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Pharm - Renal

Renal Pharmacology from First Aid 2013

Mannitol: MOA, Use, Tox MOA: osmotic diuretic Use: drug O/D, elevated intra-ocular pressure Tox: pulmonary edema, dehydration C/I in CHF, duh
Acetazolamide: MOA, Use, Tox MOA: carbonic anhydrase inhibitor -> bicarb diuresis and decreased HCO3- Use: glaucoma, urine alkalinization, altitude sickness, pseudotumor cerebri Tox: hyperchloremic metablic acidosis, NH3+ toxicity, parasthesia
Name the two major Loop diuretics. Furosemide (sulfa version) Ethacrynic acid (non-sulfa alternative)
Furosemide: MOA, effects Inhibits Na/K/2Cl co-transport Stimulates vaso-dilatory PGE at aff art. Wastes Ca, Mg paracellularly, K-wasting
Furosemide: Toxicities OH DANG! Ototoxicity, Hypokalemia, Dehydration, Allergy (Sulfa), Nephritis (Interstitial), Gout
Hydrochlorothiazide: MOA, effects Inhibits NaCl reabsorption in the early DCT and decreases Ca2+ secretion (Ca-saving). Wastes K and H+ (--> metabolic alkalosis).
Hydrochlorothiazide: Toxicities HyperGLUC: glycemia lipidemia uricemia calcemia
Name some potassium-sparing diuretics. Spironolactone, Triamterene, Amiloride
Spironolactone: MOA, side effects Competitive aldosterone receptor antagonist. Tox: hyperkalemia SFX: anti-androgenic, gynecomastia
Amiloride: MOA, Tox Blocks the Na channels in the CCT. Tox: hyperkalemia
Explain the mechanism of contraction alkalosis. Volume contraction -> inc ATII -> inc Na/H+ exchange in the PCT -> inc bicarb reabsorption
Explain how Loop and Thiazide diuretics cause metabolic alkalosis. (1) K+ loss leads to K+ exiting the cells in exchange for H+ entering into the cells. (2) In a low K-state, H+ (rather than K+) is exchanged for Na+ in the CCT, leading to alkalosis and paradoxical aciduria. (3) Contraction alkalosis.
ACE inhibitors: naming, MOA Nom: "-opril" MOA: Inhibit ACE -> dec ATII -> dec GFR by preventing constriction of eff art -> inc renin.
ACE inhibitors: Toxicities Cough (ACE breaks down bradykinin), angioedema, teratogen, inc Cr (dec GFR), Hyperkalemia, HypoTN
ACE Inhibitors: indications and contraindications Use: HTN, CHF, proteinuria, diabetic renal disease, prevent heart remodeling in HF C/I: avoid in renal artery stenosis, b/c dec in GFR will further exacerbate -> RF.
ARBs: naming, MOA, Use, Tox Nom: "-artan", e.g. losartan MOA: ATII receptor blockers Use: HTN, CHF, just like ACE-Is Tox: same mortality benefits, but no side effect of cough!
Created by: wmwebb89