First Aid: Pharmacology (ALL)

Antibiotics that block cell wall synthesis by inhibition of peptidoglycan CROSS-LINKING
Beta lactams. Penicillin, methicillin, ampicillin, piperacillin, cephalosporins, aztreonam, imipenem
Antibiotics that block peptidoglycan SYNTHESIS
bacitracin, vancomycin
Antibiotics that block nucleotide synthesis by inhibiting folic acid synthesis
sulfonamides, trimethoprim
Antibiotics that block DNA topoisomerases
Antibiotics that block mRNA synthesis
Antibiotics that damage DNA
Antibiotics that block protein synthesis at the 50S ribosomal subunit
Chloramphenicol, clindamycin, erythromycin (and other macrolides), linezolid, streptogramins (quinupristin, dalfopristin)
Antibiotics that block protein synthesis at the 30S ribosomal subunit
Aminoglycosides (gentamicin, neomycin, amikacin, tobramycin, streptomycin) and tetracyclins
Penicillin G is the ____ form; Pencillin V is the ___ form
Pen G = IV/IM
Pen V = oral

MOA: binds PBP to block peptidoglycan cross linking

Clinical use: bactericidal for gram (+) cocci/rods, gram (-) cocci (Neisseria), and spirochetes

Toxicity: hypersensitivity reactions (type II), hemolytic anemia

Oxacillin, nafcillin, dicloxacillin

MOA: binds to PBP to block peptidoglycan cross linking; beta lactamase resistant due to bulky R group

Clinical use: bactericidal, narrow spectrum- staph aureus only (except MRSA which is still resistant)

Toxicity: hypersensitivity reactions (type II), interstitial nephritis

Ampicillin, amoxicillin

MOA: binds to PBP to block peptidoglycan cross linking; wider spectrum than regular penicillin

Clinical use: bactericidal for gram (+) cocci/rods, gram (-) cocci, spirochetes; extended to cover H. influenza, E. Coli, L. monocytogenes, Proteus mirabilis, Salmonella, Shigella, enterococci

Toxicity: hypersensitivity reactions (type II), ampicillin rash, pseudomembranous colitis

Ampicillin and amoxicillin HELPSS kill enterococci
H. influenzae, E. coli, L. monocytogenes, Proteus mirabilis, Salmonella, Shigella, enterococci (extended spectrum penicillins)
Ticarcillin, piperacillin

MOA: binds to PBP to block peptidoglycan cross linking

Clinical use: extended spectrum penicillin (so already bactericidal for gram (+) cocci/rods, gram (-) cocci, and spirochetes; also covers Pseudomonas spp and gram (-) rods

Toxicity: hypersensitivity reactions (type II)

Beta lactamase inhibitors: CAST
Clavulanic Acid, Sulbactam, Tazobactam
Cefazolin, cephalexin

MOA: 1st generation beta lactam drugs that inhibit cell wall synthesis

Clinical use: bactericidal for gram (+) COCCI, PEcK: Proteus mirabilis, E. coli, Klebsiella; cefazolin used prior to surgery to prevent S. aureus wound infections

Toxicity: hypersensitivity rxns, vitamin K deficiency, potentiate nephrotoxicity of aminoglycosides

Cefoxitin, cefaclor, cefuroxime

MOA: 2nd generation beta lactam drugs that inhibit cell wall synthesis

Clinical use: bactericidal for gram (+) COCCI, HEN PEcKS- Haemophilus influenzae, Enterobacter aerogenes, Neisseria spp, Proteus mirabilis, E. coli, Klebsiella, Serratia marcescens

Toxicity: hypersensitivity rxns, vitamin K deficiency, potentiate nephrotoxicity of aminoglycosides

Ceftriaxone, cefotaxime, ceftazidime

MOA: 3rd generation beta lactam drugs that inhibit cell wall synthesis

Clinical use: bactericidal for serious gram (-) infxns resistant to other beta lactams; ceftriaxone good for meningitis and gonorrhea, ceftazidime good for pseudomonas

Toxicity: hypersensitivity rxns, vitamin K deficiency, potentiate nephrotoxicity of aminoglycosides


MOA: 4th generation beta lactam drug that inhibits cell wall synthesis

Clinical use: bactericidal w/ increased activity again Pseudomonas and gram (+) organisms

Toxicity: hypersensitivity rxns, vitamin K deficiency, potentiate nephrotoxicity of aminoglycosides

Organisms not typically covered by cephalosporins are LAME
Listeria, Atypicals (chlamydia, mycoplasma), MRSA, and Enterococci

MOA: monobactam that is resistant to beta lactamases!!!! prevents peptidoglycan cross linking by binding to PBP3

Clinical use: bactericidal for gram (-) RODS only, no activity against gram (+)s or anaerobes; good for pts w/ penicillin allergies or renal insufficiency that can’t tolerate aminoglycosides

Toxicity: no cross reactivity w/ penicillins


MOA: imipenem = beta lactamase resistant carbapenem that blocks peptidoglycan cross linking, always administered with cliastatin (inhibits renal dehydropeptidase I to slow inactivation of imipenem)

Clinical use: bactericidal for LIFE THREATENING INFECTIONS due to gram (+) cocci, gram (-) rods, and anerobes when other meds have failed (limits due to seizure potential)

Toxicity: CNS toxicity (seizures) at high plasma levels


MOA: inhibits cell wall peptidoglycan SYNTHESIS by binding D-ala D-ala portion of precursors

Clinical use: bactericidal for gram (+)s only, reserve for serious/multidrug resistant orgs such as MRSA, enterococci and C diff

Toxicity: diffuse flushing/”red man syndrome” when infused too quickly; nephrotoxicity/ototoxicity/thrombophlebitis (some)

Gentamicin, neomycin, amikacin, tobramycin, streptomycin, spectinomycin

MOA: work at the 30S ribosomal subunit to inhibit formation of the initiation complex and cause misreading of the mRNA

Clinical use: bactericidal for serious gram (-) RODS; neomycin for bowel surgery

Toxicity: nephrotoxicity, neuromuscular blockade, ototoxocity, teratogenic

“Mean” GNATSS caNNOT kill anaerobes
aMINoglycosides: Gentamicin, Neomycin, Amikacin, Streptomycin, Spectinomycin; Nephrotoxic, Neuromuscular blockade, Ototoxic, Teratogenic; can’t kill anaerobes because require O2 for uptake into the cell
Tetracycline, minocycline, doxycycline

MOA: work at the 30S ribosomal subunit to prevent attachment of charged tRNA to the A site

Clinical use: bacterioSTATIC against Borrelia burgdorferi, Mycoplasma pneumoniae, Rickettsia/Chlamydia (since drug accumulates intracellularly); **Do not take with milk, antiacids, or iron bc divalent cations inhibit absorption**

Toxicity: discoloration of teeth and inhibition of bone growth in kids, photosensitivity, CI in pregnancy
*doxycycline is fecally eliminated and can be given to ppl w/ renal impairment*

Antibiotic of the tetracycline family, but rarely used as an antibiotic. Has ADH antagonist properties, so used as a diuretic in SIADH.
Azithromycin, clarithromycin, erythromycin
MOA: binds to the 23S rRNA of the 50s ribosomal subunit to inhibit protein synthesis by blocking translocationClinical use: bacteriostatic against atypical pneumonias (mycoplasma, chlamydia, legionella), STDs (chlamydia) and gram (+) cocci

Toxicity: MACRO- Motility issues, Arrythmia (due to prolonged QT interval), acute Cholestatic hepatitis, Rash, eOsinophilia

**INHIBITOR OF P450 ENZYMES** may specifically increase serum concentration of theophyllines and oral anticoagulants


MOA: works at 50S ribosomal subunit to block the action of peptidyltransferase

Clinical use: bacterioSTATIC against meningitis (H. influenzae, N. meningitidis, S. pneumo)

Toxicity: anemia, aplastic anemia (dose independent), gray baby syndrome (in premies bc they lack liver UDP-glucuronyl transferase)


MOA: works at 50S ribosomal subunit to block peptide transfer

Clinical use: bacterioSTATIC against anaerobic infections above the diaphragm

Toxicity: C. diff colitis


MOA: PABA antimetabolites that inhibit dihydropterate synthase

Clinical use: bacterioSTATIC against gram (+), gram (-), nocardia, chlamydia; triple sulfas or just sulfamethoxazole for simple UTI

Toxicity: hypersensitivity, hemolysis in G6PD deficiency, nephrotoxicity, photosensitivity, kernicterus in infants, displaces other drugs from albumin (ESP WAFARIN)


MOA: inhibits bacterial dihydrofolate reductase

Clinical use: bacterioSTATIC use in combination w/ SMX for UTIs, Shigella, Salmonella, PJP

Toxicity: megaloblastic anemia/leukopenia/granulocytopenia (may be less w/ leucovorin rescue)

(Ie ciprofloxacin)
MOA: inhibits DNA gyrase (topo II) and topo IVClinical use: bacteriCIDAL for gram (-) rods of urinary and GI tracts, Neisseria, some gram (+)s

Toxicity: TENDON DAMAGE –> tendonitis, tendon rupture (ppl >60 yrs or on prednisone), leg cramps/myalgias, CI in pregnant women due to cartilage damage


MOA: forms free radicals in bacterial (and protozoal) cells causing DNA damage

Clinical use: PET A Gross Guy on the Metro- h. Pylori, Entamoeba, Trichomonas, Anaerobes, Giardia, Gardnerella vaginalis

Toxicity: disulfiram reaction with alcohol


MOA: inhibits synthesis of mycolic acids (only bacterial have the catalase needed to activate it)

Clinical use: TB (only one that can be used as solo prophylaxis)

Toxicity: INH Injures Neurons and Hepatocytes; also causes B6 deficiency


MOA: inhibits DNA dependent RNAP

Clinical use: TB, in combo w/ dapsone for leprosy, prophylaxis against neisseria meningitis in kids

Toxicity: Orange body fluids, induces P450 enzymes


MOA: acidifies environment of phagolysosomes of macrophages that have engulfed TB

Clinical use: TB

Toxicity: hyperuricemia, hepatotoxicty


MOA: inhibits carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase

Clinical use: TB

Toxicity: red-green colorblindness/optic neuritis (CI in kids <6yo)

Amphotericin B

MOA: binds ergosterol, forming pores in membrane that allow leakage of electrolytes

Clinical use: serious, SYSTEMIC mycoses- cryptococcus, blastomyces, coccidioides, histoplasma, candida, mucor

Toxicity: fever/chills (shake and bake), hypotension, nephrotoxicity (lessened by hydration and supplementation of K/Mg), arrhythmias, anemia, IV phlebitis


MOA: same as Ampho B, but topical only bc too toxic for systemic use

Clinical use: “swish and swallow” for oral candidiasis, topical for diaper rash or vaginal candidiasis


Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole, posaconazole

MOA: inhibit fungal sterol synthesis by inhibiting the P450 that converts lanosterol to ergosterol

Toxicity: testosterone synthesis inhibition (esp ketoconazole), liver dysfunction due to P450 inhibition

Clinical use: chronic suppression of cryptococcal meningitis in AIDS patients, candida infxns of all types
Clinical use: blastomycoses, aspergillus, coccidioides, histoplasma
Clinical use: topical fungal infections

MOA: inhibits DNA/RnA biosynthesis by conversion to 5-FU by cytosine deaminase

Clinical use: systemic fungal infections– especially cryptococcal MENINGITIS (“flu” right into the CNS) in combo w/ ampho B

Toxicity: bone marrow suppression (duh… it’s 5-FU)

Caspofungin, micafungin

MOA: inhibits cell wall synthesis by inhibiting synthesis of B-glucan (you can see right through casper the ghost)

Clinical use: “deep” infections like invasive aspergillosis, candida (you can see through casper to the deep infections)

Toxicity: flushing due to histamine release


MOA: inhibits fungal squalene epoxidase

Clinical use: dermatophytoses (esp onchomycosis)

Toxicity: abnormal LFTs, visual disturbances


MOA: interferes w/ microtubule function –> disruption of mitosis

Clinical use: oral treatment of superficial infections, inhibits growth of dermatophytes (deposits in keratin containing tissues)

Toxicity: teratogenic, carcinogenic, confusion/HA, induces P450 and warfarin metabolism


MOA: blocks detoxification of heme into hemozoin, accumulated heme is toxic to plasmodia

Clinical use: plasmodial species other than falciparum (too much resistance)

Toxicity: retinopathy

Treatment for P. falciparum
Use combo of artemether/lumifantrine or atovaquone/proguanil
Clinical use: life threatening malaria
Clinical use: toxoplamosis (often with sulfadiazine)
Clinical use: trypanosoma brucei (African sleeping sickness); suramin for blood-borne disease or melarsoprol for CNS penetration
Clinical use: trypanosoma cruzi (Chagas)
Sodium stibogluconate
Clinical use: leishmaniasis
Mebendazole, albendazole

MOA: selective inhibition of parasitic microtubules, thereby blocking the uptake of glucose and other nutrients, resulting in the gradual immobilization and eventual death of the helminths

Clinical use: roundworms (pinworms, ascaris lumbricoides, strongyloides stercoralis, toxocara canis/visceral larva migrans), hookworms (ancylostoma duodenale and necator americanus), some tapeworms (neurocysticercosis from injection of taenia solium eggs, echinococcus from dog feces)

Toxicity: CI in pregnancy

Pyrantel pamoate

MOA: neuromuscular depolarizing agent, causes contraction then paralysis in helminths (loose grip on wall of intestine and pass in stool naturally)

Clinical use: pinworms, ascaris, hookworms (ancylostoma and necator)


MOA: enhances inhibitory neurotransmission by opening glutamate gated chloride channels

Clinical use: primarily for Onchocerca volvulus (IVERmectin for rIVER blindness), also strongyloides


MOA: inhibitor of arachidonic acid metabolism in filarial microfilaria

Clinical use: Loa loa, Wuchereria bancrofti (elephantiasis)


MOA: increased cell permeability to calcium, thereby causing contraction/paralysis and allows destruction by immune system

Clinical use: tapeworms and flukes

Zanamivir, oseltamivir

MOA: inhibits influenza neuraminidase (decreasing release of new viruses)

Clinical use: treatment and prevention of influenza A AND B


MOA: competitively inhibits IMP dehydrogenase to stop synthesis of guanine nucleotides

Clinical use: RSV, chronic hep C

Toxicity: hemolytic anemia, SEVERE TERATOGEN


MOA: guanosine analog, preferentially inhibits viral DNAP bc phosphorylation by viral thymidine kinase required for activity; CHAIN TERMINATOR

Clinical use: HSV and VZV; no activity against CMV and no effect on latent forms of HSV/VZV
-Valacyclovir has better oral availability


MOA: guanosine analog, preferentially inhibits viral DNAP bc phosphorylation by viral kinase required for activity; CHAIN TERMINATOR

Clinical use: CMV, especially in immunocompromised
-Valganciclovir has better oral availability

Toxicity: leukopenia/neutropenia/thrombocytopenia, renal toxicity


MOA: inhibits viral DNA polymerase by binding to PPi binding site of enzyme, no viral kinase activation required; CHAIN TERMINATOR

Clinical use: CMV retinitis when ganciclovir fails, acyclovir resistant HSV

Toxicity: nephrotoxicity


MOA: inhibits viral DNAP, does not require viral kinase activation

Clinical use: CMV retinitis in immunocompromised patients, acyclovir reistant HSV

Toxicity: nephrotoxicity– coadminister w/ probenecid and IV saline to reduce

Protease inhibitors
“Navir tease a protease”
MOA: stops cleavage of HIV polypeptide into functional parts, thus preventing maturation of new virusesClinical use: HIV

Toxicity: hyperglycemia, GI intolerance, lipodystrophy; nephropathy, hematuria (indinavir)
-Ritonavir inhibits P450 enzymes

Tenofovir, emtricitabine, abacavir, lamivudine, zidovudine, didanosine, stavudine
MOA: competitive inhibitor of HIV reverse transcriptase (terminate DNA chain bc lack a 3′ OH)Clinical use: HIV active infection, ZDV also used for prophylaxis and during pregnancy to reduce fetal transmission

Toxicity: bone marrow suppression (alleviated by GCSF and EPO, peripheral neuropathy, lactic acidosis, rash

*if patient has concurrent Hep B infection, use tenofovir

Nevirapine, efavirenz, delavirdine
MOA: allosterically inhibit HIV reverse transcriptaseToxicity: reversible bone marrow suppression, peripheral neuropathy, lactic acidosis, rash


MOA: reversibly inhibits HIV integrase

Toxicity: hypercholesterolemia

α- chronic hep B and C, Kaposi’s sarcoma
β- MS
γ- NADPH oxidase deficiency (CGD)Toxicity: neutropenia, myopathy

Antibiotics to avoid in pregnancy– SAFe Children Take Really Good Care
Sulfonamides –> kernicterus
Aminoglycosides –> ototoxicity
Fluoroquinolones –> cartilage
Clarithromycin –> embryotoxic
Tetracylines –> discolored teeth, inhibits bone growth
Ribavirin –> teratogenic
Griseofulvin –> teratogenic
Chloramphenicol –> gray baby

MOA: binds to cyclophilins –> inhibits calcineurin –> prevents production of IL-2 –> no differentiation/activation of T cells

Clinical use: suppress organ rejection after transplant

Toxicity: nephrotoxic, HTN, hyperlipidemia, hyperglycemia, tremor, gingival hyperplasia, hirsutism

Tacrolimus (FK-506)

MOA: binds FK binding protein, inhibiting calcineurin and secretion of IL-2 (no T cell activation)

Clinical use: organ transplant recipients

Toxicity: nephrotoxic, HTN, hyperlipidemia, hyperglycemia, tremor, *NO GINGIVAL HYPERPLASIA/HIRSUTISM

Sirolimus (rapamycin)

MOA: inhibits mTOR to inhibit T cell PROLIFERATION in response to IL-2

Clinical use: immunosuppression after kidney transplant (use w/ cyclosporine and corticosteroids)

Toxicity: hyperlipidemia, thrombocytopenia, leukopenia


MOA: precursor of 6-MP, toxic to proliferating lymphocytes

Clinical use: kidney transplantation, autoimmune disoders (glomerulonephritis and hemolytic anemia)

Toxicity: BM suppression (duh); 6-MP is metabolized by xanthine oxidase so toxic effects increased when given w/ allopurinol

Muromonab-CD3 (OKT3)

MOA: monoclonal antibody that binds to CD3 on surface of T cells, blocks T cell signal transduction

Clinical use: prevents ACUTE rejection of kidney transplantation

Toxicity: mouse antibody, so use is limited till when the patient develops antibodies to the antibody

Aldesleukin (IL-2)
Clinical use: renal cell carcinoma, metastatic melanoma

Granulocyte colony stimulating factor– only granulocytes b/c “Filgrastim is Finicky”

Clinical use: bone marrow recovery


Granulocyte/macrophage colony stimulating factor

Clinical use: bone marrow recovery

Oprelvekin (IL-11)
Clinical use: thrombocytopenia
Infliximab, adalimumab

MOA: TNF α inhibtors

Clinical use: Chron’s disease, RA, psoriatic arthritis, ankylosing spondylitis (infliximab only)


MOA: inhibits Gp IIb/IIIa

Clinical use: prevent cardiac ischemia is unstable angina or pts treated w/ percutaneous coronary intervention

Clinical use: targets HER2 receptor in HER2nu positive breast cancer

MOA: targets CD20

Clinical use: B cell non-Hodgkin’s lymphoma


MOA: targets IgE

Clinical use: additional treatment for severe asthma


MOA: binds insulin receptor (tyrosine kinase activity), induces glucose–> glycogen in liver and muscle, muscles also increase protein synthesis and K+ uptake, adipose takes up TG

Clinical use: DM type 1 and 2, gestational diabetes, life threatening hyperkalemia, stress induced hyperglycemia

Toxicities: hypoglycemia

Short acting insulins versus long acting insulins
Lispro, aspart and glulisine = rapid acting
Glargine and detemir = long acting
MOA: mechanism unknown; decreases gluconeogenesis, increases glycolysis, increases peripheral glucose uptake (insulin sensitivity)Clinical use: 1st line therapy in type 2 DM, can be used in patients w/out islet function

Toxicities: lactic acidosis (contraindicated in renal failure)

Tolbutamide, Chlorpropamide
1st generation sulfonylureas
MOA: close K+ channels in β cell membrane, cell depolarizes → Ca2+ influx → insulin releaseClinical use: stimulate release of endogenous insulin in type 2 DM (useless in type 1)

Toxicities: disulfiram like effects

Glyburide, Glimepiride, Glipizide
2nd generation sulfonylureas
MOA: close K+ channels in β cell membrane, cell depolarizes → Ca2+ influx → insulin releaseClinical use: stimulate release of endogenous insulin in type 2 DM (useless in type 1)

Toxicities: hypoglycemia

Pioglitazone, Rosiglitazone

MOA: increase insulin sensitivity in peripheral tissue, binds to PPAR-γ nuclear transcription regulator

Clinical use: used as a monotherapy in type 2 DM or in combo w/ other diabetes drugs

Toxicity: weight gain, edema, hepatotoxicity, heart failure

Acarbose, Miglitol
α-glucosidase inhibitors
MOA: inhibition at intestinal brush border delays sugar hydrolysis and glucose absorption → ↓ postprandial hyperglycemiaClinical use: monotherapy in type 2 DM or w/ other diabetes drugs

Toxicities: GI upset


MOA: ↓ glucagon

Clinical use: type 1 AND 2 DM

Toxicities: hypoglycemia, nausea, diarrhea

Exenatide, liraglutide
GLP-1 analogs
MOA: ↑ insulin, ↓ glucagon releaseClinical use: type 2 DM

Toxicities: N/V, pancreatitis

Linagliptin, saxagliptin, sitagliptin
DPP-4 inhibitors
MOA: ↑ insulin, ↓ glucagon releaseClinical use: type 2 DM

Toxicities: mild UTI/URI

Propylthiouracil, methimazole

MOA: block peroxidase, inhibiting organification of iodide and coupling of thyroid hormone synthesis; propylthiouracil also blocks 5′-deiodinase so T4 can’t → T3

Clinical use: hyperthyroidism

Toxicity: agranulocytosis, aplastic anemia, hepatotoxicity (propylthiouracil)

Levothyroxine, triiodothyronine

MOA: thyroxine replacement

Clinical use: hypothyroidism, myxedema

Toxicity: tachycardia, heat intolerance, tremors, arrythmias


MOA: long acting somatostatin analog

Clinical use: acromegaly, carcinoid, gastrinoma, glucagonoma, acute variceal bleeds

Toxicity: steatorrhea

Clinical use: stimulates labor, uterine contractions, milk let down; controls uterine hemorrhage
Hydrocortisone, prednisone, triamcinolone, dexamethasone, beclomethasone

MOA: decrease the production of leukotrienes and prostraglandins by inhibiting phospholipase A2 and expression of COX2

Clinical use: addison’s disease, inflammation, immune suppression, asthma; prednisone used for cancer chemotherapy for CLL, non-Hodgkin’s lymphoma

Toxicity: iatrogenic cushing’s disease- buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin/easy bruising, osteoporosis, adrenocortical atrophy, peptic ulcers, hyperglycemia, cataracts, hypertension, psychosis

Cimetidine, ranitidine, famotidine, nizatidine
H₂ blockers (take H₂ blockers before you “dine”)
MOA: REVERSIBLY block histamine H₂ receptors → ↓ H+ secretion by parietal cellsClinical use: peptic ulcer, mild esophageal reflux

Toxicity: Cimetidine = potent inhibitor of P450 enzymes, also has antiandrogenic effects (prolactin release, gynecomastia, impotence, ↓ libido in males), can cross BBB and placenta
-Cimetidine and ranitidin ↓ renal excretion of creatinine

Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole

MOA: IRREVERSIBLY inhibits H+/K+ ATPase in stomach parietal cells

Clinical use: peptic ulcer, gastritis, esophageal reflux, Zollinger Ellison syndrome

Toxicity: increased risk of C. diff infection, pneumonia; hip fractures, decreased serum Mg2+ with long term use

Bismuth, sucralfate

MOA: bind to ulcer base, providing physical protection and allowing HCO3- secretion to reestablish pH gradient in mucous layer

Clinical use: increase ulcer healing, traveler’s diarrhea


MOA: a PGE1 analog, increases production and secretion of gastric mucous barrier, decreases acid production

Clinical use: prevention of NSAID induced peptic ulcers; maintenance of patent ductus arteriosus; induction of labor

Toxicity: CI in women of childbearing potential (abortifacient)

Aluminum hydroxide

Clinical use: antacid

Toxicity: hypokalemia (all antacids), constipation (“aluminimum” amount of feces), hypophosphatemia, proximal muscle weakness, osteodystrophy, seizures

Magnesium hydroxide

Clinical use: antacid

Toxicity: hypokalemia (all antacids), diarrhea, hyporeflexia, hypotension, cardiac arrest

Calcium carbonate

Clinical use: antacid

Toxicity: hypokalemia (all antacids), hypercalcemia, rebound acid increase

Magnesium hydroxide, magnesium citrate, polyethylene glycol, lactulose

MOA: provide osmotic load to draw water out

Clinical use: constipation; lactulose also treats hepatic encephalopathy since gut flora degrade it into lactic acid and acetic acid, which promote nitrogen excretion at NH4+

Toxicity: diarrhea/dehydration


MOA: combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid; activated by colonic bacteria

Clinical use: ulcerative colitic, Chron’s disease

Toxicity: sulfonamide toxicity, reversible oligospermia


MOA: 5-HT3 antagonist; powerful central acting antiemetic (At a party but feeling queasy? Keep ON DANCing!”)

Clinical use: control vomiting postop and in chemotherapy patients

Toxicity: headache, constipation


MOA: D2 receptor antagonist; increases resting tone, contractility, LES tone, motility (does NOT influence colon transport time)

Clinical use: diabetic and post surgery gastroparesis, antiemetic

Toxicity: increases parkinsonian effects, drug interaction with digoxin and diabetic agents; CI in patients with small bowel obstruction or parkinson’s


MOA: cofactor for the activation of antithrombin, decreases thrombin and factor Xa

Clinical use: immediate anticoagulation for pulmonary embolism, acute coronary syndrome, MI, and DVT; used during pregnancy (≠ cross placenta); follow PTT to monitor

Toxicity: bleeding, HIT (IgG antibodies against heparin bound to platelet factor 4 → platelets activated → thrombosis and thrombocytopenia), osteoporosis, drug-drug interactions

Protamine sulfate
Clinical use: rapid reversal of heparin toxicity (positively charged molecule binds negatively charged heparin)
Low molecular weight heparins
MOA: act more on factor Xa, have better bioavailability and 2-4x longer half-life; can be admin subQ and without lab monitoring; not easily reversible
Lepirudin, bivalirudin

MOA: derivatives of hirudin, the anticoagulant used by leeches- inhibits thrombin

Clinical use: alternative for heparin in patients w/ HIT


MOA: interferes w/ normal synthesis and γ-carboxylation of vitamin K dependent clotting factors II, VII, IX and X and proteins C and S; monitor PT

Clinical use: chronic anticoagulation (after STEMI, venous thromboembolism prophylaxis, and prevention of stroke in a fib); NOT used in pregnant women bc crosses the placenta

Toxicity: bleeding, teratogenic, skin/tissue necrosis, drug-drug interactions (metabolized by P450s)

Alteplase (tPA), reteplase (rPA), tenecteplase (TNK-tPA)

MOA: directly or indirectly aid conversion of plasminogen → plasmin, which cleaves thrombin and fibrin clots; ↑ PT and PTT, no changes in platelet count

Clinical use: early MI, early ischemic stroke, direct thombolysis of severe pulmonary embolism

Toxicty: bleeding (CI in patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding diatheses, or severe HTN)

Aminocaproic acid

MOA: inhibitor of fibrinolysis

Clinical use: treatment of tPA toxicity


MOA: IRREVERSIBLY inhibits COX1 and COX2 by covalent acetylation; lasts until platelets are produced; increases bleeding time, decreases TXA2 and prostaglandins

Clinical use: antipyretic, analgesic, anti inflammatory, antiplatelet (decreases aggregation)

Toxicity: gastric ulceration, tinnitus (CNVIII); chronic use can lead to acute renal failure, interstitial nephritis, upper GI bleeding; Reye’s syndrome in children with viral infxn; overdose causes mixed respiratory alkalosis (stimulation of respiratory centers → hyperventilation) and metabolic acidosis

Clopidogrel, ticlopidine, prasugrel, ticagrelor

MOA: inhibit platelet aggregation by IRREVERSIBLY blocking ADP receptors; inhibit fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen

Clinical use: acute coronary syndrome, coronary stenting, reduction of incidence or recurrence of thombotic stroke

Toxicity: ticlopidine causes neutropenia

Cilostazol, dipyridamole

MOA: phosphodiesterase III inhibitor; ↑ cAMP in platelets, thus inhibiting platelet aggregation; vasodilators

Clinical use: intermittent claudication, coronary vasodilation, prevention of stroke or TIAs, angina prophylaxis

Toxicity: facial flushing, hypotension, abd pain

Abcicimab, eptifibatide, tirofiban

MOA: bind the glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation

Clinical use: acute coronary syndrome, percutaneous transluminal coronary angioplasty

Toxicity: bleeding, thrombocytopenia


MOA: Folic acid analog that inhibits dihydrofolate reductase → ↓dTMP → ↓DNA and ↓ protein synthesis (acts on cells in the S phase)

Clinical use: leukemias, lymphomas, choriocarcinoma, sarcomas; non neoplastics- abortion, ectopic pregnancy, RA, psoriasis

Toxicity: myelosuppression (reversible w/ leucovorin rescue), macrovesicular fatty change in liver, mucositis, teratogenic

5 Fluorouracil (5-FU)

MOA: pyrimidine analog bioactivated to 5F-dUMP, which covalently complexes folic caid; complex inhibits thymidylate synthase → ↓ dTMP → ↓ DNA and protein synthesis (acts on cells in S phase)

Clinical use: colon cancer, basal cell carcinoma (topical)

Toxicity: myelosuppression (reversible w/ leucovorin), photosensitivity

Cytarabine (arabinofuranosyl cytidine)

MOA: pyrimidine analog → inhibition of DNAP (acts on cells in S phase)

Clinical use: leukemias, lymphomas

Toxicity: leukopenia, thrombocytopenia, megaloblastic anemia

Azathioprine, 6-mercaptopurine (6-MP), 6-thioguanine (6-TG)

MOA: Purine (thiol) analogs → ↓ de novo purine synthesis; activated by HGPRT (acts on cells in S phase)

Clinical use: leukemias

Toxicity: toxic to bone marrow, GI, liver; Azathioprine and G-MP metabolized by xanthine oxidase so ↑ toxicity if given w/ allopurinol (6-TG no need for dose reduction)


MOA: intercalates in DNA

Clinical use: Wilm’s tumor, Ewing’s sarcoma, rhabdomyosarcoma (childhood tumor’s, “actin” out)

Toxicity: myelosuppression

Doxorubicin (adriamycin), danurubicin

MOA: generate free radicals, noncovalently intercalate in DNA → strand breaks in DNA → ↓ replication (all phases of cell cycle susceptible)

Clinical use: solid tumors (adriamycin is the A in CAF treatment plan for breast cancer), leukemias, lymphomas

Toxicity: cardiotoxic (dilated cardiomyopathy due to free radical damage– dexrazoxane, iron chelating agent, lessens cardiotoxicity); toxic to tissues following extravasation


MOA: induces free radical damage, causing strand breaks in DNA (acts on cells in G2 phase)

Clinical use: testicular cancer (B in EBC and VBC), Hodgkin’s lymphoma (B in ABVD)

Toxicity: pulmonary fibrosis, skin changes, minimal myelosuppression

Cyclophosphamide, ifosfamide

MOA: alkylate DNA at guanine residues, causing interstrand links; requires bioactivation in liver (all phases of cell cycle susceptible)

Clinical use: solid tumors (C in CMF/CAF for breast cancer), leukemia, lymphomas and some brain cancers

Toxicity: hemorrhagic cystitis, partially prevented w/ mesna

Carmustin, lomustine, semustine, steptozocin
MOA: alkylate DNA, cross BBB → CNS; require bioactivation in liver (all phases of cell cycle susceptible)Clinical use: brain tumors (good CNS penetration), including glioblastoma multiforme

Toxicity: CNS toxicity (dizziness, ataxia)


MOA: alkylates DNA (all phases of cell cycle susceptible)

Clinical use: CML, ablation of patient’s bone marrow before BMT

Toxicity: pulmonary fibrosis, hyperpigmentation

Vincristine, vinblastine

MOA: alkaloids that bind to tubulin in M phase and block polymerization of microtubules so that mitotic spindle can’t form

Clinical use: solid tumors (vinblastine is V in VBC), leukemias (vincristine is V in VAMP for ALL), lymphoma (vinblastine is V in ABVD for hodgkins/soft tissue lymphomas, vincristine (oncovin) is O in MOPP for hodgkins/other lymphomas)

Toxicity: Vincristine (think trouble getting things moving) = neurotoxicity- areflexia, peripheral neuritis; paralytic ileus

Paclitaxel, other taxols

MOA: hyperstabilize polymerized microtubules in M phase so that mitotic spindle can’t break DOWN

Clinical use: ovarian and breast carcinomas

Toxicity: myelosuppresion and hypersensitivity

Cisplatin, carboplatin

MOA: cross links DNA (alkylating agent, non cell cycle specific)

Clinical use: testicular (C in EBC/VBC), bladder, ovary, and lung carcinomas

Toxicity: nephrotoxicity and acoustic nerve damage; prevent nephrotoxicity w/ amifostine (free radical scavenger) and chloride diuresis

Etoposide, teniposide

MOA: inhibits topoisomerase II leading to DNA degredation (acts on cells in S and G2)

Clinical use: solid tumors (E in EBC for testicular CA), leukemias, lymphomas

Toxicity: myelosuppression, GI irritation, alopecia


MOA: inhibits ribonucleotide reductase → decreased DNA synthesis (S phase specific)

Clinical use: melanoma, CML, sickle cell disease (increases HbF)

Toxicity: bone marrow suppression, GI upset

Tamoxifen, raloxifene

MOA: SERMs- receptor antagonists in breast and agonists in bone; block the binding of estrogen to estrogen receptor-positive cells

Clinical use: breast CA tx and prevention, also helps prevent osteoporosis

Toxicity: tamoxifen- partial agonist in endometrium, so increased risk of endometrial cancer, hot flashes (raloxifene is endometrial antagonist, so no increased risk)

Trastuzumab (herceptin)

MOA: monoclonal Ab against HER-2, a tyrosine kinase; helps kill breast cancer cells that overexpress HER-2 (Ab dependent cytotoxicity?)

Clinical use: HER-2 positive breast CA

Toxicity: cardiotoxicity

Imatinib (gleevec)

MOA: philadelphia chromosome bcr-abl tyrosine kinase inhibitor

Clinical use: CML, GI stromal tumors

Toxicity: fluid retention


MOA: monoclonal Ab against CD20 (found on most B cell neoplasms)

Clinical use: non-Hodgkin’s lymphoma, RA (with MTX)


MOA: small molecule inhibitor of forms of the B-Raf kinase w/ the V600E mutation

Clinical use: metastatic melanoma


MOA: monoclonal Ab against VEGF; inhibits angiogenesis

Clinical use: solid tumors

Ibuprofen, naproxen, indomethacin, diclofenac, ketorolac

MOA: reversibly inhibit COX1 and COX2, blocks prostaglandin synthesis

Clinical use: antipyretic, analgesic, anti-inflammatory; indomethacin used to close a PDA

Toxicity: interstitial nephritis, gastric ulcer (PGs protect gastric mucosa), renal ischemia (PGs vasodilate afferent arteriole)


MOA: selective reversible inhibitor of COX2 (found in inflammatory cells/vascular endothelium), but spares COX1 to help maintain gastric mucosa and has no effect on platelet function (TXA2 production is via COX1)

Clinical use: RA and osteoarthritis, patients w/ gastritis or ulcers

Toxicity: sulfa allergy


MOA: reversibly inhibits cyclooxygenase, most in CNS (inactivated peripherally)

Clinical use: antipyretic and analgesic, but NOT ANTI-INFLAMMATORY

Toxicity: overdose → hepatic necrosis (NAC is the antidote, regenerates glutathione)

Alendronate (other -dronates)
MOA: pyrophosphate analogs, bind hydroxyapatite in bone, inducing apoptosis in osteoclastsClinical use: osteoporosis, hypercalcemia, Paget’s disease of bone

Toxicity: corrosive esophagitis (1st generation), osteonecrosis of the jaw


MOA: purine analog, competitively inhibits xanthine oxidase (↓ conversion of xanthine to uric acid)

Clinical use: gout; lymphoma/leukemia to prevent tumor lysis syndrome related nephropathy

Toxicity: increases the concentration of azathioprine and 6-MP; DO NOT GIVE w/ salicylates, uric acid clearance ↓


MOA: non-purine analog allosteric inhibitor of xanthine oxidase

Clinical use: gout, lymphoma/leukemia to prevent tumor lysis syndrome

Toxicity: increases concentration of azathioprine and 6-MP (metabolized by XO)


MOA: inhibition of uric acid reabsorption in proximal collecting tubule, also inhibits secretion of penicillin

Clinical use: gout, syphilis


MOA: binds and stabilizes tubulin to inhibit polymerization, impairing leukocyte chemotaxis and degranulation

Clinical use: gout

Glaucoma drugs

α agonists: ↓ aqueous humor synthesis

β antagonists: ↓ aqueous humor synthesis

Diuretics (acetazolamide): ↓ aqueous humor synthesis via inhibition of carbonic anhydrase

Cholinomimetics: ↑ outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork

Prostaglandin (latanoprost, PGF2α): ↑ outflow of aqueous humor

Morphine, fentanyl, codeine, heroin, meperidine
(Opioid analgesics)
MOA: agonists at opioid receptors (mu = morphine, delta = enkephalin, kappa = dynorphin) to modulate synaptic transmission
** open K+ channels, close Ca2+ channels → ↓ synaptic transmission; inhibit release of ACh, NE, 5-HT, glutamate, substance PClinical use: pain, acute pulmonary edema

Toxicity: addiction, respiratory depression, constipation, miosis, additive CNS depression w/ other drugs; treat toxicity with naloxone or naltrexone


MOA: opioid receptor agonist

Clinical use: cough suppression

Diphenoxylate, loperamide

MOA: opioid receptor agonists

Clinical use: diarrhea


MOA: opioid receptor agonist

Clinical use: maintenance programs for opiate addicts


MOA: mu-opioid receptor PARTIAL agonist and kappa-opioid receptor agonist; produces analgesia

Clinical use: severe pain (migraine, labor); causes less respiratory depression that full opioid agonists

Toxicity: can cause opioid withdrawal sx if pt is also taking a full opioid agonist (competition for receptors); overdose not easily reversed w/ naloxone


MOA: very weak opioid agonist, also inhibits 5-HT and NE reuptake (works on multiple NT– “tram it all” with tramadol)

Clinical use: chronic pain

Toxicity: decreases seizure threshold


MOA: increases Na+ channel inactivation

Clinical use: 1st line drug for generalized tonic-clonic seizures
-1st line drug for prophylaxis of status epilepticus
-may also be used for simple or complex partial seizures

Toxicity: nystagmus, ataxia, diplopia, SLE like syndrome, induction of P450s; chronic use –> gingival hyperplasia in kids, peripheral neuropathy, megaloblastic anemia (↓ folate absorption), teratogenic


MOA: increases Na+ channel inactivation

Clinical use: 1st line drug for simple/complex partial seizures and tonic-clonic seizures
-also 1st line drug for trigeminal neuralgia

Toxicity: diplopia, ataxia, agranulocytosis, hepatotoxicity, teratogen, induction of P450, SIADH, steven-johnson syndrome


MOA: blocks voltage gates Na+ channels

Clinical use: simple/complex partial seizures, tonic-clonic seizures

Toxicity: stevens-johnson syndrome


MOA: primarily inhibits high-voltage activated Ca 2+ channels

Clinical use: simple/complex partial seizures, tonic-clonic seizures
-also used for peripheral neuropathy, postherpetic neuralgia, migraine prophylaxis, bipolar disorder

Toxicity: sedation, ataxia


MOA: blocks Na+ channels, ↑ GABA action

Clinical use: simple/complex partial seizures, tonic-clonic seizures
-Also used for migraine prevention

Side effects: kidney stones, weight loss


MOA: ↑ GABA(A) action

Clinical use: simple/complex partial seizures, tonic-clonic seizures
**1st line in children**

Toxicity: induction of p450

Valproic acid

MOA: ↑ Na+ channel inactivation, ↑ GABA concentration

Clinical use: *absence seizueres!*
-1st line drug for tonic-clonic seizures
-also used for simple/complex partial seizures, myoclonic seizures

Toxicity: rare but fatal hepatotoxicity, neural tube defects in fetus (CI in pregnancy), tremor, weight gain


MOA: blocks thalamic T-type Ca2+ channels

Clinical use: 1st line drug for absence seizures

Toxicity: GI distress, urticaria, stevens-johnson syndrome


MOA: ↑ GABA action by increasing the FREQUENCY of Cl- channel opening

Clinical use: 1st line for acute status epilepticus, also used for seizures of eclampsia (1st line is MgSO4)

Toxicity: dependence


MOA: inhibits GABA uptake

Clinical use: simple/complex partial seizures


MOA: IRREVERSIBLY inhibits GABA transaminase → ↑ GABA

Clinical use: simple/complex partial seizures

Phenobarbital, pentobarbital, thiopental, secobarbital

MOA: facilitate GABA(A) action by ↑ DURATION of Cl- channel opening, thus ↓ neuron firing (barbiDURATes ↑ DURATion of opening)

Clinical use: sedative for anxiety, insomnia
-thiopental for IV induction of anesthesia (high lipid solubility so action is rapidly terminated by redistribution into tissue)

Toxicity: contraindicated in porphyria patients; respiratory/cardiovascular/CNS depression, induces P450s
-overdose treatment is supportive

Triazolam, oxazepam, midazolam

MOA: short acting benzodiazepines, facilitate GABA(A) action by ↑ FREQUENCY of Cl- channel opening, ↓ REM sleep

Clinical use: anxiety, spasticity, detoxification (esp from alcohol withdrawal/DT), night terrors, sleepwalking, general anesthetic, insomnia (hypnotic effect)
-** midazolam most common IV anesthetic used for endoscopy**

Toxicity: higher additive dependence due to short half life, additive CNS depression w/ alcohol, less risk of respiratory depression and coma than w/ barbiturates


MOA: competitive antagonist at GABA benzodiazepine receptor

Clinical use: reversal of benzodiazepine and zolpidem/zaleplon/eszopiclone (nonbenzodiazepine hypnotics)

Zolpidem, zaleplon, eszopiclone

MOA: act via the BZ1 subtype of GABA receptor

Clinical use: insomnia

Toxicity: ataxia, headaches, confusion; cause only modest day-after psychomotor depression and few amnestic effects; lower dependence risk than benzodiazepines


MOA: inhaled anesthetic

Effects: myocardial/respiratory depression, nausea/emesis, ↑ cerebral blood flow (↓ cerebral metabolic demand)

Toxicity: **hepatotoxicity**, malignant hyperthermia


MOA: inhaled anesthetic

Effects: myocardial/respiratory depression, nausea/emesis, ↑ cerebral blood flow (↓ cerebral metabolic demand)

Toxicity: **proconvulsant**, malignant hyperthermia


MOA: inhaled anesthetic

Effects: myocardial/respiratory depression, nausea/emesis, ↑ cerebral blood flow (↓ cerebral metabolic demand)

Toxicity: **nephrotoxicity**, malignant hyperthermia

Nitrous oxide

MOA: inhaled anesthetics

Effects: myocardial/respiratory depression, nausea/emesis, ↑ cerebral blood flow (↓ cerebral metabolic demand)

Toxicity: expansion of trapped gas in a body cavity (no malignant hyperthermia like other inhaled anesthetics)

Isoflurane, sevoflurane

MOA: inhaled anesthetics

Effects: myocardial/respiratory depression, nausea/emesis, ↑ cerebral blood flow (↓ cerebral metabolic demand)

Toxicity: malignant hyperthermia


MOA: PCP analog that blocks NMDA receptors; cardiovascular stimulant; dissociative anesthetic

Clinical use: IV anesthetic

Toxicity: disorientation, hallucinations, bad dreams


MOA: potentiates GABA(A)

Clinical use: sedation in the ICU, rapid anesthesia induction, short procedures; less postoperative nausea than thiopental

Procaine, cocaine, tetracaine
Ester local anesthetics
MOA: block Na+ channels by binding to a specific receptor on INNER portion of the channel (most effective in rapidly firing neurons bc have to get inside a channel that has already been activated)Clinical use: minor surgical procedures, spinal anesthesia

Toxicity: CNS excitation (depression of inhibitory centers), HTN or hypotension, arrhythmias (cocaine), hypersensitivity (if allergic to esters, give amides)

Lidocaine, mepivacaine, bupivacaine
Amide local anesthetics (amide’s have two I’s)
MOA: block Na+ channels by binding to a specific receptor on INNER portion of the channel (most effective in rapidly firing neurons bc have to get inside a channel that has already been activated)Clinical use: minor surgical procedures, spinal anesthesia

Toxicity: CNS excitation (depression of inhibitory centers), HTN or hypotension, severe cardiotoxicity w/ bupivacaine

Local anesthetics principles
Principles: can be given with vasoconstrictors (usually epinephrine) to enhance local action – ↓ bleeding, ↑ anesthesia by ↓ systemic concentration
-Infected tissue is more acidic, but alkaline anesthetics are charged and cannot penetrate membrane effectively → need more anesthetic
-Size factor predominates over myelination, so order of nerve blockade = small myelinated > small unmyelinated > large myelinated > large unmyelinated
-Order of loss: (1) pain, (2) temperature, (3) touch, (4) pressure

MOA: DEPOLARIZING neuromuscular blocking drug; strong ACh receptor antagonist → produces sustained depolarization and prevents muscle contraction

Clinical use: muscle paralysis in surgery or mechanical ventilation

Toxicity: hypercalcemia, hyperkalemia, malignant hyperthermia

Reversal of succinycholine
-Phase I (prolonged depolarization): no antidote available, cholinesterase inhibitors would just potentiate the depolarization block
-Phase II (repolarized but blocked): ACh receptors are available, but desensitized; antidote = cholinesterase inhibitors (like neostigmine)

MOA: NONDEPOLARIZING neuromuscular blocking drug; competes w/ ACh for receptors

Reversal of blockade: neostigmine, edrophonium, other cholinesterase inhibitors


MOA: prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle

Clinical use: treatment of malignant hyperthermia and neuroleptic malignant syndrome

Bromocriptine, pramipexole, ropinirole

MOA: dopamine agonists

Clinical use: Parkinson’s disease (when they still have endogenous DA)


MOA: may increase dopamine release

Clinical use: Parkinson’s disease; also used as an antiviral against influenza A and rubella

Toxicity: ataxia

MOA: increase level of DA in the brain; L-dopa can cross the BBB (unlike regular DA) and is converted by dopa darboxylase in the CNS → DA
-Carbidopa = peripheral decarboxylase inhibitor, given w/ L-dopa to ↑ bioavailability of L-dopa in brain/limit peripheral side effectsClinical use: Parkinson’s disease

Toxicity: arrhythmias from increased peripheral formation of catecholamines; long term use may → dyskinesia following administration w/ akinesia between doses


MOA: selective inhibitor ofMAO-B (which preferentially metabolizes DA over NE and 5-HT), thereby ↑ availability of DA

Clinical use: adjunctive agent to L-dopa in treatment of PD

Toxicity: may enhance adverse effects of l-dopa


MOA: NMDA receptor antagonist, helps prevent excitotoxicity (mediated by Ca2+)

Clinical use: Alzheimer’s

Toxicity: dizziness, confusion, hallucinations

Donepezil, galantamine, rivastigmine

MOA: acetylcholinesterase inhibtors

Clinical use: Alzheimer’s

Toxicity: nausea, dizziness, insomnia


MOA: 5-HT 1B/1D agonist; inhibits trigeminal nerve activation; prevents vasoactive peptide release; induces vasoconstriction

Clinical use: acute migraine, cluster headache attacks

Toxicity: coronary vasospasm (CI in patients w/ CAD or prinzmetal’s angina

Tetrabenazine, reserpine

MOA: inhibit VMAT (vesicular monoamine transporter); limit DA vesicle packaging and release (since one of the problems in Huntington’s is ↑ DA)

Clinical use: Huntington’s


MOA: DA receptor antagonist

Clinical use: antipsychotic, also used in Huntington’s (since one of the problems in Huntington’s is ↑ DA)

Appropriate agents for treating ESSENTIAL HTN
Diuretics, ACE inhibitors, ARBs, calcium channel blokers
Appropriate agents for treating HTN w/ CHF
Diuretics, ACE inhibitors/ARBs, β blockers (generally only in compensated CHF), K+ sparing diuretics
Appropriate agents for treating HTN w/ DM

ACE inhibitors/ARBs, calcium channel blockers, diurectics, β blockers, α blockers

**ACE inhibitors are protective against diabetic nephropathy

Nifedipine, verapamil, diltiazem, amlodipine
Ca2+ channel blockers!
MOA: block voltage gated L type calcium channels of cardiac and smooth muscle and ∴ reduce muscle contractility
-Amlodipine and nifedipine have the most effect on vascular smooth muscle; verapamil has the most effect on the heartClinical use: HTN, angina, arrhythmias (except nifedipine), Prinzmetal’s angina, raynaud’s

Toxicity: cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation


MOA: ↑cGMP → smooth muscle relaxation; vasodilates aterioles > veins (∴ afterload reduction)

Clinical use: severe HTN, CHF. 1st line therapy for HTN in pregnancy (w/ methyldopa)

Toxicity: compensatory tachycardia (often coadministered w/ a β blocker to prevent this) — CI in patients w/ angina or CAD, fluid retention, angina, lupus-like syndrome


MOA: short acting ↑cGMP via direct release of NO

Clinical use: malignant HTN

Toxicity: can cause cyanide toxicity (releases cyanide)


MOA: D1 receptor agonist; causes coronary, peripheral, renal and splanchnic vasodilation; ↓ BP and ↑ natriuresis (excretion of sodium in the urine via action of the kidneys)

Clinical use: malignant HTN

Nitroglycerin, isosorbide dinitrate

MOA: vasodilate by releasing NO in smooth muscle, causing increase in cGMP and smooth muscle relaxation; dilates veins >> arteries (so ↓ preload)

Clinical use: angina, pulmonary edema

Toxicity: reflex tachycardia, hypotension, flushing, headache, “Monday disease”

Nitrates, effects on: EDV, BP, Contractility, HR, ejection time, MVO2
Nitrates affect preload (dilate veins >> arteries)
-EDV: ↓
-BP: ↓
-Contractility: ↑ (reflex response)
-HR: ↑ (reflex response)
-ejection time: ↓
-MV02: ↓
β blockers, effects on: EDV, BP, Contractility, HR, ejection time, MVO2
β blockers affect afterload
-EDV: ↑
-BP: ↓
-Contractility: ↓
-HR: ↓
-ejection time: ↑
-MV02: ↓
Nitrates plus β blockers, effects on: EDV, BP, Contractility, HR, ejection time, MVO2
Nitrates affect preload (dilate veins >> arteries)
-EDV: no effect or ↓
-BP: ↓
-Contractility: little/no effect
-HR: ↓
-ejection time: little/no effect
-MV02: ↓↓
Lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin

MOA: inhibit conversion of HMG-CoA to mevalonate (HMG-CoA reductase = rate limiting step in cholesterol synthesis)

Clinical use: ↓↓↓ LDL cholesterol
-↑ HDL cholesterol
-↓ TriG

Toxicity: hepatotoxicity (↑LFTs), rhabdomyolysis

Niacin (B3)

MOA: inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation

Clinical use: ↓↓ LDL cholesterol
-↑↑ HDL cholesterol (most of all options)
-↓ TriG

Toxicity: red/flushed face (↓ by aspirin or long term use), hyperglycemia (→acanthosis nigricans), hyperuricemia (exacerbates gout)

Cholestryamine, colestipol, colesevelam
Bile acid resins
MOA: prevent intestinal reabsorption of bile acids; liver must use cholesterol to make moreClinical use: ↓↓ LDL cholesterol
– slight ↑ HDL cholesterol
– slight ↑ TriG

Toxicity: patients hate it!! tastes bad, causes GI upset; ↓ absorption of fat soluble vitamins; cholesterol gallstones


MOA: prevents cholesterol reabsorption at small intestine brush border

Clinical use: ↓↓ LDL cholesterol (no effect on HDL or TriG)

Gemfibrozil, clofibrate, bezafibrate, fenofibrate

MOA: upregulate LPL to ↑ TriG clearance

Clinical use: ↓ LDL cholesterol
-↑ HDL cholesterol
-↓↓↓ TriG (most of all the options)

Toxicity: myositis, hepatotoxicity (↑ LFTs), cholesterol gallstones


MOA: DIRECT inhibition of Na+/K+ ATPase leads to INDIRECT inhibition Na+/Ca2+ exchanger/antiport; ↑ [Ca2+] intracellularly → positive inotropy (increased force of contraction); also stimulated the vagus nerve to ↓ HR

Clinical use: CHF (↑ contractility); A fib (↓ conduction at the AV node and depression of the SA node)

Toxicity: cholinergic- nausea/vomiting, diarrhea, blurry yellow vision
-ECG- ↑ PR, ↓ QT, ST scooping, T wave inversion, arrhythmia AV block
-hyperkalemia is a poor prognostic factor (shows that digoxin is significantly out competing K+ at the ATPase)
**Predisposition to overdose: renal failure (↓ digoxin excretion), hypokalemia (less competition at ATPase), quinidine (↓ digoxin clearance, displaces digoxin from tissue binding sites)

Reversal of digoxin toxicity
-slowly normalize K+
-cardiac pacer
-anti-digoxin Fab fragments
Class I antiarrhythmics are ____ channel blockers that _____ conduction by ____ the slope of phase 0 depolarization and ____ the threshold for firing in abnormal pacemaker cells. ____kalemia causes ↑ toxicity for all class I drugs.
-Na+ channel blockers
-↓ the slope of phase 0 depolarization
-↑ the threshold for firing in abnormal pacemaker cells (selectively depress tissue that is frequently depolarized, as in tachycardia)
-HYPERkalemia ↑ toxicity of class I drugs
Disopyramide, Quinidine, Procainamide
“Double Quarter Pounder”
Class IA antiarrhythmics
MOA: INCREASE AP duration, effective refractory period, and QT intervalClinical use: both atrial and ventricular arrhythmias, especially reentrant and ectopic supraventricular and ventricular tachycardia

Toxicity: quinidine – headache/tinnitus
procainamide- drug induced SLE
disopyramide- heart failure
All- thombocyotopenia, torsades de pointes due to ↑QT

Mexiletine, Lidocaine, Tocainide, Phenytoin
“Mayo, Lettuce, Tomato and Pickles”
Class IB antiarrhythmics
MOA: DECREASE AP duration;Clinical use: acute ventricular arrhythmias (especially post MI) and digitalis induced arrhythmias (preferentially affect ischemic or depolarized purkinje and ventricular tissue)

Toxicity: local anesthetics- CNS stimulation/depression, cardiovascular depression

Flecainide, propafenone
“Fries, Please!”
Class IC antiarrhythmics
MOA: NO EFFECT on AP durationClinical use: ventricular tachycardias that progress to VFib and in intractable SVT
-usually only used as a last resort in refractory tachyarrhythmias

Toxicity: proarrhythmic, especially in post MI (contraindicated), significantly prolongs refractory period in AV node

Class II antiarrhythmics
β blockers (metoprolol, propranolol, esmolol, atenolol, timolol)
MOA: decreases SA and AV nodal activity by ↓cAMP, ↓Ca2+ currents, suppress abnormal pacemakers by decreasing the slope of phase 4, ↑ PR interval bc AV node particularly sensitiveClinical use: ventricular tachycardia, SVT, slowing ventricular rate during a fib and a flutter

Toxicity: impotence, exacerbation of asthma, bradycardia, AV block, sedation, masking of hypoglycemia
-Metoprolol- dyslipidemia
-Propanolol- exacerbate Prinzmetal’s angina

Amiodarone, Ibutilide, Dofetilide, Sotalol
Class III arrhythmics
MOA: K+ channel blockers, INCREASE AP duration and ERP, ↑QT intervalClinical use: when other antiarrhythmics fail

Toxicity: sotalol- torsades de pointes, excessive β block
Ibutilide- torsades
Amiodarone- EVERYTHING! pulmonary fibrosis, hepatotoxicity, hypo/hyperthyroidism (40% iodine by weight), corneal deposits, blue/gray skin deposits that cause photodermatitis, neurologic effects, constipation, bradycardia, heart block, CHF

Class IV antiarrhythmics
Verapamil, diltiazem
MOA: decrease conduction velocity, increase ERP and PR intervalClinical use: prevention of nodal arrhythmias (like SVT)

Toxicity: constipation, flushing, edema, CHF, AV block, sinus node depression


MOA: increases K+ out of cells → hyperpolarization of the cell and decreased INTRACELLULAR Ca2+ (only lasts about 15 sec)

Clinical use: DOC in diagnosing/abolishing supraventricular tachycardia

Toxicity: flushing, hypotension, chest pain
-effects blocked by theophylline and caffeine

Clinical use: torsades de pointes digoxin toxicity

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