Renal Flashcards
Mannitol
Uses?
Osmotic diuretic
Increases tubular fluid osmolarity = increases urine flow and decreases intracranial/intraocular pressure
Uses = drug overdose and increased intracranial/intraocular pressure
Mannitol toxicities? (2)
Contraindications? (2)
Pulmonary edema
Dehydration
Contraindicated in anuria and CHF
Acetazolamide
Carbonic anhydrase inhibitor
Causes self-limited NaHCO3 diuresis and decreased total-body HCO3 stores (weak)
Uses = Glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, pseudotumor cerebri
Which diuretic is classically used in the treatment of altitude sickness?
Acetazolamide
Does acetazolamide make the urine more acidic or alkaline?
Alkaline
Is acetazolamide used in the treatment of metabolic acidosis or alkalosis? Does it cause metabolic acidosis or alkalosis?
Used in treatment of metabolic alkalosis as it causes urinary alkalinization
“ACID”azolamide causes ACIDosis
Acetazolamide toxicity
Hyperchloremic metabolic acidosis
Paresthesias
NH3 toxicity
Sulfa allergy
Where does acetazolamide act along the nephron?
Proximal convoluted tubule
Loop diuretic examples
Site of action?
Furosemide
Ethacrynic acid
Inhibit cotransport system (Na/K/2Cl) of THICK ASCENDING limb of loop of Henle
Furosemide
Sulfonamide loop diuretic = inhibits Na/K/2Cl of thick ascending loop of Henle
Abolishes hypertonicity of medulla, preventing concentration of urine
Stimulates PGE release (vasodilatory effect afferent arteriole) = blocked by NSAIDs
Increases Ca2+ excretion (Loops Lose Ca2+)
Furosemide toxicity
Inhibits Na/K/2Cl OTOTOXICITY Hypokalemia Dehydration Allergy (sulfa) Nephritis (interstitial) Gout "OH DANG"
Ethacrynic acid
Phenoxyacetic acid derivative (not a sulfonamide)
Same action as furosemide = inhibits Na/K/2Cl
Used for diuresis in patients with sulfa allergies
Can cause hyperuricemia (never use to treat gout)
Thiazide diuretic
Site of action?
Hydrochlorothiazide
Inhibits NaCl reabsorption in early DISTAL CONVOLUTED TUBULE = decreases diluting capacity of nephron
Decreases Ca2+ excretion
Hydrochlorothiazide toxicity
Thiazide diuretic Hypokalemic metabolic alkalosis Hyponatremia HyperGlycemia HyperLipidemia HyperUricemia HyperCalcemia "HyperGLUC" Sulfa allergy
K+ sparing diuretics
Spironolactone and Eplerenone
Triamterene and Amiloride
Spironolactone and Eplerenone
Site of action?
Toxicity?
K+ sparing
Competitive aldosterone receptor antagonists in the CORTICAL COLLECTING TUBULE
Toxicity = hyperkalemia (can lead to arrhythmias)
Spironolactone toxicity = endocrine effects (gynecomastia, antiandrogen effects)
Triamterene and Amiloride
Site of action?
Toxicity?
K+ sparing
Block Na+ channels in the CORTICAL COLLECTING TUBULE
Toxicity = hyperkalemia (can lead to arrhythmias)
Diuretic effects on urine NaCl
INCREASED
All diuretics except acetazolamide
Serum NaCl may decrease as a result
Diuretic effects on urine K+
Increased with loop and thiazide diuretics
Decreased with K+ sparing diuretics
Diuretic effects on urine Ca2+
Increased with loop diuretics = decreased paracellular Ca2+ reabsorption leads to hypocalcemia
Decreased with thiazides = enhanced paracellular Ca2+ reabsorption in distal tubule
Diuretics that cause acidemia (decreased blood pH)
Carbonic anhydrase inhibitors = decrease HCO3 reabsorption
K+ sparing = aldosterone blockade prevents K+ and H+ secretion
Hyperkalemia leads to K+ entering all cells (via H+/K+ exchanger) in exchange for H+ exiting cells
Diuretics that cause alkalemia (increased blood pH)
Loop diuretics and thiazides via several mechanisms:
Volume contraction = increased ATII = increased Na/K exchange in proximal tubule = increased 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”
ACE inhibitors (ACEIs)
Captopril
Enalapril
Lisinopril
“-pril”
Inhibit ACE = decreased angiotensin II = decreases GFR by preventing constriction of efferent arterioles
Levels of renin increase as a result of loss of feedback inhibition
Inhibition of ACE also prevents inactivation of bradykinin (potent vasodilator)
Angiotensin II Receptor Blockers (ARBs)
“-sartan”
Similar effect to ACEIs but do NOT increase bradykinin = decreases risk of cough or angioedema
ACEI toxicity
Cough Angioedema (contraindicated in C1 esterase inhibitor deficiency) Teratogen (fetal renal malformations) Increased creatinine (decreased GFR) Hyperkalemia Hypotension
Avoid in bilateral renal artery stenosis because ACEIs will further decrease GFR = renal failure
