Renal

Question 1

Mannitol

Uses?

Answer 1

Osmotic diuretic
Increases tubular fluid osmolarity = increases urine flow and decreases intracranial/intraocular pressure

Uses = drug overdose and increased intracranial/intraocular pressure

Question 2

Mannitol toxicities? (2)

Contraindications? (2)

Answer 2

Pulmonary edema
Dehydration
Contraindicated in anuria and CHF

Question 3

Acetazolamide

Answer 3

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

Question 4

Which diuretic is classically used in the treatment of altitude sickness?

Answer 4

Acetazolamide

Question 5

Does acetazolamide make the urine more acidic or alkaline?

Answer 5

Alkaline

Question 6

Is acetazolamide used in the treatment of metabolic acidosis or alkalosis? Does it cause metabolic acidosis or alkalosis?

Answer 6

Used in treatment of metabolic alkalosis as it causes urinary alkalinization

“ACID”azolamide causes ACIDosis

Question 7

Acetazolamide toxicity

Answer 7

Hyperchloremic metabolic acidosis
Paresthesias
NH3 toxicity
Sulfa allergy

Question 8

Where does acetazolamide act along the nephron?

Answer 8

Proximal convoluted tubule

Question 9

Loop diuretic examples

Site of action?

Answer 9

Furosemide
Ethacrynic acid

Inhibit cotransport system (Na/K/2Cl) of THICK ASCENDING limb of loop of Henle

Question 10

Furosemide

Answer 10

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+)

Question 11

Furosemide toxicity

Answer 11

Inhibits Na/K/2Cl 
OTOTOXICITY
Hypokalemia
Dehydration
Allergy (sulfa)
Nephritis (interstitial)
Gout
"OH DANG"

Question 12

Ethacrynic acid

Answer 12

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)

Question 13

Thiazide diuretic

Site of action?

Answer 13

Hydrochlorothiazide
Inhibits NaCl reabsorption in early DISTAL CONVOLUTED TUBULE = decreases diluting capacity of nephron
Decreases Ca2+ excretion

Question 14

Hydrochlorothiazide toxicity

Answer 14

Thiazide diuretic
Hypokalemic metabolic alkalosis
Hyponatremia
HyperGlycemia
HyperLipidemia
HyperUricemia
HyperCalcemia
"HyperGLUC"
Sulfa allergy

Question 15

K+ sparing diuretics

Answer 15

Spironolactone and Eplerenone

Triamterene and Amiloride

Question 16

Spironolactone and Eplerenone
Site of action?
Toxicity?

Answer 16

K+ sparing
Competitive aldosterone receptor antagonists in the CORTICAL COLLECTING TUBULE

Toxicity = hyperkalemia (can lead to arrhythmias)
Spironolactone toxicity = endocrine effects (gynecomastia, antiandrogen effects)

Question 17

Triamterene and Amiloride
Site of action?
Toxicity?

Answer 17

K+ sparing
Block Na+ channels in the CORTICAL COLLECTING TUBULE

Toxicity = hyperkalemia (can lead to arrhythmias)

Question 18

Diuretic effects on urine NaCl

Answer 18

INCREASED
All diuretics except acetazolamide
Serum NaCl may decrease as a result

Question 19

Diuretic effects on urine K+

Answer 19

Increased with loop and thiazide diuretics

Decreased with K+ sparing diuretics

Question 20

Diuretic effects on urine Ca2+

Answer 20

Increased with loop diuretics = decreased paracellular Ca2+ reabsorption leads to hypocalcemia
Decreased with thiazides = enhanced paracellular Ca2+ reabsorption in distal tubule

Question 21

Diuretics that cause acidemia (decreased blood pH)

Answer 21

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

Question 22

Diuretics that cause alkalemia (increased blood pH)

Answer 22

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”

Question 23

ACE inhibitors (ACEIs)

Answer 23

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)

Question 24

Angiotensin II Receptor Blockers (ARBs)

Answer 24

“-sartan”

Similar effect to ACEIs but do NOT increase bradykinin = decreases risk of cough or angioedema

Question 25

ACEI toxicity

Answer 25

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