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ALL THE PHARM > 547-549 - Renal Drugs > Flashcards

547-549 - Renal Drugs Flashcards

1
Q

Describe the effects of mannitol on:

  1. tubular fluid osmolarity
  2. urine flow
  3. intracranial/intraocular pressure
A
  1. ↑ tubular fluid osmolarity
  2. ↑ urine flow
  3. ↓ intracranial/intraocular pressure
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2
Q

What are the clinical uses of mannitol?

A
  1. Drug overdose

2. ↑ intracranial/intraocular pressure

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3
Q

What are the toxicities of mannitol?

A
  1. pulmonary edema

2. dehydration

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4
Q

Contraindications of mannitol use?

A
  1. anuria

2. CHF

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5
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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6
Q

What are 5 clinical uses of acetazolamide?

A
  1. Glaucoma
  2. Urinary alkalinization
  3. Metabolic alkalosis
  4. Altitude sickness
  5. Pseudotumor cerebri
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7
Q

What are the toxicities of acetazolamide?

A
  1. Hyperchloremic metabolic acidosis
  2. Paresthesias
  3. NH3 toxicity
  4. Sulfa allergy

“ACID”azolamide causes ACIDosis

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8
Q

What is furosemide?

A

A sulfonamide loop diuretic that inhibits N/K/2 Cl cotransporter of TAL

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9
Q

What effect do loop diuretics on the tonicity of the medulla of the kidney?

A

abolish the hypertonicity of the medulla → prevents concentration of urine

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10
Q

What effects do loop diuretics have on PGE release?

A

stimulates PGE release → vasodilation of afferent arteriole (inhibited by NSAIDS)

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11
Q

What effect do loop diuretics have on Ca2+?

A

↑ Ca2+ excretion (Loops Lose Calcium)

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12
Q

What are the clinical uses of loop diuretics?

A
  1. Edematous states: CHF, cirrhosis, nephrotic syndrome, pulmonary edema
  2. Hypertension
  3. Hypercalcemia
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13
Q

What are the toxicities of loop diuretics?

A
  1. Ototoxicity
  2. Hypokalemia
  3. Dehydration
  4. Allergy (sulfa)
  5. Nephritis (interstitial)
  6. Gout
    OH DANG
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14
Q

What is ethacrynic acid?

A

A loop diuretic with the same action as furosemide, but derived from phenoxyacetic acid (so not a sulfonamide). It’s used for diuresis in patients allergic to sulfa drugs.

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15
Q

What are the toxicities of ethacrynic acid?

A

similar to furosemide (OH DANG) - can cause hyperuricemia – do not use to treat gout

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16
Q

Where do thiazides work?

A

early distal tubule

17
Q

What effect do thiazides have on Ca2+?

A

↓ Ca2+ excretion

18
Q

What are the toxicities of hydrochlorothiazide?

A
  1. Hypokalemic metabolic alkalosis
  2. hyponatremia
  3. hyperGlycemia
  4. hyperLipidemia
  5. hyperUricemia
  6. hyperCalcemia
  7. Sulfa alergy

HyperGLUC

19
Q

What are the K+ sparing diuretics?

A
  1. Spironolactone
  2. Eplerenone
  3. Triamterene
  4. Amiloride
20
Q

Which drugs are competitive aldosterone receptor antagonists in the cortical collecting tubule?

A
  1. Spironolactone

2. Eplerenone

21
Q

Which drugs block Na+ channels in the CCT?

A
  1. Triamterene

2. Amiloride

22
Q

What is the clinical use of K+ sparing diuretics?

A
  1. Hyperaldosteronism
  2. K+ depletion
  3. CHF
23
Q

What are the toxicities of K+ sparing diuretics?

A
  1. Hyperkalemia (can → arrhythmias)

2. Endocrine effects (spironolactone → gynecomastia, antiandrogen effects)

24
Q

Which diuretics increase urine K+?

A

loop and thiazides

25
Q

Which diuretics increase urine NaCl?

A

All except acetazolamide

26
Q

Which diuretics cause acidemia?

A
  1. CA inhibitors (↓ bicarb reabsorption)

2. K+ sparing (aldosterone blockade prevents K+ secretion and H+ secretion; also, ↑ K+ → exchange for H+ exiting cells)

27
Q

Which diuretics cause alkalemia?

A
  1. loop diuretics

2. thiazides

28
Q

What are the 3 mechanisms by which loop and thiazide diuretics can cause alkalemia?

A
  1. contraction alkalosis
  2. K+ loss from body → loss from cells in exchange for H+ uptake
  3. K+ loss from body → H+ is exchanged rather than K+ for Na+ in CCT → alkalosis and “paradoxical aciduria”
29
Q

Which diuretics cause increased urine Ca2+?

A

loop diuretics (↓ paracellular Ca2+ reabsorption → hypocalcemia)

30
Q

Which diuretics cause ↓ urine Ca2+?

A

thiazides (enhanced paracellular Ca2+ reabsorption in distal tubule)

31
Q

Name 3 ACE inhibitors:

A
  1. Captopril
  2. Enalopril
  3. Lisinopril
32
Q

What is the mechanism of action of ACE inhibitors?

A

Inhibit ACE → ↓ angiotensin II → ↓ GFR by preventing constriction of efferent arterioles

33
Q

What are the clinical uses of ACE inhibitors?

A
  1. HTN
  2. CHF
  3. proteinuria
  4. diabetic nephropathy
  5. prevent unfavorable heart remodeling as a result of chronic HTN
34
Q

What are the toxicities of ACE inhibitors?

A
  1. Cough
  2. Angioedema (contraindicated in C1 esterase inhibitor deficiency)
  3. Teratogen (fetal renal malformations)
  4. ↑ Creatinine (↓ GFR)
  5. Hyperkalemia
  6. Hypotension
  7. Renal failure if used in bilateral renal artery stenosis (↓ GFR)

Captopril’s CATCHH

ALL THE PHARM (10 decks)

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