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Step 1 Pharmacology > Renal > Flashcards

Renal Flashcards

1
Q

What drugs act on the proximal tubule?

A

Mannitol and Acetazolamide. Mannitol also works on the descending loop of Henle and the collecting duct.

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2
Q

What drugs act on the thick ascending limb of the loop of Henle?

A

Loop diuretics (Furosemide and Ethacrynic acid)

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3
Q

What drugs act on the distal convoluted tubule?

A

Thiazides (Hydrochlorothiazide)

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4
Q

What drugs act on the cortical collecting duct?

A

K+ sparing diuretics

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5
Q

What drugs act on the collecting tubule?

A

ADH antagonists

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6
Q

What is the mechanism of Mannitol?

A

Osmotic diuretic, ↑ tubular fluid osmolarity, producing ↑ urine flow, ↓ intracranial/intraocular pressure.

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7
Q

What is the clinical use of Mannitol?

A

Drug overdose, ↑ intracranial/intraocular pressure.

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8
Q

What is the toxicity of Mannitol?

A

Pulmonary edema, dehydration. Contraindicated in anuria, CHF.

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9
Q

What is the mechanism of Acetazolamide?

A

Carbonic anhydrase inhibitor. Causes self-limited NaHCO3 diuresis and ↓ total-body HCO3− stores.

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10
Q

What is the clinical use of Acetazolamide?

A

Glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, pseudotumor cerebri.

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11
Q

What is the toxicity of Acetazolamide?

A

Hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy.

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12
Q

Loop diuretics - What is the mechanism of Furosemide?

A

Sulfonamide loop diuretic. Inhibits cotransport system (Na+/K+/2 Cl−) of thick ascending limb of loop of Henle. Abolishes hypertonicity of medulla, preventing concentration of urine.
Stimulates PGE release (vasodilatory effect
on afferent arteriole); inhibited by NSAIDs.
↑ Ca2+ excretion. Loops Lose calcium.

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13
Q

Loop diuretics - What is the clinical use ofFurosemide?

A

Edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), hypertension, hypercalcemia.

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14
Q

Loop diuretics - What is the toxicity of Furosemide?

A

OH DANG! - Ototoxicity, Hypokalemia, Dehydration, Allergy (sulfa), Nephritis (interstitial), Gout.

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15
Q

Loop diuretics - What is the mechanism of Ethacrynic acid?

A

Phenoxyacetic acid derivative (not a sulfonamide). Essentially same action as furosemide.

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16
Q

Loop diuretics - What is the clinical use of Ethacrynic acid?

A

Diuresis in patients allergic to sulfa drugs.

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17
Q

Loop diuretics - What is the toxicity of Ethacrynic acid?

A

Similar to furosemide; can cause hyperuricemia; never use to treat gout.

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18
Q

What is the mechanism of Hydrochlorothiazide?

A

Thiazide diuretic. Inhibits NaCl reabsorption in early distal tubule, ↓ diluting capacity of the nephron. ↓ Ca2+ excretion.

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19
Q

What is the clinical use of Hydrochlorothiazide?

A

Hypertension, CHF, idiopathic hypercalciuria, nephrogenic diabetes insipidus, osteoporosis.

20
Q

What is the toxicity of Hydrochlorothiazide?

A

Hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, and hypercalcemia. Sulfa allergy.

21
Q

What are the K+ sparing diuretics?

A

Spironolactone and eplerenone; Triamterene, and Amiloride.

22
Q

What is the mechanism of K+ sparing diuretics?

A

Spironolactone and eplerenone are competitive aldosterone receptor antagonists in the cortical collecting tubule. Triamterene and amiloride act at the same part of the tubule by blocking Na+ channels in the CCT.

23
Q

What is the clinical use of K+ sparing diuretics?

A

Hyperaldosteronism, K+ depletion, CHF

24
Q

What is the toxicity of K+ sparing diuretics?

A

Hyperkalemia (can lead to arrhythmias), endocrine effects with spironolactone (e.g., gynecomastia, antiandrogen effects).

25
Q

What effect do diuretics have on Urine NaCl?

A

↑ (all diuretics except acetazolamide). Serum NaCl may ↓ as a result.

26
Q

What effect do diuretics have on Urine K+?

A

↑ with loop and thiazide diuretics. Serum K+ may ↓ as a result.

27
Q

Describe how diuretics can cause acidemia.

A

↓ (acidemia): carbonic anhydrase inhibitors— ↓ HCO3− reabsorption. K+ sparing—aldosterone blockade prevents K+ secretion and H+ secretion. Additionally, hyperkalemia leads to K+ entering all cells (via H+/K+ exchanger) in exchange for H+ exiting cells.

28
Q

Describe how diuretics can cause alkalemia.

A

↑ (alkalemia): loop diuretics and thiazides cause alkalemia through several mechanisms:
▪ Volume contraction → ↑ AT II → ↑ Na+/H+ exchange in proximal tubule → ↑ 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”

29
Q

What effect do diuretics have on Urine Ca2+?

A

↑ with loop diuretics: ↓ paracellular Ca2+ reabsorption → hypocalcemia
↓ with thiazides: Enhanced paracellular Ca2+ reabsorption in distal tubule

30
Q

What are the ACE inhibitors?

A

Captopril, enalapril, lisinopril

31
Q

What is the mechanism of ACE inhibitors?

A

Inhibit ACE → ↓ angiotensin II → ↓ GFR by preventing constriction of efferent arterioles. Levels of renin ↑ as a result of loss of feedback inhibition. Inhibition of ACE also prevents inactivation of bradykinin, a potent vasodilator.
Angiotensin II receptor blockers (-sartans) have effects similar to ACE inhibitors but do not ↑ bradykinin → ↓ risk of cough or angioedema.

32
Q

What is the clinical use of ACE inhibitors?

A

Hypertension, CHF, proteinuria, diabetic nephropathy. Prevent unfavorable heart remodeling as a result of chronic hypertension

33
Q

What are the toxicities of ACE inhibitors?

A

Cough, Angioedema (contraindicated in C1 esterase inhibitor deficiency), Teratogen (fetal renal malformations), ↑ Creatinine (↓ GFR), Hyperkalemia, and Hypotension. Avoid in bilateral renal artery stenosis, because ACE inhibitors will further ↓ GFR → renal failure.

34
Q

Prostaglandins dilate the afferent arteriole (↑ RPF, ↑ GFR, so FF remains constant). What drug inhibits this?

A

NSAIDs; use may result in acute renal failure

35
Q

Angiotensin II preferentially constricts efferent arteriole (↓ RPF, ↑ GFR, so FF increases). What drug inhibits this?

A

ACE inhibitor

36
Q

What is Hartnup disease treated with?

A

High-protein diet and nicotinic acid

37
Q

What is Liddle syndrome treated with?

A

Amiloride

38
Q

What drugs shift K+ out of cell (causing hyperkalemia)

A

Digitalis and β-adrenergic antagonist

39
Q

What drugs shift K+ into cell (causing hypokalemia)?

A

β-adrenergic agonist (↑ Na+/K+ ATPase)

40
Q

What drugs cause Type 1 Renal tubular acidosis (distal, pH >5.5)?

A

Amphotericin B toxicity. Analgesic nephropathy is also a cause.

41
Q

What drugs cause Type 2 Renal tubular acidosis (proximal, pH <5.5)?

A

Carbonic anydrase inhibitors

42
Q

What drugs cause Type 3 Renal tubular acidosis (hyperkalemic, pH <5.5)?

A

K+ sparing diuretics

43
Q

What drugs cause Membranous nephropathy?

A

NSAIDs, pencillamine

44
Q

What drug is used to treat Minimal change disease (lipoid nephrosis)?

A

Excellent response to corticosteroids

45
Q

What drugs are treatments for recurrent kidney stones (Calcium)?

A

Thiazides and citrate

46
Q

What drugs cause Drug-induced interstitial nephritis (tubulointerstitial nephritis)?

A

Certain drugs (e.g., diuretics, penicillin derivatives, sulfonamides, rifampin)

47
Q

What drug causes Renal papillary necrosis?

A

Chronic phenacetin use (acetaminophen is phenacetin derivative)

Step 1 Pharmacology (18 decks)

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