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

question

Oxacillin, nafcillin, dicloxacillin

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MOA: binds to PBP to block peptidoglycan cross linking; beta lactamase resistant due to bulky R group Clinical use: bactericidal, narrow spectrum- staph aureus only (except MRSA which is still resistant) Toxicity: hypersensitivity reactions (type II), interstitial nephritis

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, pseudomembranous colitis

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

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Cefazolin, cephalexin

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MOA: 1st generation beta lactam drugs that inhibit cell wall synthesis Clinical use: bactericidal for gram (+) COCCI, PEcK: Proteus mirabilis, E. coli, Klebsiella; cefazolin used prior to surgery to prevent S. aureus wound infections Toxicity: hypersensitivity rxns, vitamin K deficiency, potentiate nephrotoxicity of aminoglycosides

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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, vitamin K deficiency, potentiate nephrotoxicity of aminoglycosides

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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, vitamin K deficiency, potentiate nephrotoxicity of aminoglycosides

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

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 Toxicity: no cross reactivity w/ penicillins

question

Imipenem/cilastatin

answer

MOA: imipenem = beta lactamase resistant carbapenem that blocks peptidoglycan cross linking, always administered with cliastatin (inhibits renal dehydropeptidase I to slow inactivation of imipenem) Clinical use: bactericidal for LIFE THREATENING INFECTIONS due to gram (+) cocci, gram (-) rods, and anerobes when other meds have failed (limits due to seizure potential) Toxicity: CNS toxicity (seizures) at high plasma levels

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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 and C diff Toxicity: diffuse flushing/"red man syndrome" when infused too quickly; nephrotoxicity/ototoxicity/thrombophlebitis (some)

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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*

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.

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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

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

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Clindamycin

answer

MOA: works at 50S ribosomal subunit to block peptide transfer Clinical use: bacterioSTATIC against anaerobic infections above the diaphragm Toxicity: C. diff colitis

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

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Trimethoprim

answer

MOA: inhibits bacterial dihydrofolate reductase Clinical use: bacterioSTATIC use in combination w/ SMX for UTIs, Shigella, Salmonella, PJP Toxicity: megaloblastic anemia/leukopenia/granulocytopenia (may be less w/ leucovorin rescue)

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, CI in pregnant women due to cartilage damage

question

Metronidazole

answer

MOA: forms free radicals in bacterial (and protozoal) cells causing DNA damage Clinical use: PET A Gross Guy on the Metro- h. Pylori, Entamoeba, Trichomonas, Anaerobes, Giardia, Gardnerella vaginalis Toxicity: disulfiram reaction with alcohol

question

Isoniazid

answer

MOA: inhibits synthesis of mycolic acids (only bacterial have the catalase needed to activate it) Clinical use: TB (only one that can be used as solo prophylaxis) Toxicity: INH Injures Neurons and Hepatocytes; also causes B6 deficiency

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Rifampin

answer

MOA: inhibits DNA dependent RNAP Clinical use: TB, in combo w/ dapsone for leprosy, prophylaxis against neisseria meningitis in kids Toxicity: Orange body fluids, induces P450 enzymes

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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)

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 and supplementation of K/Mg), arrhythmias, anemia, IV phlebitis

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, aspergillus, coccidioides, histoplasma

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 ("flu" right into the CNS) 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 (you can see right through casper the ghost) Clinical use: "deep" infections like invasive aspergillosis, candida (you can see through casper to the deep infections) Toxicity: flushing due to histamine release

question

Terbinafine

answer

MOA: inhibits fungal squalene epoxidase 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

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

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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 Clinical use: RSV, chronic hep C Toxicity: hemolytic anemia, SEVERE TERATOGEN

question

Acyclovir

answer

MOA: guanosine analog, preferentially inhibits viral DNAP bc phosphorylation by viral thymidine kinase required for activity; CHAIN TERMINATOR Clinical use: HSV and VZV; no activity against CMV and no effect on latent forms of HSV/VZV -Valacyclovir has better oral availability

question

Ganciclovir

answer

MOA: guanosine analog, preferentially inhibits viral DNAP bc phosphorylation by viral kinase required for activity; CHAIN TERMINATOR Clinical use: CMV, especially in immunocompromised -Valganciclovir has better oral availability Toxicity: leukopenia/neutropenia/thrombocytopenia, renal toxicity

question

Foscarnet

answer

MOA: inhibits viral DNA polymerase by binding to PPi binding site of enzyme, no viral kinase activation required; CHAIN TERMINATOR Clinical use: CMV retinitis when ganciclovir fails, acyclovir resistant HSV Toxicity: nephrotoxicity

question

Cidofovir

answer

MOA: inhibits viral DNAP, does not require viral kinase activation Clinical use: CMV retinitis in immunocompromised patients, acyclovir reistant HSV Toxicity: nephrotoxicity-- coadminister w/ probenecid and IV saline to reduce

question

Protease inhibitors

answer

"Navir tease a protease" MOA: stops cleavage of HIV polypeptide into functional parts, thus preventing maturation of new viruses Clinical use: HIV Toxicity: hyperglycemia, GI intolerance, lipodystrophy; nephropathy, hematuria (indinavir) -Ritonavir inhibits P450 enzymes

question

NRTIs

answer

Tenofovir, emtricitabine, abacavir, lamivudine, zidovudine, didanosine, stavudine MOA: competitive inhibitor of HIV reverse transcriptase (terminate DNA chain bc lack a 3' OH) Clinical use: HIV active infection, ZDV also used for prophylaxis and during pregnancy to reduce fetal transmission Toxicity: bone marrow suppression (alleviated by GCSF and EPO, peripheral neuropathy, lactic acidosis, rash *if patient has concurrent Hep B infection, use tenofovir

question

NNRTIs

answer

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

question

Raltegravir

answer

MOA: reversibly inhibits HIV integrase Toxicity: hypercholesterolemia

question

INFs

answer

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

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: binds to cyclophilins --> inhibits calcineurin --> prevents production of IL-2 --> no differentiation/activation of T cells Clinical use: suppress organ rejection after transplant Toxicity: nephrotoxic, HTN, hyperlipidemia, hyperglycemia, tremor, gingival hyperplasia, hirsutism

question

Tacrolimus (FK-506)

answer

MOA: binds FK binding protein, inhibiting calcineurin and secretion of IL-2 (no T cell activation) Clinical use: organ transplant recipients Toxicity: nephrotoxic, HTN, hyperlipidemia, hyperglycemia, tremor, *NO GINGIVAL HYPERPLASIA/HIRSUTISM

question

Sirolimus (rapamycin)

answer

MOA: inhibits mTOR to inhibit T cell PROLIFERATION in response to IL-2 Clinical use: immunosuppression after kidney transplant (use w/ cyclosporine and corticosteroids) Toxicity: hyperlipidemia, thrombocytopenia, leukopenia

question

Azathioprine

answer

MOA: precursor of 6-MP, toxic to proliferating lymphocytes Clinical use: kidney transplantation, autoimmune disoders (glomerulonephritis and hemolytic anemia) Toxicity: BM suppression (duh); 6-MP is metabolized by xanthine oxidase so toxic effects increased when given w/ allopurinol

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: 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

Filgrastim

answer

Granulocyte colony stimulating factor-- only granulocytes b/c "Filgrastim is Finicky" Clinical use: bone marrow recovery

question

Sargramostim

answer

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

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Oprelvekin (IL-11)

answer

Clinical use: thrombocytopenia

question

Infliximab, adalimumab

answer

MOA: TNF α inhibtors Clinical use: Chron's disease, RA, psoriatic arthritis, ankylosing spondylitis (infliximab only)

question

Abciximab

answer

MOA: inhibits Gp IIb/IIIa Clinical use: prevent cardiac ischemia is unstable angina or pts treated w/ percutaneous coronary intervention

question

Trastazumab

answer

Clinical use: targets HER2 receptor in HER2nu positive breast cancer

question

Rituximab

answer

MOA: targets CD20 Clinical use: B cell non-Hodgkin's lymphoma

question

Omalizumab

answer

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

question

Insulin

answer

MOA: binds insulin receptor (tyrosine kinase activity), induces glucose--> glycogen in liver and muscle, muscles also increase protein synthesis and K+ uptake, adipose takes up TG Clinical use: DM type 1 and 2, gestational diabetes, life threatening hyperkalemia, stress induced hyperglycemia Toxicities: hypoglycemia

question

Short acting insulins versus long acting insulins

answer

Lispro, aspart and glulisine = rapid acting Glargine and detemir = long acting

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)

question

Tolbutamide, Chlorpropamide

answer

1st generation sulfonylureas MOA: close K+ channels in β 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 β 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

question

Pioglitazone, Rosiglitazone

answer

MOA: increase insulin sensitivity in peripheral tissue, binds to PPAR-γ nuclear transcription regulator Clinical use: used as a monotherapy in type 2 DM or in combo w/ other diabetes drugs Toxicity: weight gain, edema, hepatotoxicity, heart failure

question

Acarbose, Miglitol

answer

α-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

MOA: ↓ glucagon Clinical use: type 1 AND 2 DM Toxicities: hypoglycemia, nausea, diarrhea

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Exenatide, liraglutide

answer

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

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Linagliptin, saxagliptin, sitagliptin

answer

DPP-4 inhibitors MOA: ↑ insulin, ↓ glucagon release 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 Clinical use: hyperthyroidism Toxicity: agranulocytosis, aplastic anemia, hepatotoxicity (propylthiouracil)

question

Levothyroxine, triiodothyronine

answer

MOA: thyroxine replacement Clinical use: hypothyroidism, myxedema Toxicity: tachycardia, heat intolerance, tremors, arrythmias

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Ocreotide

answer

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

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Oxytocin

answer

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

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Hydrocortisone, prednisone, triamcinolone, dexamethasone, beclomethasone

answer

MOA: decrease the production of leukotrienes and prostraglandins by inhibiting phospholipase A2 and expression of COX2 Clinical use: addison's disease, inflammation, immune suppression, asthma; prednisone used for cancer chemotherapy for CLL, non-Hodgkin's lymphoma Toxicity: iatrogenic cushing's disease- buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin/easy bruising, osteoporosis, adrenocortical atrophy, peptic ulcers, hyperglycemia, cataracts, hypertension, psychosis

question

Cimetidine, ranitidine, famotidine, nizatidine

answer

H₂ blockers (take H₂ blockers before you "dine") MOA: REVERSIBLY block histamine H₂ 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 and placenta -Cimetidine and ranitidin ↓ renal excretion of creatinine

question

Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole

answer

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

question

Bismuth, sucralfate

answer

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

answer

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)

question

Aluminum hydroxide

answer

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

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Magnesium hydroxide

answer

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

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Calcium carbonate

answer

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

question

Magnesium hydroxide, magnesium citrate, polyethylene glycol, lactulose

answer

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

answer

MOA: combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid; activated by colonic bacteria Clinical use: ulcerative colitic, Chron's disease Toxicity: sulfonamide toxicity, reversible oligospermia

question

Ondansetron

answer

MOA: 5-HT3 antagonist; powerful central acting antiemetic (At a party but feeling queasy? Keep ON DANCing!") Clinical use: control vomiting postop and in chemotherapy patients Toxicity: headache, constipation

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Metoclopramide

answer

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

question

Heparin

answer

MOA: cofactor for the activation of antithrombin, decreases thrombin and factor Xa Clinical use: immediate anticoagulation for pulmonary embolism, acute coronary syndrome, MI, and DVT; used during pregnancy (≠ cross placenta); follow PTT to monitor Toxicity: bleeding, HIT (IgG antibodies against heparin bound to platelet factor 4 → platelets activated → thrombosis and thrombocytopenia), osteoporosis, drug-drug interactions

question

Protamine sulfate

answer

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

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Low molecular weight heparins

answer

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

answer

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

answer

MOA: interferes w/ normal synthesis and γ-carboxylation of vitamin K dependent clotting factors II, VII, IX and X and proteins C and S; monitor PT Clinical use: chronic anticoagulation (after STEMI, venous thromboembolism prophylaxis, and prevention of stroke in a fib); NOT used in pregnant women bc crosses the placenta Toxicity: bleeding, teratogenic, skin/tissue necrosis, drug-drug interactions (metabolized by P450s)

question

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

answer

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)

question

Aminocaproic acid

answer

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

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Aspirin

answer

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

question

Clopidogrel, ticlopidine, prasugrel, ticagrelor

answer

MOA: inhibit platelet aggregation by IRREVERSIBLY blocking ADP receptors; inhibit fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen Clinical use: acute coronary syndrome, coronary stenting, reduction of incidence or recurrence of thombotic stroke Toxicity: ticlopidine causes neutropenia

question

Cilostazol, dipyridamole

answer

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

question

Abcicimab, eptifibatide, tirofiban

answer

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

question

Methotrexate

answer

MOA: Folic acid analog that inhibits dihydrofolate reductase → ↓dTMP → ↓DNA and ↓ protein synthesis (acts on cells in the S phase) Clinical use: leukemias, lymphomas, choriocarcinoma, sarcomas; non neoplastics- abortion, ectopic pregnancy, RA, psoriasis Toxicity: myelosuppression (reversible w/ leucovorin rescue), macrovesicular fatty change in liver, mucositis, teratogenic

question

5 Fluorouracil (5-FU)

answer

MOA: pyrimidine analog bioactivated to 5F-dUMP, which covalently complexes folic caid; complex inhibits thymidylate synthase → ↓ dTMP → ↓ DNA and protein synthesis (acts on cells in S phase) Clinical use: colon cancer, basal cell carcinoma (topical) Toxicity: myelosuppression (reversible w/ leucovorin), photosensitivity

question

Cytarabine (arabinofuranosyl cytidine)

answer

MOA: pyrimidine analog → inhibition of DNAP (acts on cells in S phase) Clinical use: leukemias, lymphomas Toxicity: leukopenia, thrombocytopenia, megaloblastic anemia

question

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

answer

MOA: Purine (thiol) analogs → ↓ de novo purine synthesis; activated by HGPRT (acts on cells in S phase) Clinical use: leukemias Toxicity: toxic to bone marrow, GI, liver; Azathioprine and G-MP metabolized by xanthine oxidase so ↑ toxicity if given w/ allopurinol (6-TG no need for dose reduction)

question

Dactinomycin

answer

MOA: intercalates in DNA Clinical use: Wilm's tumor, Ewing's sarcoma, rhabdomyosarcoma (childhood tumor's, "actin" out) Toxicity: myelosuppression

question

Doxorubicin (adriamycin), danurubicin

answer

MOA: generate free radicals, noncovalently intercalate in DNA → strand breaks in DNA → ↓ replication (all phases of cell cycle susceptible) Clinical use: solid tumors (adriamycin is the A in CAF treatment plan for breast cancer), leukemias, lymphomas Toxicity: cardiotoxic (dilated cardiomyopathy due to free radical damage-- dexrazoxane, iron chelating agent, lessens cardiotoxicity); toxic to tissues following extravasation

question

Bleomycin

answer

MOA: induces free radical damage, causing strand breaks in DNA (acts on cells in G2 phase) Clinical use: testicular cancer (B in EBC and VBC), Hodgkin's lymphoma (B in ABVD) Toxicity: pulmonary fibrosis, skin changes, minimal myelosuppression

question

Cyclophosphamide, ifosfamide

answer

MOA: alkylate DNA at guanine residues, causing interstrand links; requires bioactivation in liver (all phases of cell cycle susceptible) Clinical use: solid tumors (C in CMF/CAF for breast cancer), leukemia, lymphomas and some brain cancers Toxicity: hemorrhagic cystitis, partially prevented w/ mesna

question

Carmustin, lomustine, semustine, steptozocin

answer

Nitrosoureas MOA: alkylate DNA, cross BBB → CNS; require bioactivation in liver (all phases of cell cycle susceptible) Clinical use: brain tumors (good CNS penetration), including glioblastoma multiforme Toxicity: CNS toxicity (dizziness, ataxia)

question

Busulfan

answer

MOA: alkylates DNA (all phases of cell cycle susceptible) Clinical use: CML, ablation of patient's bone marrow before BMT Toxicity: pulmonary fibrosis, hyperpigmentation

question

Vincristine, vinblastine

answer

MOA: alkaloids that bind to tubulin in M phase and block polymerization of microtubules so that mitotic spindle can't form Clinical use: solid tumors (vinblastine is V in VBC), leukemias (vincristine is V in VAMP for ALL), lymphoma (vinblastine is V in ABVD for hodgkins/soft tissue lymphomas, vincristine (oncovin) is O in MOPP for hodgkins/other lymphomas) Toxicity: Vincristine (think trouble getting things moving) = neurotoxicity- areflexia, peripheral neuritis; paralytic ileus

question

Paclitaxel, other taxols

answer

MOA: hyperstabilize polymerized microtubules in M phase so that mitotic spindle can't break DOWN Clinical use: ovarian and breast carcinomas Toxicity: myelosuppresion and hypersensitivity

question

Cisplatin, carboplatin

answer

MOA: cross links DNA (alkylating agent, non cell cycle specific) Clinical use: testicular (C in EBC/VBC), bladder, ovary, and lung carcinomas Toxicity: nephrotoxicity and acoustic nerve damage; prevent nephrotoxicity w/ amifostine (free radical scavenger) and chloride diuresis

question

Etoposide, teniposide

answer

MOA: inhibits topoisomerase II leading to DNA degredation (acts on cells in S and G2) Clinical use: solid tumors (E in EBC for testicular CA), leukemias, lymphomas Toxicity: myelosuppression, GI irritation, alopecia

question

Hydroxyurea

answer

MOA: inhibits ribonucleotide reductase → decreased DNA synthesis (S phase specific) Clinical use: melanoma, CML, sickle cell disease (increases HbF) Toxicity: bone marrow suppression, GI upset

question

Tamoxifen, raloxifene

answer

MOA: SERMs- receptor antagonists in breast and agonists in bone; block the binding of estrogen to estrogen receptor-positive cells Clinical use: breast CA tx and prevention, also helps prevent osteoporosis Toxicity: tamoxifen- partial agonist in endometrium, so increased risk of endometrial cancer, hot flashes (raloxifene is endometrial antagonist, so no increased risk)

question

Trastuzumab (herceptin)

answer

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

question

Imatinib (gleevec)

answer

MOA: philadelphia chromosome bcr-abl tyrosine kinase inhibitor Clinical use: CML, GI stromal tumors Toxicity: fluid retention

question

Rituximab

answer

MOA: monoclonal Ab against CD20 (found on most B cell neoplasms) Clinical use: non-Hodgkin's lymphoma, RA (with MTX)

question

Vemurafenib

answer

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

question

Bevacizumab

answer

MOA: monoclonal Ab against VEGF; inhibits angiogenesis Clinical use: solid tumors

question

Ibuprofen, naproxen, indomethacin, diclofenac, ketorolac

answer

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)

question

Celecoxib

answer

MOA: selective reversible inhibitor of COX2 (found in inflammatory cells/vascular endothelium), but spares COX1 to help maintain gastric mucosa and has no effect on platelet function (TXA2 production is via COX1) Clinical use: RA and osteoarthritis, patients w/ gastritis or ulcers Toxicity: sulfa allergy

question

Acetaminophen

answer

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)

question

Alendronate (other -dronates)

answer

(Bisphosphonates) MOA: pyrophosphate analogs, bind hydroxyapatite in bone, inducing apoptosis in osteoclasts Clinical use: osteoporosis, hypercalcemia, Paget's disease of bone Toxicity: corrosive esophagitis (1st generation), osteonecrosis of the jaw

question

Allopurinol

answer

MOA: purine analog, competitively inhibits xanthine oxidase (↓ conversion of xanthine to uric acid) Clinical use: gout; lymphoma/leukemia to prevent tumor lysis syndrome related nephropathy Toxicity: increases the concentration of azathioprine and 6-MP; DO NOT GIVE w/ salicylates, uric acid clearance ↓

question

Febuoxstat

answer

MOA: non-purine analog allosteric inhibitor of xanthine oxidase Clinical use: gout, lymphoma/leukemia to prevent tumor lysis syndrome Toxicity: increases concentration of azathioprine and 6-MP (metabolized by XO)

question

Probenecid

answer

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

question

Colchicine

answer

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

question

Glaucoma drugs

answer

α agonists: ↓ aqueous humor synthesis β antagonists: ↓ aqueous humor synthesis Diuretics (acetazolamide): ↓ aqueous humor synthesis via inhibition of carbonic anhydrase Cholinomimetics: ↑ outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork Prostaglandin (latanoprost, PGF2α): ↑ outflow of aqueous humor

question

Morphine, fentanyl, codeine, heroin, meperidine

answer

(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

question

Dextromethorphan

answer

MOA: opioid receptor agonist Clinical use: cough suppression

question

Diphenoxylate, loperamide

answer

MOA: opioid receptor agonists Clinical use: diarrhea

question

Methadone

answer

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

question

Butorphanol

answer

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

question

Tramadol

answer

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

question

Phenytoin

answer

MOA: increases Na+ channel inactivation Clinical use: 1st line drug for generalized tonic-clonic seizures -1st line drug for prophylaxis of status epilepticus -may also be used for simple or complex partial seizures Toxicity: nystagmus, ataxia, diplopia, SLE like syndrome, induction of P450s; chronic use --> gingival hyperplasia in kids, peripheral neuropathy, megaloblastic anemia (↓ folate absorption), teratogenic

question

Carbamazepine

answer

MOA: increases Na+ channel inactivation Clinical use: 1st line drug for simple/complex partial seizures and tonic-clonic seizures -also 1st line drug for trigeminal neuralgia Toxicity: diplopia, ataxia, agranulocytosis, hepatotoxicity, teratogen, induction of P450, SIADH, steven-johnson syndrome

question

Lamotrigine

answer

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

question

Gabapentin

answer

MOA: primarily inhibits high-voltage activated Ca 2+ channels Clinical use: simple/complex partial seizures, tonic-clonic seizures -also used for peripheral neuropathy, postherpetic neuralgia, migraine prophylaxis, bipolar disorder Toxicity: sedation, ataxia

question

Topiramate

answer

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

question

Phenobarbital

answer

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

question

Valproic acid

answer

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

question

Ethosuximide

answer

MOA: blocks thalamic T-type Ca2+ channels Clinical use: 1st line drug for absence seizures Toxicity: GI distress, urticaria, stevens-johnson syndrome

question

Diazepam/Lorazepam

answer

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

question

Tiagabine

answer

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

question

Vigabatrin

answer

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

question

Phenobarbital, pentobarbital, thiopental, secobarbital

answer

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

question

Triazolam, oxazepam, midazolam

answer

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

question

Flumazenil

answer

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

question

Zolpidem, zaleplon, eszopiclone

answer

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

question

Halothane

answer

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

question

Enflurane

answer

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

question

Methoxyflurane

answer

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

question

Nitrous oxide

answer

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)

question

Isoflurane, sevoflurane

answer

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

question

Ketamine

answer

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

question

Propofol

answer

MOA: potentiates GABA(A) Clinical use: sedation in the ICU, rapid anesthesia induction, short procedures; less postoperative nausea than thiopental

question

Procaine, cocaine, tetracaine

answer

Ester local anesthetics MOA: block Na+ channels by binding to a specific receptor on INNER portion of the channel (most effective in rapidly firing neurons bc have to get inside a channel that has already been activated) Clinical use: minor surgical procedures, spinal anesthesia Toxicity: CNS excitation (depression of inhibitory centers), HTN or hypotension, arrhythmias (cocaine), hypersensitivity (if allergic to esters, give amides)

question

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

question

Local anesthetics principles

answer

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

question

Succinylcholine

answer

MOA: DEPOLARIZING neuromuscular blocking drug; strong ACh receptor antagonist → produces sustained depolarization and prevents muscle contraction Clinical use: muscle paralysis in surgery or mechanical ventilation Toxicity: hypercalcemia, hyperkalemia, malignant hyperthermia

question

Reversal of succinycholine

answer

-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)

question

Tubocurarine

answer

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

question

Dantrolene

answer

MOA: prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle Clinical use: treatment of malignant hyperthermia and neuroleptic malignant syndrome

question

Bromocriptine, pramipexole, ropinirole

answer

MOA: dopamine agonists Clinical use: Parkinson's disease (when they still have endogenous DA)

question

Amantadine

answer

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

question

Levodopa/carbidopa

answer

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

question

Selegiline

answer

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

question

Memantine

answer

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

question

Donepezil, galantamine, rivastigmine

answer

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

question

Sumatriptan

answer

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

question

Tetrabenazine, reserpine

answer

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

question

Haloperidol

answer

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

question

Appropriate agents for treating ESSENTIAL HTN

answer

Diuretics, ACE inhibitors, ARBs, calcium channel blokers

question

Appropriate agents for treating HTN w/ CHF

answer

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

question

Appropriate agents for treating HTN w/ DM

answer

ACE inhibitors/ARBs, calcium channel blockers, diurectics, β blockers, α blockers **ACE inhibitors are protective against diabetic nephropathy

question

Nifedipine, verapamil, diltiazem, amlodipine

answer

Ca2+ channel blockers! MOA: block voltage gated L type calcium channels of cardiac and smooth muscle and ∴ reduce muscle contractility -Amlodipine and nifedipine have the most effect on vascular smooth muscle; verapamil has the most effect on the heart Clinical use: HTN, angina, arrhythmias (except nifedipine), Prinzmetal's angina, raynaud's Toxicity: cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation

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

question

Nitroprusside

answer

MOA: short acting ↑cGMP via direct release of NO Clinical use: malignant HTN Toxicity: can cause cyanide toxicity (releases cyanide)

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: malignant HTN

question

Nitroglycerin, isosorbide dinitrate

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, pulmonary edema Toxicity: reflex tachycardia, hypotension, flushing, headache, "Monday disease"

question

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

answer

Nitrates affect preload (dilate veins >> arteries) -EDV: ↓ -BP: ↓ -Contractility: ↑ (reflex response) -HR: ↑ (reflex response) -ejection time: ↓ -MV02: ↓

question

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

answer

β blockers affect afterload -EDV: ↑ -BP: ↓ -Contractility: ↓ -HR: ↓ -ejection time: ↑ -MV02: ↓

question

Nitrates plus β 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: ↓ -ejection time: little/no effect -MV02: ↓↓

question

Lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin

answer

MOA: inhibit conversion of HMG-CoA to mevalonate (HMG-CoA reductase = rate limiting step in cholesterol synthesis) Clinical use: ↓↓↓ LDL cholesterol -↑ HDL cholesterol -↓ TriG Toxicity: hepatotoxicity (↑LFTs), rhabdomyolysis

question

Niacin (B3)

answer

MOA: inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation Clinical use: ↓↓ LDL cholesterol -↑↑ HDL cholesterol (most of all options) -↓ TriG Toxicity: red/flushed face (↓ by aspirin or long term use), hyperglycemia (→acanthosis nigricans), hyperuricemia (exacerbates gout)

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 cholesterol - slight ↑ HDL cholesterol - slight ↑ TriG 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 TriG)

question

Gemfibrozil, clofibrate, bezafibrate, fenofibrate

answer

MOA: upregulate LPL to ↑ TriG clearance Clinical use: ↓ LDL cholesterol -↑ HDL cholesterol -↓↓↓ TriG (most of all the options) Toxicity: myositis, 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

β blockers (metoprolol, propranolol, esmolol, atenolol, timolol) MOA: decreases SA and AV nodal activity by ↓cAMP, ↓Ca2+ currents, suppress abnormal pacemakers by decreasing the slope of phase 4, ↑ PR interval bc AV node particularly 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 β block Ibutilide- torsades Amiodarone- EVERYTHING! pulmonary fibrosis, hepatotoxicity, hypo/hyperthyroidism (40% iodine by weight), corneal deposits, blue/gray skin deposits that cause photodermatitis, neurologic effects, constipation, bradycardia, heart block, CHF

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

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