Renal Flashcards

1
Q

Mannitol
mech, clin use, toxicity
C/I’d in?

A
  • osmotic diuretic -> incr’d urine and decr’d intracranial/ocular P
  • drug overdose, high intracranial/ocular P
  • pulm edema, dehydration
  • C/I’d in anuria, CHF
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2
Q

Acetazolamide

mech, clin use, toxicity

A
  • CA inhib -> sm NaHCO3 diuresis, reduces total body HCO3-
  • glaucoma, urinary alkalinization, metabolic alk, altitude sickness, pseudotumor cerebri
  • hyperCl metab acidosis, paresthesias, NH3 tox, sulfa allergy
    “ACID”azolamide causes ACIDosis
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3
Q

Furosemide

type, mech, clin use, toxicity

A
  • loop diuretic (sulfa drug)
  • inhibits Na/K/2Cl in TAL of LOH, gets rid of hypertonicity of medulla so can’t conc urine, stim’s PGE release (vasodil aff art), inhib’d by NSAIDs, incr’d Ca excretion (HYPERcalciuria) (Mg and Ca aren’t reab’d)
    “Loops Lose Calcium”
  • Edema, HTN, hyperCa
  • “OH DANG!” ototox, hypoK, dehydration, allergy (sulfa), nephritis (interstitial), gout
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4
Q

Ethacrynic acid

type, mech, clin use, toxicity

A
  • loop diuretic
  • phenooxyacetic acid derivative (not a sulfonamide), blocks Na/K/2Cl transporter
  • diuresis in pt’s allergic to sulfa drugs
  • similar to furosemide, can cause hyperuricemia, never use to treat gout
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5
Q

Hydrochlorothiazide

mech, clin use, toxicity

A
  • thiazide diuretic, inhibits NaCl reab’n in early DT, reduces diluting ability of nephron, decr’d Ca excretion (HYPOcalciuria)
  • HTN, CHF, idiopathic hypercalciuria, nephrogenic DI
  • “HyperGLUG” hypoK metab acidosis, hypoNa, hyperGlc, hyperLipidemia, hyperUricemia, hyperCalcemia; sulfa allergy
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6
Q

K+-sparing diuretics
examples
mech, clin use, toxicity

A

Spironolactone and eplerenone
Triamterene and Amiloride
“The K+ STAys”
- spironolactone/eplerenone are competitive aldos R antag’s in cortical CT; triamterene/amiloride block Na+ ch’s in CCT
- hyperaldos, K+ depletion, CHF
- hyperK, endo effects w/ spironolactone (gynecomastia, antiandrogen effects)

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7
Q
Diuretics - electrolyte changes:
Urine NaCl?
Urine K+?
bl pH?
Urine Ca2+?
A
  • incr’d, serum NaCl may decr as result
  • incr’s (except w/ K+ sparing ones), serum K+ may decr
  • decr’d (acidemia) w/ CA inhib’s (less HCO3- reab’n), K+ sparing (no K+ secretion and H+ secretion, also more K+ into cells and more H+ out)
    incr’d (alkalemia) w/ loop diuretics and thiazides bc vol contraction, K+ loss so K+ out and H+ into cells, low K+ so H+ (not K+) exchanged for Na+ in CCT
  • incr’d w/ loop diuretics (decr’d paracellular Ca reab’n)
    decr’d w/ thiazides (more paracell Ca reab’n)
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8
Q

ACEIs
examples
mech, clin use, toxicity
avoid in?

A

“-pril” captopril, enalapril, lisinopril

  • inhibit ACE -> decr’d ATII -> decr’d GFR, incr’d renin, prevents inact’n of bradykinin -> vasodilation
  • HTN, CHF, proteinuria, DM renal dz
  • “Captopril’s CATCHH” Cough, Angioedema, Teratogen (fetal renal malform’s), Cr incr (decr’d GFR), HyperK, Hypotension
  • Avoid in bilat renal art stenosis bc will further decr GFR -> renal failure
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