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jknell
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Mannitol
- MOA:
- -osmotic diuretic
- -↑ tubular fluid osmolarity producing ↑ urine flow
- -↓ Intracranial/intraocular pressure
- -functions at proximal tubule
- Clinical Use:
- -drug OD
- -elevated intracranial/intraocular pressure
- Toxicity:
- -pulmonary edema
- -dehydration
- Contraindications:
- -anuria
- -CHF
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Acetazolamide
Carbonic Anhydrase Inhibitor (CAI)
- Mechanism:
- -blocks carbonic anhydrase
- -causes self-limited NaHCO3- diuresis and reduction in total body HCO3- stores
- -works at proximal tubule
- Clinical Use:
- -glaucoma
- -urinary alkalinization
- -metabolic alkalosis
- -altitude sickness
- -pseudotumor cerebri
- Toxicity:
- -hyperchloremic metabolic acidosis
- -paresthesias
- -NH3 toxicity
- -sulfa allergy
"ACIDazolamide causes ACIDosis"
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Furosemide
Loop Diuretics
- Mechanism:
- -sulfonamide loop diuretic
- -inhibits NKCC2 in thick ascending limb of the loop of Henle
- -abolishes hypertonicity of medulla (prevents concentration of urine)
- -stimulates PGE release (vasodilatory effect on afferent arteriole)
- **inhibited by NSAIDs
- -increased Ca2+ excretion
- "Loops Lose calcium"
- Clinical Uses:
- -edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema)
- -hypertension
- -hypercalcemia
- Toxicity:
- -Otoxicity
- -Hypokalemia
- -Dehydration
- -Allergy (sulfa)
- -Nephritis (interstitial)
- -Gout
- "OH DANG!"

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Ethacrynic Acid
- Mechanism:
- -phenoxyacetic acid derivative (NOT a sulfonamide)
- -essentially same action as furosemide
- Clinical Use:
- -diuresis in patients allergic to sulfa drugs
- Toxicity:
- -similar to furosemide
- -can cause hyperuricemia (NEVER USE TO TX GOUT!)
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Hydrochlorithiazide
Thiazide diuretic
- Mechanism:
- -inhibits NaCl reabsorption in early distal tubule (inhibits NCC)
- -reduces diluting capacity of the nephron
- -decreases Ca2+ excretion
- Clinical Use:
- -Hypertension
- -CHF
- -Idiopathic hypercalciuria
- -nephrogenic diabetes insipidus
- Toxicity:
- -hypokalemic metabolic alkalosis
- -hyponatremia
- -hyperGlycemia
- -hyperLipidemia
- -hyperUricemia
- -hyperCalcemia
- -Sulfa allergy
"hyper GLUC"
-
K+-Sparing Diuretics
- Spironolactone and eplerenone
- Triamterene and Amiloride
"The K+ STAys"
- Mechanism:
- -Spironolactone and eplerenone are competitive aldosterone receptor antagonists in the cortical collecting tubule
- -Triamterene and Amiloride act at CCT to block ENaC
- Clinical Use:
- -hyperaldosteronism
- -K+ depletion
- -CHF
- Toxicity:
- -hyperkalemia (arrhythmias)
- -endocrine effects with spironolactone (gynecomastia and antiandrogen effects)
-
Diuretics: Urine NaCl
Increase urine NaCl in ALL diuretics
- Serum NaCl may decrease as a result
- HYPONATREMIA
-
Diuretics: Urine K+
Increase urine K+ in all diuretics EXCEPT K-sparing diuretics
- Serum K+ may decrease as a result
- HYPOKALEMIA
-
Diuretics: blood pH
- ACIDEMIA:
- -CAI (decrease HCO2- absorption)
- -K-sparing (block aldo and prevent K+ and H+ secretion/hyperkalemia leads to K+ shift intracellularly with compensatory H+ shift out of cells)
- ALKALEMIA:
- -Loop Diuretics/Thiazide Diuretics
- 1. volume contraction → ATII → Na/H exchanger activity in PT → increased HCO3- reabsorption ("contraction alkalosis")
- 2. K+ loss leads to K+ shift out of cells in exchange for H+ entering cells
- 3. In low K+ state, H+ is exchanged for Na+ instead of K+ in the CCT leading to alkalosis and "paraxodical aciduria"
-
Diuretics: Urine Ca2+
- Increase urine Ca2+
- -loop diuretics (decrease paracellular Ca2+ reabsorption)
- -HYPOCALCEMIA
- Decrease urine Ca2+
- -thiazide diuretics (enhanced paracellular Ca2+ reabsorption in proximal tubule and loop of henle)
- -HYPERCALCEMIA
-
ACE Inhibitors
Captopril, Enalapril, Lisinopril
- Mechanism:
- -inhibit ACE
- -decrease generation of ATII → ↓GFR by preventing constriction of efferent arterioles
- -increased levels of renin due to loss of feedback inhibition
- -also prevents inactivation of bradykinin (vasodilator)
- Clinical Uses:
- -hypertension
- -CHF
- -proteinuria
- -diabetic renal disease
- *prevent unfavorable heart remodeling as a result of chronic HTN
- Toxicity:
- -Cough
- -Angioedema
- -Teratogen (fetal renal malformation)
- -Cr increase (decrease GFR)
- -Hyperkalemia
- -Hypotension
- "Captopril's CATCHH"
- Contraindicated:
- -bilateral renal artery stenosis b/c ACEI further decrease GFR → renal failure
ARBs (-sartans) have effects similar to ACE inhibitors but do not increase bradykinin (no cough or angioedema)
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