albumin (4) = normal; BRtotal = 1 = normal; PT time normal at 11.

UA within normal limits – most likely cause of conditions?

Labs involved reveal normal hepatic functon and renal functoin. JVD and peripheral edema usually occurs 2/2 RVHF or RVinfarction. Dullness to percussion and SOB indicates LSHF – therefore what would cause both LH and RH failure?


-condition where pericardium is thickened or scarred resulting in restriction of diastolic filling. Because the heart cannot fill properly during diastole, CO is compromsied and venous pressures become crhonically elevated resulting in increased JVD, severes ascites and hepatic congeston and dyspnea and weakness On exam, KUSMAULS sin, failure of JVP to decrease on inspiration. Most common causes of constrictive pericarditis are cardiat surgery, VIRAL pericarditis, and RADIATION THERAPY.

-ddx made by calcified pericardium on CXR revealing a thickened pericardium on CT or MRI scanning or by measuring pressures during cardiac catherterization. Rx with either diuretics OR pericardiectomy.

Phosphate overview
influence on phos absorp:
Normal: 3-4.5 mg/DL
location: phosphorus in bones (85%); phosphorus in intracellular soft tissues (15%) with <0.1% ECF
influ: VitaminD controls phos absption in GI; PTH controls phos excetion in kidney, PTH inc renal ohos excretion by no allowing reabsorption. Function of kidney in maintaining PO4
ALL women who are > 65 YO per the USPSTF recommends?

A one time screening of ALL women who are 65 years and older with a DEXA SCAN of the spine and pelvis. Osteoporosis refers to decreased BONE MASS and increased fragility .

Diagnosed by omparies the bone density T score of a pateint that that of a younger individual of same gender and race. (if t score of 1.5-2.5 then osteopenia) – if score less than (-2.5) then osteoporosis. Increased fracture risk.

CLinical features of decreased < 2.5 mg/dL of phosphorus

None if mild

If severe then will have:
1. Neuro-encephalopathy, confusion, numbeness
2. MUS-weakness, bone pain, ricketts
3. HEME-hemolysis; RBC/WBC dysfunctoinand platelet dys
4. CARDIAC: cardiomyo, myo depression 2/2 low ATP
5. rhabdo
-difficulty with vent weaning


Skin rash – erythema multiforme

Doesnt gram stain.

Metabolic acidosis with anion gap?
1. Anion gap = Na – (Cl- + HCO3-)
-reflrects ion in serum but unmeausred (proteins, phosphates, organic acids, sulfates)
-normals = 8-15 mEQ/L
Multiple liver masses are much more liekly to be the result of a ______ disease rather than that of and infectious causes or primary liver malignncy. Primary tumors of the ____ tract, the _____, and the _____ are the top most common diseasses that cause liver mets.
GI tract, lungs, breast
effects of acidosis v. alkalosis
1. right shift O2 -hgb curce that diminishes O2 affinitiy to Hb and drops off thus inc delivery to tissues
2. decrease CNS
3. decrease pulmonary blood flow
4. arrhythmias
-no myoardial functoin
hyperkalemic presentalkalosis
1. decreased cerebral flow
2. left shift O2 hgb so dec O2 delivery
3. arrhythmias
4. tetany, seizures

ABS interpretation
CO2 level
-if elevated, think –
-if decreased, think -HCO3
-if elevated think
-if dec think

elevated [email protected] – rep acidosis or compensation for metabolic alkalosis (inc HCO3)
low CO2 – resp alkalosis or copensation for MA (dec HCO3)If hih tihnk MAlk or comp with respiratory acidosis
If lo think m acidosis or r. alkalosis with compensation if excess base/deficient base values in ABG indicate amt of a/b needed to titrate plasmat pH to 7.4

Diagnosis of metabolic acidosis
get patient history
calculate the AG (8-15) is normal
winters formula: expected PaCo2 = 1.5 (measured HCO3) + 8 (+/-)2
-predicts the expected resp compensation of Paco2 level to metabolic acidosis
-if PaCO2 doesnt fall within acceptable range, then patient has another primary AB disorder
Why might bolus fluids be combined with dextrose or K+ for fluid replenishment?
Leads to hyperglycemia
Leads to hyperkalemia
Causes of metabolic alkalosis
1. Saline sensitive
2. Saline resistant
Saline sensitive:
1. Urine Cl- <10mEq/L with ECF contraction and hypokalemia 2. Vomiting/NG suction 3. Patient loses Hcl, gastric HCO3- generation occurs causing alkalosis 4. Diurectics = dec ecf. Because HCO33- content remains the same, but plasma HCO3- increases because ECF contraction 5. Villous adenoma of colon, diarrhea with elevated Cl- Saline R 1. Urine Cl- >20mEq/L ECF expansion and HTN due to increased mineralocorticoids
2. 2ndary to adrenal disorder like conn’s
3. Inc aldosterone, Inc resorption of Na+ and HCO3- and an excessive loss of Cl- in urine
4. expansion secondary to increased sodium
5. Cushings; severe k+ def, Barterrs syndrome; diuretic abuse
Clinical findings of hypovolemia:
1. CNS findings: AMS, sleepiness, apathy, coma
2. CV findings: due to decreased plasma volume; ortho hypotension tachycardia,decreased pulse pressure, decrease CVP and decreased PCWP
3. SKIN: poor skin turger, hypothermia, pale, dry tongue
4. Oligourina
5. Ileus, weakness
6. ARF d/t prerenal azotemia FeNa <1% or BUN/Cr >20.
constrictive pericarditis –>
decreased diastolic filling and impairment of CO. Causes include VIRAL pericarditis, radiathion therapy, and cardiac surgery.
Treatment for hypovolemia?
1. Correct volume deficit
a. Bolus to get euvolemia
b. Start with isotonic solution
c. maintain urine output @ 0.5-1.0 mL/kg/day
d. Blood loss – *replace blood loos with crystalloid at a 3:1 ratio bc 1/3 of ECF is plasma*
2. Maintainence fluid
a. D51/2NS solution with 20mEq KCl/L most common adult maintenance fluid (dextros is added to decrease muscle breakdown)

How do we know how to calculate maintenance fluid dose in patients with hypovolemia?

2 ways: 100:50:20 v. 4:2:1

100:50:20 RULE
-100mL/kg for the 1st 10kg
-50mL/kg for the 2nd 10 kg
-20mg/kg for every other 1 kg over 20kg
-divide the total by 24 for the hourly rate of fluid replenishment
If 70 kg man = 100mL (x) 10kg + 50 mL (x) 10 kg + 50kg (x) 20 mL/kg =2500mL
-2500mL/24hr = 104 mL/hr of D51/2NS4:2:1 RULE
-4mL/kg for the first 10 kg
-2mL/kg for the 2nd 10 kg
-1mL/kg for every other 1 kg over the first 20 kg
If 70 kg man = 4mL/kg (x) 10 kg + 2mL/kg (x) 10 kg + 1mL/kg (x) 50kg =110mL
-thus 110mL/hr

Causes of hypovolemia:
1. Losses due to vomiting, diarrhea, fistula damage
2. 3rd space asites, effusion, SBO, crush injury
3. Inadequate intake
4. Polyuria (DKA)
5. Sepsis, intraabdominal and retroperitoneal inflammatory process
6. Trauma, open wounds
7. Insensible losses = 75% by skin; 25% by respiratory tract
What is the diagnosis of hypovolemia
1. Monitor urine output and daily wt (if ill and cardiac/renal dys) – then start SWAN GANZ CATHEDER (check CVP and PCWP)
2. Increased serum sodium and decreased urine sodium
3. BUN:Cr ratio > 20:1 suggests hypoperfused kidneys and thus hypovolemia
4. Increased hematocrit
5. RBC/WBC/platelets and increased ECF deficits and decreased with ECF excess
What are the causes of hypervolemia
1. Iatrogenic (parenteral over hydration)
2. Fluid retaining status: CHF, nephrotic syndrome, cirrhosis, ESRD
15 YO males comes to office within one week history of fever, nonproductive cough, sore thraot and ehadaches. Today presents with skin rash. Temp 101.3, pulse 90/min. BP 115/78 and respirations are 16.min. Throat hyperemic, but there is no cervial LAD. CTAB. Note dusky red, target shaped skin leison over all four extremities. CAR reveals itnerstitial infrilates of LLL. Sputum gram stain = PMNs but no organisms. Most likely organism?

Atypical pneumonia – M. pneumo, C. pneumo, Legionella pneumophilia, coxiella, influenza

M pneumo is the msot common atypical in amualtory setting. Distinguish from progenic penumo by indolent course, nonproductive cough and higher incidence of DPS. Low grade fever and weeks worth of symptoms are consistent with indolent course. Headache, sore throat, and skin rash = EPS.


Why might someone recovering from a MVA with head trauma and on a mechanical ventilator have an ABG of 7.54/124/20/17? (pH/Pao2/Pco2/hco3-) with HIGH URINE pH?
Mechanical ventilation can force hyper or hypoventilaton. Ventilation = TV x RR. Hyperventilation caused by increased TV and or RR results in excessive CO2 lsoses and repiratory alkalosis while hyPOventilation caused by decreased TV or decreased RR results in CO2 retentionand respiratory acidosis. The patient has respiratory alkalosis as evidenced of pH value and pCO2 value and low bicarb. The low bicarb is decreased 2/2 attempted renal compensation for respiratory alkalosis – therefore the kidneys will retain increased amounts of protons (H+) and secrete excessive amounts of HCO3- in attempt to normalie serum pH. This results in an alkalotic urine
What are the basic pathophysiologic mechanisms of syncope? What are the various types?

1. Vasovagal: common fainting spell precipitated by an emotional reaction and is preceded by presyncopal dizziness and weakness and nausea

2. Autonomic dysfcn/DI-postural HypoTN: orthostatic in nature in that it occurs on standing when blood is redistributed to the dependent parts of body. When syncopye occurs without preceding change in body position (standing) then likely to NOT be orthostatic

3. Seizure: clonic jerks may occur during syncopy if it is prolong and are due to brain hypoxia. Absense of a preivous history of seizure and the description of syncope make the diagnosis of seizure LESS common.

4. Arrhythmia: onset of syncope WITHOUT warning signs, positive presense of structual heart disease (POST MI, MVR because of characteristic murmur), and frequent ectopic beats. Another clue is HcTZ in the med list that can cause electrlyte disturbance and ventricular arrhythmias.

Which situations require intubation?
1. severe acidosis
2. PaCO2 > 60 mmHg or inabiltiy to increase PaO2 with suplemental O2
3. If patient is obtunded/deteriorated mental status
4. Impending respiratory fatigue (ensures with prolonged labored breathing)
Use of NIPPV v. Mechanical ventilation and/or intubation

NIPPV should be considered in patients with COPD exacerbation ahead of intubation. NIPPV is associated with decrease complications that are a hallmark of itubation which include infections.

1. NIPPV is recommended in a patient of respiratory distress with ABGs of pH< 7.35 or PaCO2 >45mmHg or RR > 25/min
2. If pt already

Causes of respiratory alkalosis
1. anxiety
2. PE, pneumonia, asthma
3. sepsis
4. hypoxia (inc RR)
5. mechanical ventilation
6. pregnancy inc serum progesterone levels, increase hyperventilation
7. Liver dz
8. Medication (ASA tox)
9. Hyperventilation syndrome
A 20YO female presents to office for a routine check up. No complaints and PMH insignificant. Not taking any medications and denies drug abuse. Her BP is 125/65 and HR is 80. Cardiac auscultation reveals early DIASTOLIC murmur at the left sternal border. What is the next best step in management of this patient?


Diastolic and continuous murmurs revelaed on CAuscultation should always be investigated because the probability that an organic cause is present is high. Midsystolic soft murmurs (grade 1-II/IV) in an asymptomatic pt are usually benign and need no further workup. However because this was a DIASTOLIC murmur, this should be investigated by TTE.

What is the distribution of TBW (60% of body weight)
TBW = 60% body weight – 40% body weight is intracellular fluid
ICF = 2/3 of 60% = 0.40 or 40%
TBW = 60% body weight – 40% body weight is extracellular fluid
ECF = 1/3 of 60% = 0.20 or 20%Plasma is 1/3 ECF, 1/12 of TBW, 5% body weight
Interstitial fluid is 2/3 of ECF, 1/4 TBW, 15% body weight

Causes of respiratory acidosis
Alveolar hypoventilation
-prmary pulmonary disease = COPD, airway obstruction
-NM diseases = MG
-CNS malfun = brainstem
-drug induced hypoventilation = morphine, sedatives, narcotics in postop patients possibility (pinpoint)
-respiratory muscle fatigue
Clinical features of hyponatremia include
#1 Neurological symptoms:
a. H20 intoxication – osmotic water shifts, increased ICF volume, brain cell swelling or cerebral edema
b. headache, delirium, irritability
c. Muscle twitching, weakness
d. Hyperactive DTR#2 Elevated ICP; Increased seizures, coma
#3 GI/nausea, vomiting, ileus, watery diarrhea
#4 cardiovascular: elevated BP 2/2 elevated ICP (cushings)
#5 oliguria progressing to anuria

Why would administering O2 elevated by NC in patients with O2 therapy/hypercapnic/acidosis further impede the treatment of a COPD exacerbation?
Increasing O2 alone will reduce the respiratory drive. In COPD patients, PCO2 is elevated at bareline and it doesnt stimulate the respiratory ceter, unlike in formal individuals (“AIR TRAPPING” – cannot get air out). The only drive to increase the RR is that of hypoxia therefore if you just provide O2, it will WORSEN situation because will no longer have a respiratory drive 2/2 hypoxia and the baseline PaCO2 has already been compensated for. Always provide NIPPV to provide more O2 and to washout the CO2.
Venous insufficiency results from incompetent _____ within the lower extrmeity veins. Complications include ______ _ _____ _____. Therapies for such?
chronic edema, stasis dermatitis, ulcerationleg elevation, compression stocking and wound care

42 YO patient with depression, modd swings and poor sleep. Mild headaches and muscle weakness. Has two ER visits for kidney stones over past year. she denies drug use. Her BP is 160/105 and her heart rate was 85/min. Her lab findings reveal
a CBC WNL with CMP indicative of elevated serum Ca2+. Most likely cause of patients HTN?

Parathyroid gland DZ – why?

HTN, psychatric symptoms, recurrent kidney stones, and hypercalcemia

-presentation is concerning for hyperPTH. The parathyroid gland produces PTH which acts to increase serum calcium levels and decrease serum phosphate.
-stones bones mones and groans are common with hypercalcemia
-often have increased incidence of HTN although uncommon cause

Wha are the clinical factors of respiratory acidosis
1. solmnence, confusoion, myoclonus, asterixis,
2. headaches, confusion, papilledema are signs of acute O2 retentionTreatment:
1. varify patent airway
2. If low PaO2 (<60) initiate supplemental O2 (if CO2 retainers like COPD patients, O2 can exacerbate acidosis)
3. Correct reversible causes
4. Improve alveolar ventilation
5. Intubation and mechan ventilation may be necessary for relief of acidemia and hypoxia from decreased ventilation

What are the characteristics of a COPD exacerbation and how is this managed?
COPD exacerpation occurs in pts with prior DX of COPD.
-sudden loss of breath
-no fevers, chills, sweating, n/v or hemoptysis
-meds used ipratropium albuterol MC and o2 nc
-temp WNL, BP 110.65, pulse 110 and RR = 28
-ABGs show respiratory acidosisIf the patient is having acute exacerbtaiton of COPD in the refractory phase which doenst respond to standard initial management of corticosteroids and aerosolized BDilators then use NON-invasive PPV (NIPPV) ahead of intubation. This is associated with decreased complications that are hallmark of intubation (infections).

If the patient is crashing – then intubation and mechanically ventilation should be performed.

Characteristics of metabolic alkalosis

Inc pH and dec PaCO2

to maintain pH within normal limits: HCO3- must dec so renal compensation occurs (HCO3- excretion increases). Takes hours

Acute: for each 10mmHg drop in PaCO2, HCO3- decreases by 2 mEQ/L and blood pH in by 0.08

Chroni: decrease in 10mmHg in PaCO2, HCO3- decreases 5-6 and pH decreases by 0.02

When should a VENOUS blood gas be ordered?
Venous blood gas should differ very little from arterial blood gas except for the decrease in O2 levels seen in venous blood compared to arterial blood. Venous blood that contains a similar O2 content as arterial blood may indicate a disorder of respiratory metabolism such as CYANIDE poisoning.

Respiratory acidosis defined as a pH decreased 7.35 and PaCO2 > ___.

How long might renal cmpensation take to occur?

Acute v. Chronic?

> 40 mmHg

starts 12-24 hours and takes 5 days or so to complete

Acute respiratory = immediate inc in HCO3-/inc 1 mmol/L for every 10 mmHg increase PaCO2

Chronic respiratory acidosis
-renal adaptation occurs, HCO3- increases by 4 mmol/L per 10mmHg increases PaCO2
-seen in COPD patients

How does TBW change with age and obesity?
1. TBW decreases with age
2. TBW decreases with obestity because fat contains very LITTLE H2O
Neurological symptoms + ^ ICP + Nausea + HTN (d/t ICP^) + Salivation and ^ lacrimation + oligouria (may or may not be reversible) =
Hormonal control of Ca2+
PTH: inc plasma Ca2+ – inc in bone resorption
dec plasma Phos – decrease phos resorption and increase ca2+ resorptionCalcitonin: decreases plasma Ca2+; decreases plasma PO4 but acting on BONE, GUT, KIDNEY

Vitamin D: increase plasma Ca2+/increase plasma PO4

Hypernatremia and the clinical features
1. Neurologic symtoms predominante
A. AMS, restlessness, weakness, focal neurologic deficits
B. Can lead to confusion, seizure, COMA2. TIssues and mucous membranes are dry; salivation decreases

causes of serum ca2+ > 10.5 due to malignancy

….metastatic cancer due tomprostate, kidney, lung (osteolytic), bony mets result in bone destruction by osteoclastic activity

…multiple myeloma loss of bone by tumor cells release of osteoclast activity, tumors that release pthrh

pharmacologic … vitamin d intoxication, milk alkali syndrome, drugs hctz, lithium

…other includes sarcoid, inc gi absorption of ca2+, familial hypercalciuric hypercalcemia

Causes of hyponatremia
1. Hypotonic hyponatremia (TRUE)
a. Serum osmo < 280 mOSM/kg
b. Low urine sodium (<10 meq/L) – implies sodium retention by kidneys to compensate for *extra renal loss* (diarrhea, vomiting, diaphoresis, burns, third spacing (ascites/pacreatitis) of *sodium containing fluid* c. High urine sodium (>20mEq/L) – renal salt loss due to diuretics or decrease ACEi/ATN2. Euvolemia hyponatremia – no change in ECF expansion/contraction on PE
a. *SIADH* – no fluid overload/sx d/t ANP/BNP
b. Psychogenic polydypsia
c. Postop hyponatremia
d. Hypothyroidism
e. Admin/intake of relative excess, free H2O- if patient is given D5W
f. Haloperidol, cyclophosphamide, antineoplastic drugs
3. Hypervolemia hyponatremia – d/t fluid overload states stuch as nephrotic syndrome, CHF, liver disease

Calcium metabolism
1. Normal serum Ca2+
Ranges from 8.5-10.5
-Ca2+ balance is regulated by hormonal control but levels are also affected by albumin and platelets
Characteristics of hypernatremia

Defined as a plasma Na+ concentration >145mmol/L

-refers to excess Na+ in relation to h2o can result from H2O loss or sodium infusion
-assess ECF volume clinically
A. Hypovolemic hypernatremia
B. Isovolemic hypernatremia
C. Hypervolemia hypernatremia

CLinical features of serum calcium < 8.5?
1. asymptomatic
2. rickets, osteomalacia
3. increased NM irritability
-numbness/tingling – circumorol, in fingers, in toes
-tetany (hyperactive DTR, chovosteks sign, trousseaus sign)
4. Grand mal serizures
5. *BASAL GANGLIA CALCIFICATIONS* – huge clinical clue look for in geriatric population
Isotonic hyponatremia (pseudohyponatremia)

Increased plasma solid lowers plasma sodium concentration but the amount of sodium in plasma is normal (so decreased concentration but normal content) –> this is caused by elevated albumin, protein intake, or *obesity*

Caused by any condition leading to increased protein lipid levels (TG elevated; FLP elevated)

If hypoalbuminemia, the total Ca2+ is low, but the ionized Ca2+ is normal

How is ionized Ca2+ calculated:

Ionized Ca2+ = total Ca2+ – (serum albumin x 0.8)
1. Step 1, measure ______ to determine if HI, NOR, LO
2. Step 2, if < 280, LO serum OsMo; asscess ECF volume status. Then – 2. Step 2a, if HI (>295), then –
2. Step 2b, if normal (280-295), then –
If measure SERUM OSMOLARITY and normal:
-pseudohyponatremia (elevated proteins, elevated TG); confirm with FLP
If meansure serum osmolarity and HI:
-hypertonic hyponatremia (presense of osmotic substances -elevated glu, man, glycerol)
if measure serum osmolarity and low:
-THEN assess the volume status ECF
-LOW total body sodium, and HYPOVOLEMIA:
a. Measure urine Na+
b. Lo (<10) -diarrhea, diaphoresis, 3rd spacing ascites or nephrotic syn c. Hi (>20) – renal salt loss, diurentics, decreased aldosterone, ATN
-NORMAL volume status, and EUVOLEMIA:
b. Psychogenic dyspnea
c. Postop hypothy
-HIGH volume status and HYPERVOLEMIA:
a. CHF
b. Nephrotic syn
c. Liver disease
Most cases of hypernatremia are due to which types of water loss:
1. Nonrenal loss = insensible loss, GI tract (diarrhea)
2. Renal loss = osmotic diuresis, diabetes insipidis
Treatment of hypernatremia
a. Hypovolemia
b. Isovolumic
c. Hypervolemia
1. Hypo – give isotonic NaCl to restore hemodynamics
2. Patients with DI require vasopressin thus prescribe oral fluids/if cannot drink admin D5W
3. Give diuretics (ferosemid and D5W to remove excess sodium) Dialyze patients with renal FAILURE
Causes of serum calcium levels < 8.5 mg/dL

TOtal Ca2+ (serum alb x 0.8) = ionized Ca2+

1. HypoPTH – 2/2 to surgery
2. Acute pancreatitis – saponification
3. Renal insufficiency – dec hydroxylation of vit D
4. Hyperphosphatemia – inc P04 complexes calcium
5. PseudohypPTH – end organ resistance to PTH – congenital
6. Hypomagnesemia (dec PTH) – inhibits PTH
7. Vitamin D deficiency – nutritional def.
8. Malabsorption GI – short bowel syndrome/dumping
9. Transfusions – citrate in blood complexes with calcium
10. hypoalbuminemia – low albumin, binds calcium, thus measured is decreased, but ionized fraction is normal
11. DiGeorge syndrome

Treatment of hyponatremia
ISOTONIC and hypertonic hyponatremia:
1. Treat the underlying cause
2. Hyperglycemia, mannitol, glycerol
HYPOTONIC hyponatremia
1. Mild (Na+ 12-0-130) withhold free H2O and allow patient to requilibrate spontaneously
2. Moderate (110-120) – loop diuratics
3. Severe (<110 or symp) – give hypertonic saline
SYmptoms of elevated magnesium >2.5?
ecg change = prolonged QT, T wave flattened, torsades
^ NM and CNS hyperirritability
-muscle twitching, weakness, tremors
-hyperrefllexia, seizures
-mental status change
-coexist with hypocalcemia bc of decrease release of PTH and bone resistance when MG is low.
-effect on K+ levels – hypokalemia in 50%
Treatment for hypocalcemia
-provide emergency treatment – IV calcium gluconate. Make sure mag2+ is replaced (if mag down, then Ca2+ is down)LONGTERM managment
-oral ca2+ supplements (ca carbonate) and vitD

PTH deficiency
-replacement with vitamin D plus high oral Ca2+
-thiazide diuretics plus lower urinary Ca2+ and prevents urolithiasis

Redistribution leading to secondary hyperkalemia?
translocation of K+ from intra to extracellular space (metabolic acidosis)
1. MA
2. GI bleeding
3. Tissue breakdown-rhabdo, hemolysis, burns
4. Insulin def
5. BB administration
Hypertonic hyponatremia
1. Osmotic substances that cause osmotic shift of H2O out of cells
2. Substances do not cross cell membrane and create gradients
3. Causes
a. glucose hyperglycemia
b. hyperglycemia increases osmotic pressure, water shifts from cells into ECF and dilution hyponatremia
c. For every 100mg/dL increase in blood glucose – serum sodium decreases ~3mEq/L – actual sodium content is UNCHAGED (ex BS is 400; the sodium deficit is -9mEq/Lex; Mannitol, sorbitol, glycol, maltose

If K+ and ECG change, admin ____
If shift/redistribute K+ into cells: ____, ____
Remove excess from body: ____, ____, _____
IV calcium
glucose, insulin
kayexalate, hemodialysis, diuretics
Hyponatremia characteristics:
1. TOo much H2o v Na in serum
2. {PLASMA} < 135 mmol/L
3. Symp when <120mmol/L; increased ICP post head injury. As ECF osm decreases, H20 shifts into brain. Increased in ICP more; thus must keep serum Na+ normal or slightly elevated
*indication for 3% NS when sodium is <120mEq*

How might TZDs cause > 10.5 mg/dL Ca2+

How does lithium increase calcium?

inhibits renal secretion

increases pTH levels in some patients (SQUAA CC)

NS v. D51/2NS v. D5W

NS : increases intravascular volume if pt is dehydrated or lost blood; DO NOT USE IN PATIENTS WITH CHF

D51/2NS: Standard maintainence fluid (with 20 mEq) of KCl/L of fluid; glucose is contained in it so decrease muscle breakdown and H2O for insensible loss

D5W: Dilute powdered medication; corrects hypernatremia; only 1/12 remains intravascular bc goes into TBW compartment thus NOT effective in maintaining intravascular volume.

Treatment of severe hyponatremia (<Na+ <110 mmol/L) must be done with caution = why?

Hypertonic saline rapidly increases the tonicity of ECF (increases serum Na+ by 1-2 mEw/L per hour until symptoms improve)

DO NOT increase sodium more than 8 mmol/L per hour until symptoms improve
Overly rapid increase in serium concentration may cause central pontine demyelination

Excessivelyy rapid correction of hypernatremia can lead to _____ _______. Why?
Excessively rapid correction of hyponatremia can lead to?

1. Cerebral EDEMA – as H2O shifts into brain cells, therefore the rate of correction shuld not exceed 12mEw/L/day *(<8 mEq/L in the 24 hours)*

2. Central pontine demyelination – does not increase 8 mmol/L during first 24 hours

Dx of dec serum Ca2+?
Rx if serum Ca2+ is low?
1. Get bun, cr, mag, alb, ionized ca2+
2. Obtain amylase/lipases (pancreas)
3. obtain ALTS/ASTS
4. Serum phos; HIGH RENAL INSUFFICIENCY in hypoparathyroid; low if primary vitD def
5. PTH (low if primary hypoPTH)

If patient is hypovolemic hypernatremia – admin NaCl to restore hemodynamics.

If patient is unstable, what is the first step?

Correct the hypernatremia; can wait until pt is hemodynamically stable = then replace free H2o deficiency

Water def = TBW (1 – actual Na+ (+) desired Na+)

What is milk alkali syndrome?
elevated calcium, elevated pH, renal impairment d/t increased calcium intake and absorbable antacids (calcium carbonate, milk)
Causes of pseudohyperkalemia?

Artificially increased plasma K+ due to K+ movement before venipuncture (or after). Prolonged use of tournaquit +/- repeated fist clenching. Causes acidosis and K+ loss from cells, plasma (not serum) K+ is normal

Leukocytosis, hemolysis, thrombocytosis

How might changes in pH change ratio of calcium binding?
elevated pH increased binding of Ca2+ to albumin. Thus in alkaemic states (acute resp alk), total Ca2+ is normal, but ionized Ca2+ is low and the patient manifests signs and symptoms of hypocalcemia.
Location in body:
Influences on mg secretion:
Mg abs and secretion:
1.8-2.5 mg/dL
-2/3 body mg in bone; 1/3 intracellular 1% mg is extracellular
-insulin/glucagons, PTH, calcitonins, ADH, steroids influence
-30-40% dietary mg absorbed in GI but inc when Mg levels fall
-kidney can resorb Mg and is major regulation of Mg balance
Post parathyroidectomy, DKA, thyrotoxicosis, lactation or burns, pancreatitis can decrease levels of ?
D5W is not effective to maintain _____ volume. Lactated ringers solution is indicated for?

Intravascular (only 1/12 will remain within compartment – used for medication like insulin)

Lactated ringers solution is excellent replacement of intravascular vol. It is not a amaintaining fluid. It is the most common trauma resusscitation fluid. Do NOT use if hyperkalemia is a concern (contains K+)

Hospitalized patients usually have LOW serum albumin concentrations thus patients will concomitatntly hanve decreased ____. Always look at albumin lelvels in relation to decreased serum CA and adjust.
Decreased magnesium with ____ serum Ca2+ and _____ serum K+
decrease ca2+ d/t dec PTH when Mg low
decrease in 50% in muscle and myocardium, when intracellular (1/3) total Mg or K+ decreases, corresponding decrease in other cation takes place.
Water exchange: What is normal intake? Normal output?

Normal intake = 1500 mL in fluids taken PO/day; 500 mL solids or product of oxidation

Normal output = from 800-1500 mL urine/day minimum urine output to excrete products of catabolism = 500-600mL per day

250 mL from stool and 600-900 mL/day from insensible losses

causes of hypercalcemia >10 mg/dL due to endocrine
…renal failure that results in hypocalcemia but hyperpth can inc pth high enough to cause hypercalcemia
…pagets disease of the bone due to osteoclastic bone resorption
…hyperparathyroidism, acromegaly, addisons disease
CLinical features of hypercalcemia
1. Stones – nephrolithiasis, nephrocalcinosis
2. Bones – bones/ascited/pains/osteitis fibrosa cystica (brown tumors)
3. Grunts/groans-muscle pains, pancreatitis, PUD, GOUT, constipation
4. Psychiatric overtones-depression/fatigue, anorexia
5. Polydipsia, polyurea
6. HTN
7. Wt loss
8. ECG – short QT if hypercalcemia

most important effect of hyperkalemia is on the heart


Elevated or peaked T waves by 10 mm
prolonged PR
widened QRS and merged QRS with T
vFIBB cardiac arrest
Causes of hypomag

GI: malabsorption, steatorrheic states, prolonged fasting, fistulas, pt on TPN without MG2+ supplementation

Alcoholism: common cause
Renal causes: SIADH, Diuretics, Bartters syn, renal xplant, drugs like gentamycin, AMPB, cisplatin

Hypervolemia with hypotonic hyponatremia

Low urine sodium *(<10mEq/L)* due to H2O retention status. Excess H2O>Na+

B. Nephrotic syndrome
C. Cirrhosis/liver disease

Treatment of mild hypomag (<1.8)?

Treatment if severe?

Oral mag (magnesium oxide)
prenteral mg2+ (mag sulfate)
How might hyponatremia be diagnosed?

1. PLasma osmolarity will be LOW in a patient with true hyponatremia

2. Urine osmolarity will be elevated if increased levels of ADH (SIADH, CHF, hypothyroidism); or urine osmolarity will be LOW if kidneys are responding appropriately by diluting the urine and retaining the sodium via aldosterone

3. Urine sodium concentration will be low in a setting of decreased sodium serum. Urine sodium concentration > 20 mmol/L is consistant at salt wasting/diuretics
Urina [Na]>40 is consisitance with SIADH

Hypercalcemia v. Hypocalcemia on ECG?

If > 10.5 mg/dL then will have shortened QT interval

If < 10.5 mg/dL then prolonged QT interval

Method of fluid replacement therapy
1. normal saline
2. D51/2NS
3. D5W
4. Lactated ringers solution
Hypovolemic hypernatremia:
Isovolemic hypernatremia:
Hypervolemic hypernatremia:

1. Sodium stores are depleted, but more water loss than Na+ loss; renal loss from diuretics osmotic diuresis (due to glycosuria in DM type I), renal failure. Extrarenal loss from diarrhea, diaphoresis, resp losses

2. Isovolemic hypernatremia sodium stores normal H2O lost; diabetes insipidis; insensible losses respiratory (tachypnea)

3. Iatrogenic (most common) cause of hypervolemia hypernatremia; large amounts of parenteral sodium-bicarb, TPN. Cushings or saltwater drowning.

Diagnosis of hypernatremia
1. Urine volume should be low if kidneys are responding approprately to hypernatremia (want to dilute)
2. Urine osMo > 800 mOsm/kg
3. desmopresion should be given to differentiate nephrogenic from central diabetes insipidis if diabetes insipidis is suspected
How might fluid volume be assessed?
1. Tracking input and output is not an exact method bc cannot accurately calculate insensible losses = monitor urine output is VERY important becase normal URINE OUTPUT is greater than 1 mL/kg/hr.
2. Low urine output = volume depletion**Daily weights can get an accurate assessment as well

How does albumin and pH affect Ca2+?
1. Albumin = Ca2+ in plasma exists in 2 forms
a. Protein bound
b. Free ionized formA. Protein bound = most ca2+ ions bound to albumin so total ca2+ flux with protein (albumin) concentration.
B. Free ionized = physiological active fraction under tight control (PTH) independent of alb levels.

Hypoalbuminema = total Ca2+ low but ionized calcium is normal

Treatment of hyperkalemia
1. If severe or ecg change = IV CALCIUM
-stabilized resting membrane potentioal of myocardial membrane and dec excitatbilityTHEN

2. Shift K+ into intracellular compartment my admin
-glucose and insulin – glucose stimulaties insulin from b cells but exogenoush more rapid. Admin both and prevent hypoglycemia

3. Sodium bicarbonate – to increase pH level to force K+ into cells; used in emergency for severe hyperkalemia


4. Removed K+ from body
-Kayexalate – GI potassium exchange resin (Na/K+) exchange absorbs K+ in colon and prevents reabsorption in stool.

5. Hemodialysis
-most rapid and effectivel way to lower K+ in plasma; reserved for intractible hyperK and those with RF

6. Diuretics furosemide

Which three organs are responsible for calcium balance (PTH, Calcitonin, and vitamin D)?
1. Parathyroid, GUT, KIDNEY
Features of hyperMAG
nausea, weakness, facial paresthesias,* loss of DTR (CLASSICALLY THE FIRST SIGN*), ecg resembles that of hyperK with increased PR and wide QRS with elevated T waves.
-death is usually caused by respiratory or cardiac failure.-death usualy caused by resp failure or cardia arrest

Treatment of hypermag
do not admin exogenous mag
-IV calcium gluconate for emergent symptoms for cardioprotection
-admin saline and furosemide
-order dialysis in RF patients
-prepare to intubate if respiratory depression is severe
Water homeostasis

1. OsmoR in hypothalamus stimulated if plasma hypertonicity (normal >295). Activation of stimulators produces thirst

2. Hypertonic plasma increases ADH release from posterior pituitary gland to dilute the plasma. Thus ADH –> V2R –> AQP2 at collecting duct –> H2O retention

3. ADH decreases as osmolarity of plasma decreases

PTH v. Calcitonin v. Vitamin D
-PTH: high calcium resorp, dec phos resorp
-Calcitonin: dec calcium absorp; increase po resorption
-VitaminD: increase ca2+ resorp and dec phos
-PTH: vitamin d resorp
-Calcitonin: decreased postprandial o2 absorption
-VitaminD: inc Ca2+ absorption, inc po43-
-increased Ca2+ breakdown, increased po43- breakdown
-Calcitonin: dec bone turnover, inc bone breakdown
Salt and water regulation

Sodium regulation is intimately associated with H2o homeostasis; yet it is regulated by independent mechanism

1. Change in sodium concentration reflects that of water homeostasis
2. Change in sodium content reflects that of sodium homeostasis

1. Change in sodium balance = hypo/hypervolemia
2. Change in water balance = hypo/hypernatremia

Hypermagnesemia causes:
1. RF (most common)
2. Early stage burns, massive traumas, surgical stress, severe ECF volume deficit, severe acidosis
3. Excessive intake of magnesium-containing laxatives or antacids combined with renal insufficiency
4. Adrenal insufficiecy
5. Rhabdo
6. Iatrogenic-preeclam[sia or ecclampsia
Diuretics action on sodium homeostasis
Inhibits Na resorption in renal tubular system.
1. Ferosemide and other loop diuretics inhibit the Na-K-CL cotransporter in TALH;
2. HcTZ inhibits Na-Cl cotransporter at the early distal tubule.
What are the features of hypovolemia?
1. Weight gain
2. Peripheral edema
3. JVD
4. Elevated CVP and PCWP
5. Pulmonary edema/rales
6. Low HCT and albumin concentration

Decreased renal perfusion pressure results in activation of RAAS:

Aldosterone with bind to ______ receptor and result in an increase in ______ retention and ____ excretion. Also acts?

Aldosterone R
sodium retention
potassium excretion (hypokalemia)Type A intercalated cells to retain H+ ions

Diagnosis of increased Ca2+
Same labs as if hypocalcemia: BUN, Cr, CO2, Cl-, K+, amylases, lipases, LFTs
-radioimmunoassay of PTH = inc if primary hyperPTH (low in malig)
-radioimmunoassay of PTHrP = inc if malig
-Bone scan/survey to identify lytic lesions
-inc urinary cAMP = inc if hyperPTH
Features of hypokalemia?
Arrhythmias – prolongs normal cardiac conduction with muscular weakness, fatigue and paralysis, muscle cramps.
Decreased DTR-
Paralytic ileus
Makes digitalis tox worse
Why must K+ levels be monitored in patients with hypocalemia or on digoxin?
bc likely to be on diuretics as well for CHF. Thus this would cause decrease in K+ thus hypo K predisposes patients to digoxin tox – futhermore if pt who is hyperkalemic requires Calcium gluconate for cardioprotection –> D/C digoxin bc hypercalcemia also increases risk of digoxin toxicity!
Treatment of hypervolemia
1. Fluid restriction
2. Judicious use of diuretics
3. Monitor urine output and daily weights and consider swan ganz catheder placement depending upon patients condition
Cause of hypokalemia? < 3.5 mg/L
1. GI loss
-vomiting/NG drainage (decreased vol; metabolic acidosis)
-intestinal fistulas2. Renal losses
-renal tubular/parenchymal disease
-Mg2+ def
-primary and secondary hypoaldosteronsim

3.other causes
-insulin administration
-decrease dietary intake

-Bactrim or Amphotericin B

5. Trauma
-cell lysis results in release of K+ however, in trauma there are HIGH levels of epinephrine from physiologic response which results in shunting of massive amounts of K+ into cells.

What is the homeostasis of Na+

1. Sodum actively pumped out of cells is decreased and restricted to extracellular space. Osmotically active cation of the ECF

2. Increased sodium intake results in inscreased ECF volume and elevated GFR and elevated sodium exretion

3 If ECF decreases, ECF decreases, and there is a decrease in sodium excretion with an increase in sodium retention

What is Bartters syndrome?
Chronic volume depletion secondary to an AR defect in sodium reabsorption in the TALH leading to hyperplasia of JGA; increases renin which leads to secondary aldosterone hypersecretion
what are signs of volume overload
elevated JVD
pulmonary rales – due to pulmonary edema
peripheral edema
low albumin/low hct
effect of pH on calcium levels
elevated pH alkalosis will increase affinity albumin has for calcium and thus bind a larger portion of the free ionized calcium –> reducing the physiologically active form and precipitating symptoms of hypocalcemia. Adverse is true for acidosis, pt will have symptoms of hypercalcemia.
What is the diagnostic criteria for MM?
At least 10% abnormal plasma cells in bone marrow PLUS (1) of the below:
1. M-protein in the serum
2. M-protein in the urine
3. Lytic bone lesions (well-defined radioluencies on radiographs) – redominantly found in the skull and axial skeleton
What is NHL?
Occurs by the malignant transformation and growth of B and T cells or their precursors
Splenic sequestration crisis is?

The sudden pooling of blood into the spleen results in rapid development of splenomegaly and hypovolemic shock

– potentially fatal complication of SCD and b-thalassemia) curring more commonly in children because they have intact spleens.

Features of CLL:
1. Asymptomatic – found incidentally on CBC
2. Painless LAD
3. Splenomegaly
4. Frequent respiratoy or skin infections 2/2 immune deficiency
5. More advanced disease: fatigue, weight loss, pallor, skin rashes, easy bruising, bone tenderness and abdonminal pain.
Causes of thrombocytopenia:
1. Decreased production 2/2:
a. Bone marrow failure:
aquired aplastic anemia
congenital (Fanconis anemia)
congenital intrauterine rubella
b. Bone marrow invasion:
tumors, leukemia, fibrosis
c. Bone marrow injury: drugs (ethanol, gold, CA chemo agents, chloramphenicol), chemicals (benzene), radiation, infection2. Increased destruction
a. Immune: infection, DI, ITP,SLE, HIT type 2, HIV-assocaited thrombocytopenia

b. Nonimmune: disseminated intravascular coagulation dIC, Thombotic thromboy=cytopenic purpura (TTP), HIT type I

3. Sequestration from splenomegaly
4. Dilutional – after transfusions or hemorrhage
5. Pregnancy – usually an incidental finding (especially third trimester) but can also occur in setting of pre-eclampsia or eclampsia (remember HELLP syndrome)

Clinical features of Hemophilia A
1. Hemarthrosis (factor VIII) – KNEES most common site
a. progressive joint destruction can occur 2/2 recurrent hemarthrosis
b. maintaining normal factorVIII levelsby prophylactiv administration of factor VIII concentrate can minimize joint dectruction
c. SYNOVECTOMY (arthroscopic) or radiosynovectoy may be needed if recurrent hemarthrosis occurs despite optimatl medical management2. Intracranial bleeding
a. second most common cause of death (AIDS due to past history of transfusions)
3. Intramusclar hematomas
4. Retroperitoneal hematomas
5. Hematuria or hemospermia

Sickle Cell Anemia
General characteristics:
1. Autosomal recessive disorder that results when the normal hemoglobin A chain is replaced by the mutant Hb S. Sickle cell disease is caused by inheritance of two Hb S genes where as sickle cell trait is caused by the inheritance of one HbS gene (heterozygous)
What are the three major subtypes with varying severity of vWD:
1. Type 1 (most common)- decreased levels of vWF
2. Type 2 (less common)-exhibits qualitative abnormalities of vWF
3. Type 3 (least common) – absent vWF (severe dz)

Most common critically ill patients (in ICU) usually are diagnosed with >>> however it can occur in healthy patients as well

-can be acute and fatal or more gradual


Severity of thrombocytopenia and associated risk

1. Platelet count: > 100,000
2. 20,000-70,000
3. < 20,000
4. < 5,000

1. > 100k: abnormal bleeding (even after trauma or surgery) is usual
2. 20-70K: Increased bleeding hemorrhage during surgery or trauma
3. < 20K: minor spontaneous bleeding: easy bruising, petechiae, epistxis, menorrhagia, bleeding gums
4. < 5K: Major spontaneous bleeding; intracranial bleeding, heavy GI bleeding
Protein C deficiency
-autosomeal dominant inheritence
-inhibitor of factors 5 and 8 thus deficiency leads to unregulated finbrin synthesis
What are the clinical features of ITP:
1. Petechiae and ecchymoses on the skin
2. Bleeding of the mucous membranes
3. NO splenomegaly
Name one intermediate NHL
Diffuse Large-Cell Lymphoma:
1. B-cell origin
2. Middle-aged and elderly patients
3. Locally invasive; presents as large extranodal mass
4. 80% cure rate with CHOP
What is a MACROCYTIC anemia?
1. MCV > 100
2. Vitamin B12 is involved
a. Cofactor in coversion of homocysteine to methionine
b. cofactor in coversion of methylmalonyl CoA to succinyl CoA
3. Vitamin B12 stores in the liver are plentiful and can be sustained for 3 or more yrs
4. Vitamin B12 is bound to intrinsic factor (produced by gastric parietal cells), so it can be absorbed by the terminal ileum.
What is Sezary syndrome?
NHL involving the skin and bloodstream
What is the therapy for AML?

7 + 3

*Induction therapy
3. DAY 14 BMBx

IF ANC < 1000 and or platelets <100K –> 5 + 2 which includes
1. 5 days of CYTARABINE
****WAIT 7 days
3. DAY 12 BMBx

IF STILL blasts after 2nd BMBx post induction and re induction with 5+2, then performthe HiAM treatment


IF ANC > 1000 or PLT > 100K

1. Start CONSOLIDATION therapy which includes: HiDAC + Dasatinib for 21 days
2. Gets three cycles total

What is the prognosis of a patient with SCA? (sickle cell anemia)

Survival correlates with the frequency of vaso-occlusive crisis – the more frequent crisis are associated with a SHORTER LIFESPAN

If there are more than three crises per year, the median age of death is 35 years. Patients with fewer crises per year may live into their 50s. (<3/years = 50YO lifespan)


How might Hereditary spherocytosis be diagnosed? Treated?
Diagnosed: RBC osmotic fragility to HYPOtonic saline (because it tests ability of RBCS to swell in a graded series of hypotonic solutions and because of their shape, spherocytes tolerate less swelling before they rupture, thus they are OSMOTICALLY FRAGILE and undergo lysis at a HIGHER oncotic pressure.
-INCREASED retic count with elevated MCHC
-Peripheral blood smear would reveal spherocytes
-Direct coombs test result in negative which is helpful to distinguish from AIHA in which spherocytes are also seen
When might platelet transfusions be necessary:
1 unit raises platelet count by 10,000
What is the significance of ordering a SCHILLING TEST?
gives information regarding cause of b12 deficiency
-give an IM dose of unlabeled vitamin b12 to saturte binding sites
-give an oral dose of radioactive b12; measure amount of b12 in urina and plasma to determine how much b12 was absorbed
-repeat the test (oral radioactive b12) with the addition of IF. If malabsorption is the problem then adding IF will not do anything. HOWEVER if pernicious anemia is present, then adding IF will improve the serum vitamin B 12 levels.
What is the first step to perform in an anemic patient:
Assess volume status and hemodynamic stability.
If unstable, transfuse PRBCs before attempting to find the cause of the anemia
How to readily treat CLL with chemotherapy:
No current chemotherapy that can permanently treat CLL the only one we current have “treats the grass” – will continue to grow, then “debulk” by chemo but we never get rid of all the “grass” completely. Then eventally grass grows and needs to be “cut” again.

The type of lymphocyte involved and its level of differentiation determines the course of the disease and its prognosis.

B cell lymphocytes account for __% of all cases; T cell lymphocytes acct for ___% of all causes

=disease starts in the node and then spreads to blood and bone rather than node to node as seen in Hodgkins.

Treatment of essential thrombocytosis
1. Antiplatelet agents (anagrelide and low dose ASA)
2. Hydroxyurea if severeBMB will show increase MEGAKARYOCYTES

Staging system used for Hodgkins lymphoma?

Ann Arbor staging system

Stage I: confined to 1 node
Stage 2: involvvement of two or more lymph nodes but confied to same side of diaphragm
Stage 3: Both sides of diaphargm inovlvedl
Stage 4: dissemination of disease to to extralymphatic sites

What are the cell lines of the myeloid class?
RBC, platelets, granulocytes (neutro, eosino, baso)
Intravascular hemolysis v. Extravascular hemolysis (hemolytic transfusion rxns)
-very serious and life threatening – caused by ABO mismatched blood transfused into patient.
-fever, chills, n/v, pain in the flanks/back, chest pain, dyspnea
-complications include hypovolemic shock (hypotension.tachycardia), DIC, RF with hemoglobinuria
-management involves stopping the transfusion immediately and aggressively replacing the fluid to avoid shock and renal FAILURE.2. Extravascular hemolysis (also called delayed hemolytic transfusion reactions)
-extravascular hemolysis is less severe and in most cases is self-limited; it may occur withint 3-4 weeks after a transfusion
-caused by minor RBC antigen –> If patient is Kell antigen-negative and has anti-Kell IgG antibodies from a previous exposure to the antigen, reexposure of her memnory B cells to Kell antigen on RBC cells will result in synthesis of IgG anti-Kell antibodies. These AB coat all of the Kell antigen-positive donor RBCs, which will be removed extravascularly by macrophages in the spleen, liver, and bone marrow.
-Managment – none, good prog

What are the clinical features of vWD

Cutaneous and mucosal bleeding – epistaxis, easy bruising, excessive bleeding from scratches and guts with gingival bleeding.

Menorrhagia that affects more than 50% of women with vWD

GI bleeding possible

What is lymphoma?

cancers of the lymphatic system in which there are two types:

1. Hodgkins Disease
2. NHL

lymphadenopathy is usually the first finding

Myelodysplastic disoders often lead to
Why might a prolonged PT in a patient with cirrhosis be a poor prognostic factor?
Because only in SEVERE LIVER DISEASE does the PT become prolonged
What is waldenstrom’s macroglobulinemia?
proliferation of plasmacytoid lymphocytes that produce IgM paraprotein which is large and causes hyperviscosity in the blood.
-DIAGNOSIS WHEN IgM > 5G/DL; BENCE JOINES PREOTEINURI IN 10% of cases – but NOT ANY bone lesions so can r/o MM
What is the classification of NHL?
>20 different subtypes of NHL
-the “working classification system” is the most common and classifies accprding to histologic grade: low grade (indolent), intermediate grade, and HIGH grade
Teardrops on the peripheral smear with bone marrow aspirates showing marrow fibrosis that if severe enough causes a dry tap.
Agnogenic myeloid metaplasia with myelofibrosis
What is the clinical feature of Hodgkins disease:
1. Most common symptom is a painless LAD
2. Supraclavicular cervical, axillary, mediastinal lymph nodes
3. Spreads by continuity from one lymph node to adjacent lymph nodes
4. Other presentations may or may not be present, including B symptoms, pruritis and cough
What is the treatment for SCA?
1. Advise the patient to avoid high altitudes (low o2 tension can precipitate crisis)
2. Maintian fluid intake (dehydration can precipitate crisis)
3. Treat infecions PROMPTLY (infection/fever precipitates crisis)1. Early vaccination for S. pneumo; H. influ; Pneumovax, Neisseria meningitis
2. Prophylactic penicillin for children until 6YO-start at 4 months
3. Folic acid supplements (due to chronic hemolysis)
5. Management of painful crisis
-morphine for pain
-keep patient warm
-supplemental O2
6. HYDROXYUREA-enhanves HbF levels which interferes witht he sickling processing and results in reduced incidence of painful crisis and accelerates healing of leg ulcers and may reduce recurrence.
7. Blood transfusion – NOT USED UNLESS NECESSARY!! Based on clinical condition and NOT the Hb levels.
-acute chest syndrome
8. BMT-this has been performed successfully to treat SCA but is not routinely performed due to matched donor avilablilty and risk of copmlications. It may be more cost-effective in the long run that conservative therapy.

Signs of aplastic anemia
1. Fatigue and SOB
2. signs and symptos of thombocytopenia (petechieac, easy bruising
3. Inreased incidence of infections due to neutropenia
4 Can transform into acute leukemia
Causes of spherocytosis include:
1. Hereditary spherocytosis
2. G6PD deficiency
3. ABO incompatibility (but not Rh incompatibility)
4. Hyperthemia
5. AIHA (autoIMMUNE hemolytic anemia)
How is heparin administered?
Two ways:
1. Standard heparin
What makes HbS differ from HbA?
The substiution of an uncharged (neutral) valine for a negatively charged glutamic acid at the 6th position of the B chain yeilds a newly POLAR molecule that has a changed structure after the initial binding and release of O2.
Clinical features of Vitamin k deficient coagulopathy:
1. First finding is a prologed PT
2. PTT will begin to diminish as other clotting factors decrease
Fresh frozen plasma (FFP) is used for?
1. Contains all of the clotting factors
2. Contains no RBCs/WBC/platelets
3. Given in patients for high PT/PTT, coagulopathy, and deficiency of clotting factors – FFP can be administered if you cannot wait for Vitamin K to take effect, or if pateint has liver failure (in which cause VK will not work)
4. Follow up PT and PTT to assess response


a. MOA
b. Indication for use
c. Administration

a. MOA- a vitamin K antagonist – leads to a decrease in vitamin K -dependent clotting factors 2, 7, 9, 10 and protein C and S. Causes prolongation of PT (and increases INR).

** it takes 4-5 days for the anticoagulant effect to begin therefore start heparin as well if the goal is acute anticoagulation because heparin has an immediate effect. Once warfarin is therapeuic by checling INR, then stop the heparin and continue warfarin for as long as necessary.

b. same as heparin but used for LT anticoagulation
c. administered orally – must give heparin first as soon as pTT is therapeutic, inititate warfarin. Continue heparin for at least 4 days after starting warfarin. Once INR becomes therapeutic, stop heparin. THe level of INR in most causes is therapeutic from 2-3

Hemophilia A
-affects male patients primarily
-caused by deficiency or defect of factor 8 coag protein
-bleeding tendency is related to factor VIII activity
If rapid reversal of acute bleeding from warfarin is indicated, administer?
What are the clinical features associated with thrombocytopenia?
1. Cutaneous bleeding; petechiae (most common in dependent areas), eccymoses at sites of minor trauma
2. Mucosal bleeding: epistaxis, menorrhagia, hemoptysis, bleeding in GI and genitourinary tracts
3. excessive bleeding after procedures or surgery
4. ICH and heavy GI bleeding can be life threatening and occur when platelets are SEVERELY LOW
5. Unlike coagulation disorder (eg hemophilia) heavy bleeding into tissues and joints (hemarthrosis, hematomas) is not seen in thrombocytopenia!!
How can hemolytic anemias be classified?
1. Hemolytic anemia due to external factors to RBC defects (aquired)
-immune hemolysis
-mechanical hemolysis
-medications, burns, toxins
2. Hemolysis due to intrinsic RBC defects – most cases are inherited
-hemoglobin abnormality (SCA), hemoglobin C disease, thalassemia
-membrane defects: hereditary spherocytosis; paroxysmal ND (PND)
-enzyme defects: G6PD, PK deficiency
3. Hemolytic anemia INTRAVASCULAR — within circulation
4. Hemolytic anemia EXTRAVASCULAR–within the RES, primarily the spleen but can include the lymph notes, bone marrow

What is the treatment regimen for ACUTE LEUKS


1. Treatment of emergenies
a. Blood cultures and AB if infectious
b. Blood transusions for anemia anad platelet transfusion for bleeding. If needed
2. Aggressive combo chemo in HIGH doses for several weeks to obtain remission (absent leukemic cells in bone marrow). One remission occurs, maintenance therapy is used for months to years to prevent recurrance3. ALL – more than 75% children with it achieve complete remission. WHen occur (relapse) usually response to treatment with aggressive therapy adding 15 years to life. Up to 50% of all ALL patients are cured

4. AML: more difficult to treat and doesnt response well to chemotherapy Survival rates are considerably lower dspite intenive treatment. Bone marrow transplant gives the best chance of remission

5. BMT

B-Thalassemia v. A-Thalassemia

B-thal: B production is deficient but synthesis of alpha is unaffected. Excess a-chain bind to and DAMAGE the RBC membrane. Severity depends upon quantitiative amt of mutation

A-thal: there is a decrease in alpha chains which are a component of ALL tpyes of hemoglobin. The b-globin chains form tetramers which are abnormal hemoglobins. The severity depends on th number of gene loci that are deleted/mutated – it ranges from an aymptomatic carrier state to prenatal death

Causes of DIC:
1. Infection (gram neg sepsis most common like N. Meningitis)
2. Obstetrial complication
a. placenta and uterus have increased TFactor
b. amniotic fluid emboli
c. retained dead fetus
d. abruptio placenta
3. Major tissue injury – trauma , major surgery, burns, fractures
4. Malignancy – lungs, pancreas, prostate, GI tract, acute promeylocytic leukemia
5. Shock, circulatory collapse
6. Snake venum (rattlesnakes
Leukemoid reaction versus CML leukemoid reaction:
1. Usually no hepatosplenomegaly
2. Increased leukocyte alkaline phosphatase
3. History of a precipitating event (eg infection – CML
-opposite to the above findings
WHy might coag failure occur in liver?
1. Decreased synthesis of clotting factors
2. Chlestasis leads to decreased vitamin K absorption, which leads to vitamin K deficiency
3. hypersplenism (splenomegaly due to portal hypertension causing thrombocytopenia)
Name 5 causes of Normocytic (MCV 80-99) anemia with a normal to LO reticulocyte index:
1. Bone marrow fibrosis
2. Aplastic anemia
3. Tumor
4. Anemia of chronic disease
5. Renal failure
Name three types of a-thalassemia related disorders
1. Silent carriers
2. A-thalassemia trait (or minor) – mutation/deletion of two alpha loci that is common to african americans
3. HB H disease – mutation/deletion of three alpha loci
-hemolytic anemia, splenomegaly
-significant microcytic, hypochromic anemia
-hemoglobin electrophoresis shows HbH
-treatment is same as for paitnes with B thal major (continuous transfusions)
or possible splenectomy
4. Mutatoin/deletion of all found alpha loci-this is either fatal at birth (*HYDROPS FETALIS) or shortly after
Which lab studies should be ordered if suspected hemolytic anemia?
1. LDH
2. Haptoglobin
3. Bilirubin
Sideroblastic anemia usually manifests as a ______/_______ anemia simulating iron-def anemia. Only different is that iron studies will show high serum iron levels and low TIBC. In patients with an identifiably cause of vitamin b6 deficiency like _____ or _____, the administration of pyridoxine can easily correct the problem.
hypochromic, normocytic
drugs or alcohol (isonized)
What makes factor 8 unit (clotting factor)
Has two portions:
1. The coagulant portion (factor 8 coagulant protein) and an antigenic portion (factor VIII antigenic protein). The latter is synonymous with vWF
Under decreased O2 conditions, (acidosis, hypoxia, changes in termparture, dehydration and infection) the Hb molecules polymerize, causing the RBCs to sickle. How do sickled cells affect the vessels?
They cause obstruction leading to ischemia of the small vessels
Diagnosis of Hodgkins lymphoma
1. Lymph node biopsy: REED STERNBERG CELLS is required to make a diagnosis
a. Neoplastic, large cell with two or more nuclei “owl eyes”
b. B-cell phenotype
c. reed sternburg cells seen in other neoplasma2. INflammatory cell infiltrates which distinguishes it from NHL because these cells present are reactive to the RS cells. These include plasma cells, eosinophils, fibroblasts and T and B cells

3. CXR and CT scan of the chest and abdomen to detect lymph node involvment
4. Bone marrow biopsy – to evaluate bone marrow involvement
5. Laboratory findings – leukocytosis, eosinophilia; level of ESR elevation sometimes corresponds with disease activity

In elderly patients with iron deficiency anemia (normocytic with low reticulocyte) – what must be RULED OUT
Colon cancer
What is the treatment for DIC
1. management of condition that caused DIC (infection or obstetrictic or trauma or shock or snake venom)
2. supportive: FFP replaces clotting factors; platelet transfusions; cryo replaces clotting factors and fibrinogen; low dose heparin (IV or SC) inhibits clotting and can prevent consumption of clotting factors.
3. admin [email protected] and IV fluids, maintain BP and renal perfusion
How is PNH diagnosed?

Ham’s test: the patients cells are incubated in acidified serum, triggering the alternative complement pathway,, resulting in lysis of PNH cells but not normal cells

Sugar water test: patients serum mixed in sucrose. In PNH, hemolysis ensues

FLOW cytometry: anchored surface protens CD55 and CD59 are much more sensitive and specific for PNH

Chronic Lymphocytic Leukemia
Most common leukemia that occurs after age 50
-most patients are > 60YO
-most common in Western world
-unknown cause
-Monoclonal proliferation of lymphocytes that are morphologically mature but functionally defective – they do not act as functional plasma cells and produce NO antibodies
What is essential thrombocytosis?
Platelets > 600,000
-reactive (due to infection/inflammation, bleeding) and other myeloproliferative dsordes MUST BE EXCLUDED
-manifested by THROMBOSIS (CVA) or by bleeding due to defective platelet function
-LOW MORTALITY but high morbidity
What is sickle cell trait?

1 out of 12 people of african decent carry the sickle cell trait; they are heterogenous. This also appears in ITALIANS, GREEKS, SAUDI ARABIANS

-patients with SCTrait are not anemic and have a NORMAL LIFE EXPECTANCY!

Aspiraginase adminstrations should always be followed with a check for?
How does sickle cell disease affect the organs below:
1. Blood
2. Heart
3. CNS
4. GI
5. Bones
6. Lungs
7. Kidneys
8. Eyes
9. Genitalia
1. Blood – chronic HA, aplastic crisis
2. high output CF due to anemia
3. stroke
4. gallbladder disease (stones), splenic infarctions, abdominal crisis
5. painful crisis, osteomylitis, ascascular necrosis
6. Infections, acute chest syndrome
7. hematuria, papillary necrosis, renal failure
8. proliferative retinopathy, retinal infarcts
9. priapism
Protein S deficiency
1. Cofactor to protein C so a def leads to decreased protein C activity
OTHER lab tests indicative of MMyeloms
-elevated total protein in the serum due to paraproteins in blood *hyperglobulinemia
-Peripheral blood smear shows reuloux formation which resembles a stack of poker chips
-hyperglobulinemia causes the RBCs to stick together
-Urine will be elevated with BENCE JONES PROTEINS
What is the diagnosis of ITP? How do you make it? How is it treated?
1. Platelet count < 20K; remainder of the blood count is normal (unless significant bleeding has occurred in which case the HB/Hct is decreated and the reticulocyte count is increased
2. Peripheral smear shows decreased platelets
3. Bone marrow aspiration shows INCREASED MEGAKARYOCYTES
4. There is an increased amount of platelet associated IgGTreatment: Adrenal corticosteroids (cortisol) +IVIg that saturates the reticuloendothelial system binding sites for platelet bound self immunoglobulin so thre is less platelet uptake and destruction by the spleen + splenectomy + platelet transfusions for life-threatening and serious hemorrhagic episodes.

Aplastic anemia
1. Bone marrow failure leading to pancytopenia (anemia, neutropenia, thrombocytopenia)
a. Causes: IDOPATHIC – marjoity of cases
-radiation exposure
-viral infections (Human parvovirus, hepatitis C, hepatitis B, Epsetin Barr Virus (EBV), CMV, herpes zoster, HIV
-Chemicals – benzene/insectisides
Standard v. LMWH
1. STD Heparin
-therapeutic dose is usually given IV, intiated with a bolus of 70 to 80 U’kg and followed by continuous IV infusion (15-18 U/kg/hr infusion). Theraputic PTT is usually between 60-90 seconds. But this varies dependng on situation
-prophylactive dose is given subcutaneously-low dose hepatin (5000U SC every 12 hours). PTT monitoringis not necessary for SC dosing2. LMWH
-theraputic dose (give as a weight adjusted dose)
-prophylactic dose (varies dependingon type of produce)

What are the clinical findings in someone with a coagulopathy 2/2 severe LIVER disease?
-abnormal bleeding- GI is the most common primarily due to varices 2/2 portal hypertension but exacerbated by coagulopathy.
-prolonged PT and pTT especially PT
Reticulocyte index is important because:
1. Initial test to evaluate anemia – indicates whether effective erythropoiesis is occuring in the bone marrow. Effective erythropoiesis is dependent on adequate raw materials (iron, vitamin B12, folate) in bone marrow, absense of intrinsic bone marrow disease (eg asplastic anemia), adequate EPO from kidney, and survival of reticulocytes (no premature destruction before leaving the bone marrow)
Clinical features of inherited hypercoag states
1. Venous thromboembolism (DVT, and PE) are teh most comon. Hypercoaguabile stats are not fiagnosed until the patient has had sever episodes.
2. Suspect an inherited hypercoag state if one or more of the following:
a. The patient has a family history of DVT, PE, thrombotic events
b. the patient has recurrent episodes of DVT, PE or thrombotic events
c. frist thrombotic even efore age 40
d. patient experiences thombosis in usual sites (mesentary, inferior VC, renal veins, verebral veins
What are the phases of MYELOID CELL GROWTH
1. Myeloblast
2. Promyelocyte
3. Myelocyte
4. Metamyelocyte
5. Bands
6. Segmented neutrophils
How does leukemia differ from lymphoma?

Leukemia is characterized by neoplastic proliferation of abnormal WBCS in which accumulate and interfere with the production of normal WBCs as well as the production of RBC and plts resulting in both anemia and thrombocytopenia.

Two classes:
1. The type of WBC affected:
a. Granulocytes/monocytes are affected, myelogenous leukemia present
b. Lymphocytes are affected, then lymphocytic leukemia is present
2. Maturity of cells affected and the rapidity of disease progression
a. acute is rapid and affects immature cells and so immature cells proliferate before having matured.
b. chronic leuk progresses slow and affects mature cells

What are the two varients of G6PD deficiency
Mild form is present in 10% of african american men (a-variant)
-in this form, HA are self-limited beacuse they maintly involve only the OLDER RBCs and spares the younger RBCs (the younger RBCs have sufficient G6PD to prevent RBC destruction) and thus the hemolytic episodes are usually trigger by infection or by drugs like (ANTIMALARIALs, SULFUR CONTAINING AB like TMP-SMX)MORE SEVERE form is present in people of mediterranean descent. In this form, young as well as old RBCs are G6PD deficiencyt and thus severe HA occurs when exposed to FAVA beans
-Rx requires blood transfusions until drug is elimianted from the body

General characteristics of Thalassemia:
1. Inherited microcytic disorder of the RBC
2. Mutated production of alpha OR beta-globin chain
3. Classified according to chain deficiency (B thal lacks B, a-thal lacks A)
What are the clinical features of G6PD deficiency?
accumulation of unneurtalized H2O2 which denatures Hb precipitating Heinz body formation within RBCs
-HEINZ bodies attach to RBC membranes, reducing their flexibility and making them prone to sequestration by the spleen
-OFTEN DRUG induced and reports with DARK URINE and JAUNDICE on physical exam!
What is the formula for converting Hb into Hct?
Hb x 3 = Hct (IU PRBCS increased Hb level by 1 point and Hct by 3)
What is the treatment for NHL:
1. Indolent:
2. Intermediate
3. High grade
1. Indolent forms of NHL are not curable but have a 5 year survival rate of 75% thus OBSERVE, chemotherapy and radiation therapy are good options
2. Intermediate and high grade MAY be curable with aggressive treatmanets but if complete remission is not achieved, survival is less than 2 years. Aggressive treatments include: CHOP and radiation therapy
3. Very high dose chemotherapy with bone marrow transplantation is LAST resort
When might it be appropriate to be put on LT therapy of warfarin?
If two or more thromboembolic events have occured
Essential thrombocytosis on peripheral smear:
hypogranular, abnormally shaped platelets
What is polycythemia vera?

Myeloproliferative disorder in which malignant clonal proliferation of hematopoeitc stem cells leads to an excess erythrocyte production

-inc RBC mass occurs independentally of EPO
-median survival with treatment is ~ 9-14 years

What are myelodysplastic syndromes?

class of aquired clonal blood disorders that are characterized by ineffective hematopoiesis with apoptosis of myeloid precursors. This results in pancytopenia despite a normal or hypercellular bone marrow

-occurs more commonly in elderly patients are slightly more commen in men than in women


1. Platelet count
2. Bleeding time
3. PT
4. PTT

1. NL or dec
2. normal
3. normla
4. increased
Treatment for ITP
adrenal corticosteroids
IvIg to force out binding sites in spleen (competitive)
platelet transfusion
What are the epidemiological associations with NHL
Burkitts lymphoma in regions of africa
Patients with HIV and HIV associated lymphomas
Adult T cell lymphoma in japan and the carribean
1. Acute myelogenous leukemia (AML)
-neoplasm of myelogenous progenitor cells
-AML occurs mostly in adults (80% of adult acute leuks)
-risk factors include exposure to radiation, myeloproliferative syndrome, Down’s syndrome, and chemotherapy (alkylating agents)2. Acute lymphocytic leukemia (ALL)
-ALL is a neoplasm of early lymphocytic precursors with histology revealing predomiance of lymphosblasts; MOST COMMON IN CHILDREN UNDER 15 YO IN THE US
-most responsive to therapy
-poor prognostics: age <2YO or >9YO; WBC 10^5/mm^3 and/or CNS involvement
-if bcell phenotpye, LDH increase, or rapid leukemic cell proliferation – increased risk for CNS involvement.

Adverse effects of heparin?
heparin-induced thrombocytopenia *HIT-lower incidence with LMWHs
possile osteoporosis – lower incidence with LMWH
-transient alopecia
-rebound hypercoag after removal due to depression of AT3
Thrombotic thrombocytopenic purpura: ((TTP))
-disorder of platelet consumption – unknown cause
-hyaline microthombi occluse small vessels and any organ may be involved and cause mechanical damage to RBCs (schistocytes on peripheral smear)
-life threatening emergency that is responsive to therapy – if untreated – death occurs in months.Pneumonic: FATRN
2-anemia (hemolytic) microangiopathic
3-thrombocytopenia (<150K)
4-acute renal failure (mild)
5-neurological changes *AMS

In which platelet disorder are platelets abnormally large on peripheral smears?
Bernard souliers syndrome- d/o off adhesion to subendothelium due to platelets glycoprotein GPIb-IX; low platelets but large
When is heparin indicated for use?
Venous thromboembolism: DVT, PE
Acute coronary syndromes: USA, MI
Low dose standard heparin or LMWH for DVT prophylaxis
Atrial fibrillation in acute setting
After vascular bypass grafting (CABG)
B-thalassemia MINOR diagnosis? Treament?
Dx: Hemoglobin electrophoresis
Rx: Not necessary as patients are not transfusion-depending like BthalMAJOR)
What is autoimmune hemolytic anemia? (AIHA)
Production of autoantibodies to RBC resulting in destruction of RBCs – this type of AB produced is either IgG or IgM and determines the prognosis, site of RBC destruction and response to treatment.
How might hemophilia A be diagnosed?
1. Prolonged PTT
2. Low factor VIII coagulant level and normal levels of vWF
3. Detection of factor VIII inhibitor
a. If normal plasma is mixed with plasma from a hemophilliac patient, PTT will becme normal.
a. IF the PTT fails to normalize, this is diagnostic of the presnese of a factor VIII inhibitor
What is Bernard-Soulier Syndrome?
Autosomal recessive disease
-disorder of the platelets adhesion (to subendothelium)due to deficiency of platelet glycoprotein GPIb-IX
-on peripheral blood smear, platelets are abnormally large
-platelet transfusions are contraindicated
1. Platelet count
2. Bleeding time
3. PT
4. PTT
1. normal
2. increased
3. normal
4. increased
What is the MOA of Heparin?
1. Potentiates the action of antithrombin to inhibit clotting factors IIa and Xa
2. Prolongs the PTT
3. Half-life of standard heparin is 1 hour. It is longer for low moleculr weight heparins (LMWH) – longer than 2 hours and up to 24 hours depending on the product
Patient: Male with unsuspected hemorrhaging that occurs with a positive family history
Hemophilia A
How is NHL diagnosed?

Lymph node biopsy for definitive diagnosis – any lymph node > 1cm for a period > 4 weeks that cannot be attributed to infection should be biopsied

-CT scan (chest abdomen and pelvis) to dettermin the extent of disease spread and patients response to treatment
-serum LDH and B2 microglobulin are indirect indcators of tumor burden
-if ALKphos is elevated, bone or liver involvement is liekly
-if LFTs or bilirubin is elevated, liver invovlvement is likely
-Serum electrolytes, RFT
-Bone marrow biopsy

If patient is neutropenic WITH a fever, what is the goal for PLT count? What is the goal for Hb?
Plt goal is >20
Hb > 8
What is the most common type of thalassemia?
B-thalassemia minor (b-thal) is more common than alpha minor but both are mistaken with thalassemia.
1. Platelet count
2. Bleeding time
3. PT
4. PTT
1. Decreased
2. Increased
3. normal
4. normal
What are the clinical features of DIC?
Bleeding tendency (more common in acute cases)
-superficial hemorrhages
-bleeding from GI tract, urinary tract, gingival or oral mucosa
-oozing from sites of procedures
-occurs most often in chronic cases. ENd organ infarction may develop, all tissues at risk esp CNS and KIDNEY

Low molecule weight heparin (LMWH)
LMWH mostly inhibit factor Xa (equivalent inhibiton of factor Xa as STD heparin)
=less inhibition of factor IIa (thrombin) and platelet aggregation
=they cannot be monitored by PT or PTT because they do not affect either
Fevers, night sweats, anorexia, weight loss, recurrent infections, easy bruising/bleeding, symptoms of anemia, splenomegaly, hepatomegaly, lymphadenopathy
How is iron deficiency anemia treated?
1. Oral iron supplementation (watch for constipation, nausea, dyspepsia)
2. Parenteral iron replacement
a. Iron dextran (IV or IM)
b. Useful in patients with poor absorption or require > O2 than iron oral therapy can provide
3. Blood transfusion is unstable and Hb concentration is < 7
What is the diagnosis of vWD?
-clinical findings and lab information
-prolonged bleed time but normal platelet count (PTT may be prolonged)
-decreased plasma vWF, decreased factor VIII activity
-reduced ristocetin-induced platelet aggregation
While most HIV patients are prohibited from LIVE vaccinations, which vaccination should be administered to HIV + patients with CD4 count > than 200
MMR because is fatal if otherwise untreated
What are AUER RODS and when might these be present?
granules and eosinophilis rods inside malignant cells and are seen in AML but not ALL
Describe how hemolytic anemia presents in a SCA patient?
-jaundice, pallor
-gallstone disease (very common) – pigmented gallstones
-the anemia itself is well compensated and is rarely transfusion dependent
-high-output heart failure may ovver over time (secondary to anemia)-many adults eventually die of CHF
-aplastic crisis: these are provoked by viral infection such as human parvovirus B19, which reduces the ability of the bone marow to compensate. Rx: blood transfusion – the patient recovers in 7-10 days
What is the treatment of HODGKINS lymphoma?

Chemotherapy + radiation therapy to the involved field.

Stage I, II, IIIA can be treated by radiation along
-some will use chemo adjuvant therapy

Stage IIIB or IV require chemo

***chemo+radiation therapy in combination achieve cure rates of over 70% in hodgkins disease

If anemia develops rapidly, what symptoms develop?

If anemia develops gradually?

Rapidly: then symptoms are much more likely to be present bc little time for compensation

Gradually: compensatory mechanisms are able to maintain oxygen delivery and symptoms may be minimal or ABSENT

What is the treatment for PNH?

Glucocorticoids (prendnisone) are the usual initial therapy, but many patients do not respond thus will administer…


Diagnosis of myelodysplastic syndrome:
-dysplastic marrow cells
-blasts/ringed sideroblastsCBC WITH PERIPHERAL SMEAR
-normal or elevated MCV
-low retics

What is the least aggressive type of leukemia with the highest rate of survivial?
CLL; and most survive longer than those with acute leuks or those with CML. The course is variable but typically follows a prolonged indolent course.
Presense of “smudge cells” in peripheral smear is diagnostic for?
More than 75% of patients with hemophilia A and 50% of patients with hemophilia B are _____-positive. These values should be decreasing with time 2/2 modern screening of donor blood. (>1985)
Only instance in which WHOLE BLOOD is used
massive blood loss
What is monoclonal gammopathy of undetermined significance (MGUS)? How does this differ from MM?
Common in the elderly (up to 10% in patients > 75 Yrs of age)
-diagnosis: IgG spike < 3.5g; less than 10% plasma cellsin bone marrow; bence jones proteinuria < 1g/24 hours.
-fewer than 20% develops MM in 10-15 years
-no treatment necessary; close observation is suggested
Diagnosis of iron deficiency anemia:
1. Decreased serum ferritin – most reliable test available
3. Elevated transferrin levels
4. Decreased serum IRON
5. Microcytic, hypochromic RBCs on peripheral smear
6. Bone marrow biopsy-GOLD STD
7. Guaiac stool test – if GI bleed is suspected
What are the two forms of ITP?

1. Acute form: seen in children, preceded by a viral infection (in most cases); usually self-limited – 90% resolve spontaneously within 6 months

2. Chronic form: seeen in adults most commonl women between 20-40 YO; spontaneous remissions are rare

Antiphosphoslipid AB syndrome
1. Aquired
2. Presents with arterial or venous thrombi
What is the prognosis of multiple myeloma with treatment? WIthout treatment? 5 year survival rate?
With treatment = 2-4years
Without treatment = 6 months
5 year survival = 10%
What are the clinical features of MM?
1. Bone pain due to osteolytic lesions in the low back or chest (ribs) and jaw (mandible)
2. Pathological fractures
3. Loss of height 2/2 collapse of vertebraeAnemia (normocytic normochromic)-present in most patients due to bone marrow infiltration adn renal failure

Renal failure – mainly due to:
1. Myeloma nephrosis = immunoglobulin precipitation in renal tubules leads to tubular casts of Bence Johnees protein and hypercalcemia also plays a role in renal dcompensation

Recurrent infections – 2/2 deprivation of normal Ig; therfore hemoral immunity is affected

What is the treatment of AIHA?
1. No treatment necessary in either type of AIHA because the hemolysis is MILD. If it is more severe, the erapeutic approach depends upon the typ of autoantibody causing it.
-WARM AIHA: glucocorticoids are the mainstay of therapy.
-splenectomy – use for patienst whose condition does not responds to glucocorticoids
-immunosuppression (AZA/cyclophosphamide.
-RBC transfusions
-folic acid supplementation
-COLD AIHA: avoiding cold exposure prevents hemolysis and anemia
-RBC transfusions if absolutely necessary
-various chemotherapeutic agents
-steroids are NOT beneficial
Treatment of aplastic anemia
Bone marrow transplant
Transfusion of PRBCs and platelets, if necessary *use judiciously
Thrombocytopenia can result in clinical features that includes:
ecchymosis, nasal bleeding, mouth ulceration/gum bleeding, GI tract, ICH
Lo reticulocye (<2%) with macrocytic anemia (>100)
1. Check B12 and folate levels
2. Abnormal B12/folate –> diagnostic
3. Normal – then suspect LIVER DISEASE
What is the diagnosis of Hb and Hct:

1. Formula to convert Hb to Hct: Hb x 3 = Hct (1 unit of packed RBCs [PRBCs]) increases Hb level by 1 point and Hct by 3 points

2. If patient has good cardiac function and intravascular volume is adequate, low Hb and Hct levels are tolderated even an Hb of 7 or 8 provides sufficient O2 carryng capacity for most patients however anemia is not tolerated as well in patients with impaired cardiac function

How is SCA diagnosed?
1. Anemia is the most common finding.
2. Peripheral smear – sickle shaped RBCs
3. Hemoglobin electrophoresis is REQUIRED for diangosis in most casis, diagnosis is made from newborn screening tests!
Diagnosis of CLL
CLL: a cancer of B-lymphocytes
-to diagnose CLL – there is NOT ONE PARTICULAR GENETIC ABNORMALITY THAT IS PATHOPNEUMONIC (unlike that of CML in which has the t(9; 22) genetic abnormality)
-We do not have a molecular-marker, instead look at pattern (Look @ CD19, 20, 23
-Find B cells that have abnormal expression of CD5 (t cell marker) in normal cells – shouldn’t have both CD20 and cd5 positive B cells because abnormal to express a T CELL marker CD5
-Thus can make diagnosis by FLOW cytometry of the peripheral blood.
-Look for population of cells that has the t cell markers 50% of the time gets diagnosed incidentally asymptomatic usually but if they do — will have the origniation of b cells in bone marrow then go to lymph nodes and cause to swell
-if too many CLL cells in marrow, can cause some pancytopenias due to proliferation
A reticulocyte index of < 2% implies?
Inadequate RBC production produced by the bone marrow
What is the difference between HIT type I versus type II?

HIT type I = heparin directly causes platelet aggregation seen < 48 hours after initiating heparin; no treatment needed (NONIMMUNE)

HIT type II = heparin induces antibody-mediated injury to paltelet; seen 3-12 days after intiiating heparin; discontinue HEPARIN IMMEDIATELY!

How is hemoglobin S distinguished from Hb A?
By electrophoresis
What are the clinical features of irondeficiency anemia:
dyspnea on exertion
orthostatis lightheadedness
hypotension, if acute, tachycardia
Disorders of blood coagulation:
1. von Willebrands Disease (vWD)
-autosomal dominant d/o with deficiency or defec of factor VIII-related antigen (vWF)
-vWF enhances platelet adhesion and aggregation (first two steps in platlet flot formation)
-carrier of factor VIII (8) in blood****MOST COMMON INHERITED BLEEDING D/O (1-3% OF US)

PT v. PTT v. Thrombin time v. Bleeding time
PT: reflects extrinsic pathway (prolonged by warfarin)
PTT: reflects the intrinsic pathway (prolonged by heparin – factor X)
thrombin time: measures fibrinoen concentratoin
bleeding time: reflects platelet function
What is the treatment of/for CLL

Chemotherapy has little effect on survival but good for symptoms.

1. FLUDARABINE AND CHLORAMBUCIL have been shown to be of some benefit.

Major clinical features associated with SCA?
1. Severe lifelong hemolytic anemia
2. Findings secondary to vasal occlusion
a. Painful crisis
b. Hand-foot syndrome (dactylitis)
c. Acute chest syndrome
d. repeated episodes of splenic infarctions
e. avascular necrosis of joints
f. priapism
g. CVAs
h. Opthalmologic complications
i. Renal papillary necrosis with hematuria *painless
j. Chronic leg ulcers
k. abdominal crisis
3. infectious complications
a. functional asplenia results in increased susceptibility to infections of encap
bacteria that includes (S. pneumo, H. Influ)
b. predisposition to that of salmonella osteomyelitis (also due to splenic malfunction)
4. Delayed growth and sexual maturation, especially in boys.
Hyperviscosity, headache, dizziness, weakness, pruritis, visual impairment, dyspnea
with thrombotic phenomena (DVT, PE, VIA, MI, portal vein thrombosis) or BLEEDING -GI or GU bleeding with HTN
Polycythemia vera
High-grade NHL (name 2)

1. Lymphoblastic lymphoma: T-cell lymphoma; more common to children, can progress to T-ALL in which 50% have B symptoms; aggressive with rapid dissemination

2. Burkitts (small non-cleaved cell) lymphome: T cell lymphoma common to children. Two types (one in AA involving face and jaw and the other that is american with hepatomegaly and abdominal masses with LAD). AA linked with EBV infection and assicated with t(8; 14)

1. IgG spike < 3.5g
2. Less than 10% plasma cellsin bone marrow
3. Bence jones proteinuria < 1g/24 hours. -fewer than 20% develops MM in 10-15 years -no treatment necessary; close observation is suggested MM: 1. >10% abnormal plasma cells in marrow
2. Mprotein in serum, urine
3. lytic bone lesions
Causes of myelodysplastic syndromes:
1. idiopathic
2. radiation
3. immunosuppressive agents
4. Toxins
1. Platelet count
2. Bleeding time
3. PT
4. PTT
1. NL
2. NL
3. Increased
4. NL
HIV-associated lymphomas include:
Not a discrete entity; usually Burkitts *high grade, or diffuse large t cell *intermediate grade
What is autologous stem cell transplant and when is this used?
Autologous HSCT requires the extraction (apheresis) of haematopoietic stem cells (HSC) from the patient and storage of the harvested cells in a freezer. The patient is then treated with high-dose chemotherapy with or without radiotherapy with the intention of eradicating the patient’s malignant cell population at the cost of partial or complete bone marrow ablation (destruction of patient’s bone marrow function to grow new blood cells). The patient’s own stored stem cells are then returned to his/her body, where they replace destroyed tissue and resume the patient’s normal blood cell production. Autologous transplants have the advantage of lower risk of infection during the immune-compromised portion of the treatment since the recovery of immune function is rapid. Also, the incidence of patients experiencing rejection (graft-versus-host disease) is very rare due to the donor and recipient being the same individual. These advantages have established autologous HSCT as one of the standard second-line treatments for such diseases as lymphoma.[15] However, for others such as Acute Myeloid Leukemia, the reduced mortality of the autogenous relative to allogeneic HSCT may be outweighed by an increased likelihood of cancer relapse and related mortality, and therefore the allogeneic treatment may be preferred for those conditions.[16] Researchers have conducted small studies using non-myeloablative hematopoietic stem cell transplantation as a possible treatment for type I (insulin dependent) diabetes in children and adults. Results have been promising; however, as of 2009 it was premature to speculate whether these experiments will lead to effective treatments for diabetes.[17]
What is the diagnosis for patiens iwth suspected inherited hypercoag states
Functional assays are available for at3 AB, protein C, S, factor V leigen, prothrobin gene adn hyperhomocystinemia
What is the INITIAL clinical finding of SCA
What is WARM versus COLD AIHA?
Warm AIHA = most common
-autoantibody is IgG which bindsoptimally to RBC membranes at 37 degrees
-results in extravascular hemolysis – primary site of RBC sequestions is the spleen. Splenomegaly is a common feature.
-causes: idiopathic; secondary to lymphomas, leukemias (CLL) and other leukemias, malignancies, CVD (especially SLE!!), and drugs such as alpha-methyldopaCOLD AIHA = autoantibody is IgM which optimally binds to RBC membrane at cold temperatures (usually 0-5 degrees)
-produces compleent activation and intravascular hemolysis and the primary site of RBC sequestration is that of the LIVER
-causes: idiopathic (elderly) or due to infection (such as mycoplasma pneumonia infection or infectious mononucleosis).

WHat are the options for DVT prophylaxis?
2. Low dose unfractionated heparin (UFH)
3. Pneumatic compression boots
What type of anemia can lead to CHF (with symptoms of hemochromatosis)? Why?
B-thalassemia major because requires continuous transfusions leading to IRON overload that can develop. If untreated, these patients are at risk for severe cardiac issues and are often treated with desferrioxamine A CHELATNG AGENT THAT ELIMINATES EXCESS IRON)
What is the treatment for patients diagnosed with B12 deficiency?
Parenteral therapy if preferred – cyanocobalamin (vitamin B12) IM once per month
Lab tests to diagnose hemolytic anemia:
Elevated reticulocyte count
Elevated LDH
Decreased haptoglobin
Decreased hemoglobin/hct
Common cause of death 2/2 DIC?

Intracranial hemorrhaging


Fibrosis of bone marrow resulting in pancytopenia and extramedullary hematopoiesis. Not surprisingly, massive splenomegaly is usually present. Other manifestations are secondary to pancytopenia (fatigue, bleeding, infection)
Agnogenic Meyloid Metaplasia with Myelofibrosis
Hodgkin type A or Hodgkin type B
Type A: No symptoms
Type B: Fever, weight loss, night sweats, (constitutional symptoms worsens the prognosis)
When are PRBCs transfused? (no plt or clotting factors)
1. MIX with NS to infuse faster (not with lactated ringers solution because calcium causes coagulation with the IV line.
2. Each UNIT of PRBC raises Hct by 3-4 points
3. Admin 2U – each U may be given to adult over 90-120 minutes
4. Check CBC after the transfusion is completed
How is macrocytic anemia diagnosed?
Peripheral blood smear
-megaloblastic anemia (macrocytic RBCs – MCV > 100)
-hypersegmented neutrophils
Serum bitamin B12 is low (<100 pg/mL)
Serum methylmalonic acid and homocysteine levels – elevated in vitamin B12 deficiency and are useful if B12 is borderline. Will notice if treatment with folate.
What does the RDW measure?
the variation in RBC size. RDW is usually abnormal in irondef anemia but is generally normal in all of the other microcytic anemias.
What is the pathology of hereditary spherocytosis?
Autosomal dominant inheritance of a defect in gene coding for the SPECTRIN and other RBC proteins. Spectrin content is deeased but is not totally absent. There is a loss of RBC membrane surface area without a reduction in RBC volume. Necessitating a spherical shape. The spherical RBCs become trapped and destroyed in the spleen by macrophages hence the term extravascular hemolysis
Inherited hyperCOAG states?
1. Antithrombin III deficiency
2. Antiphospholipid antibody syndrome
3. Protein C deficiency
4. Protein S deficiency
5. Factor V leiden
6. Prothrombin gene mutation
7. Hyperhomocystinuria
Features of NHL?
-b symptoms
-recurrent infections
-superior vena cava obstruction, respiratory involvement, bone pain
Treatment for Angogenic myeloid metaplasia with myelofibrosis?

Supportive with transfusions, eruthropoitin and splenectomy for palliative relief of painful splenomegaly

BMT is sometimes appropriate

Normal PT:
Normal PTT:
Normal bleeding time:
1. 11-15 seconds = PT (2, 7, 9, 10, C, S)
2. 25-40 secondar = PTT (factor X = intrinsic)
3. 2-7 minutes = bleeding time (PLATELETS)
What is CML
-neoplastic clonal proliferation of myeloid stem cells (plt, erythro, granulo)
-pt >40YO
-CML is indolent *chronic course for many years before it transforms into ACUTE leuks.
-end point of diesase is usually acute phase or a “BLAST CRISIS”
-associated with t(9;22) phildelphia chromosome that is present in >>>>90% of patients
What is the treatment for the anemia type in the below picture (what is the most important step in treatment)?
1. avoid drugs that precipitate hemolysis
2. maintain hydration
3. perform RBC transfusion when necessary
Treatment of vWD
1. DDVAP (demopressin) induces endothelial cels to secrete vWF.
-rx of choice for type 1 vWD
-some with type 2 may respond but not if type 3
2. Factor VIII concentrates with high molecular weight vWF
-give to all patients with vWD of any type after trauma or during surgery
-good for type III and type II not responding to DDVAP
3. Cryoprecipitate is NOT recommened as treatment because it carries a risk of VIRAL transmission
4. do not use ASA/NSAIDS – exacerbates bleeding tendency
Treatment of vitamin K deficiency
1. Vit K replenishment (oral or SQ) – may take a few days for PT to return to normal
2. If bleeding is severe and emergency treatment is necessary, FFPshould be transfused
In patients with prior heart disease, what hemoglobin level should be maintained?
Hgb > 10
admin 1U pRBC if abnormally low
Acquired disorder
-affects hematopoietic stem cells and cells of all blood lineages
-caused by a deficiency of anchor proteins that link complement-inactivating proteins to blood cell membranes. The deficiency of this achoring mechansim results in an unusal susceptibility to completment -mediated lysis of RBCs, WBCs and platelets.
Microcytic Anemia: cause due to IRON DEFICIENCY
Causes = chronic blood loss
1. Most common cause of iron deficiency anemia in adults
2. Menstrual blood loss is the msot common source (in the absense of menstrual bleeding, GI blood loss is most likelyCauses = dietary deficiency/increased iron requirements-primarily seen in these three age groups:
1. Infants and toddlers- occurs is diet is predominantly human milk (low in iron). Children in this age group also have increased requirements for iron because of accelerated growth. Most common between 6mo-3YRS
2. Adolescents-rapid growth increases iron req. Adolescent women are at high risk of irondeficiency microcytic anemia
3. Pregnant women – increases iron req

Adverse effects of warfarin
1. Hemorrhage
2. Skin necrosis is a rare but serious complication caused by rapid decrease in protein C *a vitamin K dependent inhibitor of factor 5 and 8a
3. Teratogenic during pregnancy
4. should not be given to alcoholics or to any patient prone to frequent falls because intracranial bleed in a patient on warfarin can be catastrophic
How might VB12 and folate deficiency differ in clinical symptoms:
1. SImilar to those in vitamin b12 deficiency without the neurological symptoms

Potential complication of chemotherapy seen in acute leukemia and high grade NHL (burkitts)

-Rapid cell death leads to the release of intracellular contents that causes hyperkalemia, hyperphosphaemia and hyperuricemia

What is the treatment of thrombocytopenia?
Treat the underlying cause
-platelet transfusion- use depending on he cause and severity of thrombocytopenia
-discontinue NSAIDS and other antiplatets agents and anticoags
WARM AIHA is often seen in which type of leuks?
Patients with CML, the course of CML is mroe aggressive than CLL
How is hemolytic anemia diagnosed?
1. Hb/Hct level depends upon degree of hemolysis and reticulocytosis
2. Elevated reticulocyte count due to increased RBC production
3. Peripheral smear (schistocytes or helmet cells)
4. Haptoglobin levels – low in HA – haptoglobin binds to hemoglobin so its absense means that hemoglobin was destroyed.
5. Direct coombs test (detects AB or completment on RBC membrane) – positive in autoimmune HA
6. Osmotic fragility
Treatment of myelodysplasic syndromes:
-RBC and platlet transfusions
-EPO may help to reduce the number of blood transfusions necesary
-Granulocyte colony-stimulating factor can be an effective adjunctive tretament for neuropenic patients
-vitamin supplementatin particularly with B6, 12, folate, is important gievn the large turnover of marrow cells.Pharmocologic therapy has variable results:
1. Immunosuppressive therapy
2. chemo
3. Androgenic steroids

BMT is the only cure

What is the purpose of the MCH and MCHC?
Little value clinically. THey are neither sensitive nor specific for any diagnosis however the MCV is very valuable in diagnosing the cause of anemia.
How is B-thalassemia MAJOR diagnosed? Treated?

Diagnosis: Hemoglobin electrophoresis (HbF elevated); peripheral blood smear (microcytic hypochromic anemia

Treatment: Frequent PRBC transfusions to sustain life

What is multiple myeloma?
Neoplastic proliferation of a single plasma cell line that produces monocloncal immunoglobulins. This leads to enormous copies of one specific immunoglobulin (IgG or IgA) in the over 50YO individual.
-most common in african americans
-as the disease progesses, bone marrow elements are replaced by the malignant plasma cells therefore anemia, leucopenia and thrombocytopenia may be present in advanced disease.
Vincristine as an antineoplastic med can result in?
Diagnostic criteria for polycythemia vera

Must have all three major criteria or any two major and 2 minor to be diagnosed:

1. Elevated RBC (men > 36; females >32)
2. Aterial O2 sat > 92%
3. Splenomegaly

1. Thrombocytosis (>400 platelet count
2. Leukocytosis > 12 x 10^9/L
3. Leukocyte alk phosphatase (>100) without fever or infection
4. Serum vitamin b12>900

What is the treatment of Hemolytic anemia:
1. Treat underlying cause
2. Transfusion of PRBCs if severe anemia is present or patient is hemodynamically 3. compromised
Folate supplementation (folate is depleted in hemolysis)
What is considered thrombocytopenia?
A platelet count of <150,000
What are the clinical features of anemia
1. Nonspecific complaints (headache, fatigue, poor concentration, diarrhea, causea, vague abdominal discomfort
2. pallor – best noted at conjunctive
3. Hypotension and tachycardia
4. Signs of the underlying cause – jaundice if HA, blood in stool if GI bleeding.
Treatment of choice for hereditary spherocytosis
Splenectomy is the treatment of choice
Vitamin K deficiency:
Vitamin K is required for: 2, 7, 9, 10, protein C/S
-process is post translational modification
-source of vitamin K is by diet leafy greens and bacteria in the gut
-CAUSES of VITA K deficiency:
a. broad spec AB that suppressed gut flora in patients who are NPO
b. Patients on TPN (unless vitamin K delivered)
c. Malabsorption of fat solubl vitamins in the (SBO, inflammatory disease, celiac, pancreatits, jaundice)
d. Warfarin – a vitamin K antagonist (causes production of INACTIVE clotting factors)
Reversal of heparin versus reversal of warfarin:
Warfarin – d/c and administer vitamin K
-halflife of warfarin is much longer than that of heparin and it takes 5 days to correct the effects of warfarin on stopping the medication. Vitamin K infusion corrects the abnormal PT within 4-10 hours if thepatient has normal liver function
-giving vitamin K makes it difficult to return the patient to therapeutic INR levels if anticoagulation is to be continued
A reticulocyte index > 2% implies
excessive RBC destruction or loss. The bone marrow is responding to increased RBC requirement
What are the general characteristics of anemia?
1. Reduction in EITHER hematocrit or hemoglobin
2. When red cell mass (as measured by Hb or less precisely by Hct) decreases, several compensatory mechanisms maintain oxygen delivery to the tissues.
a. increased CO (heart rate and stroke volume)
b. Increased extraction ratio
c. Rightward shift of the oxyhemoglobin curve (increased 2,3DPG)
d. Expansion of plasma volume
3. Blood transfusions are not recommended unless <7 g/dL Hgb or the patient requires increased O2 carrying capacity (patients with coronary artery disease or some other cardiopulmonary disease)
Liver disease
1. Platelet count
2. Bleeding time
3. PT
4. PTT
1. Normal
2. Normal
3. Increased
4. Increased
Diagnosis for apastic anemia
Perform a bone marrow biopsy for definitive diagnosis-this reveals hypocellular marrow and in the absense of progenitors of all three hematopoietic cell lines.
What is DIC?
characterized by the abnormal activation of the coag sequence, leading to formation of microthrombi throughout the microcirculation. This causes consumption of platelets, fibrin, and coagulation factors Fibrinolytic mechanisms are activated leading to hemorrhage. Therefore, bleeding and thrombosis occur simultaneously
Secondary causes of hypercoaguable states or risk factors
1. Malignancy
2. Antiphospholipid antibody syndrome
3. Pregnancy
4. Immobilization, causign stasis of blood
5. Myelo[rpliferative disorders
6. OCP
7. Postoperative state (especially after ortho procedures)
8. Trauma
9. Nephrotic syndrome
10. HIT or DIC
11. PNH
12. CHF – stsis of blood
vWF (Factor 8-related antigenic protein)
1. produced in endothelial cells and megakaryocytes
2. platelet adhesion – mediates the adhesion of platelets to the injured vessel walls (ie reacts with platelet GPIbIX and subendothelium)
3. Binds the factor 8 coagulant protein and protects it from degradation
4. inheritance pattern of vWF – AD
5. vWD has low vWF
6. Hemophilia is NORMALFactor 8 coag protein
1. produced in the liver
2. functions as fibrin clot formation
3. Xlinked recessive
4. vWF is reduced but not low
6. VERY LOW hemophilia

Treatment of CML:
1. Chemo to control symptoms before acute phase blast crisis develops
2. Blast crisis is usually terminal with high dose chemo may be used to return dz to chornic
3. Alkylating agent or antimetaolic can be used
3. Bone marrow or stemp cell transplate becase most cases will eventaully become an acute phase.

Low hemoglobin, high calcium, high serum protein, and poor renal function suggest multiple myeloma.


1. Bone marrow replacement by plasma cells
2. PTHrP and degradation
3. High protein content to due immunoglobulins and poor renal function with light chains being passed through the glomerular capsule.
Values of serum ferritin/iron/TIBC/RDW in:
1. Iron def anemia
2. Anemia of chronic disease
3. Thalassemia
1. Low ferritin, low iron, high TIBC and HI RDW
2. Normal to HI, lo serum iron, low TIBC and normal RDW
3. Normal to HI serum ferritin, normal/high iron, normal TIBC, RDW normal to HI
Which aggressive NHL with rapid dissemination responds well to combination chemotherapy?
Lymphoblastic lymphoma
How is polycythemia vera treated?
1. Phlebotomy to lower hematocrit
2. Myelosuppression with hydroxyurea or recombinant interferon alpha (rIFNa)
1. Platelet count
2. Bleeding time
3. PT
4. PTT
1. Decreased
2. increased
What are the stages of CLL?
Stage 0 CLL – just lymphocytosis :
-because small, no proteins on outside to make sticky – do not “smudge” in blood so no symptoms thus is NOT a reason to start treatment – DO NOT TREAT BASED ON WBC countStage I CLL – lymphocytosis with LAD:
-Not all LAD are symptomatic from it if symptoms LAD then this is a reason to pull the trigger to start chemo.

Stage II CLL – lymphocytosis with SPLENOMEGALY
-not all splenomegaly causes symptoms but if regurgitation, n/v, early satiety 2/2 enlargement – then reason to put on chemo

Stage III CLL – anemia Hb < 11; with lymphocytosis
-ONLY USE CHEMO if anemia is 2/2 increased proliferation of lymphocytes.
-IF 2/2 iron def/b12/folate/HA then the chemotherapy will NOT treat the CLL
Do a bone marrow and look at to see if low levels of precursor cells with lymphocytosis anemia specifically due to the CLL not to iron impaired normal hematopoeisis – reason to treat!

Stage IV CLL – thrombocytopenic specificially 2/2 CLL always check iron, b12, etc.; Always check ITP, AIHA; AIHA – LDH bili hapto and direct and UA – ITP

Success rate of splenectomy:
Induces remission in 70-80% of the cases of CHRONIC ITP
For the diagnosis of CML, what is required for diagnosis?

For CML – MUST HAVE T(9; 22) to make diagnosis or else NOT CML


-BUT IF THE HEMATOPOEITIC STEM CELL GETS A SIGNAL, CAN GET ACTIVATED AND START DOWN THE LYMPOID too which results in the diagnosis of CML with lymphoid crisis (so will have a 210kDA breakpoint with t(9;22) and > 90% lymphoblasts)

*****normally, shouldnt see immature cells in the blood. If you see blasts then bc too many to fit and growing at such rapid rate.
THe peripheral blood of CML in a patient looks like that of the normal bone marrow biopsy in a patient
-genetic abnormality (9; 22) – philadelphia chromosome
even though change by genetics, will STILL get maturation

What are the clinical features of Acute leuks?
1. Anemia, increased risk of infection 2/2 neurtropenia
2. Pneumonia, UTI, cellulitis pharyngitis, esophagitis
high mortality and morbiditiy
3. Abnormal mucosal or cutaneous bleeding (2.2 thrombocytopenia)
5. Bone and joint pain
6. CNS involvment – diffuse or focla neurologic dysfunction (meningitis)
7. Testicular involvement (ALL)
8. Anterior mediastinal mass (Tcell ALL)
9. Skin nodules (AML)
Dark urine + jaundice + heinz bodies on blood smear = by ingestion of which drugs?
Cryoprecipitate is transfused in a case of?
For patients with hemophilia A, decreased fibrinogen (DIC), and vWD. Contains factor VIII and fibrinogen
What is CHOP therapy and when is it used?

CHOP – intermediate/high grade lymphoma (NHL)

C- cyclophosphamide
H- hydroxydaunomycin (doxorubicin – can cause cardiomegaly)
O- oncovin (vincristine)
P- prednisone

Which clotting factor has the shrotest halflife and thus makes the first laboratory finding be a prolonged +++
Factor VII has the shortest half life of (3-5) hours so the PT will be prolonged first to >11-15 seconds
How is DIC diagnosed?

Elevated PT, PTT, bleeding time and TT, Fibrin split products (activation of fibrinolytic system), D-dimer

Decreased fibrinogen, platelet count, peripheral smear reveals schistocytes (damage from RBCs as they go through the microcirculation with microthrombi)

Why might a burning sensation be noted in patients with essential thrombocytosis
erythromelagia is a burnging pain and erythemia of the extremeitie due to microvascular occlusions.
In TTP, there is no consumption of ____ ______, so the PT and PTT will be NORMAL. What are the signs of TTP? OR what are the signs of HUS?
CLotting factors are fine – liver still producing them
1. TTP = HUS + fever + AMS
2. HUS = Thrombocytopenia + acute renal failure + hemolytic anemia (microangio)
Distribution of Hodgkins lymphoma?
Bimodal – 15-30YO and >50YO
-lymph node histology divides disease into four subtypes
a. Lymphocyte predominance 10-20% – few reed sternburg cells and Bcells
b. Nodular sclerosis (40-60%) occurs more frequently in women with bands of collagen envelope pools of RS cells
c. Mixed cellularity (20-40%) large number of RS cells in pleomorphic background.
d. lymphocyte depletion (1-10%)-lacking in mix of reactive cells, associated with the worst progonsis
Normocytic anemias: Anemia of chronic disease
1. Occurs in the setting of chronic infection (TB, HIV, lung abscess), cancer (lung, breast, Hodgkins disease), inflammation (RA, SLE) or trauma.
2. The release of inflammatory cytokines which has a suppressive effect on eryothropoiesis.Lab findings: low serum iron and low TIBC, and low serum transferrin levels occur. Serum ferritin levels are increased

How to diagnose the cause of anemia:
1. Look at the _______ index if >2 or <2% 2. If elevated (>2%) then the anemia is due to either _____ or ______.
3. If normal or (<2%) then look at the ______
4. Three types of MCV include:
5. If MCV < 80, what is next to be checked? Leads to result into:
1. Reticulocyte
2. Blood loss or Hemolytic anemia
3. MCV
4. Microcytic (<80); Normocytic (80-99); Macrocytic (>100)
5. Check iron studies: look at both IRON and TIBC
-If <80 MCV, and iron studies show decreased iron and decreased TIBC then diagnosis is probably ANEMIA OF CHRONIC DISEASE
-If <80 MCV, and iron studies show decreased iron and increased TIBC, then diagnosis is IRON DEFICIENCY ANEMIA
-If <80 MCV and studies show normal Fe2+ and TIBC that is low or decreasing: lead poisoning or thalassemia
What is pseudoanemia:
Decrease in hemoglobin and hematocrit secondary to dilution (secondary to acute volume infusion or overload)
AT3 deficiency doesnt repond to Rx of heparin, why?

Because heparin requires the presense of AT3 to anticoagulate. If AT3 is defieienct (what directly inhibits thrombin) then increased thrombi can form

Autosomal dominant

Folate deficiency and the general characteristics as a macrocytic anemia
1. Folic acid stores limited
2. Inadequate intake of folate over a 3-month period can lead to deficiency
3. Green vegetables are the main source of folate. Overcooking vegetables can remove folate
What are the risk factors for NHL?
History of EBV or HTLV-1
History of H. pylori gastritis
autoimmune disease (Hashimotos, SLE, SS, MALT)
General evaluation in patients with LEUKEMIA (acute or chronic)
1. Evidence of infection
2. Evidence of bleeding or easy bruising
3. Lymphadenopathy
4. Hepatosplenomegaly
5. Signs of anemia
6. Fatigue and weight loss.
what causes macrocytic anemia?
pernicious anemia (lack of IF)
poor diet
crohns disease, ileal resection (terminal ileum)
organisms: diphyllobothrium latum infestation (tapeworm), blind-loop syndrome *bacterial overgrowth******
Why is a TTE ordered for a leukemic pt on admission?
Because can result in abnormal ejection fraction 2/2 AML
Contraindications to heparin:
1. Previous HIT
2. Active bleeding, GI bleeeding, intracranial bleeding
3. Hemophilia, thrmbocytopenia
3. Severe HTN
4. Recent surgery on eyes, spine and brain
Causes of folate deficiency leading to macrocytic anemia?
1. Inadequate dietary intake “tea and toast”
2. Alcoholism
3. LT use of oral AB
4. Increased demand
5. Pregnancy
6. Hemolysis
7. Use of folate antagonists such as MTX
8. Anticovulsant medicatiosn (phenytoin)
9. Hemodialysis
Relavant findings in patient history regarding hemolytic anemia:
1. Jaundice
2. ethnic background
3. family background
4. medications
What is the treatment for TTP:
1. Plasmaphoresis (large volume)
2. Begin as soon as dianosis is established (delay in treatment if life-threatening)-response is usually good (monitor platelet count) which should increase
3. Corticosteroids and splenectomy – may be of benefit in some cases
4. Platelet transfusions are contraindicated
Autosomeal recessive d/o (like Bernard Souliers Syndrome)
-disorder of platelet aggregation due to DEFICIENCY in platelet glycoprotein GPIIb-IIIa *on the actual platelet itself that doesnt allow it to bind to R on other cells)
-will prolong the bleeding time because platelets will not adhere or clot
-the platelet count will be normal because no damage to platelet is being done – it is a lack of receptor ON the platelet (in bernard souliers, is lack of receptor on the subendo)
How might heparin/LMWH be reversed?
1. The half life of STD heparin is short (one hour) so it will cease to have an effect within four hours of its cessation.
2. Can give PROTAMINE SULFATE to reverse the effects of heparin if necessary (effectiveness isnot proven)
3. LMWH has a longer half-life than STD heparin, so it takes longer for the effects to fade
-administer FFP if severe bleeding occurs for patients on either warfarin or heparin
What is the treatment for hemophilia A
1. acute hemarthrosis
-analgesics (codeine with or without acetominophen) avoiding all ASA/NSAIDS
-immobilize joint, ice package , non weight bearing movements
2. CLotting factor replacement
-factor 8 concentrate is the mainstay of therapy (both plasma derived and recombinant factor 8 are available)-for acute bleeding episodes and before surgery or dental work.
-cryoprecipitate and FFP are not recommended 2/2 the risk of viral transmission
3. DDVAP – helpful in patients with mild disease. it can increase the levels of factor 8 up to 4x
4. Gene therapy is the next step in future for rx
Coagulopathy of the LIVER disease
1. All clotting factors are produced by the liver (except vWF)
2. Liver disease must be severe for coagulopathy to develop. Therefore if the coagulopathy is due to liver failure the overrall prognosis for the patient is very poor.

*****normally, shouldnt see immature cells in the blood. If you see blasts then bc too many to fit and growing at such rapid rate.


The peripheral blood of CML in a patient looks like that of the normal bone marrow biopsy in a patient

genetic abnormality (9; 22) – philadelphia chromosome
even though change by genetics, will STILL get maturation
Diagnosis of acute leukemias
1. Variable WBC count but there will be a significant number of blast cells (immature) preset in peripheral blood
2. Anemia
3. Thrombocytopenia
4. Granulocytopenia
5. Electrolyte disturbances (hyperuricemia, hyperkalemia, hyperphosphatemia)*****REQUIRES BONE MARROW BIOPSY FOR DIAGNOSIS! Replacement of marrow by blasts should be the finding

T or F: ALL causes of anemia are initially normocytic because it takes some time for the abnormal sized RBCs to outnumber the normal-sized ones
How might someone with PNH present? (Clinically)
1. chronic intravascular hemolysis – results in chronic paroxysmal hemoglobinuria with elevated LDH
2. Normochromic, normocytic anemia unless iron deficiency anemia is present
3. Pancytopenia
4. Thrombosis of venous systems can occur for example if the hepatic veins (BUDD CHIARI) syndrome.
5. May evolve into aplastic anemia, myelodysplasia, myelofibrosis, and acute leukemia
6. abdominal pain, back pain, and MSK pain
1. Platelet count
2. Bleeding time
3. PT
4. PTT
1. Decreased
2. increased
3. normal
4. normal
Sideroblastic anemia
Caused by abnormality in RBC iron metabolism
1. Can be hereditary or acquired-
a. Acquired causes include DRUGS (chloramphenicol, INH, alcohol, lead exposure, collagen vascular disease, neoplastic disease (myelodysplastic syndromes)
b. clinical findings: increased serum iron, ferritin, normal TIBC; ringered siderolasts in bone marrow. Traetment remove offending agents (consider pyridoxine.
Why is it imperative that megaloblastic anemia 2/2 folate versus b12 deficiency?
Treatment by folate suplement can improve the anemia of b12 deficiency but not the neurologic impariment. If the b12 deficiency remains untreated, irreversible neurologic disease results
What blood products are capable of being transfused?
1. Packed RBCs (no platelets or clotting factors)
2. Fresh frozen plasma
3. Cyroprecipitate
4. Platelet transfusions
5. Whole blood
clinical features of myelodysplastic syndromes?
Asymptomatic in early stages
-pancytopenia may be an incidental findingon a routine blood test
-anemia thrombocytopenia, neutropenia
Diagnosis of CLL:
1. CBC: shows WBC of 50-200,000
2. Anemia, thrombocytopenia, and neutropenia common
3. Peripheral blood smear
a. Absolute lymphocytosis -almsot ALL of the WBCs are mature, small lymphocytes
b. Small smudge cells – leukemic cells that are “beaten up” in the blood.
2. Bone marrow biopsy with the presnse of infiltrating leukumic cells in the marrow.
What are the clinical features of macrocytic anemia?
1. Anemia
2. SOre tongue (stomatitis and glossitis)
3. neuropathy – can distinguish etween vitamin B12 deficiency and folate deficiency.
a. demyelination in posterior columns, in lateral corticospinal tracts and spinocerebellar trats that ultimately leads to a loss of position/virbatory sensation in lower extremities, ataxia and UMB signs like increased DTR, spasticity, weakness, babinski sigh
4 leads to urinary and fecal inontinence, impotence
5. leads to dementia
3. HEINZ BODIES (after the removal of the Heinz bodies look as if they are/have had bites taken out of them. The bitten areas are secondary to phagocytosis of heinz bodies by splenic macrophages recognizing them as foreign).
-heinz bodies are abnormal hemoglobin precipatites within RBCs that are visible with special stains
4. Deficient NADPH formation on G6PD assay
5. Measurement of G6Pd is diagnostic!
How is thrombocytopenia diagnosed?
CBC – platelet count
-BLEEDING TIME, PROTHROMBIN TIME (PT), partial thromboplastic time (PTT)
-to determine cause, the following may be helpful:
-exmaination of peripheral blood smear or bone marrow biopsy
Name two low grade or INDOLENT NHL:
1. Small lymphocytic lymphoma – related to CLL, elderly pts, indolent course
2. Follicular, predominant small, cleaved cell lymphoma – most common form of NHL with age of 55; diffuse, large cell, t(14; 18), indolent, PAINLESS LAD
1. Platelet count
2. Bleeding time
3. PT
4. PTT
1. normal
2. normal
3. normal
4. increased
What are the clinical features of waldenstoms macroglobulinemia?
1. Lymphadenopathy
2. Splenomegaly
3. Anemia
4. Abnormal bleeding
5. Hyperviscosity syndrome (due to elevated IgM)
6. THere is no definitive cure – use chemo, and plasmapheresis for hyperviscosity syndromes – some retinal vessel dilation with resulting hemorrhage and possible blindness because of elevated IgM which is already very LARGE
A t-cell lymphoma of the skin that presents with eczematoid skin lesions that progress to generalized erythroderma with CRIBRIFORM SHAPED lymphcytes.
Mycosis fungiodes
Mechanical heart valves can hemolyze RBCs and lead to HA but which cause?
Extrinsic factors (mecanical hemolysis – heart valves or MAHA)
What is the treatment for MM?
1. ONLY begin treatment when: hypercalcemia, bone pain, and spinal cord compression begins
2. Systematic chemotherapy is the intial treatment with alkylating agents
3. Radiation therapy – if no response to chemotherapy and if disabling pain is present
3. Transplantation – autologous peripheral blood stem cell transplantation is preferred of bone marrow transplant
Screening can identify asymptomatic carriers (SCT) for who ____ couseling SHOULD BE PROVIDED
Diagnosis of CML
1. Marked leukocytosis – WBC 50-2000L with left shift toward granulocytes
2. Small amt of blasts/promyelocytes
3. Eosinophila
4. Peripheral smear – leukemic cells in the peripherl blood: myelocytes, metamyelocytes ,bands and semented forms
5. Decreased leukocyte alk phos activity.
6. BMB shows leukemic cells
How is AIHA diagnosed?
1. Direct coombs test
a. If RBCs are coated with IgG (positive direct Coombc test), then the diagnosis if warm AIHA
b. If RBCs are coated with complement along, then the diagnosis if cold AIHA
c. If there is a positive cold agglutinin titer, then the diagnosis is cold AIHA
d. Spherocytes may e present in warm HA
Historical findings to consider in patients with anemia
1. Family history of hemophilia, G6PD deficiency, thalassemia
2. Bleeding (melena, recent trauma/surgery, hematemesis)
3. Chronic illness (eg recent failure)
4. ALcoholism (folate/b12/iron deficiency)

Physcial injury to RBCs leads to the presnese of fragmented RBCs called SCHISTOCYTES or HELMET cells on the blood smear that can occurs in (TTP, DIC, and patients with prosthetic heart valves.

T or F

Normal platelet counts:
150-400,000 platets
What is ristocetin?
The ristocetin-induced platelet aggregation (RIPA) is an ex vivo assay for live platelet function to aggregate with help of von Willebrand factor and exogenous antibiotic ristocetin added in a graded fashion[1] used to diagnose von Willebrand disease. It is similar to the ristocetin cofactor activity but has the added benefit in that it can diagnose type 2B vWD and Bernard-Soulier syndrome because it uses patients live endogenous platelets, whereas Ristocetin Cofactor Assay tests function of only the VWF but not the platelets. Riscocetin cofactor assay uses platelet poor plasma (with VWF but no platelets) and adds ristocetin and exogenous formalin fixed platelets which can passively agglutinate (but not actively “aggregate”, as they are dead).
In an unknown fashion, the antibiotic ristocetin causes von Willebrand factor to bind the platelet receptor glycoprotein Ib (GpIb), so when ristocetin is added to normal blood, it causes agglutination of fixed platelets or initiates the initial agglutination phase of aggregation of live platelets. In von Willebrand disease, where von Willebrand factor is absent or defective, abnormal agglutination occurs:
In type 1 vWD: hypoactive agglutination occurs
In type 2A vWD: hypoactive agglutination occurs
In type 2B vWD: hyperactive agglutination occurs
In type 2M vWD: hypoactive agglutination occurs activity[2]
In type 2N vWD: normal agglutination occurs
In type 3 vWD: no agglutination occurs
What is the pathophysiology behind that of vaso-occlusive crisis?

Obstruction of microcirculation by sickeled RBCs. This leads to ischemia in various organs, producing the characteristic “painful crises”.

1. Painful crisis including BONE often the tibia, humerus, femur and can be bilateral. lasts 2-7 days
2. Hand-foot syndrome (dactylitis) painful swelling of dorsa of hands and feet seen in infancy and early childhood (4-6 months). FIRST MANIFESTATION OF SCDISEASE. Caused by avascular necrosis of the metacarpal and metatarsal bones.
3. ACUTE chest syndrome: due to repeated episodes of pulmonary infarctions; clinical presentation is similar to pneumonia and associated with chest pain repiratory disress and pulmonary infiltrates and hypoxia.
4. Avascular necrosis of joints most common in the hip with decreased blood supply to femoral head and shoulder and decreased blood supply to humeral head.
5. Priapism-erection due to vaso-occlusion, usually lasting between 30 minutes to 3 hours. treatment with NIFEDIPINE (also used in cases for prevention of vasospasm post MI) or a trial of hydralazine can prevent further episodes.

Which hepatitis vaccine is generally administered to travelers? Those who are exposed to hepatitis _ will likely receive what?
HAV, passive immunization can be given to people exposed to the virus
Someone with acute hepatitis is is likely to present with which clinical features:
1. Jaundice
2. Dark-colored urine
3. RUQ pain
4. N/v
5. Fever/malaise
6. HSM may be present
How is rabies diagnosed?
1. Virus/viral antigen can be indentified in infected tissue and can be isolated to saliva as well
2. Four-fold increase in serum AB titers
3. Indentification of Negri bodies histologically
4. PCR detection of virus RNA
If a patients presents with inflammation, erythema, warmth, pain and swelling at an atraumatic site on skin – your clinical suspicion should lead to to dx?
Cellulitis secondary to a bacterial infection (GAS, S. Aureus)
Two primary clinical features associated with CRYPTOCOCCUS NEOFORMANS
1. CNS disease –> BIGTIME in patients with HIV
2. Isolated pulmonary infection
Most common cause of death due to infection worldwide
Clinical features of infectious mononucleosis:
1. LAD that is found in > 90% patients. Tonsillar or cervial (especially posterior cervical) lymph nodes that are enlarges, painful and tender
2. Pharyngeal erythema and/or exudate
3. Splenomegaly
4. Maculopapular rash (15% of patients but HIGHER if AMPICILLIN is administered)
5. Hepatomegaly (10%)
6. Palatal petechiae and eyelid (periorbital edema) may occur in a minority of cases
Complications that are commonly associated with gonorrheal infections?
1. PID
2. Salpingitis
3. Ectopic pregnancy
4. Fitz-Hugh-Curtis Syndrome (peri-hepatitis) with RUQ pain and elevated LFTs
5. Epididymitis, Prostatitis
6. Disseminated gonococcal infection
Which viral infection that can replicate in the dermis and epidermis, travel to the DRG via sensory nerves and reside as a latent infection, is associated with Bell’s Palsy?
-empiric treatment with oral BACTRUM (TMP/SMX) for 3 days
-use of a CIPROFLOXACIN (FLUOROQUINOLONE) for 3 days is appropriate if resistance rate is high in community to BACTRUM
-amoxacillin not used as much due to high resistance
Hepatitis A serology: Acute versus chronic
Hepatitis A antibody (anti-HAV)
1. Anti-HAV is detectable during acute and chronic phase; cannot distinguish
2. IgM-specific anti-HAV denotes ACUTETherefore anti-HAV + means acute and/or chronic HAV infection
Therefore IgM anti-HAV + means acute and active HAV

Treatment of RMSF
Doxycycline – adminstered 7 days; given IV if the patient is vomiting
Chloramphenicol – CNS manifestations or pregnant patients
How does an HIV+ patient differ from a patient with full-blown AIDS?

AIDS criteria: marked immune suppression leads to disseminated opportunistic infections and malignancies;

1. CD4 count < 200
2. Pulmonary, GI, neuro, cutaneous, and systemic symptoms are common

What is the diagnostic tool for intra-abdominal absesses using IMAGING:
CT scan or ultrasound
What does the Hepatitis B core antibody indicate? (anti-HBc)
Assay of IgM and IgG combined
1. During “window’ period of HBV infection, this is the only marker present
2. Doesnt distinguish between acute and chronic NOR immunity
How is malaria diagnosed?
peripheral blood smear, must have GIEMSA STAINS
Prophylaxis Rx for TB in patients with dx HIV
Screen annually with PPD test.
Prescribe INH and pyridoxine if patient has postitive PPD
Female risk factors versus male risk factors for UTI

Females: shorter urethra and gainal colonization of bacteria, sexual intercourse secondary to the use of diaphragms and spermicides increases rsk further and alters vaginal colonization, pregnancy

Males: uncircumcised males due to bacterial colonization of foreskin, anal intercourse, vaginal intercourse with a femal colonized with uropathogens, BPH, incomplete voiding, indwelling catheders

What indicates a “positive” PPD test?
1. >/= 15 mm if healthy individual
2. 10 mm –> High risk population (high prevalence, Homeless, prisonmates, HCW)
3. 5 mm –> HIV patients or those in close contact with active TB or evidence of primary TB on CXR
What are the most common risk factors for brain abscesses?
AIDS, immunosuppression, bone marrow transplant, bacterial meningitis
Which three areas of the united states are most commonly affected by lyme disease?
NE seaboard; Midwest; West coast (N. Cali)
How is necrotizing fasciitis treated?
Rapid surgical exploration and excision of devitalized tissue is necessary with BROAD SPEC AB parenterally.
A patient presents with lethargy, malaise for a period of 3 days to 2 weeks with other symptoms including: fever, sweats, headaches, arthralgias, diarrhea, sore throat, LAD, and a truncal maculopapular rash. The patient states that the majority of his symptoms have lessened to a minimum, and wants to know if his possible blood transfusion after he was diagnosed with SCA may have been what spawned it?

This is a typical presentation of someone with PRIMARY INFECTION of HIV. Currently, the patient had 3days-2 weeks of flu-like/mono-like symptoms. HIV has an incubation period of 2-4 weeks after its initial infection before its viral load is high enough to have an effect.

It is important BUT difficult to catch patients with primary HIV because of the benefits of early antiretrovirl therapy.

Treatment of chronic HBV:
treat with interferon (IFNalpha)
treat with lamivudine (nucleoside analog)
Risk factors for diffuse inflammation of the brain parenchyma (encephalitis) include:
1. AIDS: those with AIDS are at risk for toxo when count < 400
2. immunosuppression (chemo)
3. Travel in underdeveloped countries
4. Exposure to mosquitos (vectors) from endemic areas
5. Exposure to wild animals (BATS) in an endemic area for rabies
CLINICAL features of acute bacterial arthritis (SEPTIC arthritis)
1. Swollen, warm, painful
2. ROM active and passive is limited
3. Constitutional symptoms such as fever, chills, and malaise are common
Diagnosis of infectious mononucleosis is made by:
1. Serology
-Monospot test for detection of heterophile AB
-Heterophile antibodies are positive within 4 weeks of infection with EBV mononucleosis and are undetectable by 6 months. Thus a positive monospot test indicates acute infection with EBV mononucleosis.
-Heterophile antibodies are negative and do not form in CMV mononucleosis
EBV specific antibody testing is performed in cases inw hich diagnosis is not straightforward and dont by ELISA.2. Peripheral blood smear: revelas lymphoctoc leukocytosis with large atypical lympocytes
3. Throat culture – perform if pharyngitis is present to rule out a secondary infection with B-hemolytic streptococciwith B-hemolytic stretococci

Toxoplasmosis prophylaxis in HIV patient:
If CD4 < 100 administer BACTRUM (tmp-smx)
How might vaginal candidiasis be treated?
1. Miconazole
2. Clotrimazole cream
Primary syphilis includes
Painless chancre (indurated, hard with clean base)
-crater like lesion that appears on the genitalia 3-4 weeks post exposure
-heals in 14 weeks
-highly infectious
Two recommendations for prevention of pneumonia
1. Influenza vaccination given annually to people at increased risk for complications and health care workers
2. Pneumococcal vaccine – for patients > 65YO and for younger people with SCA, heart disease, pulmonary disease (COPD), DM, alcoholics cirrhosis, asplenic individuals.
Treatment of acute prostatitis
1. If septic: hosptalize patient and start IV AB
2. If mild: treat on OUTPT basis with AB: BACTRUM, CIPRO, or DOXY for 4-6 wks
How is lymphadenitis treated for?
penicillin G, antistaph penicillin (naf or oxa), cephalosporin, warm compresses
Neutropenia is defined by absolute neutrophil count (ANC) < 1500/mm2. What does ANC represent?
Combination of bands and mature neutrophils
What causes a CHANCROID?
Haemophlius ducreyi, a gram-negative ROD
Women v. Men who are symptomatic for Chlamydia?
Females: purulent urethral discharge, intermenstral or post coital bleeding, dysuria
Males: dysuria, purulent uretral dischange, scrotal pain and swelling, fever
When should a CT scan of the head be ordered in patients with suspected acute bacterial meningitis?
Recommended before LP is there are focal neurological signs OR if there is evidence of a space-occurpying lesion with elevations in ICP (noted papilledema, ETC)
Major risk factors for developing OSTEOMYELITIS
1. Open fractures
2. DM
3. Use of illicit drugs (IV)
4. Sepsis
How is disseminated/systemic candida treated?
ORAL fluconazoleNew agents include: voriconazole as CASPOFUNGIN

How long does genital herpes last for (symptoms)?
3 weeks
Most likely bacteria to result from aspirations pneumonia?
Oral anaerobes: Prevotella, Peptostreptococcus, Dusobacterium, Bacteroides
Others S. aureus, S pneumo, aerobic gram negative bacilli
In nursing home residents, the most common nosocomial pathogen with predilectation to the upper lobes?
Pseudomonas Aeruginosa
DIAGNOSIS of pyelonephritis:
1. UA: pyuria, bacteriuria, WBC casts
2. Urine culture: get from all patients with pyelo
3. Blood culture: get from all ill appearing pts and hospitalized patients
4. CBC: left shift with leukocytosis
5. RFT: should be preserved; impairment can be reversible
6. Imaging studies: if Rx fails or if pt with complicated pyelo. Get renal US, then CT, IVP, or retrograde ureterogram.
What is Erysipelas? How does this differ from an uncomplicated cellulitis?

Erysipelas is a cellulitis that is usually confined to the dermis and lymphatics. This is caused by GAS with a presentation of well-demarcated, RED, PAINFUL lesion on the lower extremities and the face.

Unlike that of cellulitis, erysipelas often has predisposing factors of lympatic obstruction (pst radical mastectomy) local trauma or ascess, fungal infections, DM or alcoholism.

CHRONIC HEPATITIS is more likely to occur in acute hepatitis 1-10% of patients with Hepatitis __ virus versus patients diagnosed with Hepatitis __ virus whose chance is between 80-90%.
HBV has 10% chance of becoming chronic
HCV has 80-90% chance of becoming chronic
Oval budding yeasts known for their formation of hyphae and long pseudohyphae.
Candida species
Toxic-shock syndrome (TSS) is most commonly associated with?
Menstruating women and tampon use but can occur in both male and females secndary to surgical wounds, burnes, infected insect bites. This is due to an enterotoxin by S. Aureus or less frquently an exotoxin of GAS.
What are the clinical findings of patients with C. Trachomatis L1-L3 (lymphogranuloma venereum)?
PAINLESS ulcer at site of inoculation that can often go unnoticed. A few weeks post infection, it will have spread to inguinal lymph node and developed unilateral tenderness and can result in more severe issues that can resemble that of ulcerative colitis and/or orther IBDs. For example, PROCTOCOLITIS may develop with perianal fissures and rectal stricture resulting in the obstruction of lymphatics and elephantitis of the genitals.
Pathophysiology of HIV:
a. Most common virus assciated iwth HIV is the HIV type 1 human retrovirus
b. Attaches to surface of CD4+ T cells (target of HIV-1)-enters cell by binding to GP120 and entering GP40 the cell-uncoating-transcribing RNA into DNA using host machinery and OWN reverse transcriptase.
c. Particles are produced each day by activated CD4 cells. When the virus enters into the lytic phast of infection, the CD4+ cells are destroyed and its depletion of the bodys arsenal of CD4 cells weakens the cellular immunity of the host.
How should one approach a patient with recurrent UTI infections?

If relapse occurs within 2 weeks of cessation of treatment, continue treatment fr 2 more weeks then get a urine culture


Treatment for uncomplicated cystitis – if patient has more than two UTIs per year:
1. Give chemoprophylaxis (one dose of TMP/SMX after intercourse or at the first signs of symptoms)
2. Alternative lowdose prophylactic AB for 6 mo (TMP/SMX)

Empiric treatment for ACUTE BACTERIAL MENINGITIS for infants
Etiology: GBS, E. Coli, Klebsilla spp., Listeria monocytogenes
Empiric Treatment: Cefotaxime + amp + VANC
DO aminoglycoside < 4 weeks
OM of the vertebral bodydue to M. TB is called _____ ______.
Potts Disease
Transmission of Hepatitis A, B, C, D, E?
HEP A: Fecal/oral
HEP B: Sexually or Parenterally
HEP C: Associated with cryoglobulinemia and IV drug abuse
HEP D: requires the outer envelope of HEP BsAg for replication or as a superinfection in a chronic HBV carrier
HEP E: Fecal/oral route and are more prevalent in developing countries
Atypical pneumonia syndrome is associated with which pathogens?
CAP can be either typical (S. Pneumo) or atypical in presentation. Those which are commonly associated with atypical include: Mycoplasma pneumonia, Chlyamydia pneumonia, Legionella, Coxiella Burnetti (Q Fever), and chlyamydia psittachi. Viruses are included in the atypical presentation
RMSF is characterized by the intracellular bacteria
Rickettsia rickettsii
Vector: ticks
Most common areas affected by mucocutaneous growth of candida?
1. Oropharynx – (“thrush”) with thick, white plaques that ahere to the oral mcosa, painless, unexplained thrush shuld rasie suspicion of HIV infection
2. Vagina-“yeast” infection
3. Cutaneous candidiasis-erythematous, eroded patches of satellite lesions
4. GI tract (esophagus) -esp in HIV; odynophagia can result
Second stage of syphilis
Develops 4-8 weeks post that of the primary infection that resples spontaneously. Maculopapular rash forms in this stage
What tests diagnose a lung abscess and how is this treated once tests confirm?
1. Order CXR: receals thick walled cavitation with air fluid levels
2. Order CT scan: differentiated between abscess and empyema
3. Sputum stain and culture low sensitivity so get bronchoscopy or transtracheal aspiration to avoid expetoration thats contaminated with oral flora.Rx: Drainage if necessary should be performed first and foremost.
1. AB regimens:
-cover gram positive cocci = amp or amoxi/clav acid(zosyn), vanc for s. aureus
-cover anaerobes = clindamycin/metronidazole
-cover gram negatives = fluoroquinolones or ceftazidime
2. Duration: until cavity is gone or CXR improved significantly – can take months.

HIV + patients with contrast enhanced mass lesions in the BG and subcortical white matter (greater than three)?
Toxoplasmosis gondii (cause of noninfectious encephalopathy)
Complications for pneumonia
# 1 = pleural effusion (“parapneumonic effusion”
1. Seen in > 50% patients with CAP on routine CXR
2. Most uncomplicated courses and resolve with treatment of the pneumoia with AB however if it is complicated with an empyema – thoracentensis should be performed if LL decubitius film shows >1cm fluid. Get grain stain, culture, pH and cell count. Then determine amt of glucose, protein and LDH to differentiate between an exudative versus nonexudative
If patient is very ill, elderly, pregnany, or unable to tolerate oral medications for that of a pyelonephritis, how should patients be treated?
1. Hospitaliation with IV fluids
2. Administer AB first parenterally (broad spec) AMP-GENT or CIPRO
3. If blood cultures (-) –> not urosepsis –> Rx IV AB for 24 hours until patient is afebrile. Then give oral AB to complete 14-21 day regimen
4. If blood cultures (+) –> UROSEPSIS –> Rx: IV AB for 2-3 weeks.
Two forms of botulism
1. From ingestion of preformed toxin – adminster antitoxin if known
2. Wound contamination – clean and administer penicillin
Acute meningitis versus Chronic meningitis
Acute: onset within hours to days and are BACTERIAL (OFTEN)
Chronic: onset within weeks to months (commonly due to mycobacteria, fungi, parasites, Lyme disease)
What is more sensitive than the HCV antibody?
VIRAL LOAD: HCV RNA measured by PCR. Detectable 1-2 weeks after infection
Rabies is contracted from a bite or scratch of an infected animal and can result in a deadly viral _______ if not treated early.
Diagnosis of TSS
High index of clinical suspicion, blood cultures are usually negative

Neurosyphilis is characterised by: ________, ___________, ________


Dementia, personality change, tabes dorsalis

Rx. penicillin

Complications in males secondary to Chlamydia v. females?
Males: prostatitis, epididimitis
Females: Fits-Hugh-Curtis Syndrome (inflammation of liver with elevated LFTS), Pelvic inflammatory disease (PID), salpingitis, tubo-ovarian abscess, ectopic pregnancy
Three primary malignancies associated with HIV
1. Kaposis sarcoma (HHV8)
2. NHL — rapidly growing lesion in CNS
3. Primary CNS lymphoma
Healthy patients who are positive for TB exposure and a positive PPD test without ACTIVE TB should be treated with which medications?
Isonizid only
Diagnosis of UTI requires the use of which tests:
1. Urinary dipstick
-positive urine leukocyte esterase test-rapid screen for pyuria
-positive nitrite test for presense of bacteria (gram -)
2. UA
-clean catch void; epithelial squamous cells indicates vulvular or urethral contamination
-Bacteriuria > 1 organism per oil-immersio
-pyuria: > 8 WBC/HPF
3. Urine gram stain
-count greater than 10^5 organisms/mL represents significant bacteriuria
4. Urine culture
-confirms diagnosis with high specificity: if >/= 10 CFU/mL or urine from clean-catch
5. Blood culture
6. IVP cytoscopy
What would an LP show to indicate encephalitis secondary to a viral infection?
1. Lymphocytosis: >5 WBC/uL with normal glucose is consistent with viral encephalitis (similar CSF as in viral meningitis)
2. Negative CSF cultures
3. CSF PCR: most specific and sensitive test for diagnosing many various viral encephalitis, including HSV-1, CMV, EBV, VZV
Medical treatment of acute bacterial arthritis in a relatively healthy adult: will be empircal treatment for:

S. aureus

1. Parenteral B-lactamase resistant penicillin (oxa/naf) or first gen ceph x 4 weeks
2. Parenteral VANC if MRSA suspected

What is the purpose of the CD4 count in patients with HIV?
Best indicator of the status of the immune system and of the risk for opportunistic infections and disease progression
In acute hepatitis, ALT is usually > _____, however drug induced hepatitis is much higher.
Acute hepatitis will normally have elevated ALT > 1000
Chronic hepatitis will normally have ALT < 1000
Headache that worsens when lying down; fevers; n/v; stiff, painful neck, malaise
What makes FULMINANT hepatitis different from ACUTE hepatitis?
Fulminant hepatitis: where acute hepatitis turns into liver failure with complications (hepatic encephalopathy, hepatorenal syndrome, bleeding diathesis)
What is “cellulitis” and what are the two most common causes?

Cellulitis is an inflammation of skin and subcutaneous tissue that is caused bya wide vareity of bacteria – most common being that of:

1. GAS
2. S. Aureus

What is the treatment of RABIES postexposure?
2. If wildlife bite (bat/raccoon) – capture animal if possible, destroy it, send to lab for immunofluorescence of brain tissue
3. If bitten by healthy dog/cat in endemic area, capture animal and observe for 10 days. If not change in animal condition then rabies is not present.
4. IF KNOWN rabies exposure then perform both of below:
-Passive immunization: admin human rabies Ig to patients into wound and into the gluteal region
-Administer the antirabies vaccine in 3 doses IM via the deltoid or thigh over a period of 28 days.
What diagnostic tests should be ordered to workup an ill neutropenic patient?
1. CXR
2. PAN culture (blood, urine, sputum, line tips, wound)
3. CBC
4. Complete metabolic panel
5. Place the patient on reverse isolation precautions (positive pressure rooms with masks and strict handwashing)
6. Give broad spectrum antibacterial agents immediately after cultures are drawn
7. If fever persists greater than 4-5 days despite broad spectrum antibacterial therapy, give antifungal agents like IV AMP B.**CONSIDER ADMIN OF G-CSF to stimulate growth factors to produce WBC

Unlike that of C. Trachomatis, how does N. Gonorrhea present in males versus females?
Males: SYMPTOMATIC – purulent d/c, dysuria, erythema, edema, erethral meatus, frequency of urination
Females: ASYMPTOMATIC – cervicitis, urethreitis
How is Herpes Simplex transmitted?
Contact with people who have the ACTIVE ULCERATIONS OR SHEDDING OF VIRUS from the mucous membrane. HSV-1 is usually nonsexually transmitted whereas HSV-2 is sexually transmitted nearly 100% of the time.
Duration of treatment for acute uncomplication cystitis?
Most cost-effective duration is 3 days;
1. Single-dose treatment has a higher recurrence rate
2. 7 day course has too many side effects.
Define encephalitis:
diffuse inflammation of the brain parenchyma and is often seen SIMULTANEOUSLY with that of meningitis
Pathophysiology of RMSF:
Organisms enter host by tick bites –> multiply in the vascular endothelium, spread to different layers of vasculature, damage vascular endothelium and results in increased vascular permeability –> activation of compliment –> microhemorrhages –> microinfarcts
Which countries have an elevated prevalence of HEV?
India, Pakistan, SE Asia, parts of Africa
If a patient has a history of <3 doses, unknown status or > 10 YR sincle last “booster” of tetanus, what should be done for wound management in clean/minor wounds? Other wounds?
If clean, minor – administer active immunication with tetanus/dip toxoid (Td)
Do not provide TIG is clean, minor woundIf other wounds, administer both TIG and Td

Diagnosis of HIV requires which tests?
Two are required:
1. ELISA – screening test for detecting antibody to HIV; becomes positive 1-12 weeks after infection. These tests are 99% sensitive (and thus a negative ELISA excludes HIV as long as the patient hasnt had prior exposure before testing – hence seroconversion). A positive ELISA wins the patient another test…2. Western blot – performed after a positive ELISA for confirmation. This is a highly specific test >99% thus will rule out if negative.

DDx for food-borne botulism includes:
Guillian Barre syndrome –> ASCENDING muscle paralysis
Eaton-Lambert syndrome
Myasthenia gravis-EM studies differentiate
Diptheria toxin
Tick paralysis (RMSF)
What does the Hepatitis B e Antigen represent?
Infectivity of the virus. If HBeAg positive, then highly infectious and actively replicating. Will appear shortly after HBsAg
Fever pattern varies depending upon the cause:
1. P. falciparum –> A
2. P. ovale and P. vivax –> B
3. P. Malariae –> C
A. Fever is constant
B. Fever spikes every 48 hours
C. Fever spikes every 72 hours
How is menitigitis diagnosed?
CSF examination (LP) – must perform; also note the opening pressure
-Cloudy: pyogenic leukocytosis
-CSF sent for: cell count, chemistry (protein, glucose), gram stain, culture (AFB included), cryptococcal antigen OR india ink stain for cryptococcus sporidium
Most common bacteria associated with osteomyelitis?
S. Aureus and coag-negatice staphylococcus (epidermidis)
Cryptococcus neoformans is a budding, round yeast with a thick _ capsule. Cryptococcus is most commonly associated with ____ droppings and seen in patients with advanced HIV. Infection is often secondary to inhalation of fungus into lungs – hematogenous spread may involve the brain and meninges.
polysaccharide, pigeons
What is HAART?
Triple drug regimen used in patients with HIV
1. Regimen 1: two nucleoside reverse transcriptase inhibitors + NNRI or protease inhibitor
Treatment for Herpes Simplex?

NO CURE, this will forever ly dormant. Antiviral treatment provides relief from symptoms and reduces duration but doesnt inhibit flares.

-rx with acyclovir

What is the most common form of UTI?
UNCOMPLICATED acute cystitis which is more common in women than in men and are ASCENDING from the urethra.
Chronic pyelonephritis can result in ______ of the kidneys long-term
Necrotizing fasciitis is common two which two bacterial causes?
1. C. Perfringens
2. S. Pyogenes
What are the top three common agents for CAP?
S. Pneumonia
H Influenza
Aerobic gram negative rods
S. Aureus
Symptoms of progressive primary TB into secondary TB (active)
Initially asymptomatic with possible effusion. Then the pulmonary and consititutional symptoms of TB develop (fever, night sweats, weight loss, malaise) and the cough progresses from dry to purulent sputum Hemoptysis suggests advanced disease as well as apical RALES.
Which patients should be tested for HIV infection because they are considered to be “high risk”
1. Homosexual males/bisexual men
2. IV drug users
3. Blood transfusion receipients before 1985 (widespread donor screening)
4. Heterosexual contacts of HIV+ patients
5. Unborn/newborn babies of patients with HIV+ mothers
Fever of Unknown Origin (FUO) defined:
1. Fever >101.3F
2. Continuing “on several occasions” for at least 2 weeks
3. No diagnosis over this time period despite 1 week of inpatient workup
What is a common STD that results in “pubic lice”
Pediculosis pubis (“crabs”) is a common STD caused by Phthirus pubis that is transmitted by sex, clothing, towels that are shared.
Patients with active TB should be treated in which order and with which medications?
1. ISOLATION! (Until sputum is negative for AFB
2. FIrst line therapy: the 4 drugger regimen RIPE
Ethambutol OR streptomycin
3. 4 drug regimen lasts 2 months then the last 4 months is INH and RIFAMPIN only

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