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Renal Pharmacology

  1. 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
  2. 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"
  3. 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!"
    • Image Upload 1
  4. 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!)
  5. 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

    "hyperGLUC"

    Image Upload 2
  6. 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)

    Image Upload 3
  7. Diuretics: Urine NaCl
    Increase urine NaCl in ALL diuretics

    • Serum NaCl may decrease as a result
    • HYPONATREMIA
  8. Diuretics: Urine K+
    Increase urine K+ in all diuretics EXCEPT K-sparing diuretics

    • Serum K+ may decrease as a result
    • HYPOKALEMIA
  9. 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"
  10. 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
  11. 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)
Author
jknell
ID
206255
Card Set
Renal Pharmacology
Description
Step I
Updated

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