Review-Arthritis SLE MS Fibromyalgia

What is arthritis?
Inflammation of ?1 joints

There are about 100 types of arthritis, but what are the 2 most common types?
Osteoarthritis-normal wear & tear
Rheumatoid-auto immune disorder

What questions should you ask when assessing musculoskeletal pain?
Location-articular or nonarticular
Character-crampy, throbbing, etc
Quantity- scale of 1-10
Course- onset, duration, progression
Aggravating/alleviating factors
Setting- repetitive activity, rest
Associated manifestations-local, constitutional, emotional

By what age do 90% of all people have some sort of joint problems?
By age 40

What are some risk factors for osteoarthritis?
What are some risk factors for osteoarthritis?
Joint trauma
Age
Obesity, overuse
Weak muscles and joints
Congenital musculoskeletal disorders

What is the clinical presentation of osteoarthritis?
Gradual onset
Morning stiffness, or stiffness after prolonged immobility
Crepitus & occasional joint effusions
Grating or catching sensation with movement
Joint deformities

What osteoarthritic joint is considered the most painful and disabling?
The hip joint

What joints are most affected by osteoarthritis?
DIP
PIP
1st metacarpophalangeal
knees
hips
cervical & lumbar spine

What joint is most commonly symptomatic for osteoarthritis?
The knees

What is a Heberden's node?
What is a Heberden’s node?
Bony bumps at the distal interphalangeal joint (DIP)

What are Bouchard's nodes?
What are Bouchard’s nodes?
Bony bumps at the proximal interphalangeal joint (PIP)

If a pt complains of asymmetric, poorly localized pain, stiffness that lasts up to 30 min, and no constitutional symptoms-what should you suspect?
Osteoarthritis

Describe the focused exam for osteoarthritis
Inspect the joint
ROM
Palpate for crepitus, warmth, edema, & tenderness
Observe muscles for atrophy
Evaluate joint stability

What are some diff’s of osteoarthritis?
Bone dx-osteopenia, osteoporosis, malignancy
Tendinitis
Bursitis
Neuropathy
RA
Gout
Vascular dx like vasculitits

These tests can be ordered, to rule out other etiologies, when working up osteoarthritis. But if it is OA, they should all be normal
CBC
RF
ESR
CMP
Uric Acid

Why should you order x-rays for the diagnosis of osteoarthritis?
Good for baseline
Can see progression
Narrowed joint space
Sclerosis of subchondral bone
Bony cysts
Osteophytes

What is the goal of treatment for osteoarthritis?
The goal is to control pain, maintain function, maximize independence & minimize complications.

Every 1lb of weight lost takes how much pressure off of each knee?
1lb of weight loss results in 4lbs of pressure taken off each knee

What are some non-pharmacologic treatments for osteoporosis?
Lose weight
Lessen weight bearing
Community support groups
PT/OT
Exercise program
Assistive devices-canes, jar openers, scooters

What medications can be used for osteoarthritis?
NSAIDs-target inflammation
Analgesics-treat only the pain
Topicals-temprorry relief of pain or swelling
Injectables-aim to replace joint fluid

Cox 2 inhibitors are from what drug class?
NSAIDs
Celebrex, Mobic

Ibuprofen is the 1st NSAID that should be tried for tx of osteoarthritis. If that is ineffective, what are 2 other NSAID options?
Naprosyn, Diclofenac (Voltaren XR)

What 2 analgesics should be used for osteoporosis?
Tylenol & Tramadol

What 2 injectable treatments are available for osteoarthritis?
Hyaluronic acid-pain relief, improves mobility
Steroid injection- used with signs of inflammation, effusion or substantial pain

What are some alternative treatment options for osteoarthritis?
Glucosamine/chondroitin
Acupuncture
Massage
Hydrotherapy
Copper bracelets

Can surgically repair or replace damaged joints, but they must commit to rehabbing the joint

What is the follow-up for osteoarthritis?
If on prescribed meds-monitor lab work:
CBC, CMP, hemoccult if on NSAIDs
LFT’s if on Tylenol
Return to office if no response to tx within 4-6wks, or with flare-up

What is rheumatoid arthritis?
What is rheumatoid arthritis?
An autoimmune disease where the immune system attacks joints causing inflammation that damages joints and organs. Women>Men 3:1

What is the average age of onset for RA?
Women 30-60yo, older for men

What is the pathogenesis of RA?
Inflammation of synovial membranes result in thickened synovium which adheres to articular cartilage and later erodes cartilage & underlying bone.
Adhesions & cysts can develop

For classification of RA, a pt must have 4 of these complaints, at least 1 of which has been present ?6 weeks.
For classification of RA, a pt must have 4 of these complaints, at least 1 of which has been present ?6 weeks.
Morning Stiffness
Arthritis to ?3 joints
Arthritis of hand joints
Symmetric arthritis
Rheumatoid nodules
Serum rheumatoid factor
Radiographic changes

Does OA or RA have diffuse warmth & redness?
Does OA or RA have diffuse warmth & redness?
RA

What are some systemic manifestations of RA?
Fatigue
Morning stiffness
Vasculitis
Scleritis
Sjogren’s syndrome
Lymphadenopathy
Peripheral neuropathy
Pleuritis
Interstitial lung fibrosis
Pericarditis
Amyloidosis
Splenomegaly
Felty’s syndrome

Rheumatoid nodules
Rheumatoid nodules

What are some diff’s of RA?
Polymyalgia Rheumatica
Reiter’s syndrome
SLE
Gouty arthritis
Psoriatic arthritis
Lyme disease
Acute rheumatic fever
Ulcerative colitis or Crohn’s disease

What tests should you order to work-up RA?
CBC with diff
RF
ESR
CMP
Synovial fluid analysis
UA
X-rays

Could also get ANA, CH50, immunoglobulins, CRP

How is RA treated?
Initially treated by rheumatology
Pt education
Early referral for PT/OT
Hot/cold therapy
Ultrasound therapy
TENS
Visual imagery
Massage
Acupuncture
Hypnosis
Medications

What does DMARDS stand for?
Disease-modifying-antirheumatic-drugs
These drugs work slowly to modify the course of the disease. Methotrexate is the most common, but there are about 12 in all.

What drugs are used in the treatment of RA?
NSAIDs
DMARDS
Biologic agents
Immunosupressive agents
Systemic corticosteroids
Combo DMARDS
Experimental agents
Combo of other drugs- analgesics, antidepressants, etc

How do biologic agents work in the treatment of RA?
There are currently 6 drugs, they block specific steps in the inflammation process.

These 3 biologic agents are called TNF-a inhibitors because they block the cytokine called tumor necrosis factor-alpha
Adalimumab – Humira
Etanercept – Enbrel
Infliximab – Remicade

Name the 6 biologic agents now available for the treatment of RA
Abatacept – Orenica blocks activation of T cells
Adalimumab – Humira blocks TNF-a
Anakinra – Kineret blocks interlukin-1
Etanercept – Enbrel blocks TNF-a
Infliximab – Remicade blocks TNF-a
Rituximab – Rituxan blocks B cells

What benefit do the biologic agents have that other RA meds don’t have?
Biologic agents target a specific step in the inflammation process, but they don’t wipe out the entire immune response like other RA drugs

When should systemic corticosteroids be used in the treatment of RA?
Use them only to get potentially damaging inflammation under control.

What are some common side effects of DMARDS?
Skin: rash, pruritis, exfoliation
GI: N, diarrhea, abd cramping, oral ulcerations
Pulm: fibrosis
Liver: fibrosis
Immune: immunocompromised, risk of Ca
Renal: proteinuria, increased creatinine
Blood: thrombocytopenia, leukopenia, elevated LFT’s

What are some common side effects of TNF-a inhibitors?
Nausea, diarrhea, hair loss, immunocompromised

When should you use biologic agents for the treatment of RA?
Moderate to severe RA that has not responded well to other treatments.
All but 1 are injections

What survival options are available for RA?
Total joint replacement
Tendon repair
Joint fusion

What topics should be discussed for pt education on RA?
Regular exercise
Heat/cold therapy
Relaxation
Maintain ideal body weight
Assistive devices

What is the follow-up for a pt with RA?
What is the follow-up for a pt with RA?
They should be followed by rheumatology
Be sure lab work is being done & monitored
Goal is to control condition, maintain/improve function, prevent deformities, psychosocial support, pt education, self-mgmgt

What gender is most affected by juvenile arthritis? And what are the causes?
Girls more often affected.
Caused by genetic, viral
Treatment is similar to RA

What is one of the only artropathies seen more commonly in men?
Ankylosing spndylitis
Chronic inflammatory disease causing pain and inflammation to the joints between vertebrae & pelvis. Eventually causes fusion to the spine.

What is psoriatic arthritis?
What is psoriatic arthritis?
Form of arthritis that affects some people with psoriasis. Usually psoriasis appears 1st.
Will see involvement in the spine, sacroiliac, & a distal asymmetric pattern.

Psoriatic arthritis can be symmetric or asymmetric, which is typically associated with more severe psoriasis?
Symmetric psoriatic arthritis is typically is associated with more severe psoriasis.
Usually affects ?5 of the same joints on both sides of the body.

Describe the joint involvement of asymmetric psoriatic arthritis.
Usually affects joints on only 1 side of the body, or different joints on each side.
Usually involve ?5 joints, & they’re often red and tender.

What is the most severe, destructive, form of psoriatic arthritis?
Arthritis mutilans. Occurs in about 5% of people with psoriatic arthritis. Results in severe osteolytis, ultimately destroying the small bones of the hands.

Distal interphalangeal (DIP) joint predominant psoriatic arthritis is rare, but occurs mostly in what gender?
Distal interphalangeal (DIP) joint predominant psoriatic arthritis is rare, but occurs mostly in what gender?
Men

If you can’t see, pee, or climb a tree- it’s probably this type of arthritis…
Reactive arthritis (Reiter’s syndrome)

What is the classic triad of Reiter’s syndrome?
Conjunctivitis
Urethritis
Arthritis

This type of arthritis is triggered by an infection that occurs elsewhere in the body
Reactive arthritis
Usually caused by a UTI or STD.
Symptoms usually come & go, and disappear within 12 months.

What is scleroderma?
A group of rare, progressive diseases that involve hardening and tightening of the skin and connective tissue.

What are the 2 main types of scleroderma?
Localized- only the skin
Systemic scleroderma- skin & internal organs

What are the 2 types of localized scleroderma?
Morphea
Linear

What is morphea localized scleroderma?
What is morphea localized scleroderma?
Oval shaped, thickened patches of skin that are white in the middle, with a purple border.

What is linear localized scleroderma?
What is linear localized scleroderma?
Bands or streaks of hardened skin in 1 or both arms, legs, or forehead.
Seen more commonly in children.

What is CREST syndrome?
A muiltisystem connective tissue disorder, that is a limited cutaneous form of systemic sclerosis.
C- calcinosis
R- Raynaud phenomenon
E- esophageal dysmotility
S- sclerodactyly
T- telangiectasia

What is sclerodactyly?
What is sclerodactyly?
A localized thickening and tightness of the fingers and toes

What is telangiectasia?
What is telangiectasia?
Spider veins

What meds are used in the treatment of scleroderma?
BP meds to dilate the blood vessels to prevent lung & kidney problems & improve Raynaud’s.
Immunosupressant meds may reduce scleroderma symptoms.

What is polymayalgia Rheumatica?
An inflammatory disorder causing muscle pain and stiffness, typically bilateral & symmetric to neck, upper arms, and hips.
Most often in pt’s >60yo
Related to giant cell arteritis (Temporal arteritis)
Symptoms begin quickly, ?2 wks

What is polymyositis/dermatomyositis?
An uncommon connective tissue disorder with inflammation of the muscles.
Most notable characteristic is skeletal muscle weakness. May have dysphagia, dyspnea, aspiration.
More common in blacks. More common in women.
Remission is rare.
Will have elevated CPK, abnormal EMG

What are some sources of pain in rheumatic diseases?
Inflammation
Articular cartilage loss
Muscle spasm
Nerve irritation or compression
Bone fracture or spur
Stretched or torn tissue
Referred pain
Reflex sympathetic dystrophy

What is fibromyalgia?
A chronic condition characterized by widespread pain in muscles, ligaments and tendons, as well as fatigue and multiple tender points.

Name the 18 tender points of fibromyalgia
Name the 18 tender points of fibromyalgia
Occiput (bilat)
Low cervical (bilat)
Trapezius (bilat)
Supraspinatus (bilat)
Second rib (bilat)
Lateral epicondyle (bilat)
Gluteal (bilat)
Greater trochanter (bilat)
Knee (bilat)

How do you test the tender points of fibromyalgia?
Apply 5-10lbs of firm pressure to the points

Many pt’s with fibromyalgia have coexisting conditions. Name some
Chronic fatigue
Depression
IBS
Lupus
Restless leg
Raynaud’s
POTS
Headaches
OA/RA
PTSD

What is the American College of Rheumatology criteria for the classification of fibromyalgia?
Hx of widespread pain, must be present for 3 months.
Pain in 11 of 18 tender points on digital palpation

In addition to a thorough MS exam, what other parts of the exam should you focus on to work-up fibromyalgia?
Neck for thyromegaly
Mental status/psych

What are some diff’s of fibromyalgia?
Chronic fatigue -won’t have pain
RA
SLE
Somatization
Depression
PMR
Severe hypothyroid

What labs can you order for fibromyalgia?
New test for fibromyalgia FMA, just starting to be used.
CBC
ESR
CPK
TSH
RF

What drug classes can be used to treat fibromyalgia?
Analgesics-acetaminophen, NSAIDs, tramadol
Antidepressants- amitryptyline, fluoxetine, duloxetine, milnacipran
Antiseizures-gabapentin, pregabalin

Other than meds, what other treatments may help fibromyalgia?
PT
Massage
Acupuncture
Stress Mgmt
Relaxation techniques
TENS
Lido injection to tender points
Medical marijuana
Melatonin
5HT
St. John’s wort
SAM-E

Is fibromyalgia progressive?
no, but it can lead to sleep disturbances and depression

How often should fibromyalgia pts follow-up?
Depends on the pt, severity of their symptoms, and their coping skills

What is gout?
What is gout?
An inflammatory disease of peripheral joints caused by monosodium irate crystal deposits.

What is the cause of Primary gout?
An inborn error in production or excretion of uric acid

What is the cause of Secondary gout?
Can develop secondary to other disease, like leukemia or renal insufficiency.
Can develop as a result from drugs like salicylates, diuretics, ETOH, or nicotinic acid.
Can be from a diet high in purines like anchovies, organ meats, liver, spinach, mushrooms, asparagus, oatmeal, cocoa, or sweetbreads.

What is tophi?
What is tophi?
Uric acid deposits that can form on the skin, around a joint, or in the external ear. Usually seen after 10 years of having gout.

When does gout usually begin for men? Women?
Men >30yo
Rare in women until menopause

Describe the acute phase of gout
Sudden onset of joint inflammation and EXCRUCIATING pain, typically in 1 joint, often the MP joint of the big toe.

What is podagra?
What is podagra?
Gout, when it involves the big toe

When does the 1st attack of gout usually begin?
At night or early morning.
Pain usually peaks within 24-36 hrs

What is chronic gout?
Gout attacks happen more often, and more joints are involved.

What are some extra-articular manifestations of chronic gout?
Low-grade fever
Chronic gouty neuropathy
Nephrolithiasis
Acute uric nephropathy

What is tophaceoud gout?
What is tophaceoud gout?
Visible nodules of tophi

What meds can cause or make gout worse?
Tzd’s
Nicotinic acid
ASA

What history should you obtain for a gout work-up?
Precipitating factors like meds, ETOH, diet
Family hx (for primary gout)
#, duration & characteristics of attacks
Associated symptoms for chronic gout

What are some diff’s of gout?
Pseudogout-something other than uric acid
RA/OA
Cellulitis
Infectious arthritis
Bursitis secondary to a bunion

Pseudogout typically affects the elderly and rarely involves
Tophi
Because there is no build up of uric acid

What is the gold standard for diagnosing gout?
Joint aspirate for smear and culture and to identify urate crystals.
Gold standard, but painful & not required!

Not the Gold Standard for diagnosing gout, but this is usually sufficient to establish the diagnosis.
Hyperuricemia & a typical history of monoarticular acute arthritis

What labs can you order to work up arthritis?
Uric acid >7.0 supports dx of gout
ESR & WBC’s will be elevated during acute attack
RF to rule out RA
Consider 24h urine to measure uric acid excretion

What will you see on x-ray with tophaceous gout?
What will you see on x-ray with tophaceous gout?
Punched-out lesions

What is the acute phase treatment for gout?
NSAIDs are 1st line tx, high-dose for 2-3 days, then decrease for 3-5 days.
Indomethacin
Naproxen
Colchicine (Colcrys) 1.2 at 1st sign of attack, then 0.6qh, 1.2q2h, or 0.6q2-3h until relief.
Low-dose steroids

How do you treat the inter critical phase of gout?
1 attack/yr: colchicine 0.6mg 3-4x/wk
>1 attack/yr: 0.6mg daily
>1 attack/yr that are severe: 0.6 BID or TID

If a pt has just had an acute attack of gout, do not start this med for 2-4 weeks
Urate lowering medications

How do you treat chronic gout?
Treat with a irate lowering agent or hypouricemic
Allopurinol (Zyloprim)-reduces uric acid production
Probenecid (Benemid)-increases renal excretion
Febuxostat (Uloric)-reduces uric acid production

Urate lowering agents or hypouricemics are indicated when these conditions are met
>3 attacks a year that are considered disabling
Tophi
Destructive joint dx as seen on x-ray
Recurrent urolithiasis
Severe hyperuricemia (>10 in females, >13 in males, >15 in renal pts)
Severe uric acid overproduction (urinary uric acid excretion >1100mg/day)
Pts with high tumor burden about to receive cytoxic tx

Before starting irate lowering meds, you need to order these labs
BUN/Cr
Lipids
CBC

When using irate lowering meds, what is the target value for uric acid?
<6.5mg/dL

Between probenecid and allopurinol, which one is not recommended with renal impairment?
Allopurinol

What is the pt education for gout?
Gradual wt loss
Reduce ETOH, ASA, purines
Avoid hi fructose corn syrup
Try to drink 3L/day
Acute attack should have follow-up in 4wks
Chronic is individualized, but should have at least yearly uric acid level

What is multiple sclerosis MS?
A disease in which the body’s immune system breaks down the protective sheath covering nerves (myelin sheath). This disrupts communication between the mind & the body & can lead to irreversible deterioration of the nerves. Affects the brain, spinal cord, & optic nerve.

How is MS diagnosed?
Should be based on ?2 neurologic signs that are localized to the brain or spinal cord & are disseminated in time & space.
Generally separated by >30 days, & 2 different parts of the CNS.
MRI with contrast, during or after 1st attack can show lesions. 2nd MRI @ 3 months later can show new lesions.

What is the average age of onset for MS?
30-50
Female> Male 2:1

What are some risk factors for MS?
Age 20-40
Female
Caucasian
Living in temperate climate -further from Equator
Certain infections
Other autoimmune disorders

What are the 4 classifications of MS?
Relapsing Remitting MS (RRMS) least severe, most common
Secondary Progressive MS (SPMS)
Primary Progressive MS (PPMS)
Relapsing Progressive MS (RPMS) most severe, least common

Listed from least to most severe, but most to least common

What are the 3 variations of MS?
Clinically Isolated Syndrome (CIS)
Neuromyelitis Optica (NMO)
Acute Disseminated Encephalomyelitis (ADEM)

This variation of MS is a post-viral dysfunction of CNS. It is most common in pediatrics
Acute disseminated encephalomyelitis (ADEM)

Devic Syndrome is another name for this
Neuromyelitis Optica
Severe relapses involving the spinal cord & optic nerve

What is Lhermitte’s sign?
An electrical shock down back and legs with flexion of the neck. A clinical feature of MS

What are paroxysmal symptoms?
Temporary neurological disturbances, such as muscle spasms (tonic spasms), paresthesias, slurred speech, and ataxia. Unlike MS attacks that last days to weeks, these, often precursors to MS, last seconds to 2 minutes.

What are extrapyramidal symptoms?
Various movement disorders such as dystonia, pseudoparkinsonism, akinesia (inability to initiate movement), and akathisia (inability to remain motionless).

Know MS vs non-MS symptoms
Know MS vs non-MS symptoms

This symptom is VERY specific to MS
Useless hand syndrome (of Oppenheim). The useless hand is functionally impaired by proprioceptive sensory loss.

How does MS usually present or begin?
N beginning in 1 foot, ascending ipsilaterally, then contra laterally.
Sensory symptoms may ascend to the trunk.

What are some diff’s of MS?
Fibromyalgia
Myelopathy 2ndary to cervical spondylosis
Sleep disorders
POTS
Sjogren Syndrome
Vit B12 deficiency
Stroke
Peripheral Neuropathy
Lymphoma
Sarcoidosis
Guillian-Barre Syndrome -b/c it ascends
ALS
Mitochondrial Disease

What are some complications of MS?
Muscle spasms or stiffness
Paralysis- usually in legs
Bladder/bowel dysfunction
Sexual dysfunction
Depression
Forgetfulness
Difficulty concentrating
Epilepsy
Osteoporosis

What is Chaddock’s sign?
Similar to babinski sign, but the outside of the foot is stimulated

What should be included in the Neuro exam for MS?
Sensation
Vibration, proprioception
Reflexes, including abdominal
Babinski sign
Chaddock’s sign
Fundoscopic, EOM, nystagmus
Lhermitte’s sign

These 5 symptoms are the common presentation of early MS
Ascending numbness, starting at the feet
Bilateral hand numbness- useless hand syndrome
Hemiparesthesia
Dysethesia in 1 of the above areas
Generalized heat intolerance

***Objectively THE most common sensory findings indicative of MS are
Dorsal column signs. Dorsal column is part of ascending pathway and is responsible for well-localized fine touch like vibration, as well as proprioception and stereognosis.

What tests are used to work-up MS?
NO specific test to diagnose MS
CBC
CMP
TSH
Vit B12
ANA, ESR
RPR, Lyme titer
Anti-NMO antibody
CSF eval by lumbar puncture
MRI brain & spinal cord
Evoked potential- by EEG or EMG

What are Dawson's fingers?
What are Dawson’s fingers?
Lesions around the ventricle-based veins of MS pts

What is the treatment for MS?
No cure
Treatment is to manage exacerbations
Corticosteroids
Plasma Exchange/Plasmapheresis

What can be done for symptom mgmt with MS?
PT/OT
Muscle relaxants
Meds to reduce fatigue
Meds for depression
Meds for bowel/bladder dysfunction
Ampyra to improve walking speed- SE of seizures

What lifestyle changes could help manage symptoms of MS?
Rest
Exercise-but don’t run a marathon!
Temperature control
Balanced diet
Stress Mgmt
Bee stings (to restore sensation)
Medical marijuana
Removal of Amalgam dental fillings

What is the prognosis for MS?
50% will need help walking within 15yrs of onset
# of lesions does NOT correlate with dx progression
Some have normal pregnancies, some get worse with pregnancies, it varies.

****What are the FAVORABLE prognostic indicators of MS?
Early age of onset
Female
Optic neuritis as presenting episode
Sensory symptoms as presenting episode
Little residual disability after each exacerbation
Long inter exacerbation period

**** What are unfavorable prognostic indicators of MS?
Later age of onset
Progressive course from onset
Male
Frequent exacerbations
Poor recovery from exacerbations
Involvement of cerebellar or motor functions

What is Systemic Lupus Erythematous?
A chronic autoimmune disease where the immune system attacks the body’s cells and tissue, resulting in inflammation and tissue damage.

Patients may inherit a predisposition to lupus, but not lupus itself. So how do they develop lupus?
People with inherited predisposition come into contact with something in the environment that can trigger lupus like meds, or a virus.

What are the 4 types of lupus?
Systemic Lupus erythematosus
Discoid lupus erythematosus
Drug-induced jujus erythemstosus
Neonatal lupus

What is discoid lupus erythematosus?
Also called cutaneous lupus.
It only affects the skin, usually a circular rash on the face, neck, and scalp.

What is drug-induced lupus erythemstosus?
Occurs after taking certain prescription meds. S/S usually go away when the med is stopped.

What is neonatal lupus?
Rare form of lupus that affects newborns. Baby may get a rash within the 1st few weeks after birth, and last about 6 months.

What are the risk factors for lupus?
Women
Age 20 – 45
AA or Asian
Sunlight exposure
Exposure to mercury and silica
EBV
Certain meds – chlorpromazine, hydralazine, isoniazid, procanimide

What is it called when a person with lupus has worsening S/S that eventually improve or disappear for a time?
Flares

What are the derm symptoms of lupus?
No 2 cases are alike.
May see:
Butterfly rash or discoid rash.
Alopecia.
Symptoms appear or worsen with sun exposure.
Leg, nasal, or oropharyngeal ulcers.
Livedo reticularis- pallor from anemia.
Petechiae- from thrombocytopenia.

What is a butterfly rash?
What is a butterfly rash?
Erythematous rash over the malar eminences, but the nasolabial folds are often spared.
Seen in SLE

What is a discoid rash?
What is a discoid rash?
Raised erythematous patches with subsequent edematous plaques and adherent scales.
Seen in SLE

What are the musculoskeletal symptoms of SLE?
Joint tenderness, swelling, and possibly effusions.

What are the cardiac symptoms of SLE?
Pericardial rub- in pt’s with pericarditis.
Heart murmurs-if endocarditis or valvular thickening or dysfunction.
Chest pain.

Name some constitutional/general symptoms of SLE
Fever
Conjunctivitis
Dry eyes
Dry mouth
Abd tenderness
Wt loss/gain
Raynaud’s
Easy bruising
Anxiety/depression
Memory loss

What are some diff’s of SLE?
Other connective tissue disorders like RA, MCTD (mixed connective tissue disease), progressive systemic sclerosis.
Mets neoplasm
Infection

How is SLE diagnosed?
Must have any 4 of:
1. Butterfly rash
2. Discoid rash
3. Photosensitivity
4. Oral ulcers
5. Arthritis
6. Serositis (pleuritis, pericarditis)
7. Renal disorder
8. Neurologic disorder (seizures, psychosis)
9. Hematologic disorders (hemolytic anemia, leukopenia, lymphopenia, thrombocytopenia)
10. Immunologic disorder (+ SLE cell prep, Anti-DNA, Anti-SM, false + STS known to be + for 6 months
11. Abnormal ANA

What lab tests can be done to test for SLE?
Immunologic: ANA, Anti-DNA antibody, Anti-SM antibody, ESR.
CBC with Diff.
Platelet count (Coomb’s test if anemia detected).
UA (24h for protein if proteinuria present).
PTT & anticardiolipin antibodies in pt’s with thrombotic events.
CMP to evaluate kidney & liver fx

What imaging studies can be done to test for SLE?
CXR-pulm involvement like effusions or infiltrates.
EKG- eval causes of chest pain.
Echo-screen for significant valvular heart dx (present with 18% of SLE pt’s), detect valvular thickening/dysfunction.

What is 1 of the leading causes of death in SLE pt’s?
#1 Infection
#2 Nephritis
#3 CNS causes

Name some complications of SLE
Pulm: pleurisy, effusions, infiltrates.
Cardiac: inflammation of heart muscle-myocarditis, endocarditis, pericarditis, coronary vasculitis. Also greatly increases risk of cardio dx and MI’s.
CNS: headaches, dizziness, memory probe, behavior changes, seizures.
Heme-oncological: anemia, bleeding or clotting disorders, vasculitits (inflammation of blood vessels), cancers, esp. Non-Hodgkin’s lymphoma.
Renal: kidney damage/failure.
Immunological: susceptibility to infection d/t dx and tx.
Pregnancy: increased risk of miscarriage, flares, pre-eclampsia, pre-term birth.

How is SLE treated?
Depends on S/S:
1st line tx is NSAID’s and lifestyle changes like diet, avoiding sunlight, smoking cessation, adequate rest, & exercise.
Antimalarials like Plaquenil
Immunosupressants like cytoxan, Imuran, Cellcept, & methotrexate.

What are some side-effects of NSAID’s?
Stomach bleeding, kidney problems, increased risk of heart problems.

What are some side-effects of anti-malarials?
Upset stomach, and rarely-damage to the retina.

What are some side-effects of corticosteroids?
Long term use can cause weight gain, easy bruising, osteoporosis, HTN, DM, and increased risk of infection.
Risk increases with dosage and length of use.

What are some side-effects of immunosupressants?
Increased risk of infection, liver damage, decreased fertility, increased risk of cancer.

Anti-malarials can be used for these manifest ions of SLE
Joint pain and mild serositis

Plaquenil can be used for SLE…what is the normal dosage?
Start with 400 daily or bid, then maintenance of 200-400 daily.

What are the tx options for cutaneous manifestations of SLE?
Topical corticosteroids.
Intradermal corticosteroids.
Anti-malarials.
Sunscreens.
Immunosupressives like methotrexate 2.5mg 3x/week (max dosage of 20mg/week)

What are the tx options for renal manifestations of SLE?
* High pulsed doses of cyclophosphamide given at monthly intervals.
* Glucocorticoids.
* Plasmapheresis in combo with immunosupressive agents (for rapidly progressing renal fx or life-threatening vasculitis).
* Azanthioprine maintenance regimen with corticosteroids.

What are the tx options for CNS manifestations of SLE?
* Corticosteroid therapy-usually reserved for organic brain syndrome.
* Anticonvulsants and antipsychotics.
* Headaches treated symptomatically.
* Cyclophosphamide
* IVIG
* Plasmapheresis

How is thrombocytopenia treated?
Initial tx usually corticosteroids

Why is DHEA being used in lupus clinical trials?
Because supplements containing DHEA have been shown to reduce the dose of steroids needed to stabilize symptoms of lupus.

How is flex seed helpful in the tx of SLE?
Flaxseed contains a fatty acid called alpha linolenic acid that may decrease inflammation. Studies show it may improve kidney function.

What racial/ethnic groups have a worse prognosis for SLE?
Hispanics and AA’s

What is a major predictor of irreversible organ damage & death in SLE?
Antiphospholipid syndrome with thrombotic manifestations

What referrals should be made for SLE pt’s?
Rhematology for all SLE pt’s
Hematology for hematologic probs
Nephrology for significant renal probs

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