FA - Renal Pharmacology Flashcards
What is the osmolarity in Bowman’s capsule?
290 mOsm (isotonic)
What is the osmolarity in PCT?
290 mOsm (isotonic)
What diuretics act on the PCT?
Acetazolamide (CA inhibitor)
What is the osmolarity in the proximal straight tubule?
600 mOsm
What diuretics act on the proximal straight tubule?
Mannitol
What is the osmolarity in the thin descending limb of Henle?
800 mOsm
What is the osmolarity at the bottom of the loop of Henle?
1200 mOsm
What is the osmolarity in the TAL?
600 mOsm
What diuretics act on the TAL?
Loop diuretics (furosemide, torsemide), ethacrynic acid
What is the osmolarity in the DCT?
80-100 mOsm
What diuretics act on the DCT?
Thiazides
What is the osmolarity in the CD?
50 - 1200 mOsm (depends on action of ADH)
What diuretics act on the CD?
Potassium-sparing diuretics (spironolactone, eplerenone, amiloride, triamterene)
What is the MOA of mannitol?
Osmotic diuretic –>increases tubular fluid osmolarity producing increased urine flow, decreased ICP/IOP
What are the clinical uses of mannitol?
Drug overdose, elevated ICP/IOP
What are the AEs of mannitol?
Pulmonary edema, dehydration, dilutional hyponatremia, hyperkalemia, metabolic acidosis
What are the contraindications for mannitol use?
Anuria, CHF
What is the MOA of acetazolamide?
CA inhibitor; causes self-limited NaHCO3 diuresis and reduction in total-body HCO3- stores
What are clinical uses of acetazolamide?
Glaucoma (decreased aqueous humor production), urinary alkalinization, altitude sickness, pseudotumor cerebri, drug-induced edema, CHF
What are the AEs of acetazolamide?
Hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy, hypokalemia
What is the MOA of loop diuretics?
Inhibits co-transport system (Na+, K+, 2Cl-) of TAL. Abolishes hypertonicity of medulla, preventing concentration of urine.
Stimulates PGE release –>aff arteriole dilation (effect also inhibited by NSAIDs)
Increases Ca++ excretion
What are the clinical uses of loop diuretics?
Edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), hypertension, hypercalcemia
What are the AEs of loop diuretics?
Ototoxicity, hypokalemia, dehydration, allergy, nephritis, gout (OH DANG)
Hyperuricemia, hypocalcemia, hypomagnesemia, and metabolic (contraction) alkalosis
What is the MOA of ethacrynic acid?
Phenoxyacetic acid derivative; works similarly to furosemide
What is the clinical use of ethacrynic acid?
Diuresis in patients allergic to sulfa drugs
What are the AEs of ethacrynic acid?
Similar to furosemide; can cause hyperuricemia so do not use to treat gout. Also may generate PVCs if given with digoxin.
What is the MOA of thiazide drugs?
Inhibits NaCl reabsorption in the early distal tubule, reducing diluting capacity of the nephron –>decreased Ca++ excretion
What are the clinical uses of thiazides?
HTN (including isolated systolic HTN), CHF, idiopathic hypocalciuria, nephrogenic DI
What are the AEs of thiazides?
Hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia, sulfa allergy
What is the MOA of K+ sparing diuretics?
Spiro and eplerenone: competitive MR antagonists
Amiloride and triamterene: block Na+ channels in CCTs
What are the clinical uses of K+ sparing diuretics?
Hyperaldosteronism, K+ depletion, CHF (spiro used to prevent aldosterone-mediated adverse remodeling in stage III/IV HF)
What are the AEs of K+ sparing diuretics?
Hyperkalemia, endocrine effects with spironolactone (gynecomastia, antiandrogenic effects)
How is urine NaCl affected with diuretic use?
Increased, may also see decreased serum NaCl
How is urine K+ affected with diuretic use?
Increased (except for K+ sparing), serum K+ may decreased as a result
How is blood pH affected by diuretic use?
Acidemia with CA inhibitors and K+ sparing diuretics, alkalemia with loop diuretics and thiazides
How is urine Ca++ affected by diuretic use?
Increases with loop diuretics, decreases paracellular Ca++ reabsorption –>hypocalcemia
Decreases with thiazide use, enhances paracellular Ca++ reabsorption in PCT and loop of Henle
What is the MOA of ACE inhibitors?
Inhibit ACE –>decrease ANGII –>decrease GFR by preventing efferent arteriole constriction
Also prevents inactivation of bradykinin –>vasodilator
Results in increased renin production
What are the clinical uses of ACEi?
HTN, CHF, diabetic renal dz, prevents unfavorable heart remodeling as a result of chronic HTN
What are the AEs of ACEi’s?
Cough, angioedema, teratogen (fatal renal malformations), creatinine increase as a result of dec. GFR, hyperkalemia, hypotension (esp. 1st dose)
Avoid in bilateral renal artery stenosis due to dec GFR effect
What is the MOA of ARBs?
Prevent action of ANGII at AT1 receptor; no effect on bradykinin
What are the clinical uses of ARBs?
Similar to ACEi
What are the AEs of ARBs?
Similar to ACEi, risk of cough is reduced
