USMLE

Description:	Comprehensive Pharm 1
Category:	USMLE
Created by:	Asclepius on 2008-10-22

Question	Answer
MOA mannitol	creates an osmotic diuresis because it can't leave the tubule inhibits Na and Cl reabsorption in PC and ascendin loop
clinical uses of mannitol	to decrease intractranial pressure or intraocular pressure through volume depletion
side effects of mannitol	can cause pulmonary edema d/t extracellular volume expansion, pulling water out of cells hypernatremia
contraindications of mannitol	CHF pulmonary edema anuria severe renal failure severe dehydration
how is mannitol administered?	parenterally (poorly absorbed PO)
MOA spironolactone	K sparing diuretic, antagonizes aldosterone in the DCT, inhibiting Na reabsorption
what effect does spironolactone have on Ca	decreases serum Ca levels by directly inhibiting its transport in the DCT
clinical uses of spironolactone	HTN pulmonary edema edema from CHF or cirrhosis, nephrotic syndrome primary hyperaldosteronism
side effects of spironolactone	gynecomastia (and other anti-androgenic effects) hyperkalemia hyponatremia hypochlroemic acidosis (blocks aldosterone's effect on Na/H antiporter)
MOA amiloride	K sparing diuretic, directly inhibits Na reabsorption, independent of aldosterone increased Ca reabsorption
uses of amiloride	treats ca stones
differences between amiloride and triamterene?	MOA similar, but triampterene has shorter t1/2
MOA furosemide	loop diuretic, blocking NKCC increased urinary excretion of K, Mg, Ca increases RBF without altering GFR
clinical uses for furosemide	edema to increase urine output in ARF (although it doesn't alter the course of ARF) hypercalcemia hyperkalemia
side effects of furosemide	K wasting metabolic alkalosis Mg depletion ototoxicity hyperuricemia
why does hyperuricemia result from furosemide use?	increases urate reabsorption d/t increased proximal Na reabsorption
contraindication of furosemide	sulfa allergy
which is the only loop diuretic without a sulfa group?	ethacrynic acid
MOA HCTZ?	block NaCl transport at the DCT Enhanced Ca reaborption (because Na and Ca compete for ATP dependent reabsorption at DCT)
clinical uses of HCTZ?	HTN edema DI (by inducing mild volume depletion) to stop recurrent renal calcium stones
contraindication of HCTZ	sulfa allergy
side effects of HCTZ	hyperglycemia hyperlipidemia hyperuricemia hypercalcemia melabolic alkalosis Mg depletion
MOA acetazolamide	Carbonic anhydrase inhibitor so it inhibits the reabsorption of HCO3- in PCT also CA is in ciliary body of eye and in choroid plexus cells, so it decreases aqueous humor production and increases CSF production
uses for acetazolamide	acute altitude sickness glaucoma treatment for alkalosis facilitate eexcretion of weak acid (as seen in tumor lysis syndrome)
side effects of acetazolamide	encephalopathy (from decreased excretion of NH3 in urine) renal stones b/c calcium phosphate is less soluble in alkaline urine hyperchloremic metabolic acidosis
contraindications of acetazolamide	sulfa allergy hepatic or renal dz hyperchloremic acidosis hyponatremia hypokalemia
what effect does furosemide have on the following serum levels: K HCO3 Ca Mg urate	decreased increased decreased decreased increased
what effect does thiazide have on the following serum levels: K HCO3 Ca Mg urate	decrease increase increased decreased increased
what effect does spironolactone have on the following serum levels: K HCO3 Ca Mg urate	increased decreased decreased none none
what effect does amiloride have on the following serum levels: K HCO3 Ca Mg urate	increased decreased increased none none
what effect does acetazolamide have on the following serum levels: K HCO3 Ca Mg urate	decreased decreased none none none
which diuretics decrease Mg?	furosemide HCTZ
which diuretics increase urate?	furosemide HCTZ
contraindication of spironolactone	acute renal failure
MOA nitroprusside	vasodilation of arteries and veins contact with RBC --> decomposition of drug and release of NO NO, via activation of guanylate cyclase --> vasodilation
clinical uses of nitroprusside	HTN crisis aortic dissection (must be given with B blocker) CHF
side effects of nitroprusside	hypotension reflex tachy CN release
contraindications for nitroprusside	known inadequate cerebral circulation hepatic/renal dz (increases thiocyanate toxicity)
MOA nitroglycerine	via guanylate cyclase --> increase cGMP which activates cAMP protein dependent kinases and leads to dephosphorylation of myosin light chains and decreased intracellular Ca --> relaxation of veins and increased venous capacitance
uses of nitroglyceride	treats angina (decresae coronary asospasm) CHF HTN
side effects of nitroglycerine	hypotension, tachycardia, throbbing HA from meningeal arterial dilation
MOA captopril	ACE inhibitor blocks formation of AII and degradation of bradykinin so, inhibits constriction of efferent arteriole, and potentiates vasodilation caused by bradykinin also causes venous vasodilation
uses of captopril	HTN CHF ischemic heart disease decreases proteinuria and progression of nephropathy in diabetics
side effects of captopril	cough from increased bradykinin can cause renal insufficiency b/c GFR is not increased in low volume states
contraindications of captopril	renal insufficiency bilateral renal artery stenosis
MOA losartan	AII receptor blocker
uses of losartan	HTN CHF
side effects of losartan	no cough can't maintain GFR by vasodilation of efferent arterioles
MOA milrinone	inhibits PDE III --> dilation of arteries and veins PDE III inactivates cAMP, so this process is inhibited --> increased Ca reflux in myocardium, with increased cardiac contractility
uses of milrinone	refractory CHF can increase mortality, and should ONLY be used if diuretics, digoxin, and vasodilators have failed a-fib
side effects of milrinone	ventricular arrhythmias hypotension hepatotoxicity
MOA sildenafil	blocks PDE V action (thus potentiating the action of cGMP dependent kinases that activate phosphatases that encourage the relaxation of smoooth muscle) also decreases the Ca concnetration --> smooth muscle relaxation
MOA digoxin	blocks the Na-K pump --> increased Na intracellularly this inhibits the Na concentration gradient from forming, blocking the Ca from leaving the cells this improves cardiac contractility also slows the conduction through AV node
uses of digoxin	CHF a fib, a flutter (slows conduction through AV node)
side effects of digoxin	narrow therapeutic window visual disturbances, nausea, blurred vision a-tac and AV block can result
contraindication of digoxin	hypokalemia 2nd/3rd degree heart block WPW who develop a-fib --> increased impulses through accessory pathway --> VF
what abnormalities can be seen on the EKG on a person taking digoxin	incresaed PR, decreased QT, scooping of ST segments, T wave inversion