Renal Pharmacology Flashcards
Aliskiren MOA? Use? AE?
MOA: Direct Renin Inhibitor (think it Ali’s Renin)=>blocks Angiotensinogen to angiotensin IUSE: HTNAE: Hyperkalemia (No aldosterone)
ACE Inhibitor MOA? Use? Result?
MOA: Blocks formation of AT2 and degradation of bradykininUse: Diabetic Nephropathy, CHFResult: Increased AT1, Increased Bradykinin, decreased aldosterone release
ARBs (Losartan)
MOA: Block AT1 Receptors; Does not interfere with BradykininUse: Diabetic Nephropathy, CHF
ACE Inhibitor AE?
Dry Cough and Angioedema (Bradykinin)!, Hyperkalemia (No aldosterone), Contra in Bilateral renal stenosis=>ARF
ACE Inhibitor (Captopril) MOA? Use? Result?
MOA: Blocks formation of AT2 and degradation of bradykinin
Use: Diabetic Nephropathy, CHF=>Result: Increased AT1, Increased Bradykinin, decreased aldosterone release
ACE Inhibitor AE?
Dry Cough and Angioedema (Bradykinin)!
Teratogen (Renal) problems,
Increased Creatinine, Hyperkalemia (No aldosterone), Contra in bilateral renal Stenosis=>ARF, “CATCHS cough”
Mannitol MOA? Use?
MOA: Osmotic diuretic=>increase urine flow
Use: Rhadbdomyolysis (myoglobinuria)
Acetazolamide MOA? Use?
Carbonic anhydrase inhibitor=> decreased HCO3− stores.
Use: High Altitude Sickness
Acetazolamide AE?
Hyperchloremic metabolic acidosis, paresthesias=>hypokalemia, Renal Stones
Loop Diuretics MOA? Use?
MOA: 1. Sulfonamide loop diuretics. Inhibit cotransport system (Na+/K+/2Cl−)
2. Stimulate PGE release
Use: DOC for HF, cirrhosis, nephrotic syndrome, pulmonary edema
Loop Diuretics AE?
Ototoxicity, Hypokalemia, Dehydration, Allergy (sulfa), Nephritis (interstitial), Gout.
Why use Ethacrynic acid?
Diuresis in patients allergic to sulfa drugs.
Thiazide MOA?
MOA: Inhibit NaCl reabsorption in early DCT diluting capacity of nephron. Decreased Ca2+ excretion
Thiazide AE?
HyperGLUC
Spironolactone and eplerenone MOA?
competitive aldosterone receptor antagonists in cortical collecting tubule
