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Pharm - Renal
Renal Pharmacology from First Aid 2013
| Question | Answer |
|---|---|
| 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
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