Term
|
Definition
MOA: Osmotic diuresis; increase tubular fluid osmolarity, producing increased urine flow, decreased intracranial/intraocular pressure
Use: drug overdose, elevated intracranial/intraocular pressure
Toxicity: pulmonary edema, dehydration. CI in anuria, CHF |
|
|
Term
|
Definition
MOA: CA inhibitor; causes self-limited NaHCO3 diuresis & reduction in total body HCO3- stores
Use: glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, pseudotumor cerebri
Toxicity: hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy |
|
|
Term
|
Definition
MOA: sulfonamide loop diuretic. Inhibits cotransport (Na/K/2Cl) of thick ascending limb of loop of Henle. Abolishes hypertonicity of medulla, preventing concentration of urine. Stimulates PGE release (vasodilatory effect on afferent arteriole); inhibited by NSAIDs. Increases Ca2+ excretion; loops lose Ca2+
Use: edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), HTN, hypercalcemia
Toxicity: ototoxicity, hypokalemia, dehydration, allergy (sulfa), nephritis (interstitial), gout |
|
|
Term
|
Definition
MOA: phenoxyacetic acid derivative (not a sulfonamide). Loop diuretic.
Use: Diuresis in patients allergic to sulfa drugs.
Toxicity: similar to furosemide, can cause hyperuricemia, never use to treat gout |
|
|
Term
|
Definition
MOA: thiazide diuretic. Inhibits NaCl reabsorption in early distal tubule, reducing diluting capacity of the nephron. Decrease Ca2+ excretion.
Use: HTN, CHF, idiopathic hypercalciuria, nephrogenic DI
Toxicity: hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia, sulfa allergy |
|
|
Term
| Spironolactone, eplerenone |
|
Definition
MOA: competitive aldosterone R antagonists in the cortical collecting tubule
Use: hyperaldosteronism, K+ depletion, CHF
Toxicity: hyperkalemia (can lead to arrhythmia), endocrine effects of spironolactone (gynecomastia, antiandrogen effects) |
|
|
Term
|
Definition
MOA: Act at corical collecting tubule blocking ENaC Na channels
Use: hyperaldosteronism, K+ depletion, CHF
Toxicity: hyperkalemia (can lead to arrhythmia), endocrine effects of spironolactone (gynecomastia, antiandrogen effects) |
|
|
Term
| Ace Inhibitors: Captopril, enalapril, lisinopril |
|
Definition
MOA: Inhibit ACE causing decreased angiotensin II, dec GFR by preventing constriction of efferent arterioles. Levels of renin increases as a result of loss of feedback inhibition. Inhibition of ACE also prevents inactivation of bradykinin (vasodilator)
Use: HTN, CHF, proteinuria, diabetic renal disease. Prevent unfavorable heart remodeling as a result of chronic HTN
Toxicity: Cough, angioedema, teratogen (fetal renal malformations), creatinine increase (dec GFR), hyperkalemia, hypotension. Avoid in bilateral renal artery stenosis, because ACE inhibitor will further decrease GFR leading to renal failure. |
|
|
