| Question | Answer |
|---|
| Where does acetazolamide work | PCT |
| Where does mannitol work | thick descending |
| Where does loop diuretics work | thick ascending |
| Where do thiazides work | DCT |
| Where do potassium sparing diuretics work | collecting tubule |
| Where do ADH antagonists work | collecting duct |
| MOA of mannitol | osmotic diuretic. Increases solute load forces water out of cells. |
| Clinical use of mannitol | acute glaucoma, increased ICP |
| A/E of mannitol | pulmonary edema, dehydration. Contraindicated in anuria and HF. |
| MOA of acetazolamide | carbonic anhydrase inhibitor in the PCT. Leads to decrease in HCO3 stores. |
| Clinical of use of acetazolamide | acute angle closure glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, pseudotumor cerebri, uric acid and cysteine stones (by alkalinizing urine) |
| A/E of acetazolamide | hypercholermic metabolic acidosis, NH3 toxicity (retention of ammonia), sulfa allergy. |
| MOA of loop diuretics | inhibits co-transport system (Na/K/2Cl) of thick ascending limb of loop of henle. Abolishes hypertonicity of medulla preventing concentration of urine. Causes calcium lost. |
| Clinical use of loop diuretics | edematous states |
| Toxicity of loop diuretics | OH DANG (ototoxicity, hypokalemia, dehydration, allergy (sulfa), nephritis, gout (hyperuricemia), metabolic alkalosis and hypomagnesimia. |
| Loop diuretics and prostaglands | stimulate prostaglandin release and increase GFR. do not use NSAIDS with loops |
| MOA of ethacrynic acid | essential same as furosemide |
| Clinical use of ethacrynic acid | diuresis in patients with sulfa allergies |
| Toxicity | similar to furosemide |
| MOA of thiazides | inhibit NACL reabsorption in early DCT |
| Clinical use of thiazides | Hypertension!!! Nephrogenic diabetes insipidus, osteoporosis. |
| Toxicity of thiazides | hyperGLUC (hyperglycemia, hyperlipidemia, hyperuricemia, hypercalemia.) Sulfa allergy. Also causes metabolic alkalosis and hypokalemia. |
| Aldosterone antagonists | spironolactone and eplerenone |
| ENAC inhibitors | triamtrene and amiloride |
| Lithium induced nephrogenic diabetes inspidus | amiloride |
| Hyperaldosteronism | spironolactone and eplernone |
| A/E spironolactone | gynecomastia, antiandrogen effects. |
| ARBS | losartan, candesartan, valsartan. |
| Mechanism of ARBS | selectively blocks binding of angiotensin II to receptor. Effects: increase renin, increase angiotensin I, increase angiotensin II decrease in aldosterone. No change bradykinin. |
| Clinical use of ARBS | hypertension, HF, proteinuria, diabetic nephropathy with intolerance to ACEi |
| A/E of ARBS | hyperkalemia. Teratogen. |
| MOA of ACEi | inhibit ACE decreases ATII decreases GFR by dilating efferent arteriole. |
| Relationship between ACEi and bradykinin | inhibition ACE prevents inactivation of bradykinin, a potent vasodilator. |
| Clinical use of ACE i | hypertension, proteinuria, diabetic nephropathy. |
| What is the relationship between ACEi, ARBS and bilateral renal artery stenosis | ACE inhibitors further decrease GFR by dilating efferent arteriole so contraindicated! |
| What are A/E of ACEi think | CAPTOPRIL (Cough, Angioedema, Pregnancy, metallic Taste, hypOtension Potassium elevation, Rash, Increased Renin, Lowered Angiotensin II) |
| MOA of aliskiren | direct re nin inhibitor, blocks conversion of angiotensiongen to angiotensin I. |
| Clinical use of aliskiren | hypertension. |
| A/E of aliskiren | contraindicated in diabetes taking ARBS or ACEi. |
| Which drug could you give to help with calcium nephroliathisis | thiazides |
| why use azetazolamide in altitude sickness | in high altitudes will hyperventilate causing a respiratory alkalosis. To counteract the respiratory alkalosis, azetazolamide will induce a metabolic acidosis. |
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