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USMLE
Comprehensive Pharm 1
| 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 |
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