Comprehensive Pharm 1
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| MOA mannitol | creates an osmotic diuresis because it can't leave the tubule inhibits Na and Cl reabsorption in PC and ascendin loop
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| clinical uses of mannitol | to decrease intractranial pressure or intraocular pressure through volume depletion
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| side effects of mannitol | can cause pulmonary edema d/t extracellular volume expansion, pulling water out of cells hypernatremia
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| contraindications of mannitol | CHF pulmonary edema anuria severe renal failure severe dehydration
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| how is mannitol administered? | parenterally (poorly absorbed PO)
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| MOA spironolactone | K sparing diuretic, antagonizes aldosterone in the DCT, inhibiting Na reabsorption
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| what effect does spironolactone have on Ca | decreases serum Ca levels by directly inhibiting its transport in the DCT
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| clinical uses of spironolactone | HTN pulmonary edema edema from CHF or cirrhosis, nephrotic syndrome primary hyperaldosteronism
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| side effects of spironolactone | gynecomastia (and other anti-androgenic effects) hyperkalemia hyponatremia hypochlroemic acidosis (blocks aldosterone's effect on Na/H antiporter)
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| MOA amiloride | K sparing diuretic, directly inhibits Na reabsorption, independent of aldosterone increased Ca reabsorption
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| uses of amiloride | treats ca stones
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| differences between amiloride and triamterene? | MOA similar, but triampterene has shorter t1/2
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| MOA furosemide | loop diuretic, blocking NKCC increased urinary excretion of K, Mg, Ca increases RBF without altering GFR
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| clinical uses for furosemide | edema to increase urine output in ARF (although it doesn't alter the course of ARF) hypercalcemia hyperkalemia
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| side effects of furosemide | K wasting metabolic alkalosis Mg depletion ototoxicity hyperuricemia
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| why does hyperuricemia result from furosemide use? | increases urate reabsorption d/t increased proximal Na reabsorption
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| contraindication of furosemide | sulfa allergy
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| which is the only loop diuretic without a sulfa group? | ethacrynic acid
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| MOA HCTZ? | block NaCl transport at the DCT Enhanced Ca reaborption (because Na and Ca compete for ATP dependent reabsorption at DCT)
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| clinical uses of HCTZ? | HTN edema DI (by inducing mild volume depletion) to stop recurrent renal calcium stones
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| contraindication of HCTZ | sulfa allergy
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| side effects of HCTZ | hyperglycemia hyperlipidemia hyperuricemia hypercalcemia melabolic alkalosis Mg depletion
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| 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
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| uses for acetazolamide | acute altitude sickness glaucoma treatment for alkalosis facilitate eexcretion of weak acid (as seen in tumor lysis syndrome)
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| 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
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| contraindications of acetazolamide | sulfa allergy hepatic or renal dz hyperchloremic acidosis hyponatremia hypokalemia
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| what effect does furosemide have on the following serum levels: K HCO3 Ca Mg urate | decreased increased decreased decreased increased
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| what effect does thiazide have on the following serum levels: K HCO3 Ca Mg urate | decrease increase increased decreased increased
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| what effect does spironolactone have on the following serum levels: K HCO3 Ca Mg urate | increased decreased decreased none none
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| what effect does amiloride have on the following serum levels: K HCO3 Ca Mg urate | increased decreased increased none none
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| what effect does acetazolamide have on the following serum levels: K HCO3 Ca Mg urate | decreased decreased none none none
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| which diuretics decrease Mg? | furosemide HCTZ
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| which diuretics increase urate? | furosemide HCTZ
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| contraindication of spironolactone | acute renal failure
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| MOA nitroprusside | vasodilation of arteries and veins contact with RBC --> decomposition of drug and release of NO NO, via activation of guanylate cyclase --> vasodilation
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| clinical uses of nitroprusside | HTN crisis aortic dissection (must be given with B blocker) CHF
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| side effects of nitroprusside | hypotension reflex tachy CN release
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| contraindications for nitroprusside | known inadequate cerebral circulation hepatic/renal dz (increases thiocyanate toxicity)
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| 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
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| uses of nitroglyceride | treats angina (decresae coronary asospasm) CHF HTN
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| side effects of nitroglycerine | hypotension, tachycardia, throbbing HA from meningeal arterial dilation
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| 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
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| uses of captopril | HTN CHF ischemic heart disease decreases proteinuria and progression of nephropathy in diabetics
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| side effects of captopril | cough from increased bradykinin can cause renal insufficiency b/c GFR is not increased in low volume states
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| contraindications of captopril | renal insufficiency bilateral renal artery stenosis
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| MOA losartan | AII receptor blocker
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| uses of losartan | HTN CHF
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| side effects of losartan | no cough can't maintain GFR by vasodilation of efferent arterioles
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| 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
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| uses of milrinone | refractory CHF can increase mortality, and should ONLY be used if diuretics, digoxin, and vasodilators have failed a-fib
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| side effects of milrinone | ventricular arrhythmias hypotension hepatotoxicity
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| 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
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| 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
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| uses of digoxin | CHF a fib, a flutter (slows conduction through AV node)
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| side effects of digoxin | narrow therapeutic window visual disturbances, nausea, blurred vision a-tac and AV block can result
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| contraindication of digoxin | hypokalemia 2nd/3rd degree heart block WPW who develop a-fib --> increased impulses through accessory pathway --> VF
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| 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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