Usmle Step 1 Fa Renal Pharmacology

Front 1

Mannitol
(a) mechanism
(b) clinical use
(c) toxicity

Back 1

(a) osmotic diuretic; incr tubular fluid osmolarity preventing reabsorption in proximal tubule; produce incr urine flow
(b) increase urine flow in solute overload, shock, drug overdose, decr intracranial/intraocular pressure
(c) pulmonary edema, dehydration (contraindicated in anuria and CHF)

Front 2

Acetazolamide
(a) mechanism
(b) clinical use
(c) toxicity

Back 2

(a) carbonic anhydrase inhibitor; causes self limited bicarb diuresis and reduction in total body bicarb stores
(b) glaucoma, urinary alkalinization (eliminates acidic drugs), metabolic alkalosis, altitude sickness

Front 3

Furosemide
(a) mechanism
(b) clinical use
(c) toxicity

Back 3

(a) Inhibit Na/K/2Cl transporter in thick ascending loop of henle; abolishes hypertonicity of medulla preventing concentration of urine
(b) edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), HTN, hypercalcemia
(c) ototixicity, hypokalemia, dehydration, allergy (allergy), nephritis (interstitial), gout

Front 4

Ethacrynic acid
(a) mechanism
(b) clinical use
(c) toxicity

Back 4

(a) phenoxyacetic acid derivative (NOT a sulfonamide); essentially the same action as furosemide
(b) diuresis in patients allergic to sulfas
(c) similar to furosemide; can be used in hyperuricemia, acute gout (NEVER use to treat gout)

Front 5

Hydrachlorathiazide
(a) mechanism
(b) clinical use
(c) toxicity

Back 5

(a) inhibits NaCl reabsorption in early distal tubule (Na/Cl transporter) reducing diluting capacity of nephron. Also decr Ca2+ loss
(b) HTN, edematous states (CHF), idiopathic hypercalciuria, nephrogenic diapetes insipidus
(c) hypokalemic metabolic alkalosis
Hyponatermia
Hyperglycemia
Hyperlipidemia
Hypercalcemia
Hyperuricemia
Sulfa allergy

Front 6

Spironolactone, eplerenone,
(a) mechanism
(b) clinical use
(c) toxicity

Back 6

(a) block aldosterone receptor
(b) adjunct w/other diuretics to prevent K+ loss (HTN, CHF), hyperaldosteronism (spironolactone), antiandrogen (spironolactone)
(c) hyperkalemia, endocrine effects (gynecomastia, antiandrogen effects)

Front 7

Triamterene, Amiloride
(a) mechanism
(b) clinical use
(c) toxicity

Back 7

(a) block sodium channels
(b) adjunct with other diuretics to prevent K+ loss; Hyperaldosteronism; K+ depletion; CHF
(c) hyperkalemia (arrythmias)

Front 8

Which diuretics increase urine K+? (mechanism)

Back 8

All except K+ sparing diuretics (spironolactone, eplerenone, triamterene, amiloride)

Front 9

Whichdiuretics decrease blood pH? (mechanism)

Back 9

CA inhibitors (decr bicarb reabsorption_
K+ sparing (hyperkalemia leads to K+ entering as H+ exits)

Front 10

Which diuretics can lead to alkalemia? (mechanism)

Back 10

Loop diuretics and thiazides
(1) volume contraction (incr ATII causing incr bicarb reabsorption)
(2) K+ loss leads to K+ exit in exchange for H+ entering
(3) in low K+ states, H+ rather than K+ is exchanged for Na+ in principle cells leading to alkalosis and paradoxical aciduria

Front 11

Which diuretics increase urine calcium? (mechanism)

Back 11

Loop diuretics: abolish lumen positive potential in TALH decr paracellular Ca++ absorption

Front 12

Which diuretics decrease urine calcium? (mechanism)

Back 12

Thiazides: block luminal Na/Cl cotransport in distal convoluted tubule causing increased Na gradient leading to increased interstitial Na/Ca exchange leading to hypercalcemia

Front 13

ACE Inhibitor
(a) clinical use
(b) toxicity

Back 13

(a) HTN, CHF, Diabetic renal disease
(b) cough, angioedema, proteinuria, taste changes, hypotension, pregnancy problems, rash, increased renin, lower angiotensin II, alko hyperkalemia. Avoid in bilateral renal artery stenosis b/c ACEI b/c they will significantly decrease GFR by preventing constriction of efferent arterioles.