First Aid Pharmacology (complete)

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

MOR: ?-lactamase

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 bc alters PBP)

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(often with mononucleosis infection- reaction-not an allergy), pseudomembranous colitis

MOR: ?-lactamase

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

Add to aminopenicillins and antipseudomonals

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, disulfiram-like runs, vitamin K deficiency, potentiate nephrotoxicity of amino glycosides

MOR: structural change in PBP

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, disulfiram-like runs, vitamin K deficiency, potentiate nephrotoxicity of amino glycosides

MOR: structural change in PBP

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, disulfiram-like runs, vitamin K deficiency, potentiate nephrotoxicity of amino glycosides

MOR: structural change in PBP


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

Clinical use: bactericidal w/ increased activity again Pseudomonas and gram (+) organisms
-Use in patients with neutropenic fever

Toxicity: hypersensitivity rxns, disulfiram-like runs, vitamin K deficiency, potentiate nephrotoxicity of amino glycosides

MOR: structural change in PBP


MOA: 5th generation beta lactam drug that inhibits cell wall synthesis

Clinical use: broad gram (+) and gram (-) coverage including MRSA; does NOT cover pseudomonas

MOR: structural change in PBP

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

no cross allergenicity w/ penicillins

Imipenem/cilastatin, meropenem, ertapenem, doripenem

MOA: imipenem = beta lactamase resistant carbapenem that blocks peptidoglycan cross linking, always administered with cilastatin (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 (NOT VRE) and C diff

Toxicity: diffuse flushing/”red man syndrome” when infused too quickly (can prevent with antihistamines and slow infusion rate); nephrotoxicity/ototoxicity/thrombophlebitis (“NOT trouble free”)

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*

MOR: bacterial transferase enzymes

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

MOR: methylation of 23S rRNA-binding site


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

Clinical use: bacterioSTATIC against meningitis (H. influenzae, N. meningitidis, S. pneumo) and Rocky Mountain spotted fever (Rickettsia rickettsii)

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

MOR: plasmid-encoded acetyltransferase


MOA: works at 50S ribosomal subunit to block translocation

Clinical use: bacterioSTATIC against anaerobic infections above the diaphragm
-Aspiration pneumonia, lung abscess, oral infxns

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
-Dapsone (lepromatous leprosy) closely related

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

MOR: altered enzyme, ? uptake, or ?PABA synthesis


MOA: inhibits bacterial dihydrofolate reductase

Clinical use: bacterioSTATIC use in combination w/ SMX for UTIs, Shigella, Salmonella, Pneumocystitis jirovceii pneumonia tx and prophylaxis, toxoplasmosis prophylaxis

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, QT interval prolongation, CI in pregnant women due to cartilage damage

MOR: chr-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps


MOA: lipopetide that disrupts cell membrane of gram (+) cocci

Clinical use: skin infections (esp MRSA), VRE, bacteremia, endocarditis
**Not used for pneumonia b/c inactivated by surfactant

Toxicity: myopathy, rhabdomylosis (?CPK)


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

Clinical use: Giardia, Entamoeba, Trichomonas, Garderella vaginalis, Anaerobes below diaphragm (“GET GAP on the Metro with metronidazole!)

Toxicity: disulfiram reaction with alcohol


MOA: inhibits synthesis of mycolic acids ( bacteria have the catalase-KatG-needed to activate it)

Clinical use: TB (only one that can be used as solo prophylaxis)
-Different INH half-lives in fast vs. slow acetylators

Toxicity: INH Injures Neurons and Hepatocytes(10-20%), lupus ; also causes B6 deficiency (give pyridoxine to prevent neurotox&sideroblastic anemia)

MOR: underexpression of KatG catalase


MOA: inhibits DNA dependent RNA poly

Clinical use: TB, in combo w/ dapsone for leprosy, prophylaxis against neisseria meningitis in kids & Haemophilus influenzae type B

Toxicity: “Rifamin 4 R’s”
-RNA polymerase inhibitor, Ramps up CYP450, Red/orange body fluids, Rapid resistance used alone

MOR: mutations of RNA poly


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)( supplementation of K/Mg), arrhythmias, anemia, IV phlebitis. AMPHOTERRIBLE


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, coccidioides, histoplasma (the systemic mycoses)
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 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

Clinical use: invasive aspergillosis, candida

Toxicity: flushing due to histamine release


MOA: inhibits fungal squalene epoxidase ? inhibit production of lanosterol

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
Quinidine, artesunate
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 (IMP ? GMP)

Clinical use: RSV (palivizumab preferred in children), chronic hep C

Toxicity: hemolytic anemia, SEVERE TERATOGEN

Acyclovir, famciclovir, valacyclovir

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

Clinical use: HSV and VZV (HSV lesions/encephalitis); no activity against CMV and no effect on latent forms of HSV/VZV
-Valacyclovir (prodrug) has better oral availability
-Use famcicylovir for herpes zoster

MOR: mutated viral thymidine kinase

Ganciclovir, valganciclovir

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

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

Toxicity: leukopenia/neutropenia/thrombocytopenia, renal toxicity

MOR: mutated viral thymidine kinase


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

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

Toxicity: nephrotoxicity, seizures due to electrolyte abnormalities, anemia

MOR: mutated DNA polymerase


MOA: inhibits viral DNA poly, 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” (HIV-1 protease (pol) cleaves polypeptide products of HIV mRNA)
MOA: stops cleavage of HIV polypeptide into functional parts, thus preventing maturation of new virusesClinical use: HIV

Toxicity: hyperglycemia, GI intolerance, lipodystrophy (buffalo hump); nephropathy, hematuria (indinavir)
-Ritonavir inhibits P450 enzymes
-pancreastitis(ritonavir), Increased Bilirubin (atazanavir)

Tenofovir (only nucleotide), emtricitabine, abacavir, lamivudine, zidovudine(ZDZ, AZT), didanosine, stavudine (others nucleoside analogs and need activation ie triphosphate form)
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 -up to 40%(alleviated by GCSF and EPO), peripheral neuropathy, lactic acidosis(nucleosides, anemia (ZDV), pancreatitis & Hepatic steatosis (didanosine, stavudine), life-threatening rash (abacavir)

*if patient has concurrent Hep B infection, use tenofovir

Nevirapine, efavirenz, delavirdine
MOA: allosterically inhibit HIV reverse transcriptase; do not require phosphyrlationToxicity: rash(SJS), hepatotoxicity (life-threatening hepatic failure +encephalopathy in first 6 weeks)
-Efavirenz: vivid dreams and CNS symptoms
-Delavirdine and efavirenz CI in pregnancy

Integrase inhibitor
MOA: reversibly inhibits HIV integraseToxicity: ? creatine kinase, hypercholesterolemia

Fusion inhibitor
MOA: binds gp41, inhibiting viral entry (into uninfected CD4+ Cells)Toxicity: skin reaction at injection site

Fusion inhibitor
MOA: bindins CCR-5 on surface of T cells/monocytes, inhibiting interaction with gp120
?- chronic hep B and C, Kaposi’s sarcoma, hairy cell leukemia, condyloma acuminatum, renal cell carcinoma, malignant melanoma
?- MS
?- NADPH oxidase deficiency (CGD)Toxicity: neutropenia, myopathy


MOA: HCV protease inhibitor; prevents viral replication

Clinical use: chronic hep C in combination with ribavirin and peg interferon alfa
-Do not use as mono therapy

Toxicity: photosensitivity, rash


MOA: inhibits HCV RNA-dependent RNA polymerase acting as a chain termiantor

Clinical use: chronic HCV in combination with ribavirin,+/- peginteferon alfa
-Do not use as mono therapy

Toxicity: fatigue, headache, nausea

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: calcineurin inhibitor; binds *cyclophilin*. Blocks T cell activation by preventing IL-2 transcription.

Clinical use: transplant rejection prophylaxis, psoriasis, rheumatoid arthritis.

Toxicity: *nephrotoxicity*,
hypertension, hyperlipidemia, hyperglycemia, tremor, hirsutism, gingival hyperplasia.

Tacrolimus (FK-506)
MOA: Calcineurin inhibitor; binds *FK506 binding protein (FKBP*).
Blocks T cell activation by preventing IL-2 transcription.
10x more potent than cyclosporineClinical use: transplant rejection prophylaxis, topical (eczema)

Toxicity: similar to cyclosporine, ? risk of diabetes and neurotoxicity, also pleural effusion; no gingival hyperplasia or hirsutism

Sirolimus (rapamycin)

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

Clinical use: kidney transplant rejection prophylaxis
-Also used in drug eluting stents

Toxicity: anemia, thrombocytopenia, leukopenia, insulin resistance, hyperlipidemia; *non-nephrotoxic*

Daclizumab, basiliximab

MOA: monoclonal antibodies; block IL-2R

Clinical use: kidney transplant rejection prophylaxis

Toxicity: edema, HTN, tremor


MOA: precursor of 6-MP; inhibits lymphocyte proliferation by blocking NT synthesis

Clinical use: transplant rejection prophylaxis, RA, Crohn disease, glomerulonpehritis

Toxicity: BM suppression; 6-MP degraded by xanthine oxidase so toxicity ? by 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: Cytokine release syndrome, HSN rxn, CNS effects
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
Epoetin alfa (erythropoietin)
Clinical use: anemias (esp renal failure)

Granulocyte colony stimulating factor

Clinical use: bone marrow recovery


Granulocyte/macrophage colony stimulating factor

Clinical use: bone marrow recovery

Romiplostim, eltrombopag


Clinical use: thrombocytopenia

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

MOA: TNF ? inhibtors

Clinical use: IBD, RA, ankylosing spondylitis, psoriasis


MOA: inhibits Gp IIb/IIIa

Clinical use: anti platelet for prevention of ischemic complications in pts undergoing PCI

Clinical use: targets HER2 receptor in HER2nu positive breast cancer (Herceptin)

MOA: targets CD20

Clinical use: B cell non-Hodgkin’s lymphoma, CLL, RA, ITP


MOA: targets IgE

Clinical use: additional treatment for severe asthma


MOA: targets CD52

Clinical use: CLL (“Alymtuzumab”)


MOA: targets VEGF

Clinical use: colorectal cancer, renal cell carcinoma


MOA: targets EGFR

Clinical use: stage IV colorectal cancer, head and neck cancer


MOA: targets complement protein C5

Clinical use: paroxysmal nocturnal hemoglinuria


MOA: targets ?4-integrin

Clinical use: MS, Crohn disease


MOA: targets RANKL

Clinical use: osteoporosis (inhibits osteoclast maturation)

Digoxin immune Fab

MOA: targets digoxin

Clinical use: antidote for digoxin toxicity


MOA: targets RSV F protein

Clinical use: RSV prophylaxis for high-risk infants

Ranibizumab, bevacizumab

MOA: targets VEGF

Clinical use: neovascular age-related macular degeneration

MOA: binds insulin receptor (tyrosine kinase activity)
-Liver: increase glycogen synthesis
-Muscle: increase glycogen, protein synthesis; increase K+ uptake
-Fat: increase TG storageClinical use: DM type 1 and 2, gestational diabetes, life threatening hyperkalemia, stress induced hyperglycemia

Toxicities: hypoglycemia

Insulin, rapid acting
Aspart, glulisine, lispro
Insulin, short acting
Insulin, intermediate acting
Insulin, long acting
Detemir, glargine
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), GI upset

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

Toxicities: hypoglycemia
favors lipogenesis (weight gain)

Pioglitazone, Rosiglitazone

MOA: increase insulin sensitivity in peripheral tissue, binds to PPAR-? 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, ?risk of fractures
Metabolism: Liver (better for renal failure Pt)

Acarbose, Miglitol
?-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

Amylin analog
MOA: ?gastric emptying, ? glucagonClinical use: type 1 AND 2 DM (with insulin only)

Toxicities: hypoglycemia, nausea, diarrhea

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

Toxicities: N/V, pancreatitis

Exenitide, liraglutide
GLP-1 analogs
MOA: ? insulin, ? glucagon release
(induce satiety, decrese gastric emptying, insulin release from Beta cells)
Clinical use: type 2 DMToxicities: pancreatitis, nausea, vomiting

SGLT-2 inhibitors (sodium glucose cotransporter 2)
MOA: block reabsorption of glucose in PCTClinical use: type 2 DM

Toxicities: glucosuria, UTIs, vaginal yeast infections, hypotension
CI in renal impairment (obviously!)

Linagliptin, saxagliptin, sitagliptin
DPP-4 inhibitors (DPP-4 inhibits GLP-1)
MOA: ? insulin, ? glucagon release
(activates incretins)Clinical 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 (ie peripheral with PTU)

Clinical use: hyperthyroidism

Toxicity: agranulocytosis, aplastic anemia, hepatotoxicity (propylthiouracil)
-**Methimazole is a possible teratogen (aplasia cutis)
(ANCA- associated vasculitis with PTU-rare)

Levothyroxine, triiodothyronine

MOA: thyroxine replacement

Clinical use: hypothyroidism, myxedema

Toxicity: tachycardia, heat intolerance, tremors, arrythmias4

note: can prevent MR in neonate if admin w/in 2 weeks of delivery


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
Beclomethasone, dexamethasone, fludrocortison (mineralocorticoid + glucocorticoid activity), hydrocortisone, methylprednisolone, prednisone, traimcinolone

MOA: Metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements, inhibition of phospholipase A2, and inhibition of transcription factors such as NF-?B

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

Toxicity: Iatrogenic Cushing syndrome (buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis (treat with bisphosphonates), adrenocortical atrophy, peptic ulcers, diabetes (if chronic).
-Adrenal insufficiency when drug stopped abruptly after chronic use.


MOA: sensitizes Ca2+ sensing receptor (CaSR) in parathyroid gland to circulating Ca2+ ? ? PTH

Clinical use: hypercalcemia due to 1° or 2° hyperparathyroidism

Toxicity: hypocalcemia

Cimetidine, ranitidine, famotidine, nizatidine
H? blockers (take H? blockers before you “dine”)
MOA: REVERSIBLY block histamine H? 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 (headache,confusion, dizziness) 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 (hypermagnesemia toxicities)

Calcium carbonate

Clinical use: antacid

Toxicity: hypokalemia (all antacids), hypercalcemia, rebound acid increase
can chelate and decrease effect of other drugs (tetracyclines)

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, Crohn’s disease, RA

Toxicity: sulfonamide toxicity, reversible oligospermia


MOA: 5-HT3 antagonist; decrease vagal stimulation; 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, QT prolongation


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: inhibits gastric and pancreatic lipase ? ?breakdown and absorption of dietary fats

Clinical use: weight loss

Toxicity: steatorrhea, ?absorption of fat-soluble vitamins


MOA: activator 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)
Enoxaparin, dalteparin, fondaparinux

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, argatroban, dabigatran

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 ?-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)-especially with Protein C toxicity

Reversal of warfarin toxicity?
1) Vitamin K
2) Fresh frozen plasma for rapid reversal
Apixaban, rivaroxaban

MOA: direct factor Xa inhibitors

Clinical use: treatment and prophylaxis for DVT and PE (rivaroxaban); stroke prophylaxis in patients with a-fib

Toxicity: bleeding (no reversal agent)

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 ? prevent expression of gp IIb/IIIa on platelet surface

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

Toxicity: ticlopidine causes neutropenia (monitor CBC)

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

Abciximab, 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

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: ? risk of thrombosis, 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 (advise pts to take with water and remain upright for 30 min), osteonecrosis of the jaw


MOA: recombinant PTH analog given subQ, ? osteoblastic activity

Clinical use: osteoporosis, causes ? bone growth compared to antiresorptive therapies (e.g., bisphosphonates)

Toxicity: transient hypercalcemia

Drugs for acute gout
1st line NSAIDS – naproxen, indomethacin
Drugs for chronic gout
Allopurinol, febuxostat

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

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

Toxicity: increases the concentration of azathioprine and 6-MP (both normally metabolized by xanthine oxidase)


MOA: non-purine analog allosteric inhibitor of xanthine oxidase

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

Toxicity: see allopurinol

use: safer in patients with renal dysfunction


MOA: recombinant uricase that catalyzes metabolism of uric acid to allantoin (more water-soluble)

Clinical use: chronic gout


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

Clinical use: acute and prophylactic value in gout

Toxicity: GI


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

Clinical use: chronic gout, syphilis

Toxicity: uric acid calculi

Glaucoma drugs
? agonists: ? aqueous humor synthesis
**Cause mydriasis -> do not use in closed-angle glaucoma? antagonists(tim,betax, carte-): ? aqueous humor synthesis

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

Cholinomimetics(direct/inderect): ? outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork. Use pilocarpine in emergencies (open canal of schlemm)–Miosis/ciliary m contraction)

Prostaglandin (latanoprost, PGF2?): ? outflow of aqueous humor-darkens iris color

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 ? ? GI motility

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, serotonin syndrome


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, SJS, osteopenia, peripheral neuropathy, megaloblastic anemia (? folate absorption), teratogenic (fetal hydantoin syndrome)


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/aplastic anemia, 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
-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, sedation, tolerance, dependence

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: EthosuximideFGHIJ (Fatigue, GI distress, Headache, Itchiness, 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 (respirations/blood pressure)

Alprazolam, 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, hallucination and bad dreams

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.
not LT use bc increases TG. Myoclonus & pain at injection site

Procaine, cocaine, tetracaine
Ester local anesthetics (all only have one “i”
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)
Metabolized in Blood (esters)

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 agonist ? produces sustained depolarization and prevents muscle contraction

Clinical use: muscle paralysis in surgery or mechanical ventilation

Toxicity: hypercalcemia, hyperkalemia (esp with burn victims), 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 (think inhaled anesthetics&succinylcholine) and neuroleptic malignant syndrome

Bromocriptine, pramipexole, ropinirole
MOA: dopamine agonists
Bromo (ergot),
pramipexole (kidney elim)/ropinerole(liver elim) (non-ergot) preferredClinical 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, livedo reticularis

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 = blocks peripheral conversion of L-dopa to dopamine by inhibiting DOPA decarboxylase, 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 (“on-off” phenomenon)
Vit B6 will increase the peripheral metabolism of L-Dopa.

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-dopaentacapone/tolcapone- COMT inhibitors also used to decrease breakdown


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)

Methylphenidate, dextroamphetamine, methamphetamine

CNS stimulants

MOA: ? catecholamines in synaptic cleft, especially norepinephrine and dopamine

Clinical use: ADHD, narcolepsy, appetite control

Haloperidol, trifluoperazine, fluphenazine
High potency antipsychotics (“Try to Fly High)
MOA: block D2 receptors (?cAMP)Clinical use: schizophrenia (primarily + symptoms), psychosis, acute mania, Tourette syndrome

-All antipsychotics: highly lipid soluble and slow to be removed from body; hyperprolactinemia; QT prolongation
-High potency antipsychotics: EPS, neuroleptic malignant syndrome

Neuroleptic malignant syndrome

Think FEVER (Fever, Encephalopathy, Vitals, Enzymes ?, Rigidity of muscles)

Rigidity, myoglobinuria, autonomic instability, hyperpyrexia

Tx: dantrolene, D2 agonists (e.g., bromocriptine)

EPS side effects
4 hr acute dystonia (muscle spasms, stiffness, oculogyric crisis)
4 day akathisia (restlessness)
4 wk bradykinesia (parkinsonism)
4 mo tardive dyskinesia (stereotypic oral-facial movements)
Thioridazine, chlorpromazine

Low potency antipscyhotics (“Cheating Thieves are low)

Clinical use: schizophrenia (primarily + symptoms), psychosis, acute mania, Tourette syndrome

-All antipsychotics: highly lipid soluble and slow to be removed from body; hyperprolactinemia; QT prolongation
-Low potency antipsychotics: block muscarinic, ?1, and histamine receptors

Olanzapine, clozapine, quetiapine, risperidone, aripiprazole, ziprasidone

MOA: effects on 5-HT2, dopamine, ?1, and H1 receptors

Clinical use: schizophrenia (both + and – symptoms), bipolar disorder OCD, anxiety disorder, depression, mania, Tourette syndrome

Toxicity: fewer EPS and anticholinergic effects than traditional antipsychotics; QT prolongation
-Olanzapine/clozapine: weight gain
-Clozapine: agranulocytosis (require WBC monitor)/seizures
-Risperidone: hyperpolactinemia
-Ziprasidone: prolong QT interval


MOA: not established

Clinical use: mood stabilizer for bipolar; SIADH

Toxicity: LMNOP (Lithium, Movement, Nephrogenic DI, hypOthyroidism, Pregnancy problems)
-Ebstein abnormality if taken during pregnancy
-Thiazide use implicated in lithium toxicity
-**Narrow therapeutic window
others: heart block, edema,
-Most is reabsorbed in the PCT (following Na+ reabsorption)


MOA: stimulates 5-HT1A receptors

Clinical use: generalized anxiety
-1-2 weeks to see effect

Toxicity: does not cause sedation, addiction, or tolerance
-Does not interact with alcohol (vs. barbiturates, benzos)

Fluoxetine, paroxetine, sertraline, citalopram
MOA: 5-HT-specific reuptake inhibitorsClinical use: depression, generalized anxiety disorder, panic disorder, OCD, bulimia, social phobias, PTSD
-Takes 4-8 weeks to see effect

Toxicity: fewer than TCAs
-SIADH, sexual dysfunction
-Serotonin syndrome

Serotonin syndrome

With any drug that ?5-HT (e.g., MAO inhibitors, SNRIs, TCAs)

Hyperthermia, confusion, myoclonus, CV instability, flushing diarrhea, seizures

Tx: cyproheptadine (5-HT2 receptor antagonist)

Venlafaxine, duloxetine
MOA: inhibit 5-HT and norepinephrine uptakeClinical use: depression
-Venlafaxine for generalized anxiety disorder, panic disorder, PTSD
-Duloxetine for peripheral neuropathy

Tx: ?BP

Amitriptyline, nortriptyline, imipramine, despramine, clomipramine, doxepin, amoxapine
Tricylic antidepressants
MOA: block reuptake of 5-HT and norepinphrineClinical use: major depression, OCD (clomipramine), peripheral neuropathy, chronic pain, migraine prophylaxis, bedwetting (imipramine)

Toxicity: sedation; ?-1 blocking effects; anticholinergic effects (Ami>Nor); QT prolongation
-Tri-C’s: Convulsions, Coma, Cardiotoxicity (tx: NaHCO3 to prevent arrhythmia)
-Respiratory depression and hyperpyexia
-Despramine is less sedating with a higher seizure threshold

Tranylcypromine, phenelzine, isocarboxazid, selegiline
MOA: nonselective MAO inhibition ?levels of amine neurotransmitters (NE, 5-HT, dopamine)
Selegiline (selective MAO-B inhibition
Clinical use: atypical depression, anxiety, hypochondriasisToxicity: hypertensive crisis with ingestion of tyramine (found in wine and cheese)
-CNS stimulation
-CI with SSRIs, TCAs, St. John’s wort, meperidine, detromethorphan to prevent serotonin syndrome

Atypical antidepressant, also smoking cessation
MOA: ? norepinephrine and dopamine via unknown mechanismsToxicity: stimulant effects (tachycardia, insomnia), headache
-Seizures in anorexic/bulimic patients
NO sexual side effects

atypical antidepressant
blocks NE reuptake
tox: sedation, orthostatic hypoTN
Atypical antidepressant (high doses), primary use is insomnia
MOA: Primarily inhibits 5HT reuptakeClinical use: insomnia

Toxicity: priapism (trazo*bone*), postural hypotension, nausea, sedation

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

ACE inhibitors/ARBs, calcium channel blockers, thiazide diuretics, ? blockers

**ACE inhibitors are protective against diabetic nephropathy

Appropriate agents for treating HTN in pregnancy
Hydralazine, labetalol, methyldopa, nifedipine
Amlodipine, clevidipine, nicardipine, nifedipine, nimodipine

Dihydropyridine Ca2+ channel blockers, act on smooth muscle

MOA: block voltage-independent L-type Ca2+ channels of smooth muscle ? ? contractility
Vascular smooth muscle–amlodipine = nefidipine > diltiazem > verapamil

Clinical use: HTN, angina (including Prinzmetal), Raynaud phenomenon
-Nimodipine: subarachnoid hemorrhage (prevent cerebral vasopasm)
-Clevidipine: hypertensive urgency or emergency

Toxicity: cardiac depression, peripheral edema, flushing, dizziness, constipation, gingival hyperplasia

Diltiazem, verapamil

Non-dihydropyridine Ca2+ channel blockers, act on heart

MOA: block voltage-independent L-type Ca2+ channels of smooth muscle ? ? contractility
Heart–verapamil > diltiazem > amlodipine = nifedipine

Clinical use: hypertension, angina, a-fib/flutter

Toxicity: cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation, gingival hyperplasia
-Hyperprolactinemia with verapamil


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 ? blocker to prevent this; thus CI in patients w/ angina or CAD), fluid retention, angina, lupus-like syndrome

Drugs used in hypertensive emergency
Clevidipine, fenoldopam, labetalol, nicardipine, nitroprusside

MOA: short acting ?cGMP via direct release of NO

Clinical use: hypertensive emergency

Toxicity: can cause cyanide toxicity (releases cyanide)
-Tx: sodium thiosulfate


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: hypertensive emergency

Nitroglycerin, isosorbide dinitrate, isosorbide mononitrate (almost 100% oral availability)

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

Clinical use: angina, acute coronary syndrome, pulmonary edema

Toxicity: reflex tachycardia, hypotension, flushing, headache, “Monday disease”
-**Use with PDE inhibitors (e.g., sildenafil) CI due to risk of SEVERE HYPOTENSION

Nitrates, effects on: EDV, BP, Contractility, HR, ejection time, MVO2
Nitrates affect preload (dilate veins >> arteries)
-EDV: ?
-BP: ?
-Contractility: no effect
-HR: ? (reflex response)
-ejection time: ?
-MV02: ?
? blockers, effects on: EDV, BP, Contractility, HR, ejection time, MVO2
? blockers affect afterload
-EDV: no effect or ?
-BP: ?
-Contractility: ?
-HR: ?
-ejection time: ?
-MV02: ?
Nitrates plus ? 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: no effect or ?
-ejection time: little/no effect
-MV02: ??
Lovastatin, pravastatin (not metabolized by CYP450), simvastatin, atorvastatin, rosuvastatin

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

Clinical use: ??? LDL
-? HDL
-? TG

Toxicity: hepatotoxicity (?LFTs), rhabdomyolysis (esp when used with fibrates or niacin)
-? toxicity with CYP450 inhibitors

Niacin (B3)

MOA: inhibits lipolysis in adipose tissue; reduces hepatic VLDL synthesis

Clinical use: ?? LDL
-?? HDL cholesterol (most of all options)
-? TG

Toxicity: red/flushed face (? by aspirin or long term use since mediated by prostaglandns), 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
– slight ? HDL
– slight ? TG

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 TG

Toxicity: rare ? LFTs, diarrhea

Gemfibrozil, clofibrate, bezafibrate, fenofibrate

MOA: upregulate LPL to ? TG clearance; activates PPAR-? to induce HDL synthesis

Clinical use: ? LDL cholesterol
-? HDL
-??? TG (most of all the options)

Toxicity: myopathy (? risk with statins), 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
? 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 ? 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

Cholinomimetic – direct agonist

Clinical use: postop ileus, neurogenic ileus, urinary retention

Action: Activates bowel and bladder smooth muscle; resistant to AChE.
“Bethany, call (bethanecol) me to activate your bowels and bladder.”


Cholinomimetic – direct agonist

Clinical use: glaucoma; constricts pupil and relieves intraocular pressure

Action: carbon copy of acetylcholine


Cholinomimetic – direct agonist

Clinical use: challenge test for asthma (Decrease FEV1 ;20%= bronchial asthma)

Action: stimulates muscarinic recpetors in airway


Cholinomimetic – direct agonist

Clinical use: open- and close-angle glaucoma; potent stimulator of sweat, tears, and saliva

Action: contracts ciliary muscle of eye (open-angle glaucoma, pupillary sphincter (close-angle glaucoma); resistant to AChE.
“You cry, drool, and sweat on your ‘pilow.'”

Donepezil, galantamine, rivastigmine

Cholinomimetic – indirect agonist (anticholinesterase)

Clinical use: Alzheimer

Action: ?ACh


Cholinomimetic – indirect agonist (anticholinesterase)

Clinical use: diagnosis of myasthenia gravis
-Myasthenia gravis now diagnosed by anti-AChR Ab test

Action: ?ACh


Cholinomimetic – indirect agonist (anticholinesterase)

Clinical use: postop and neurogenic ileum and urinary retention, myasthenia gravis, reversal of neuromuscular junction blockade (postop)

Action: ?ACh
-Neo CNS = no CNS penetration


Cholinomimetic – indirect agonist (anticholinesterase)

Clinical use: anticholinergic toxicity
-Crosses blood-brain barrier ? CNS

Action: ?ACh
“Physostigmine ‘phyxes’ atropine overdose.”


Cholinomimetic – indirect agonist (anticholinesterase)

Clinical use: myasthenia gravis (long acting)
-Does not penetrate CNS

Action: ?ACh; ?muscle strength
“Pyridostigmine gets rido of myasthenia gravis.”

Conditions aggravated by all cholinomimetic agents
asthma, COPD, peptic ulcers
Cholinesterase inhibitor poisoning

Organophosphates (ex: parathion) -; irreversible inhibition of AChE

*DUMBBELSS* – diarrhea, urination, miosis, bradycardia, bronchospasm, excitation of skeletal muscle and CNS, lacrimation, sweating, salivation

Reversed by atropine (competitive inhibitor) + pralidoxime (regenerates AChE if given early)

Atropine, homatropine, tropicamide

Muscarinic antagonists

Organ systems: eye

Clinical use: mydriasis and cycloplegia


Muscarinic antagonists

Organ systems: CNS

Clinical use: Parkinson, acute dystonia
“park my Benz”


Muscarinic antagonists

Organ system: GI, respiratory

Clinical use:
-Parenteral: prep use to reduce airway secretions
-Oral: drooling, peptic ulcer

Hyoscyamine, dicyclomine

Muscarinic antagonists

Organ system: GI

Clinical use: antispasmodics for irritable bowel syndrome

Oxybutynin, solifenacin, tolterodine

Muscarinic antagonists

Organ system: GU

Clinical use: overactive bladder


Muscarinic antagonists

Organ system: CNS

Clinical use: motion sickness


Muscarinic antagonist. Used to treat bradycardia and for ophthalmic applications.

Organ system effects:
-Blocks DUMBBeLSS (skeletal muscle and CNS excitation mediated by nicotinic receptors)
-Eye (?pupil dilation, cycloplegia), airway (?secretions), stomach (?acid secretion), gut (?motility), bladder (?urgency in cystitis)

Toxicity: ?body temp; rapid pulse; dry mouth; dry, flushed skin; cycloplegia; constipation; disorientation; urinary retention
-*Can cause acute angle-closure glaucoma in elderly (due to mydriasis)*

Jimson weed (Datura)
Gardener’s pupil due to mydriasis
Albuterol, salmeterol
Direct sympathomimetic
?2>?1Clinical use:
-Albuterol for acute asthma
-Salmeterol for long-term asthma or COPD

Direct sympathomimetic
?1>?2, ?Clinical use: HF (isotropy > chronotropic), cardiac stress testing

Direct sympathomimetic
D1=D2>?>?Clinical use: unstable bradycardia, HF, shock
-Inotropic and chronotropic ? effects predominate at high doses

Direct sympathomimetic
?>?Clinical use: anaphylaxis, asthma, open-angle glaucoma
-? effects predominate at high doses
-*Significantly stronger ?2 effects than NE*

Direct sympathomimetic
?1=?2Clinical use: electrophysiologic evaluation of tachyarrhythmias
-Can worsen ischemia

Direct sympathomimetic
?1>?2>?1Clinical use: hypotension (but ?renal perfusion)
-*Significantly weaker ?2 effects than epinephrine*

Direct sympathomimetic
?1>?2Clinical use: hypotension (vasoconstrictor), ocular procedures (mydriatic), rhinitis (decongestant)


Indirect sympathomimetic

Effect: Indirect general agonist, reuptake inhibitor, also releases stored catecholamines

Clinical use: narcolepsy, obesity, ADHD


Indirect sympathomimetic

Effect: Indirect general agonist, reuptake inhibitor

Clinical use: causes vasoconstriction and anesthesia
-*Never give ?-blockers if suspected cocaine intoxication b/c can lead to unopposed ?1 activation -> extreme hypertension*


Indirect sympathomimetic

Effect: Indirect general agonist, release stored catecholamines

Clinical use: nasal decongestion, urinary incontinence, hypotension


Sympatholytic (?2 agonist)

Clinical use: hypertensive urgency (does not decrease renal blood flow), ADHD, Tourette syndrome

Toxicity: CNS depression, bradycardia, hypotension, respiratory depression, miosis


Sympatholytic (?2 agonist)

Clinical use: hypertension in pregnancy

Toxicity: direct Coombs + hemolysis, SLE-like syndrome


?-blocker – nonselective, irreversible

Clinical use: pheochromocytoma (used preop to prevent hypertensive crisis)

Toxicity: orthostatic hypotension, reflex tachy


?-blocker – nonselective, reversible

Clinical use: give to pts on MAO inhibitors who eat tyramine-containing foods ? avoid hypertensive crisis

Toxicity: orthostatic hypotension, reflex tachy

Prazosin, terazosin, doxazosin, tamsulosin

?1 selective blocker

Clinical use: urinary symptoms of BPH; PTSD (prazosin); hypertension (except tamsulosin)

Toxicity: 1st-dose orthostatic hypotension, dizziness, headache


?2 selective blocker (also potent 5-HT2 and 5-HT3 receptor antagonist)

Clinical use: depression

Toxicity: sedation, ? serum cholesterol, ? appetite (weight gain-may help elderly/anorexic)

MOA: GnRH analogue
-Agonist properties when used in pulsatile fashion
-Antagonist when used in continuous fashion (down regulates GnRH receptor in pituitary ? ?FSH/LH)Clinical use: infertility (pulsatile), prostate CA (continuous use following androgen receptor blockade with *flutamide*), uterine fibroids (continuous), precocious puberty (continuous), endometriosis (continuous), dysfunctional uterine bleeding (continuous)

Toxicity: antiandrogen, nausea, vomiting

Estrogens (ethinyl estradiol, DES, mestranol)

MOA: bind estrogen receptors

Clinical use: hypogonadism or ovarian failure, menstrual abnormalities, hormone replacement
-Use in men with androgen-dependent prostate CA

Toxicity: ?risk of endometrial cancer, bleeding in postmenopausal women, ?risk of thrombi
-*Clear cell adenocarcinoma of vagina in females exposed to DES in utero*
-CI in ER+ breast cancer, history of DVTs

-Antagonist at estrogen receptors in hypothalamus ? prevent normal feedback inhibition and ?release of LH and FSH from pituitary ? ovulationClinical use: infertility due to anovulation (e.g., PCOS)

Toxicity: hot flashes, ovarian enlargement, *multiple simultaneous pregnancies*, visual disturbances

Hormone replacement therapy
-Used for relief or prevention of menopausal sx (e.g., hot flashes, vaginal atrophy), osteoporosis (?estrogen, ?osteoclast activity)
-**Unopposed estrogen replacement ?risk of endometrial cancer, so progesterone is added
-Possible increased cardiovascular risk

MOA: aromatase inhibitor

Clinical use: postmenopausal women with ER+ breast cancer


MOA: bind progesterone receptors, ?growth and ?vascularization of endometrium

Clinical use: oral contraceptives, endometrial cancer tx, abnormal uterine bleeding

Mifepristone (RU-486)

MOA: competitive inhibitor of progestins at progesterone receptors

Clinical use: termination of pregnancy
-Administered with *misoprostol (PGE1)* ? cervical ripening and uterine contractions

Oral contraception (synethetic progestins, estrogen)
-Estrogen and progestins inhibit LH/FSH ? no estrogen surge ? no LH surge ? no ovulation
-Progestins cause thickening of cervical mucus
-Progestins also inhibit endometrial proliferation ? endometrium less suitable for embryo implantation-CI: smokers >35 y/o (?risk of CV events), hx of thromboembolism and stroke, hx of estrogen-dependent tumor

Terbutaline, ritodrine (tocolytics)

MOA: ?2 agonists that relax the uterus

Clinical use: ?contraction frequency in women during labor; prevent preterm labor


MOA: synthetic androgen that acts as a partial agonist at androgen receptors

Clinical use: endometriosis, hereditary angioedema

Toxicity: weight gain, edema, acne, hirsutism, masculinization, ?HDL, hepatoxicity

Testosterone, methyltestosterone

MOA: agonists at androgen receptors

Clinical use: hypogonadism; development of 2° sex characteristics; stimulation of anabolism to promote recovery after burn or injury

-Masculinization in females
-?intratesticular testosterone in males by inhibiting release of LH (via negative feedback) ? gonadal atrophy
-Premature closure of epiphyseal plates


MOA: 5?-reductase inhibitor (?conversion of testosterone to DHT)

Clinical use: BPH, male-pattern baldness

Flutamide, cyproterone

MOA: competitive inhibitor androgen receptors

Clinical use: prostate CA


MOA: inhibits steroid synthesis (inhibits 17,20-desmolase)

Clinical use: reduce androgenic symptoms in PCOS

Toxicity: gynecomastia, amenorrhea


MOA: inhibits steroid binding, 17?-hydroxylase, and 17, 20-desmolase

Clinical use: reduce androgenic symptoms in PCOS

Toxicity: gynecomastia, amenorrhea

Azathioprine, 6-mercaptuptopurine (6-MP), 6-thioguanine (6-TG)
Cladribine (2-CDA)
Cytarabine (arabinofuranosyl cytidine)
5-fluorouracil (5-FU)
Methotrexate (MTX)
Azathioprine, 6-mercaptopurine (6-MP), 6-thioguanine (6-TG)
MOA: *Purine analog -> dec de novo purine synthesis*
Activated by HGPRT. Azathioprine is metabolized into 6-MP.Use: Prevent organ rejection, rheumatoid arthritis, IBD, SLE; wean pts off steroids in chronic disease and to treat steroid-refractory dz

Tox: Myelosuppression, GI, liver. Azathioprine and 6-MP metabolized by xanthine oxidase -> inc toxicity with allopurinol or febuxostat (rx tumor lysis syndrome)

Increase toxicity with allopurinol or febuxostat
Azathioprine, 6-MP, 6-TG
Cladribine (2-CDA)

MOA: *Purine analog -> multiple mech* (e.g., inhibition of DNA poly, DNA strand breaks)

Clinical use: *hairy cell leukemia*

Tox: Myelosuppression, nephrotoxicity, neurotoxicity

Cytarabine (arabinofuranoysl cytidine)

MOA: *Pyrimidine analog* -> inhibition of DNA polymerase

Clinical use: Leukemia (AML), lymphoma

Tox: Leukopenia, thrombocytopenia, megaloblastic anemia
CYTarabine causes panCYTopenia

5-fluorouracil (5-FU)

MOA: Pyrimidine analog bioactivated to 5F-dUMP -> forms complex with folic acid -> *inhibits thymidylate synthase* -> dec dTMP -> dec DNA synthesis

Use: Colon cancer, pancreatic cancer, basal cell carcinoma (topial)

Tox: Myelosuppression (NOT reversible with leucovorin)

Methotrexate (MTX)

MOA: Folic acid analog that competitively *inhibits dihydrofolate reductase* -> dec dTMP -> dec DNA synthesis

Cancers: luekemias (ALL), lymphomas, *choriocarcinoma*, sarcomas.
Non-neooplastic: *ectopic pregnancy*, *medical abortion* (with misoprostol), rheumatoid arthritis, psoriasis, IBD, vasculitis

Tox: Myelosuppression (reversible with *leucovorin rescue*), hepatoxicity, mucositis, *pulmonary fibrosis*

Myelosuppression reversible with leucovorin
*Antitumor antibiotics*
Dactinomycin (actinomycin D)
Anthracyclines: doxorubicin, daunorubicin

MOA: *Free radical formation -> DNA strand breaks*

Use: Testicular cancer, Hodgkin lymphoma

Tox: *Pulmonary fibrosis*, skin hyper pigmentation, mucositis. *Minimal myelosuppression*

Dactinomycin (actinomycin D)

MOA: *Intercalates in DNA*

Use: *Childhood tumors* such as Wilms tumor, Ewing sarcoma, rhabdomyosarcoma
(“children *act* out”)

Tox: Myelosuppression

Give ____ to prevent cardiotoxicity of doxorubicin/daunorubicin.
Anthracyclines: doxorubicin, daunorubicin
MOA: *Free radical formation*.
*Intercalate in DNA* -> breaks in DNA -> dec replicationUse: Solid tumors, leukemias, lymphomas

Tox: *Cardiotoxicity* (dilated cardiomyopathy). *Dexrazoxane* (iron chelating agent), used to prevent cardiotoxicity.
*Extravasation* -> redness, necrosis. Do NOT give IM/SC.
Myelosuppression, alopecia.

*Alkylating agents*
Cyclophosphamide, ifosfamide
Nitrosoureas (carmustine, lomustine, semustine, streptozocin)

MOA: *Cross-links* DNA

Use: CML. Also used to ablate bone marrow before bone marrow transplant.

Tox: *Severe myelosuppression* (in almost all cases), *pulmonary fibrosis*, hyper pigmentation

Cyclophosphamide, ifosfamide

MOA: *Cross-link DNA* at guanine N-7. Require bioactivation by liver.

Use: Solid tumors, leukemia, lymphomas

Tox: Myelosuppression; *hemorrhagic cystitis*, partially prevented with *mesna* (binds toxic metabolites-acrolein)

Give _____ to avoid hemorrhage cystitis with cyclophosphamide.
Mesna (binds toxic metabolites)
(carmustine, lomustine, semustine, streptozocin)
MOA: *Cross-link DNA*
*Cross blood-brain barrier -> CNS*
Require bioactivation.Use: *Brain tumors* (including glioblastoma multiform)

Tox: CNS (convulsions, dizziness, ataxia)

*Microtubule inhibitors*
Paclitaxel, other taxols
Vinca alkaloids: vincristine, vinblastine
Paclitaxel, other taxols
MOA: *Hyperstabilize polymerized microtubules* in M phase -> mitotic spindle can’t break down -; anaphase can’t occur
“It is *tax*ing to stay polymerized.”Use: *Ovarian* and *breast* carcinomas

Tox: Myelosuppression, alopecia, hypersensitivity

Vinca alkaloids: vincristine, vinblastine

MOA: Bind beta-tubulin and *inhibit polymerization* into microtubules -> prevent mitotic spindle formation (M-phase arrest)

Use: Solid tumors, leukemias, Hodgkin (vinblastine) and non-Hodgkin (vincristine) lymphomas

Vincristine: *neurotoxicity* (areflexia, peripheral neuritis, paralytic ileus)
Vinblastine: bone marrow suppression. Vin*blast*ine *blasts* *b*one marrow.

Cisplatin, carboplatin

MOA: *Cross-link DNA*

Use: Testicular, bladder, ovary, and lung carcinomas

*Nephrotoxicity* – prevent with *amifostine* (free radical scavenger) and chloride (saline) diuresis.

Prevention of cisplatin/carboplatin related nephrotoxicity? (2 steps)
1) Amifostine (free radical scavenger)
2) Chloride (saline) diuresis
Etoposide, teniposide

MOA: *Inhibits topoisomerase II* -> inc DNA degradation

Use: Solid tumors (particularly testicular and small cell lunger cancer), leukemias, lymphomas

Tox: Myelosuppression, GI upset, alopecia

Irinotecan, topotecan

MOA: *Inhibit topoisomerase I” -> prevent DNA unwinding and replication

Use: Colon cancer (irinotecan); ovarian and small cell lunger cancers (topotecan)

Tox: Severe myelosuppression, diarrhea


MOA: *Inhibits ribonucleotide reductase* -> dec DNA synthesis (S-phase specific)

Use: Melanoma, CML, *sickle cell disease (inc HbF)*

Tox: Severe myelosuppression, GI upset

Prednisone, predinosolone

MOA: Various; bind intracytoplasmic receptor -> alter gene transcription

Use: Used in CLL, non-Hodgkin lymphoma (part of combination chemotherapy regimen).
Also used as immunosuppressants (e.g., in autoimmune disease)

Tox: *Cushing-like sx*; weight gain, central obesity, muscle breakdown, cataracts, acne, osteoporosis, hypertension, peptic ulcers, hyperglycemia, psychosis


MOA: Monoclonal Ab against *VEGF* -> inhibit angiogenesis

Use: Solid tumors (colorectal cancers, renal cell carcinoma)

Tox: Hemorrhage, blood clots, and impaired wound healing


MOA: EGFR tyrosine kinase inhibitor

Use: *Non-small cell lung carcinoma*

Tox: Rash


MOA: *Tyrosine kinase inhibitor of BCR-ABL* (Philadelphia chr fusion gene in *CML*) and *c-kit* (*GI stromal tumors*)

Use: *CML, GI stromal tumors*

Tox: Fluid retention


MOA: Monoclonal Ab against *CD20*, which is found on most *B cell neoplasms*

Use: Non-Hodgin lymphoma, CLL, IBD, rheumatoid arthritis

Tox: inc risk of *progressive multifocal leukoencephalopathy*

Tamoxifen, raloxifene

MOA: SERM – receptor *agonists in breast* and *agonists in bone*. Block the binding of estrogen to ER+ cells.

Use: Breast cancer tx (tamoxifen only) and prevention.
Raloxifene used to prevent osteoporosis.

Tamoxifen – partial *agonist* in endometrium -> *inc risk endometrial cancer*; hot flashes
Raloxifene – *antagonist* in endometrium -> no risk of endometrial cancer

Trastuzumab (Herceptin)

MOA: Monoclonal Ab against *HER-2, a tyrosine kinase receptor*. Helps kills cancer cells that *overexpress HER-2* thru inhibition of HER2-initiated cellular signaling and Ab-mediated cytotoxicity.

Use: *HER2+ breast cancer and gastric cancer*

Tox: *Cardiotoxicity*. “*Heart*ceptin” damages the *heart*.


MOA: Small molecular inhibitor of *BRAF oncogene+ melanoma*

Use: Metastatic melanoma

Common chemotoxicities
Cisplatin/Carboplatin tox
nephrotoxic and acoustic nerve damage
Vincristine tox
peripheral neuropathy
Bleomycin, Busulfan tox
pulmonary fibrosis
Trastuzumab tox
Cyclophosphamide tox
hemorrhagic cystitis
MOA: Decrease thymidine synthesis
MOA: Decrease de novo purine synthesis
MOA: Cross-link DNA
Alkylating agents
MOA: DNA strand breakage
MOA: DNA intercalators
MOA: Inhibit topoisomerase II
Etoposide, teniposide
MOA: Inhibit topoisomerase I
Irinotecan, topotecan
MOA: Inhibit microtubule formation
Vinca alkaloids: vinblastine, vincristine
MOA: Inhibit microtubule breakdown
Paclitaxel, other taxols
Diuretics: site of action
Diuretics: site of action

MOA: Osmotic diuretic. Increased tubular fluid osmolarity -> increased urine flow, decreased intracranial/intraocular pressure.

Clinical Use: Drug overdose, elevated intracranial/intraocular pressure.

Toxicity: Pulmonary edema, dehydration. Contraindicated in anuria, HF.


MOA: Carbonic anhydrase inhibitor. Causes self-limited NaHCO3 diuresis and decreased total body HCO3- stores.

Clinical Use: Glaucoma, altitude sickness, metabolic alkalosis, urinary alkalization, pseudo tumor cerbri.

Toxicity: Hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity (in acidosis, compensatory NH3 production by PCT cells), sulfa allergy.

Loop diuretics: furosemide, bumetanide, torsemide

MOA: Sulfonamide loop diuretics. Inhibit cotransport system (Na+/K+/2Cl-) of thick ascending limb of loop of Henle. Abolish hypertonicity of medulla, preventing concentration of urine. Stimulate PGE release (vasodilatory effect on afferent arteriole); inhibited by NSAIDs. Increase Ca2+ excretion.

Clinical Use: Edematous states (HF, cirrhosis, nephrotic syndrome, pulmonary edema), HTN, hypercalcemia.

Toxicity: Ototoxicity, Hypokalemia, Dehydration, Allergy (sulfa), Nephritis (interstitial), Gout

Loop diuretics: ethnacrynic acid

MOA: Phenoxyacetic acid derivative (not a sulfonamide). Essentially same action as furosemide.

Clinical Use: Diuresis in pts allergic to sulfa drugs.

Toxicity: Similar to furosemide; can cause hyperuricemia; never use to treat gout.

Thiazide diuretics

Chlorthalidone, hydrochlorothiazide

MOA: Inhibit NaCl reabsorption in early DCT -> increased diluting capacity of nephron. Decrease Ca2+ excretion.

Clinical Use: HTN, HF, idiopathic hypercalciuria, nephrogenic diabetes insipidus, osteoporosis.

Toxicity: Hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia, HyperLipidemia, hyperUricemia, hyperCalcemia. Sulfa allergy.


K+-sparing diuretics

Spironolactone and eplerenone; triameterene and amiloride

Mechanism: Spironolactone and epleronone are competitive aldosterone receptor antagonists in cortical collecting tubule. Triamterene and amiloride act at same part of the tubule by blocking Na+ channels in the cortical collecting tubule.

Clinical Use: Hyperaldosteronism, K+ depletion, HF.

Toxicity: Hyperkalemia (can lead to arrhythmias), endocrine effects with spironolactone (e.g., gynecomastia, anti androgen effects)

Urine NaCl changes with diuretics
Increase with all diuretics except acetazolamide. Serum NaCl may decrease as a result.
Urine K+ changes with diuretics
Increase with loop and thiazide diuretics. Serum K+ may decrease as a result.
Blood pH changes with diuretics

Decreases (academia): Carbonic anhydrase inhibitors: decreased HCO3- absorption. K+ sparing: aldosterone blockade prevents K+ secretion and H+ secretion. Additionally, hyperkalemia leads to K+ entering all cells (via H+/K+ exchanger) in exchange for H+ exiting cells.

Increases (alkalemia): loop diuretics and thiazdides cause alkalemia through:
1) Volume contraction -> Increased ATII -> Increased Na+/H+ exchange in PCT -> Increased HCO3- reabsorption (“contraction alkalosis”)
2) K+ loss leads to K+ exiting all cells (via H+/K+ exchange) in exchange for H+ entering cells
3) In low K+ state, H+ (rather than K+) is exchanged for Na+ in cortical collecting tubule -> alkalosis and “paradoxical aciduria”

Urine Ca2+ changes with diuretics

Increase with loop diuretics: decreased paracellular Ca2+ reabsorption -> hypocalcemia.

Decreased with thiazides: enhanced Ca2+ reabsorption in DCT.

ACE inhibitors

Captopril, enalapril, lisinopril, ramipril

MOA: Inhibit ACE -> Decreased ATII -> Decreased GFR by inhibiting constriction of efferent arterioles. Levels of renin increases as a result of loss of feedback inhibition. Inhibition of ACE also prevents inactivation of bradykinin, a potent vasodilator.

Clinical Use: HTN, HF, proteinuria, diabetic nephropathy. Prevent unfavorable heart remodeling as a result of chronic HTN.

Toxicity: Cough, Angioedema (contraindicated in C1 esterase inhibitor deficiency), Teratogen (fetal renal malformation), increased Creatinine (decreased GFR), Hyperkalemia, and Hypotension. Avoid in bilateral renal artery stenosis because ACE inhibitors will further decrease GFR -> renal failure.

Captopril’s CATCHH

Angiotensin II receptor blockers

Losartan, candesartan, valsartan

MOA: Selectively block binding of angiotensin II to AT1 receptor. Effects similar to ACE inhibitors, but ARBs do NOT increase bradykinin.

Clinical Use: HTN, HF, proteinuria, or diabetic nephropathy with intolerance to ACE inhibitors (e.g., cough, angioedema)

Toxicity: Hyperkalemia, decreased renal function, hypotension, teratogen.


MOA: Direct renin inhibitor, blocks conversion of angiotensinogen to angiotensin I.

Clinical Use: HTN

Toxicity: Hyperkalemia, decreased renal function, hypotension. Contraindicated in diabetics taking ACE inhibitors or ARBs.

TNF-alpha inhibitor (fusion protein, aka decoy receptor used for RA,Psoriasis, ankylosing spondylitis

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