question

Antibiotics that block cell wall synthesis by inhibition of peptidoglycan CROSS-LINKING

answer

Beta lactams. Penicillin, methicillin, ampicillin, piperacillin, cephalosporins, aztreonam, imipenem

question

Antibiotics that block peptidoglycan SYNTHESIS

answer

bacitracin, vancomycin

question

Antibiotics that block nucleotide synthesis by inhibiting folic acid synthesis

answer

sulfonamides, trimethoprim

question

Antibiotics that block DNA topoisomerases

answer

Fluroquinolones

question

Antibiotics that block mRNA synthesis

answer

Rifampin

question

Antibiotics that damage DNA

answer

Metronidazole

question

Antibiotics that block protein synthesis at the 50S ribosomal subunit

answer

Chloramphenicol, clindamycin, erythromycin (and other macrolides), linezolid, streptogramins (quinupristin, dalfopristin)

question

Antibiotics that block protein synthesis at the 30S ribosomal subunit

answer

Aminoglycosides (gentamicin, neomycin, amikacin, tobramycin, streptomycin) and tetracyclins

question

Penicillin G is the ____ form; Pencillin V is the ___ form

answer

Pen G = IV/IM Pen V = oral

question

Penicillin

answer

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

question

Oxacillin, nafcillin, dicloxacillin

answer

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

question

Ampicillin, amoxicillin

answer

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

question

Ampicillin and amoxicillin HELPSS kill enterococci

answer

H. influenzae, E. coli, L. monocytogenes, Proteus mirabilis, Salmonella, Shigella, enterococci (extended spectrum penicillins)

question

Ticarcillin, piperacillin

answer

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)

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Beta lactamase inhibitors: CAST

answer

Clavulanic Acid, Sulbactam, Tazobactam Add to aminopenicillins and antipseudomonals

question

Cefazolin, cephalexin

answer

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

question

Cefoxitin, cefaclor, cefuroxime

answer

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

question

Ceftriaxone, cefotaxime, ceftazidime

answer

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

question

Cefepime

answer

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

question

Ceftaroline

answer

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

question

Organisms not typically covered by cephalosporins are LAME

answer

Listeria, Atypicals (chlamydia, mycoplasma), MRSA, and Enterococci

question

Aztreonam

answer

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

question

Imipenem/cilastatin, meropenem, ertapenem, doripenem

answer

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

question

Vancomycin

answer

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")

question

Gentamicin, neomycin, amikacin, tobramycin, streptomycin, spectinomycin

answer

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

question

"Mean" GNATSS caNNOT kill anaerobes

answer

aMINoglycosides: Gentamicin, Neomycin, Amikacin, Streptomycin, Spectinomycin; Nephrotoxic, Neuromuscular blockade, Ototoxic, Teratogenic; can't kill anaerobes because require O2 for uptake into the cell

question

Tetracycline, minocycline, doxycycline

answer

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

question

Demeclocyline

answer

Antibiotic of the tetracycline family, but rarely used as an antibiotic. Has ADH antagonist properties, so used as a diuretic in SIADH.

question

Azithromycin, clarithromycin, erythromycin

answer

(Macrolides) MOA: binds to the 23S rRNA of the 50s ribosomal subunit to inhibit protein synthesis by blocking translocation Clinical 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

question

Chloramphenicol

answer

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

question

Clindamycin

answer

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

question

Sulfonamides

answer

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

question

Trimethoprim

answer

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)

question

Fluroquinolones

answer

(Ie ciprofloxacin) MOA: inhibits DNA gyrase (topo II) and topo IV Clinical 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

question

Daptomycin

answer

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)

question

Metronidazole

answer

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

question

Isoniazid

answer

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

question

Rifampin

answer

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

question

Pyrazinamide

answer

MOA: acidifies environment of phagolysosomes of macrophages that have engulfed TB Clinical use: TB Toxicity: hyperuricemia, hepatotoxicty

question

Ethambutol

answer

MOA: inhibits carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase Clinical use: TB Toxicity: red-green colorblindness/optic neuritis (CI in kids <6yo) "Eyethambutol"

question

Amphotericin B

answer

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

question

Nystatin

answer

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

question

Azoles

answer

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

question

Fluconazole

answer

Clinical use: chronic suppression of cryptococcal meningitis in AIDS patients, candida infxns of all types

question

Itraconazole

answer

Clinical use: blastomycoses, coccidioides, histoplasma (the systemic mycoses)

question

Clotrimazole/Miconazole

answer

Clinical use: topical fungal infections

question

Flucytosine

answer

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)

question

Caspofungin, micafungin

answer

MOA: inhibits cell wall synthesis by inhibiting synthesis of B-glucan Clinical use: invasive aspergillosis, candida Toxicity: flushing due to histamine release

question

Terbinafine

answer

MOA: inhibits fungal squalene epoxidase ? inhibit production of lanosterol Clinical use: dermatophytoses (esp onchomycosis) Toxicity: abnormal LFTs, visual disturbances

question

Griseofulvin

answer

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

question

Chloroquine

answer

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

question

Treatment for P. falciparum

answer

Use combo of artemether/lumifantrine or atovaquone/proguanil

question

Quinidine, artesunate

answer

Clinical use: life threatening malaria

question

Pyrimethamine

answer

Clinical use: toxoplamosis (often with sulfadiazine)

question

Suramin/melarsoprol

answer

Clinical use: trypanosoma brucei (African sleeping sickness); suramin for blood-borne disease or melarsoprol for CNS penetration

question

Nifurtimox

answer

Clinical use: trypanosoma cruzi (Chagas)

question

Sodium stibogluconate

answer

Clinical use: leishmaniasis

question

Mebendazole, albendazole

answer

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

question

Pyrantel pamoate

answer

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)

question

Ivermectin

answer

MOA: enhances inhibitory neurotransmission by opening glutamate gated chloride channels Clinical use: primarily for Onchocerca volvulus (IVERmectin for rIVER blindness), also strongyloides

question

Diethylcarbamazine

answer

MOA: inhibitor of arachidonic acid metabolism in filarial microfilaria Clinical use: Loa loa, Wuchereria bancrofti (elephantiasis)

question

Praziquantel

answer

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

question

Zanamivir, oseltamivir

answer

MOA: inhibits influenza neuraminidase (decreasing release of new viruses) Clinical use: treatment and prevention of influenza A AND B

question

Ribavirin

answer

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

question

Acyclovir, famciclovir, valacyclovir

answer

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

question

Ganciclovir, valganciclovir

answer

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

question

Foscarnet

answer

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

question

Cidofovir

answer

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

question

Protease inhibitors

answer

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

question

NRTIs

answer

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

question

NNRTIs

answer

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

question

Raltegravir

answer

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

question

Enfuvirtide

answer

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

question

Maraviroc

answer

Fusion inhibitor MOA: bindins CCR-5 on surface of T cells/monocytes, inhibiting interaction with gp120

question

INFs

answer

?- 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

question

Simeprevir

answer

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

question

Sofosbuvir

answer

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

question

Antibiotics to avoid in pregnancy-- SAFe Children Take Really Good Care

answer

Sulfonamides --> kernicterus Aminoglycosides --> ototoxicity Fluoroquinolones --> cartilage Clarithromycin --> embryotoxic Tetracylines --> discolored teeth, inhibits bone growth Ribavirin --> teratogenic Griseofulvin --> teratogenic Chloramphenicol --> gray baby

question

Cyclosporine

answer

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.

question

Tacrolimus (FK-506)

answer

MOA: Calcineurin inhibitor; binds *FK506 binding protein (FKBP*). Blocks T cell activation by preventing IL-2 transcription. 10x more potent than cyclosporine Clinical use: transplant rejection prophylaxis, topical (eczema) Toxicity: similar to cyclosporine, ? risk of diabetes and neurotoxicity, also pleural effusion; no gingival hyperplasia or hirsutism

question

Sirolimus (rapamycin)

answer

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*

question

Daclizumab, basiliximab

answer

MOA: monoclonal antibodies; block IL-2R Clinical use: kidney transplant rejection prophylaxis Toxicity: edema, HTN, tremor

question

Azathioprine

answer

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

question

Muromonab-CD3 (OKT3)

answer

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

question

Aldesleukin (IL-2)

answer

Clinical use: renal cell carcinoma, metastatic melanoma

question

Epoetin alfa (erythropoietin)

answer

Clinical use: anemias (esp renal failure)

question

Filgrastim

answer

Granulocyte colony stimulating factor Clinical use: bone marrow recovery

question

Sargramostim

answer

Granulocyte/macrophage colony stimulating factor Clinical use: bone marrow recovery

question

Romiplostim, eltrombopag

answer

Thrombopoietin Clinical use: thrombocytopenia

question

Oprelvekin (IL-11)

answer

Clinical use: thrombocytopenia

question

Infliximab, adalimumab

answer

MOA: TNF ? inhibtors Clinical use: IBD, RA, ankylosing spondylitis, psoriasis

question

Abciximab

answer

MOA: inhibits Gp IIb/IIIa Clinical use: anti platelet for prevention of ischemic complications in pts undergoing PCI

question

Trastazumab

answer

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

question

Rituximab

answer

MOA: targets CD20 Clinical use: B cell non-Hodgkin's lymphoma, CLL, RA, ITP

question

Omalizumab

answer

MOA: targets IgE Clinical use: additional treatment for severe asthma

question

Alemtuzumab

answer

MOA: targets CD52 Clinical use: CLL ("Alymtuzumab")

question

Bevacizumab

answer

MOA: targets VEGF Clinical use: colorectal cancer, renal cell carcinoma

question

Cetuximab

answer

MOA: targets EGFR Clinical use: stage IV colorectal cancer, head and neck cancer

question

Eculizumab

answer

MOA: targets complement protein C5 Clinical use: paroxysmal nocturnal hemoglinuria

question

Natalizumab

answer

MOA: targets ?4-integrin Clinical use: MS, Crohn disease

question

Denosumab

answer

MOA: targets RANKL Clinical use: osteoporosis (inhibits osteoclast maturation)

question

Digoxin immune Fab

answer

MOA: targets digoxin Clinical use: antidote for digoxin toxicity

question

Palivizumab

answer

MOA: targets RSV F protein Clinical use: RSV prophylaxis for high-risk infants

question

Ranibizumab, bevacizumab

answer

MOA: targets VEGF Clinical use: neovascular age-related macular degeneration

question

Insulin

answer

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

question

Insulin, rapid acting

answer

Aspart, glulisine, lispro

question

Insulin, short acting

answer

Regular

question

Insulin, intermediate acting

answer

NPH

question

Insulin, long acting

answer

Detemir, glargine

question

Metformin

answer

(Biguanide) 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

question

Tolbutamide, Chlorpropamide

answer

1st generation sulfonylureas MOA: close K+ channels in ? cell membrane, cell depolarizes ? Ca2+ influx ? insulin release Clinical use: stimulate release of endogenous insulin in type 2 DM (useless in type 1) Toxicities: disulfiram like effects

question

Glyburide, Glimepiride, Glipizide

answer

2nd generation sulfonylureas MOA: close K+ channels in ? cell membrane, cell depolarizes ? Ca2+ influx ? insulin release Clinical use: stimulate release of endogenous insulin in type 2 DM (useless in type 1) Toxicities: hypoglycemia favors lipogenesis (weight gain)

question

Pioglitazone, Rosiglitazone

answer

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)

question

Acarbose, Miglitol

answer

?-glucosidase inhibitors MOA: inhibition at intestinal brush border delays sugar hydrolysis and glucose absorption ? ? postprandial hyperglycemia Clinical use: monotherapy in type 2 DM or w/ other diabetes drugs Toxicities: GI upset

question

Pramlintide

answer

Amylin analog MOA: ?gastric emptying, ? glucagon Clinical use: type 1 AND 2 DM (with insulin only) Toxicities: hypoglycemia, nausea, diarrhea

question

Exenatide, liraglutide

answer

GLP-1 analogs MOA: ? insulin, ? glucagon release Clinical use: type 2 DM Toxicities: N/V, pancreatitis

question

Exenitide, liraglutide

answer

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

question

Canagliflozin

answer

SGLT-2 inhibitors (sodium glucose cotransporter 2) MOA: block reabsorption of glucose in PCT Clinical use: type 2 DM Toxicities: glucosuria, UTIs, vaginal yeast infections, hypotension CI in renal impairment (obviously!)

question

Linagliptin, saxagliptin, sitagliptin

answer

DPP-4 inhibitors (DPP-4 inhibits GLP-1) MOA: ? insulin, ? glucagon release (activates incretins) Clinical use: type 2 DM Toxicities: mild UTI/URI

question

Propylthiouracil, methimazole

answer

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)

question

Levothyroxine, triiodothyronine

answer

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

question

Ocreotide

answer

MOA: long acting somatostatin analog Clinical use: acromegaly, carcinoid, gastrinoma, glucagonoma, acute variceal bleeds Toxicity: steatorrhea

question

Oxytocin

answer

Clinical use: stimulates labor, uterine contractions, milk let down; controls uterine hemorrhage

question

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

answer

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.

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Cinalcet

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MOA: sensitizes Ca2+ sensing receptor (CaSR) in parathyroid gland to circulating Ca2+ ? ? PTH Clinical use: hypercalcemia due to 1° or 2° hyperparathyroidism Toxicity: hypocalcemia

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Cimetidine, ranitidine, famotidine, nizatidine

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H? blockers (take H? blockers before you "dine") MOA: REVERSIBLY block histamine H? receptors ? ? H+ secretion by parietal cells Clinical 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

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Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole

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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

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Bismuth, sucralfate

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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

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Misoprostol

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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)

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Aluminum hydroxide

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Clinical use: antacid Toxicity: hypokalemia (all antacids), constipation ("aluminimum" amount of feces), hypophosphatemia, proximal muscle weakness, osteodystrophy, seizures

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Magnesium hydroxide

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Clinical use: antacid Toxicity: hypokalemia (all antacids), diarrhea -hyporeflexia, hypotension, cardiac arrest (hypermagnesemia toxicities)

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Calcium carbonate

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

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Magnesium hydroxide, magnesium citrate, polyethylene glycol, lactulose

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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

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Sulfasalazine

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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

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Ondansetron

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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

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Metoclopramide

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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

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Orlistat

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MOA: inhibits gastric and pancreatic lipase ? ?breakdown and absorption of dietary fats Clinical use: weight loss Toxicity: steatorrhea, ?absorption of fat-soluble vitamins

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Heparin

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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

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Protamine sulfate

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Clinical use: rapid reversal of heparin toxicity (positively charged molecule binds negatively charged heparin)

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Enoxaparin, dalteparin, fondaparinux

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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

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Lepirudin, bivalirudin, argatroban, dabigatran

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MOA: derivatives of hirudin, the anticoagulant used by leeches- inhibits thrombin Clinical use: alternative for heparin in patients w/ HIT

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Warfarin

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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

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Reversal of warfarin toxicity?

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1) Vitamin K 2) Fresh frozen plasma for rapid reversal

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Apixaban, rivaroxaban

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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)

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

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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)

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Aminocaproic acid

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MOA: inhibitor of fibrinolysis Clinical use: treatment of tPA toxicity

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Aspirin

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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

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Clopidogrel, ticlopidine, prasugrel, ticagrelor

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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)

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Cilostazol, dipyridamole

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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

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Abciximab, eptifibatide, tirofiban

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MOA: bind the glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation Clinical use: acute coronary syndrome, percutaneous transluminal coronary angioplasty Toxicity: bleeding, thrombocytopenia

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Ibuprofen, naproxen, indomethacin, diclofenac, ketorolac

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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)

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Celecoxib

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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

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Acetaminophen

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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)

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Alendronate (other -dronates)

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(Bisphosphonates) MOA: pyrophosphate analogs, bind hydroxyapatite in bone, inducing apoptosis in osteoclasts Clinical 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

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Teriparatide

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MOA: recombinant PTH analog given subQ, ? osteoblastic activity Clinical use: osteoporosis, causes ? bone growth compared to antiresorptive therapies (e.g., bisphosphonates) Toxicity: transient hypercalcemia

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Drugs for acute gout

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1st line NSAIDS - naproxen, indomethacin Glucocorticoids Colchicine

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Drugs for chronic gout

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Allopurinol, febuxostat Pegloticase Probenecid

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Allopurinol

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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)

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Febuxostat

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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

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Pegloticase

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

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Colchicine

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MOA: binds and stabilizes tubulin to inhibit microtubule polymerization, impairing neutrophil chemotaxis and degranulation Clinical use: acute and prophylactic value in gout Toxicity: GI

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Probenecid

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MOA: inhibition of uric acid reabsorption in proximal collecting tubule, also inhibits secretion of penicillin Clinical use: chronic gout, syphilis Toxicity: uric acid calculi

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Glaucoma drugs

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? 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

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Morphine, fentanyl, codeine, heroin, meperidine

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(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 P Clinical use: pain, acute pulmonary edema Toxicity: addiction, respiratory depression, constipation, miosis, additive CNS depression w/ other drugs; treat toxicity with naloxone or naltrexone

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Dextromethorphan

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MOA: opioid receptor agonist Clinical use: cough suppression

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Diphenoxylate, loperamide

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MOA: opioid receptor agonists ? ? GI motility Clinical use: diarrhea

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Methadone

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MOA: opioid receptor agonist Clinical use: maintenance programs for opiate addicts

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Butorphanol

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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

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Tramadol

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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

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Phenytoin

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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)

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Carbamazepine

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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

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Lamotrigine

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MOA: blocks voltage gates Na+ channels Clinical use: simple/complex partial seizures, tonic-clonic seizures Toxicity: stevens-johnson syndrome

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Gabapentin

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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

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Topiramate

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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

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Phenobarbital

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MOA: ? GABA(A) action Clinical use: simple/complex partial seizures, tonic-clonic seizures **1st line in children** Toxicity: induction of p450, sedation, tolerance, dependence

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Valproic acid

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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

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Ethosuximide

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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)

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Diazepam/Lorazepam

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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

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Tiagabine

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MOA: inhibits GABA uptake Clinical use: simple/complex partial seizures

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Vigabatrin

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MOA: IRREVERSIBLY inhibits GABA transaminase ? ? GABA Clinical use: simple/complex partial seizures

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Phenobarbital, pentobarbital, thiopental, secobarbital

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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)

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Alprazolam, triazolam, oxazepam, midazolam

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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

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Flumazenil

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MOA: competitive antagonist at GABA benzodiazepine receptor Clinical use: reversal of benzodiazepine and zolpidem/zaleplon/eszopiclone (nonbenzodiazepine hypnotics)

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Zolpidem, zaleplon, eszopiclone

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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

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Halothane

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MOA: inhaled anesthetic Effects: myocardial/respiratory depression, nausea/emesis, ? cerebral blood flow (? cerebral metabolic demand) Toxicity: **hepatotoxicity**, malignant hyperthermia

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Enflurane

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MOA: inhaled anesthetic Effects: myocardial/respiratory depression, nausea/emesis, ? cerebral blood flow (? cerebral metabolic demand) Toxicity: **proconvulsant**, malignant hyperthermia

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Methoxyflurane

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MOA: inhaled anesthetic Effects: myocardial/respiratory depression, nausea/emesis, ? cerebral blood flow (? cerebral metabolic demand) Toxicity: **nephrotoxicity**, malignant hyperthermia

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Nitrous oxide

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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)

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Isoflurane, sevoflurane

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MOA: inhaled anesthetics Effects: myocardial/respiratory depression, nausea/emesis, ? cerebral blood flow (? cerebral metabolic demand) Toxicity: malignant hyperthermia

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Ketamine

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MOA: PCP analog that blocks NMDA receptors; cardiovascular stimulant; dissociative anesthetic, hallucination and bad dreams Clinical use: IV anesthetic Toxicity: disorientation, hallucinations, bad dreams

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Propofol

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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

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Procaine, cocaine, tetracaine

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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)

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Lidocaine, mepivacaine, bupivacaine

answer

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

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Local anesthetics principles

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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

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Succinylcholine

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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

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Reversal of succinycholine

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-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)

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Tubocurarine

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MOA: NONDEPOLARIZING neuromuscular blocking drug; competes w/ ACh for receptors Reversal of blockade: neostigmine, edrophonium, other cholinesterase inhibitors

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Dantrolene

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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

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Bromocriptine, pramipexole, ropinirole

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MOA: dopamine agonists Bromo (ergot), pramipexole (kidney elim)/ropinerole(liver elim) (non-ergot) preferred Clinical use: Parkinson's disease (when they still have endogenous DA)

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Amantadine

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MOA: may increase dopamine release Clinical use: Parkinson's disease; also used as an antiviral against influenza A and rubella Toxicity: ataxia, livedo reticularis

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Levodopa/carbidopa

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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 effects Clinical 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.

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Selegiline

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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 entacapone/tolcapone- COMT inhibitors also used to decrease breakdown

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Memantine

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MOA: NMDA receptor antagonist, helps prevent excitotoxicity (mediated by Ca2+) Clinical use: Alzheimer's Toxicity: dizziness, confusion, hallucinations

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Donepezil, galantamine, rivastigmine

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MOA: acetylcholinesterase inhibtors Clinical use: Alzheimer's Toxicity: nausea, dizziness, insomnia

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Sumatriptan

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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)

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Tetrabenazine, reserpine

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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

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Haloperidol

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MOA: DA receptor antagonist Clinical use: antipsychotic, also used in Huntington's (since one of the problems in Huntington's is ? DA)

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Methylphenidate, dextroamphetamine, methamphetamine

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CNS stimulants MOA: ? catecholamines in synaptic cleft, especially norepinephrine and dopamine Clinical use: ADHD, narcolepsy, appetite control

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Haloperidol, trifluoperazine, fluphenazine

answer

High potency antipsychotics ("Try to Fly High) MOA: block D2 receptors (?cAMP) Clinical use: schizophrenia (primarily + symptoms), psychosis, acute mania, Tourette syndrome Toxicity: -All antipsychotics: highly lipid soluble and slow to be removed from body; hyperprolactinemia; QT prolongation -High potency antipsychotics: EPS, neuroleptic malignant syndrome

question

Neuroleptic malignant syndrome

answer

Think FEVER (Fever, Encephalopathy, Vitals, Enzymes ?, Rigidity of muscles) Rigidity, myoglobinuria, autonomic instability, hyperpyrexia Tx: dantrolene, D2 agonists (e.g., bromocriptine)

question

EPS side effects

answer

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)

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Thioridazine, chlorpromazine

answer

Low potency antipscyhotics ("Cheating Thieves are low) Clinical use: schizophrenia (primarily + symptoms), psychosis, acute mania, Tourette syndrome Toxicity: -All antipsychotics: highly lipid soluble and slow to be removed from body; hyperprolactinemia; QT prolongation -Low potency antipsychotics: block muscarinic, ?1, and histamine receptors

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Olanzapine, clozapine, quetiapine, risperidone, aripiprazole, ziprasidone

answer

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

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Lithium

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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)

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Buspirone

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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)

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Fluoxetine, paroxetine, sertraline, citalopram

answer

SSRIs MOA: 5-HT-specific reuptake inhibitors Clinical 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

question

Serotonin syndrome

answer

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)

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Venlafaxine, duloxetine

answer

SNRIs MOA: inhibit 5-HT and norepinephrine uptake Clinical use: depression -Venlafaxine for generalized anxiety disorder, panic disorder, PTSD -Duloxetine for peripheral neuropathy Tx: ?BP

question

Amitriptyline, nortriptyline, imipramine, despramine, clomipramine, doxepin, amoxapine

answer

Tricylic antidepressants MOA: block reuptake of 5-HT and norepinphrine Clinical 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

question

Tranylcypromine, phenelzine, isocarboxazid, selegiline

answer

MOA: nonselective MAO inhibition ?levels of amine neurotransmitters (NE, 5-HT, dopamine) Selegiline (selective MAO-B inhibition Clinical use: atypical depression, anxiety, hypochondriasis Toxicity: 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

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Bupropion

answer

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

question

Maprotiline

answer

atypical antidepressant blocks NE reuptake tox: sedation, orthostatic hypoTN

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Trazodone

answer

Atypical antidepressant (high doses), primary use is insomnia MOA: Primarily inhibits 5HT reuptake Clinical use: insomnia Toxicity: priapism (trazo*bone*), postural hypotension, nausea, sedation

question

Appropriate agents for treating ESSENTIAL HTN

answer

Thiazide diuretics, ACE inhibitors, ARBs, dihydropyridine calcium channel blokers

question

Appropriate agents for treating HTN w/ CHF

answer

Diuretics, ACE inhibitors/ARBs, ? blockers (generally only in compensated CHF), K+ sparing diuretics

question

Appropriate agents for treating HTN w/ DM

answer

ACE inhibitors/ARBs, calcium channel blockers, thiazide diuretics, ? blockers **ACE inhibitors are protective against diabetic nephropathy

question

Appropriate agents for treating HTN in pregnancy

answer

Hydralazine, labetalol, methyldopa, nifedipine

question

Amlodipine, clevidipine, nicardipine, nifedipine, nimodipine

answer

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

question

Diltiazem, verapamil

answer

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

question

Hydralazine

answer

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

question

Drugs used in hypertensive emergency

answer

Clevidipine, fenoldopam, labetalol, nicardipine, nitroprusside

question

Nitroprusside

answer

MOA: short acting ?cGMP via direct release of NO Clinical use: hypertensive emergency Toxicity: can cause cyanide toxicity (releases cyanide) -Tx: sodium thiosulfate

question

Fenoldopam

answer

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

question

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

answer

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

question

Nitrates, effects on: EDV, BP, Contractility, HR, ejection time, MVO2

answer

Nitrates affect preload (dilate veins >> arteries) -EDV: ? -BP: ? -Contractility: no effect -HR: ? (reflex response) -ejection time: ? -MV02: ?

question

? blockers, effects on: EDV, BP, Contractility, HR, ejection time, MVO2

answer

? blockers affect afterload -EDV: no effect or ? -BP: ? -Contractility: ? -HR: ? -ejection time: ? -MV02: ?

question

Nitrates plus ? blockers, effects on: EDV, BP, Contractility, HR, ejection time, MVO2

answer

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: ??

question

Lovastatin, pravastatin (not metabolized by CYP450), simvastatin, atorvastatin, rosuvastatin

answer

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

question

Niacin (B3)

answer

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)

question

Cholestryamine, colestipol, colesevelam

answer

Bile acid resins MOA: prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more Clinical use: ?? LDL - slight ? HDL - slight ? TG Toxicity: patients hate it!! tastes bad, causes GI upset; ? absorption of fat soluble vitamins; cholesterol gallstones

question

Ezetimibe

answer

MOA: prevents cholesterol reabsorption at small intestine brush border Clinical use: ?? LDL cholesterol -No effect on HDL or TG Toxicity: rare ? LFTs, diarrhea

question

Gemfibrozil, clofibrate, bezafibrate, fenofibrate

answer

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

question

Digoxin

answer

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)

question

Reversal of digoxin toxicity

answer

-slowly normalize K+ -lidocaine -cardiac pacer -anti-digoxin Fab fragments -Mg2+

question

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.

answer

-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

question

Disopyramide, Quinidine, Procainamide

answer

"Double Quarter Pounder" Class IA antiarrhythmics MOA: INCREASE AP duration, effective refractory period, and QT interval Clinical 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

question

Mexiletine, Lidocaine, Tocainide, Phenytoin

answer

"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

question

Flecainide, propafenone

answer

"Fries, Please!" Class IC antiarrhythmics MOA: NO EFFECT on AP duration Clinical 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

question

Class II antiarrhythmics

answer

? 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 sensitive Clinical 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

question

Amiodarone, Ibutilide, Dofetilide, Sotalol

answer

"AIDS" Class III arrhythmics MOA: K+ channel blockers, INCREASE AP duration and ERP, ?QT interval Clinical 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

question

Class IV antiarrhythmics

answer

Verapamil, diltiazem MOA: decrease conduction velocity, increase ERP and PR interval Clinical use: prevention of nodal arrhythmias (like SVT) Toxicity: constipation, flushing, edema, CHF, AV block, sinus node depression

question

Adenosine

answer

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

question

Mg2+

answer

Clinical use: torsades de pointes digoxin toxicity

question

Bethanechol

answer

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."

question

Carbachol

answer

Cholinomimetic - direct agonist Clinical use: glaucoma; constricts pupil and relieves intraocular pressure Action: carbon copy of acetylcholine

question

Methacholine

answer

Cholinomimetic - direct agonist Clinical use: challenge test for asthma (Decrease FEV1 ;20%= bronchial asthma) Action: stimulates muscarinic recpetors in airway

question

Pilocarpine

answer

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.'"

question

Donepezil, galantamine, rivastigmine

answer

Cholinomimetic - indirect agonist (anticholinesterase) Clinical use: Alzheimer Action: ?ACh

question

Edrophonium

answer

Cholinomimetic - indirect agonist (anticholinesterase) Clinical use: diagnosis of myasthenia gravis -Myasthenia gravis now diagnosed by anti-AChR Ab test Action: ?ACh

question

Neostigmine

answer

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

question

Physostigmine

answer

Cholinomimetic - indirect agonist (anticholinesterase) Clinical use: anticholinergic toxicity -Crosses blood-brain barrier ? CNS Action: ?ACh "Physostigmine 'phyxes' atropine overdose."

question

Pyridostigmine

answer

Cholinomimetic - indirect agonist (anticholinesterase) Clinical use: myasthenia gravis (long acting) -Does not penetrate CNS Action: ?ACh; ?muscle strength "Pyridostigmine gets rido of myasthenia gravis."

question

Conditions aggravated by all cholinomimetic agents

answer

asthma, COPD, peptic ulcers

question

Cholinesterase inhibitor poisoning

answer

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)

question

Atropine, homatropine, tropicamide

answer

Muscarinic antagonists Organ systems: eye Clinical use: mydriasis and cycloplegia

question

Benzotropine

answer

Muscarinic antagonists Organ systems: CNS Clinical use: Parkinson, acute dystonia "park my Benz"

question

Glycopyrrolate

answer

Muscarinic antagonists Organ system: GI, respiratory Clinical use: -Parenteral: prep use to reduce airway secretions -Oral: drooling, peptic ulcer

question

Hyoscyamine, dicyclomine

answer

Muscarinic antagonists Organ system: GI Clinical use: antispasmodics for irritable bowel syndrome

question

Oxybutynin, solifenacin, tolterodine

answer

Muscarinic antagonists Organ system: GU Clinical use: overactive bladder

question

Scopolamine

answer

Muscarinic antagonists Organ system: CNS Clinical use: motion sickness

question

Atropine

answer

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)*

question

Jimson weed (Datura)

answer

Gardener's pupil due to mydriasis

question

Albuterol, salmeterol

answer

Direct sympathomimetic ?2>?1 Clinical use: -Albuterol for acute asthma -Salmeterol for long-term asthma or COPD

question

Dobutamine

answer

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

question

Dopamine

answer

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

question

Epinephrine

answer

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

question

Isoproterenol

answer

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

question

Norepinephrine

answer

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

question

Phenylephrine

answer

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

question

Amphetamine

answer

Indirect sympathomimetic Effect: Indirect general agonist, reuptake inhibitor, also releases stored catecholamines Clinical use: narcolepsy, obesity, ADHD

question

Cocaine

answer

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*

question

Ephedrine

answer

Indirect sympathomimetic Effect: Indirect general agonist, release stored catecholamines Clinical use: nasal decongestion, urinary incontinence, hypotension

question

Clonidine

answer

Sympatholytic (?2 agonist) Clinical use: hypertensive urgency (does not decrease renal blood flow), ADHD, Tourette syndrome Toxicity: CNS depression, bradycardia, hypotension, respiratory depression, miosis

question

?-methyldopa

answer

Sympatholytic (?2 agonist) Clinical use: hypertension in pregnancy Toxicity: direct Coombs + hemolysis, SLE-like syndrome

question

Phenoxybenzamine

answer

?-blocker - nonselective, irreversible Clinical use: pheochromocytoma (used preop to prevent hypertensive crisis) Toxicity: orthostatic hypotension, reflex tachy

question

Phentolamine

answer

?-blocker - nonselective, reversible Clinical use: give to pts on MAO inhibitors who eat tyramine-containing foods ? avoid hypertensive crisis Toxicity: orthostatic hypotension, reflex tachy

question

Prazosin, terazosin, doxazosin, tamsulosin

answer

?1 selective blocker Clinical use: urinary symptoms of BPH; PTSD (prazosin); hypertension (except tamsulosin) Toxicity: 1st-dose orthostatic hypotension, dizziness, headache

question

Mirtazapine

answer

?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)

question

Leuprolide

answer

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

question

Estrogens (ethinyl estradiol, DES, mestranol)

answer

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

question

Clomiphene

answer

MOA: SERM -Antagonist at estrogen receptors in hypothalamus ? prevent normal feedback inhibition and ?release of LH and FSH from pituitary ? ovulation Clinical use: infertility due to anovulation (e.g., PCOS) Toxicity: hot flashes, ovarian enlargement, *multiple simultaneous pregnancies*, visual disturbances

question

Hormone replacement therapy

answer

-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

question

Anastrazole/exemestane

answer

MOA: aromatase inhibitor Clinical use: postmenopausal women with ER+ breast cancer

question

Progestins

answer

MOA: bind progesterone receptors, ?growth and ?vascularization of endometrium Clinical use: oral contraceptives, endometrial cancer tx, abnormal uterine bleeding

question

Mifepristone (RU-486)

answer

MOA: competitive inhibitor of progestins at progesterone receptors Clinical use: termination of pregnancy -Administered with *misoprostol (PGE1)* ? cervical ripening and uterine contractions

question

Oral contraception (synethetic progestins, estrogen)

answer

-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

question

Terbutaline, ritodrine (tocolytics)

answer

MOA: ?2 agonists that relax the uterus Clinical use: ?contraction frequency in women during labor; prevent preterm labor

question

Danazol

answer

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

question

Testosterone, methyltestosterone

answer

MOA: agonists at androgen receptors Clinical use: hypogonadism; development of 2° sex characteristics; stimulation of anabolism to promote recovery after burn or injury Toxicity: -Masculinization in females -?intratesticular testosterone in males by inhibiting release of LH (via negative feedback) ? gonadal atrophy -Premature closure of epiphyseal plates -?LDL, ?HDL

question

Finasteride

answer

MOA: 5?-reductase inhibitor (?conversion of testosterone to DHT) Clinical use: BPH, male-pattern baldness

question

Flutamide, cyproterone

answer

MOA: competitive inhibitor androgen receptors Clinical use: prostate CA

question

Ketoconazole

answer

MOA: inhibits steroid synthesis (inhibits 17,20-desmolase) Clinical use: reduce androgenic symptoms in PCOS Toxicity: gynecomastia, amenorrhea

question

Spironolactone

answer

MOA: inhibits steroid binding, 17?-hydroxylase, and 17, 20-desmolase Clinical use: reduce androgenic symptoms in PCOS Toxicity: gynecomastia, amenorrhea

question

*Antimetabolites*

answer

Azathioprine, 6-mercaptuptopurine (6-MP), 6-thioguanine (6-TG) Cladribine (2-CDA) Cytarabine (arabinofuranosyl cytidine) 5-fluorouracil (5-FU) Methotrexate (MTX)

question

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

answer

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)

question

Increase toxicity with allopurinol or febuxostat Drug?

answer

Azathioprine, 6-MP, 6-TG

question

Cladribine (2-CDA)

answer

MOA: *Purine analog -> multiple mech* (e.g., inhibition of DNA poly, DNA strand breaks) Clinical use: *hairy cell leukemia* Tox: Myelosuppression, nephrotoxicity, neurotoxicity

question

Cytarabine (arabinofuranoysl cytidine)

answer

MOA: *Pyrimidine analog* -> inhibition of DNA polymerase Clinical use: Leukemia (AML), lymphoma Tox: Leukopenia, thrombocytopenia, megaloblastic anemia CYTarabine causes panCYTopenia

question

5-fluorouracil (5-FU)

answer

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)

question

Methotrexate (MTX)

answer

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

question

Myelosuppression reversible with leucovorin Drug?

answer

MTX

question

*Antitumor antibiotics*

answer

Bleomycin Dactinomycin (actinomycin D) Anthracyclines: doxorubicin, daunorubicin

question

Bleomycin

answer

MOA: *Free radical formation -> DNA strand breaks* Use: Testicular cancer, Hodgkin lymphoma Tox: *Pulmonary fibrosis*, skin hyper pigmentation, mucositis. *Minimal myelosuppression*

question

Dactinomycin (actinomycin D)

answer

MOA: *Intercalates in DNA* Use: *Childhood tumors* such as Wilms tumor, Ewing sarcoma, rhabdomyosarcoma ("children *act* out") Tox: Myelosuppression

question

Give ____ to prevent cardiotoxicity of doxorubicin/daunorubicin.

answer

Dexrazoxane

question

Anthracyclines: doxorubicin, daunorubicin

answer

MOA: *Free radical formation*. *Intercalate in DNA* -> breaks in DNA -> dec replication Use: 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.

question

*Alkylating agents*

answer

Busulfan Cyclophosphamide, ifosfamide Nitrosoureas (carmustine, lomustine, semustine, streptozocin)

question

Busulfan

answer

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

question

Cyclophosphamide, ifosfamide

answer

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)

question

Give _____ to avoid hemorrhage cystitis with cyclophosphamide.

answer

Mesna (binds toxic metabolites)

question

Nitrosoureas (carmustine, lomustine, semustine, streptozocin)

answer

MOA: *Cross-link DNA* *Cross blood-brain barrier -> CNS* Require bioactivation. Use: *Brain tumors* (including glioblastoma multiform) Tox: CNS (convulsions, dizziness, ataxia)

question

*Microtubule inhibitors*

answer

Paclitaxel, other taxols Vinca alkaloids: vincristine, vinblastine

question

Paclitaxel, other taxols

answer

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

question

Vinca alkaloids: vincristine, vinblastine

answer

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

question

Cisplatin, carboplatin

answer

MOA: *Cross-link DNA* Use: Testicular, bladder, ovary, and lung carcinomas Tox: *Nephrotoxicity* - prevent with *amifostine* (free radical scavenger) and chloride (saline) diuresis. *Ototoxocicity*

question

Prevention of cisplatin/carboplatin related nephrotoxicity? (2 steps)

answer

1) Amifostine (free radical scavenger) 2) Chloride (saline) diuresis

question

Etoposide, teniposide

answer

MOA: *Inhibits topoisomerase II* -> inc DNA degradation Use: Solid tumors (particularly testicular and small cell lunger cancer), leukemias, lymphomas Tox: Myelosuppression, GI upset, alopecia

question

Irinotecan, topotecan

answer

MOA: *Inhibit topoisomerase I" -> prevent DNA unwinding and replication Use: Colon cancer (irinotecan); ovarian and small cell lunger cancers (topotecan) Tox: Severe myelosuppression, diarrhea

question

Hydroxyurea

answer

MOA: *Inhibits ribonucleotide reductase* -> dec DNA synthesis (S-phase specific) Use: Melanoma, CML, *sickle cell disease (inc HbF)* Tox: Severe myelosuppression, GI upset

question

Prednisone, predinosolone

answer

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

question

Bevacizumab

answer

MOA: Monoclonal Ab against *VEGF* -> inhibit angiogenesis Use: Solid tumors (colorectal cancers, renal cell carcinoma) Tox: Hemorrhage, blood clots, and impaired wound healing

question

Erlotinib

answer

MOA: EGFR tyrosine kinase inhibitor Use: *Non-small cell lung carcinoma* Tox: Rash

question

Imatinib

answer

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

question

Rituximab

answer

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*

question

Tamoxifen, raloxifene

answer

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

question

Trastuzumab (Herceptin)

answer

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*.

question

Vemurafenib

answer

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

question

Cisplatin/Carboplatin tox

answer

nephrotoxic and acoustic nerve damage

question

Vincristine tox

answer

peripheral neuropathy

question

Bleomycin, Busulfan tox

answer

pulmonary fibrosis

question

Trastuzumab tox

answer

cardiotoxicity

question

Cyclophosphamide tox

answer

hemorrhagic cystitis

question

5-FU

answer

myelosuppression

question

6-MP

answer

myelosuppression

question

Methotrexate

answer

myelosuppression

question

MOA: Decrease thymidine synthesis Drugs?

answer

MTX 5-FU

question

MOA: Decrease de novo purine synthesis Drugs?

answer

6-MP

question

MOA: Cross-link DNA Drugs?

answer

Alkylating agents Cisplatin

question

MOA: DNA strand breakage Drugs?

answer

Bleomycin

question

MOA: DNA intercalators Drugs?

answer

Dactinomycin Doxorubicin/daunorubicin

question

MOA: Inhibit topoisomerase II Drugs?

answer

Etoposide, teniposide

question

MOA: Inhibit topoisomerase I Drugs?

answer

Irinotecan, topotecan

question

MOA: Inhibit microtubule formation Drugs?

answer

Vinca alkaloids: vinblastine, vincristine

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MOA: Inhibit microtubule breakdown Drugs?

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Paclitaxel, other taxols

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Mannitol

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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.

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Acetazolamide

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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.

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Loop diuretics: furosemide, bumetanide, torsemide

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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 OH DANG!

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Loop diuretics: ethnacrynic acid

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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.

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Thiazide diuretics

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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. HyperGLUC

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K+-sparing diuretics

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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)

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Urine NaCl changes with diuretics

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Increase with all diuretics except acetazolamide. Serum NaCl may decrease as a result.

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Urine K+ changes with diuretics

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Increase with loop and thiazide diuretics. Serum K+ may decrease as a result.

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Blood pH changes with diuretics

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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"

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Urine Ca2+ changes with diuretics

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Increase with loop diuretics: decreased paracellular Ca2+ reabsorption -> hypocalcemia. Decreased with thiazides: enhanced Ca2+ reabsorption in DCT.

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ACE inhibitors

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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

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Angiotensin II receptor blockers

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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.

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Aliskiren

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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.

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Etanercept

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

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