USMLE Pharmacoloy

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calcium channel blocker associated with accelerated progression of CHF?: verapamil
drug to slow ventricular response in Wolff-Parkinson White?: ibutilide
hypersensitivity angiitis or microscopic polyarteritis nodosa (can be caused by penicilin): leukocytoclastic angiitis
in which part of the systemic circulation does the greatest decrease in blood pressure occur?: arterioles
vasodilator with lupus-like syndrome as side effect?: hydralazine
mechanism of hydralazine?: increases cGMP - smooth muscle relaxation; vasodilates arterioles > veins; reduces afterload
what calcium channel blocker is most selective for peripheral vasculature?: nifedipine
mechanism of calcium channel blockers?: block voltage-dependent L-type calcium channels of cardiac and SM and thereby reduce contractility
which calcium channel blocker is not used to treat arrhythmias?: nifedipine
what is the goal of antianginal therapy?: reduce myocardial O2 consumption by decreasing 1 or more of the determinants of MVO2: EDV, BP, HR, contractility, ejection time
what do nitrates affect in antianginal therapy?: preload
what happens to contractility and HR in nitrate therapy?: increase - reflex response
what do beta blockers affect in antianginal therapy?: afterload
how do nitrates affect ejection time and MVO2?: decrease
how do beta blockers affect ejection time?: increase it
what do beta blockers do to EDV?: increase it
what do beta blockers do to BP, contractility, and HR?: decrease them
what is digitoxin used for?: CHF (increases contractility) and atrial fibrillation (decreases conduciton at the AV node)
toxicities of digitoxin are increased by what?: renal failure, hpokalemia, and quinidine
blurry yellow vision is side effect of what?: digitoxin
what is the antidote for digitoxin?: slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments
lupus-like syndrome is associated with what class IA antiarrythmic?: procainamide
what are the class IA antiarrythmics?: Na+ channel blockers: quinidine, amiodarone, procainamide, disopyramide (queen amy proclaims disco pyramids)
this class IA antiarrhythmic can cause cinchonism (headache, tinnitus, thrombocytopenia), torsades de pointes (due to increased QT interval): quinidine
what class of antiarrhythmics are contraindicated post-MI: class IC - proarrhythmic
what beta blocker is very short acting?: esmolol
what is the antiarrhythmic action of beta blockers?: decrease cAMP and calcium currents; suppress abnormal pacemaker by decreasing slope of phase 4 - AV node particularly sensitive - increased PR interval
toxicity of amiodarone?: pulmonary fibrosis, hepatotoxicity, hypo/hyperthroidism;corneal deposits, skin deposits resulting in photodermatitis, neuro effects, constipation, bradycardia, heart block, CHF
K+ channel blockers that can cause torsades de pointes: soltalol, ibutilide
K+ channel blocker that can cause new arrhythmias and hypotension?: bretylium
wha type of cells do Ca2+ channel blockers primarily affect?: AV nodal cells
what type of antiarrhythmics are used for prevention of nodal arrhythmias?: class IV - Ca2+ channel blockers
what class IV antiarrhythmic can cause torsades de pointes?: bepridil
what is the drug of choice for diagnosing/abolishing AV nodal arrhythmias?: adenosine
what depresses ectopic pacemakers, especially in digitoxin toxicity?: K+
Mg+ is effective for treating what?: torsades de pointes and digitoxin toxicity
drug for hypertension in patient with PKD?: ACE inhibitor
anti-hypertesive for pregnant woman?: methyldopa
in patients with wolff parkinson white and atrial fibrillation, what can digitoxin do?: enhance transmission through accessory pathways that can predispose to v tac
when is mannitol contraindicated?: anuria, CHF
clinical use of mannitol?: shock, drug overdose, decrease intracranial/intraocular pressure
how does mannitol work?: increases tubular fluid osmolarity, producing increased urine flow
mechanism of acetazolamide?: carbonic anhydrase inhibitor - causes self-limited NaHCO3 diuresis and reduction in total body HCO3- stores
where does acetazolamide act?: proximal convoluted tubule
toxicity of acetazolamide?: hyperchloremic metabolic acidosis, neuropathy, NH3 toxicity, sulfa allergy
clinical use of acetazolamide?: glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness
mechanism of furosemide?: sulfonamide loop diuretic - inhibits NKCC of thick ascending limb; abolishes hypertonicity of medulla, preventing concentration of urine
what effect does furosemide have on calcium excretion?: increases it - Loops Lose calcium
clinical use of furosemide?: edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), hypertension, hypercalcemia
toxicity of furosimide?: OH DANG: ototoxicity, hypokalemia, dehydration, allergy (sulfa), nephritis (interstitial), gout
drug for diuresis in patients allergic to sulfa drugs?: ethacrynic acid
diuretic that can be used in hyperuricemia, acute gout?: ethacrynic acid
mechanism of hydrochlorothiazide?: inhibits NaCl reabsorption in distal convoluted tubule, reducing diluting capacity of the nephron, decreases calcium excretion
clinical use of hydrochlorothiazide?: hypertension, CHF, idiopathic hypercalciuiria, nephrogenic diabetes insipidus
diuretic used in nephrogenic diabetes insipidus?: hydrochlorothiazide
toxicity of hydrochlorothiazide?: hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia, hyperLipidemia, hyperUricemia, and hyperCalcemia (sulfa alergy)
what are the potassium sparing diuretics?: Spironolactone, Triamterene, Amiloride, eplercone (the K+ STAys)
mechanism of spironolactone?: competitive aldosterone receptor antagonist in cortical collecting tubule
how do triamterene and amiloride act?: cortical collecting tubule - block Na+ channels
clinical use of K+ sparing diuretics?: hyperaldosteronism, K+ depletion, CHF
toxicity of K+ sparing diuretics?: hyperkalemia, endocrine effects (e.g. spironolactone causes gynecomastia, antiandrogen effects)
diuretics causing acidosis?: carbonic anhydrase inhibitors, K+ sparing diuretics
diuretics causing alkalosis?: loop diuretics, thiazides
diuretic that increases urine calcium?: loop diuretics
diuretics that decrease urine calcium?: thiazides
name 3 ACE inhibitors: captopril, enlapril, lisinopril
mechanism of Losartan?: AT II receptor antagonist - not ACE inhibitor and so doesn't cause cough
toxicity of ACE inhibitors?: CATOPRIL: cough, angioedema, proteinuria, taste changes, hypOtension, pregnancy problems (fetal renal damage), rash, increased renin, lower angiotensin II; hyperkalemia
serious cardiac arrhythmias/torsades de pointes can occur with erythromycin and what?: cisapride
what type of drug are omeprazole, lansoprazole?: proton pump inhibitors
action of misoprostol?: PGE1 analog - increases production and secretion of gastric mucous barrier, decreases acid production
drug that can be used to prevent NSAID-induced peptic ulcers, maintain a PDA, and induce labor: misoprostol
action of pirenzepine, propantheline?: muscarinic antagonists - block M1 receptors on ECL cells (decrease histamine secretion) and M3 receptors on parietal cells (decrease H+ secretion) - used for peptic ulcer
monoclonal antibody to TNF-alpha: infliximab
sulfasalazine?: combination of sulfapyradine (antibacterial) and mesalamine (antinflammatory) activated by colonic bacteria; Rx for Crohn's and UC
mechanism of ondansetron?: 5-HT3 antagonist - powerful central-acting antiemetic
overuse of aluminum hydroxide?: constipation and hypophosphatemia
overuse of magnesium hydroxide?: diarrhea
overuse of calcium carbonate?: hypercalcemia, rebound acid increase
all antacids can cause what metabolic disturbance?: hypokalemia
antiemetic that can cause Parkinsonian symptoms?: metoclopramide
how does cimetidine impact P-450 system?: potent inhibitor
H2 blocker with antiandrogenic effect that can decrease renal excretion of creatinine?: cimetidine
A patient presents with HA, tinnitis, vomiting,and confusion ⬦ you are concerned about and overdose of what common medication?: Aspirin
Aspirin overdose will manifest as a respiratory _____ and a metabolic ______?: Aspirin overdose will manifest as a respiratory alkalosis and metabolic acidosis
At a [CO] of 30% a patient will experience HA, and SOB because of hypoxia of what area of the brain?: gray matter
at a [co] of 50% there is hypoxia of the globus pallidus leading to what symptoms and signs?: loss of conciousness, convulsions, and coma
which mushroom is typically lethal, amanita muscaria or amanita phalloides?: phalloides - the toxin inhibits RNA polymerase and can lead to ab pain, vomiting, diarrhea, and fulminant hepatitis with extensive liver necrosis
"garlic scented breath": arsenic poisioning
what are Mees lines?: transverse band on fingernails that may indicate chronic arsenic poisioning
what are the long term complications of chronic arsenic poisioning?: squamous cell carcinoma of lungs and skin
what is the most common chrnoic metal poisioining in the united states?: lead
lead poisionign ALWAYS involves: CNS toxicity
what is the mechanism of lead toxicity?: lead interferes with heme production by inhibiting d-aminolevulinic acid dehydratase and ferrochelatase
A patient presents with wrist and foot drop, microcytic anemia with basophillic stippling, and dark lines on their gums ⬦ you suspect ⬦: lead poisioning
"bitter almond" scented breath: cyanide poisioing
what is the mechanism of cyanide poisioning: blocks cellular respiration by binding cytocrhome oxidase
what are the top 3 causes of death in smokers: 1. heard disease, 2. lung cancer, 3. copd
T or F: stopping smoking for 15 years will reduce the risk of dying to almost the level of a non-smoker: TRUE
a patient presents with a perforation in the nasal septum and dilated cardiomyopathy ⬦ you suspect chronic use of what chemical?: cocain
what causes "track marks" of a IVDU: the healing of skin abscesses
mechanism of amantadine?: blocks viral penetration/uncoating; may buffer pH of endosome. also causes the release of dopamine from intact nerve terminals
clinical use of amantadine?: prophylaxis and treatment for influenza A; Parkinson's disease
toxicity of amantadine?: ataxia, dizziness, slurred speech
mehcanism of zanamivir, oseltamivir?: inhibit influenza neuraminidase
clinical use of zanamivir & oseltamivir?: both influenza A & B
mechanism of ribavirin?: inhibits synthesis of gruanine nucleotides by competitively inhibiting IMP dehydrogenase
clinical use of ribavirin?: RSV, chronic hepatitis C
toxicity of ribavirin?: hemolytic anemia, severe teratogen
mechanism of acyclovir?: preferentially inhibits viral DNA polymerase when phosphorylated by viral thymidine kinase; guanine analog
clinical use of acyclovir?: HSV, VZV, EBV; mucocutaneous and genital herpes lesions; prophylaxis in immunocompromised patients
toxicity of acyclovir?: delerium, tremor, nephrotoxicity
mechanism of ganciclovir?: phosphorylation by viral kinase; preferentially inhibits CMV DNA polymerase
clinical use of ganciclovir?: CMV, especially in immunocompromised patients
toxicity of ganciclovir?: leukopenia, neutropenia, thrombocytopenia, renal toxicity; more toxic to host enzymes then acyclovir
mechanism of foscarnet?: viral DNA polymerase inhibitor that binds to the pyrophosphate binding site of the enzyme; does not require action by viral kinase
clinical use of foscarnet?: CMV retinitis in immunocompromised patients when ganciclovir fails; acyclovir-resistant HSV
toxicity of foscarnet?: nephrotoxicity, hypoglycemia, hypomagnesia
saquinavir, ritonavir, indinavir, nelfinavir, and amprenavir are what type of drugs?: protease inhibitors - used in HIV therapy
mechanism of protease inhibitors?: inhibit assembly of new virus by blocking protease enzyme
toxicity of protease inhibitors?: GI intolerance (nausea, diarrhea), hyperglycemia, lipid abnormalities
protease inhibitor that can cause thrombocytopenia?: indinavir
zidovudine, didanosine, zalcitabine, stavudine, lamivudine, and abacavir are what type of drug?: nucleoside RT inhibitors
nevirapine, delaviridine, and efavirenz are what type of drug?: non-nucleoside RT inhibitors
mechanism of reverse transcriptase inhibitors?: preferentially inhibit RT of HIV; prevent incorporation of viral genome into host DNA
toxicity of RT inhibitors?: bone marrow suppression (neutropenia, anemia), peripheral neuropathy
what type of reverse transcriptase inhibitors can cause lactic acidosis?: nucleosides - zidovudine, didanosine, zalcitabine, stavudine, lamivudine, and abacavir
what type of RT inhibitors can cause rash?: non-nucleosides -nevirapine, delaviridine, and efavirenz
nucleoside RT inhibitor that can cause megaloblastic anemia?: AZT (zidovudine)
what HIV drug is used during pregnancy to reduce the risk of fetal transmission?: AZT
interferon-alpha is used for what?: chronic hepatitis B andC, Kaposi's sarcoma
interferon beta is used in what disease?: MS
interferon gamma is used in what disease?: NADPH oxidase deficiency
toxicity of interferons?: neutropenia
these are glycoproteins from human leukocytes that block various stages of viral RNA and DNA synthesis: interferons
drug used for giardiasis, amebic dysentery, bacterial vaginitis, trichomonas?: metronidazole
drug used for giant roundworm (asarcis), hookworm (necator/ancylostoma), and pinworm (enterobius)?: pyrantel pamoate
drug used for trematode/fluke (schistosomes, paragnimus, clornorchis), and cysticercosis?: praziquantel
drug used for cestode/tapeworm (e.g. diphyllobothrium latum, taenia species) infections except cysticercosis?: niclosamide
drug used for onchocerciasis?: ivermectin (rIVER blindness)
drug used for nematode/roundworm (e.g. pinworm, whipworm) infections?: mebendazole/thiabendazole
block cell wall synthesis by inhibition of peptidoglycan cross-linking: penicillin, ampicillin, ticarcillin, piperacillin, imipenem, aztreonam, cephalosporins
block peptidoglycan synthesis: bacitracin, vancomycin, cycloserine
disrupt bacterial/fungal cell membranes: polymyxins
disrupt fungal cell membranes: amphotericin B, nystatin, fluconazole/azoles
block nucleotide synthesis: sulfonamides, trimethoprim
block DNA topoisomerases: quinolones
block mRNA synthesis: rifampin
block protein synthesis at 50S ribosomal subunit: chloramphenicol, erythromycin/macrolides, lincomycin, clindamycin, streptogramins (quinupristin, dalfopristin), linezolid
block protein synthesis at 30S ribosomal subunit: aminoglycosides, tetracyclines
bacteriacidal antibiotics (6): penicilin, cephalosporins, vancomycin, aminoglycosides, fluoroquinolones, metronidazole
penicillin mechanism: bind PBPs, block transpeptidase cross-linking of cell wall; activate autolytic enzymes
penicillin toxicity: hypersensitivity reactions, hemolytic anemia
mechanism of methicillin, nafcillin, dicloxacillin: bind PBPs, block transpeptidase cross-linking of cell wall - penicillinase resistant because of bulkier R group
methicillin toxicity: interstitial nephritis
ampicillin, amoxicillin toxicity: hypersensitvity, ampicillin rash (esp. in pts. w/ mono), pseudomembranous colitis
ticarcillin, carbenicillin, piperacillin usage: pseudomonas (Takes Care of Pseudomonas)
mechanism of cephalosporins: beta-lactam drugs that inhibit cell wall synthesis - less susceptible to penicillinases
antibiotic for penicillin-allergic patients and patients w/ renal toxicity who can't tolerate aminoglycosides: aztreonam (synergistic w/ aminoglycosides)
drug of choice for enterobacter: imipenem/cilastin
antibiotic that can cause seizures at high plasma levels: imipenem/cilastin
mechanism of vancomycin: inhibits cell wall mucopeptide formation by binding D-ala D-ala portion of cell wall precursors
mechanism of resistance to vancomycin: amino acid change of D-ala D-ala to D-ala D-lac
vancomycin toxicity: well tolerated in general - does NOT have many problems: nephrotoxicity, ototoxicity, thrombophlebitis
aminoglycosides: streptomycin, gentamicin, tobramycin, amikacin - bacteriacidal
mechanism of action of aminoglycosides: inhibit 30S subunit - inhibit formation of initiation complex and cause misreading of mRNA
are aminoglycosides effective agains anaerobes?: no! require O2 or uptake
aminoglycosides cause nephrotoxicity especially when used in combination with _________: cephalosporins
aminoglycosides cause ototoxicity especially when used with_________: loop diuretics
are aminoglycosides safe to use in pregnancy?: no! teratogenic
which tetracycline can be used in patients with renal failure?: doxycycline because it is fecally eliminated
can you take tetracyclines with milk?: no! nor atacids or iron-containing preparations because divalent cations inhibit its absorption in the gut
tetracycline toxicity: discoloration of teeth and inhibition of bone growth in children, photosensitivity
mechanism of action of macrolides: inhibit protein synthesis by blocking translocation - bind to 23S rRNA of the 50S subunit
name 3 macrolides: erythromycin, azithromycin, clarithromycin
when can sulfonamides cause hemolysis?: G6PD deficiency
most common cause of noncompliance with macrolides: GI discomfort
macrolides increase the serum concentration of what drugs?: theophyllines, oral anticoagulants
acute cholestatic hepatitis & eosinophilia are toxicities of which class of antibiotics?: macrolides
clinical use of chloramphenicol: meningitis - H. flu, neisseria, strep pneumo
why does chloramphenicol cause gray baby syndrome?: because infants lack liver UDP-glucoronyl transferase
is the aplastic anemia seen with chloramphenicol dose dependent?: no! the anemia is, however
mechanism of action of chloramphenicol: inhibits 50S peptidyltransferase
what is the clinical use of clindamycin?: treatment of anaerobic infections - B. frag, C. perfringfens
clindamycin toxicity: pseudomembranous colitis - destroys normal GI flora
mechanism of action of sulfonamides (sulfamethoxazole, sulfisoxazole, triple sulfas, etc.): PABA antimetabolites inhibit dihydropteroate synthase
what side effect can sulfonamides cause in infants?: kernicterus
mechanism of action of trimethoprim: inhibits bacterial dihydrofolate reductase
trimethoprim toxicity: megaloblastic anemia, leukopenia, granulocytopenia (may alleviate with supplemental folinic acid)
mechanism of action of fluoroquinolones: inhibit DNA gyrase (topoisomerase II)
what class of antibiotics can cause cartilage damage in kids?: fluoroquinolones
what drug is associated with a disulfiram-like reaction with alcohol and a metallic taste: metronidazole
what can prevent the neurotoxicity associated with INH?: pyridoxine (vitamin B6)
INH toxicity: hemolysis if G6PD deficient, neurotoxicity, hepatotoxicity, SLE-like syndrome
mechanism of action of rifampin: inhibits DNA-dependent RNA polymerase
what drug delays resistance to dapsone when used for leprosy?: rifampin
resistance mechanism for penicillins/cephalosporins: beta-lactamase cleavage of beta lactam ring
resistance mechanism for aminoglycosides: modification via acetylation, adenylation, or phosphorylation
resistance mechanism for chloramphenicol: modification via acetylation
resistance mechanism for macrolides: methylation of rRNA near erythromycin's ribosome binding site
resistance mechanism for tetracycline: decreased uptake or increased transport out of cell
resistance mechanism for sulfonamides: altered enzyme (bacterial dihydropteroate synthetase), decreased uptake, or increased PABA synthesis
mechanism of action of amphotericin B: binds ergosterol (unique to fungi); forms membrane pores that allow leakage of electrolytes and disrupt homeostasis
drug of choice for systemic mycoses: amphotericin B
amphotericin B toxicity: fever/chills, hypotension, nephrotoxicity, arrhythmias, hypochromic normocytic anemia
do ketoconazole and ampho B act synergistically?: no - they antagonize each other's actions, so should never be used together
which has greater oral availability - amoxicillin or ampicillin?: amOxicillin
spectrum of ampicillin, amoxicillin: HELPS kill enterococci: h. flu, e. coli, listeria, proteus, salmonella, enterococci
cefazolin and cephalexin are what generation cephalosporins?: first
coverage of cefazolin and cephalexin?: proteus, e. coli, klebsiella and gram +
cefoxitin, cefaclor, cefuroxamine are what generation?: second
coverage of cefoxitin, cefaclor, cefuroxamine?: h. flu, enterobacter, neisseria, proteus, e. coli, klebsiella
ceftriaxone, cefotaxime, and ceftazidime are what generation?: third
use of ceftriaxone, cefotaxime, and ceftazidime?: serious gram-negative infections resistant to other beta lactams; meningitis; ex. ceftazidime for pseudomonas, ceftriaxone for gonorrhea
cefepime, cefpiramide belong to what generation?: fourth
use of cefepime, cefpiramide?: increased activity against pseudomonas and gram-positive organisms
serum-like sickness in infants and kids can be seen with what cephalosporin?: ceflacor (2nd generation)
this is an inhibitor of renal dihydropeptidase I: cilastin - decreases inactivation of imipenem in renal tubules
why are aminoglycosides ineffective against anaerobes?: require O2 for uptake
drug used for bowel surgery?: neomycin
this tetracycline is an ADH antagonist - acts as a diuretic in SIADH: demeclocylcine
clinical use of tetracyclines?: VACUUM THe BedRoom: vibrio cholerae, acne, chlamydia, ureaplasma urealyticum, mycoplasma, tularemia, h. pylori, borrelia burgdorferi, rickettsia
this drug treats anaerobes above the diaphragm: clindamycin
these drugs can cause leg cramps and myalgias in kids: fluoroquinolones
used for anaerobes below the diaphragm: metronidazole
how does nystatin work?: binds to ergosterol, disrupting fungal membranes (too toxic for systemic use)
mechanism of the -azoles?: inhibit fungal steriod (ergosterol) synthesis
toxicities of -azoles?: hormone synthesis inhibition (gynecomastia), liver dysfunction (inhibition of P450), fever, chills
this antifungal inhibits DNA synthesis by conversion to fluorouracil, which competes with uracil: flucytosine
toxicity of flucytosine: nausea, vomiting, diarrhea, bone marrow suppression
mechanism of caspofungin?: inhibits cell wall syntehsis
use of caspofungin?: invasive aspergillosis
toxicity of caspofungin?: GI upset, flushing
this antifungal inhibits the fungal enzyme squalene epoxidase: terbinafine
use of terbinafene?: used to treat dermatophytoses (especially onychomycosis)
mechanism of griseofulvin?: interferes with microtubule function; disrupts mitosis; depostis in keratin-containing tissues (e.g. nails)
clinical use of griseofulvin?: oral treatment of superficial infections; inhibits growth of dermatophytes (tinea, ringworm)
toxicity of griseofulvin?: teratogenic, carcinogenic, confusion, headaches, increases warfarin metabolism
actions of insulin/insulin-like drugs?: TK activity: liver (increase glucose stored as glycogen), muscle (increase glycogen and protein synthesis, K+ uptake), fat (aids TG storage)
what type of drug: tolbutamide & chlorpropamide?: first generation sulfonylureas
what type of drug: glyburide, glimepiride, glipizide?: second generation sulfonylureas
mechanism of action of sulfonylureas?: close K+ channel in beta cell membrane so cell depolarizes, triggering of insulin release via Ca2+ influx
what are sulfonylureas used for?: stimulate release of endogenous insulin in type 2 DM; require some islet function so useless in type 1
side effects of first generation sulfonylureas?: disulfiram-like reactions
side effect of second generation sulfonylureas?: hypoglycemia
what is the most grave side effect of metformin?: lacti acidosis
can metformin be used in patients without islet function?: yes
action of pioglitazone and rosiglitazone?: increase target cell response to insulin
action of acarbose and miglitol?: alpha glucosidase inhibitors - inhibit intestinal brush border alpha glucosidases; delayed sugar hydrolysis and glucose and glucose absorption lead to decreased postprandial hyperglycemia
mechanism of propylthiouracil, methimazaole?: inhibit organification and coupling of thyroid hormone synthesis - used for hyperthyroidism

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