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Renal Pharmacology

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navyy's version from 2017-09-10 20:02

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Mannitol mechanismOsmotic diuretic, ↑tubular fluid osmolarity. producing ↑urine flow
Mannitol clinical useShock (with Furosemide: Acute Renal Insufficiency in shock), drug overdose, increased ICP/Intraocular pressure - used to ↓ extracellular fluid volume
Mannitol toxicityPulmonary edema, dehydration . Contraindicated in anuria, CHF
Acetazolamide mechanismCarbonic anhydrase inhibitor. Causes self-limited NaHCO3 diuresis and reduction in total-body HCO3 stores.
Acetazolamide clinical useGlaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness
Acetazolamide toxicityHyperchloremic metabolic acidosis, neuropathy, NH3 toxicity, sulfa allergy
Furosemide MechanismSulfonamide loop diuretic. Inhibits cotransport system (Na+, K+, 2 CI-) of thick ascending limb of loop of Henle. Abolishes hypertonicity of medulla, preventing concentration of urine. ↑Ca2+ excretion. Loops lose calcium.
Furosemide clinical useEdematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), HTN, hypercalcemia
Furosemide ToxicityOtotoxicity, Hypokalemia, Dehydration, Allergy (sullfa), Nephritis (interstitial), Gout - OH DANG
Ethacrynic acid mechanismPhenoxyacetlc acid derivative (NOT a sulfonamide). Essentially same action as furosemide.
Ethacrynic acid clinical useDiuresis in patients allergic to sulfa drugs
Ethacrynic toxicitySimilar to furosemide, cause hyperuricemia, acute gout (never used to treat gout)
HCTZ mechanismInhibits NaCI reabsorption in early distal tubule, reducing diluting capacity of the nephron . ↓ Ca2+ excretion.
HCTZ clinical useHypertension, CHF, idiopathic hypercalciuria (IH)- Decreases Ca in urine by reabsorbing it, nephrogenic diabetes Insipidus (creates a little hypovolemia to induce reabsorption by tubules)
HCTZ toxicityHypokalemic metabolic alkalosis, hypponatremla, hyperGlycemia, hyperLipidemla, hyperUricemia, and Hypercalcemia. Sulfa allergy. . - HyperGLUC
K+ sparing diureticsSpironolactone, Triamterene, Amiloride, eplerenone
Spironolactone mechanisma competitive aldosterone receptor antagonist in the cortical collecting tubule (CCT)
Triamterene and amiloride mechanism act atCCT by blocking Na+ channels in the CCT.
K+ sparing diuretics clinical useHyperaldosteronism, K+ depletion, CHF
K+ sparing diuretics toxicityHyperkalemia (can lead to arrhythmias), endocrine effects with aldosterone antagonists (e.g.,spironolactone causes gynecomastia, antiandrogen effects).
Diuretic effects on Urine NaCl↑(all diuretics-carbonic anhydrase inhIbitors, loop diuretics, thiazides, K+-sparing diuretics). Serum NaCI may ↓ as a result.
Diuretic effects on Urine K+↑ (all except K+ sparing) - serum K+ may decrease as a result
Diuretic that cause acidemia Carbonic anhydrase inhibitors, ↓HC03- reabsorption. K+ sparing aldosterone blockade prevents K+ secretion and H+ secretion. Additionally. hyperkalemia leads to K+ entering all cells (via H+/K+ exchanger) in exchange for H+ exiting cells.
Diuretics that cause alkalemiaLoop diuretics and thiazides cause alkalemia through several mechanisms: 1. Volume contraction → ↑AT II → ↑ Na+/H+ exchange in proximal tubule → ↑ HCO3 ("contraction alkalosis") 2. K+ loss leads to K+ exiting all cells (via H+/K+ exchanger) in exchange for H+ entering cells 3. In low K+ state, H+ (rather than K+) is exchanged for Na+ in cortical collecting tubule, leading to alkalosis and "paradoxical aciduria”
Diuretics that increase urine Caloop diuretics: Abolish lumen-positive potential in thick ascending Iimb of loop of Henle →↓ paracellular Ca+ reabsorption → hypocalcemIa, ↑ urinary Ca
Diuretics that decrease urine Cathiazides: Volume depletion → upregulation of sodium reabsorption→ enhanced paracellular Ca reabsorption in proximal tubule and loop of Henle. Thiazide also block luminal Na+/CI- co transport in distal convoluted tubule → ↑NA+ gradient →↑ interstitial Na+/Ca exchange → hypercalcemia.
ACE inhibitorsCaptopril, enalapril, lisinopril
ACE inhibitor mechanismInhibit angiotensin -converting enzyme, reducing levels of angiotensin II and preventing inactivation of bradykinin, a potent vasodilator. Renin release is ↑ due to loss of feedback inhibition
Losartan (ARB)
mechanism
angiotensin II receptor antagonist - is not an ACE inhibitor - does not cause cough
ACE inhibitor clinical useHTN, CHF, diabetic renal disease
ACE inhibitor ToxicityCough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy prob lems (fetal renal damage), Rash, Increased renin, Lower angiotensin II . Also hyperkalemia. Avoid with bilateral renal artery stenosis because ACE Inhibitors significantly ↓ GFR by preventing constriction of different arterioles. CAPTOPRIL
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