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USMLE Step I Pharmacology > Renal Pharmacology > Flashcards

Renal Pharmacology Flashcards

1
Q

mannitol–mechanism

A
  • osmotic diuretic
    • increase tubuar fluid osmolarity –> increase urine flow, decrease intracranial/intraocular pressure
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2
Q

mannitol–use

A
  • drug overdose
  • elevated intracranial/intraocular pressure
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3
Q

mannitol–toxicity

A
  • pulmonary edema
  • dehydration
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4
Q

what are contraindications for mannitol?

A
  • anuria
  • HF
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5
Q

acetazolamide–mechanism

A
  • carbonic anhydrase inhibitor
  • causes self limited NaHCO3 diuresis and decrease in total body HCO3- stores
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6
Q

acetazolamide–use

A
  • glaucoma
  • urinary alkalinization
  • metabolic alkalosis
  • altitude sickness
  • pseudotumor cerebri
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7
Q

acetazolamide–toxicity

A
  • proximal renal tubular acidosis
  • paresthesias
  • NH3 toxicity
  • sulfa allergy
    • “ACIDazolamide causes ACIDosis”
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8
Q

name the 4 loop diuretics

A
  • furosemide
  • bumetanide
  • torsemide
  • ethacrynic acid
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9
Q

furosemide, bumetanide, torsemide–mechanism

A
  • inhabit contransport system (Na/K/2Cl) of thick ascending limb of loop of Henle
  • abolishes hypertonicity of medulla which prevents concentration of urine
  • increase Ca2+ excretion
    • Loops Lose Ca2+
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10
Q

furosemide, bumetanide, torsemide–what type of loop diuretic?

A
  • sulfonamide loop diuretic
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11
Q

what does furosemide, bumetanide, torsemide stimulate and what is the effect?

A
  • stimulates the release of PGE
    • vasodilatory effect on afferent arteriole
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12
Q

what is furosemide, bumetanide, torsemide inhibited by?

A

NSAIDs

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13
Q

furosemide, bumetanide, torsemide–use

A
  • edematous states
    • HF
    • cirrhosis
    • nephrotic syndrome
    • pulmonary edema
  • hypertension
  • hypercalcemia
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14
Q

furosemide, bumetanide, torsemide–toxicity

A
  • OH DANG
    • ​Ototoxicity
    • Hypokalemia
    • Dehydration
    • Allergy (sulfa) and Metabolic Alkalosis
    • Nephritis (interstitial)
    • Gout
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15
Q

ethacrynic acid–mechanism

A
  • nonsulfonamide inhibitor of cotransport system (Na/K/2Cl) of thinck ascending limb of loop of Henle
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16
Q

ethacrynic acid–use

A
  • diuresis in patients allergic to sulfa drugs
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17
Q

ethacrynic acid–toxicity

A
  • similar to furosemide
    • more ototoxic
      • “Loop earrings hurt your ears”
  • hyperuricemia
    • never use to treat gout
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18
Q

name the diuretics that work at the PCT:

A
  • mannitol
  • acetazolamide
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19
Q

name the diuretics that work at the loop of Henle:

A
  • furosemide
  • bumetanide
  • torsemide
  • ethacrynic acid
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20
Q

name the diuretics that work at the DCT:

A
  • hydrochlorothiazide
  • chlorthalidone
  • metolazone
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21
Q

name the diuretics that work at the collecting duct:

A
  • K+ sparing diuretics
    • spironolactone
    • eplerenon
    • triamterene
    • amiloride
22
Q

name the thiazide diuretics:

A
  • hydrochlorothiazide
  • chlorthalidone
  • metolazone
23
Q

hydrochlorothiazide, chlorthalidone, metolazone–mechanism

A
  • inhibit NaCl reabsorption in early DCT –> decrease diluting capacity of nephron
    • decrease Ca2+ excretion
24
Q

hydrochlorothiazide, chlorthalidone, metolazone–use

A
  • hypertension
  • HF
  • idiopathic hypercalciuria
  • nephrongenic diabetes insipidus
  • osteoporosis
25
Q

hydrochlorothiazide, chlorthalidone, metolazone–toxicity

A
  • hypokalemic metabolic alkalosis
  • hyponatremia
  • hyperGlycemia
  • hyperLipidemia
  • hyperUricemia
  • hyperCalcemia
    • HyperGLUC
  • sulfa allergy
26
Q

name the potassium sparing diuretics

A
  • Spirinolactone and eplerenone
  • Triamterene
  • Amiloride
    • “the K+ STAys”
27
Q

spironolactone and eplerenone–mechanism

A
  • (K+ sparing)
  • spironolactONE and eplerenONE are competitive aldosterONE receptor antagonists in cortical collecting tubule
28
Q

triamterene and amiloride–mechanism

A
  • (K+ sparing)
  • act at the same part of the tubule by blocking Na+ channels in the cortical collecting tubule
29
Q

K+ sparing diuretics–use

A
  • hyperaldosteronism
  • K+ depletion
  • HF
  • hepatic ascites (spironolactone)
  • nephrongenic DI (amiloride)
30
Q

K+ sparing diuretics–toxicity

A
  • hyperkalemia–can lead to arrhythmias
  • endocrine effects with spironolactone
    • gynecomastia
    • antiandrogen effects
31
Q

diuretic induced electrolyte change: urine NaCl

A
  • inc with all diuretics
    • strength varies on potency of diuretic effect
  • serum NaCl may decrease as a result
32
Q

diuretic induced electrolyte change: urine K+

A
  • inc especially with loop and thiazide diuretics
  • serum K+ may dec as a result
33
Q

diuretic induced electrolyte change: decreased blood pH (acidemia)

A
  • carbonic anhydrase inhibitors
    • decrease HCO3- reabsorption
  • K+ sparing:
    • aldosterone blockade prevents K+ secretion adn H+ secretion
  • hyperkalemia –> K+ entering all cells via H/K exchanger in exchange for H exiting cells
34
Q

diuretic induced electrolyte change: increase in blood pH (alkalemia)

A
  • loop diuretics and thiazides cause alkalemia through severeal mechanisms:
    • volume contraction –> increase AT II –> increase Na/K exchange in PCT –> inc HCO3- reabsorption
      • “contraction alkalosis”
    • K+ loss leads to K+ exiting all cells (via H+/K+ exchanger) in exchange for H+ entering cells
    • in low K+ state, H+ (rather than K+_ is exchanged for Na+ in cortical collecting tubule –> alkalosis and “paradoxical aciduria”
35
Q

diuretic induced electrolyte change: urine Ca2+

A
  • increase with loop diuretics:
    • decrease paracellular Ca2+ reabsorption –> hypocalcemia
  • decrease with thiazides:
    • enhanced Ca2+ reabsorption
36
Q

name the angiotensin converting enzyme inhibitors

A
  • captopril
  • enalapril
  • lisinopril
  • ramipril
37
Q

ACE inhibitors–mechanism

A
  • inhibit ACE –> decrease AT II –> decrease GFR by preventing constriciton of efferent arterioles
  • increase renin due to loss of negative feedback
  • inhibition of ACE also prevent inactivation of bradykinin, a potent vasodilator
38
Q

ACE inhibitors–use

A
  • HTN
  • HF (dec mortality)
  • proteinuria
  • diabetic neuropathy
39
Q

what are 2 things that ACE inhibitors can prevent?

A
  • unfavorable heart remodeling
  • diabetic neuropathy
    • increase intraglomerular pressure, slows GBM thickening
40
Q

ACE inhibitors–toxicity

A
  • “Captopril’s CATCHH”
    • Cough
    • Angiodema
      • due to increased bradykinin
    • Teratogen
      • fetal renal malformation
    • increased Creatinine
      • decrease GFR
    • Hyperkalemia
    • Hypotension
41
Q

what are contraindications for ACE inhibitors?

A
  • CI esterase inhibitor deficiency
  • bilateral renal artery stenosis
42
Q

why are ACE inhibitors contraindicated in bilateral renal artry stenosis?

A
  • b/c ACE inhibitors further decrease GFR –> renal failure
43
Q

name the 3 Angiotensin II receptor blockers (ARBs)

A
  • losartan
  • candesartan
  • valsartan
44
Q

Angiotensin II Receptor Blockers–mechanism

A
  • selectively block binding of angiotensin II to AT1 receptor
  • effects similar to ACE inhibitors
    • but ARBs do not increase bradykinin
45
Q

Angiotensin II Receptor Blockers–use

A
  • HTN
  • HF
  • proteinuria
  • diabetic neuropathy with intolerance to ACE inhibitors
    • ie. cough, angioedema
46
Q

Angiotensin II Receptor Blockers–toxicity

A
  • hyperkalemia
  • decrease GFR
  • hypotension
  • teratogen
47
Q

Aliskiren–mechanism

A
  • direct renin inhibitor
  • blocks conversion of angiotensinogen to angiotensin I
48
Q

Aliskiren–use

A
  • hypertension
49
Q

Aliskiren–toxicity

A
  • hyperkalemia
  • decrease GFR
  • hypotension
50
Q

what is a contraindication for aliskiren?

A
  • patients already taking ACE inhibitors or ARBs

USMLE Step I Pharmacology (17 decks)

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