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Renal Pharmacology > Diuretics > Flashcards

Diuretics Flashcards

15.18-15.20

1
Q

What are the 3 carbonic anhydrase inhibitors?

A
  1. Acetazolamide
  2. Methazolamide
  3. Dichlorphenamide
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2
Q

What are the 4 osmotic agents?

A
  1. Mannitol
  2. Isosorbide
  3. Glycerin
  4. Urea
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3
Q

What are the 4 loop diuretics?

A
  1. Furosemide
  2. Bumetanide
  3. Ethacrynic acid
  4. Torsemide
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4
Q

What are the 11 thiazide diuretics?

A
  1. Hydrochlorothiazide
  2. Chlorothiazide
  3. Methyclothiazide
  4. Bendroflumethiazide
  5. Hydroflumethiazide
  6. Polythiazide
  7. Trichlormethiazide
  8. Indapamide
  9. Chlorthalidone
  10. Quinethazone
  11. Metolazone
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5
Q

What are 4 potassium-sparing diuretics?

A
  1. Triamterene
  2. Amiloride
  3. Spironolactone
  4. Eplerenone
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6
Q

What is the diuretic agent that is a natriuretic peptide?

A

Nesiritide

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7
Q

Acetazolamide; Methazolamide; Dichlorphenamide - MOA (2)

A
  1. Carbonic anhydrase inhibitor –> luminal inhibition prevents H2CO3-> H20+CO2 so less entry into cell and intracellular inhibition prevents HCO3- formation –> decreases basolateral Na+ reabsorption via Na/HCO3- (1:3) symport
  2. Acts at PCT-> Low diuretic b/c of tubuloglomerular feedback (TGF) activation in macula densa –> decrease in RBF/GFR –> self-limited diuresis
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8
Q

Acetazolamide; Methazolamide; Dichlorphenamide - Potency

A

Acetazolamide < methazolamide < dichlorphenamide (30X more potent that acetazolamide)

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9
Q

Acetazolamide; Methazolamide; Dichlorphenamide - Uses (3)

A

Glaucoma, urinary alkalinization; metabolic alkalosis (b/c of increased bicarbonate excretion)

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10
Q

Acetazolamide; Methazolamide; Dichlorphenamide - SE/Toxicity (4)

A

Metabolic acidosis; Ca-Ph (renal) stone formation; hypokalemia; allergic sulfur rxn

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11
Q

Mannitol, Isosorbide, Glycerin, Urea - MOA (3)

A

Osmotic diuretic

  1. Limit Na+ and water reabsorption
  2. Increase urinary excretion of nearly all electrolytes including Na+, K+, Ca+2, Mg+2, Cl-, phosphate
  3. Increases oncotic P and pulls water from ICF to expand extracellular fluid volume –> causes decreased renin release and increased RBF which causes medullary washout and thus diuresis (decreased concentrating ability)
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12
Q

Mannitol, Isosorbide, Glycerin, Urea - Formulation

A

Isosorbide/Glycerin –> oral

Mannitol/Urea –> IV –> more for increased intracranial P

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13
Q

Mannitol, Isosorbide, Glycerin, Urea - Uses (3)

A
  1. Acute renal failure
  2. Reduction of intracranial/intraocular P
  3. Dialysis disequilibrium (loss of solutes causes shift from ECF –> ICF)
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14
Q

Mannitol, Isosorbide, Glycerin, Urea - SE/Toxicity (3)

A
  1. Pulmonary edema
  2. Expansion of extracellular volume problem w/CHF
  3. Electrolyte loss
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15
Q

What is the special SE associated w/Glycerin?

A

Hyperglycemia

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16
Q

Urea/Mannitol - C/I (2)

A

Mannitol/Urea w/ intracranial bleeding

Urea w/ liver dysfunction

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17
Q

Furosemide, Bumetanide, Ethacrynic acid, Torsemide - MOA (4)

A

Loop diuretic in thick ascending limb (TAL)

  1. Inhibits Na-K-2Cl symport –> increased luminal [salt] = decreased water reabsorption
  2. Inhibits macula densa sensing mechanism –> interprets this as low luminal [NaCl] –> thus block TGF and do not decrease GFR
  3. Loss of interstitial gradient from medullary washout –> decreased urine concentrating abilities –> diuresis
  4. Increased urinary excretion of Na, Cl, K, and Ca/Mg (less positive lumen so decrease electrical gradient)
18
Q

Furosemide, Bumetanide, Ethacrynic acid, Torsemide - Potency (2)

A
  1. Ethacrynic acid < furosemide < torsemide < bumetanide

2. Dose-response curve shift to R w/ chronic renal failure (impaired drug secretion into PCT)

19
Q

Furosemide, Bumetanide, Ethacrynic acid, Torsemide - Uses

A

Pulmonary edema and other edematous states (e.g. CHF), HTN, acute renal failure

20
Q

Furosemide, Bumetanide, Ethacrynic acid, Torsemide - SE

A

Ototoxicity (esp. Ethacrynic acid); electrolyte loss; metabolic alkalosis; allergic sulfur reaction (not w/ Ethacrynic acid); hyperglycemia, hyperuricemia

21
Q

Furosemide, Bumetanide, Ethacrynic acid, Torsemide - D/I

A

Compounded ototoxicity w/ aminoglycosides, cisplatin/carboplatin, paclitaxel

22
Q

Hydrochlorothiazide, Chlorothiazide, Methyclothiazide , Bendroflumethiazide, Hydroflumethiazide, Polythiazide, Trichlormethiazide, Indapamide, Chlorthalidone, Quinethazone, Metolazone - MOA (3)

A

Thiazide diuretics

  1. Inhibit Na/Cl symport in distal convoluted tubule (DCT) => decreased water reabsorption = diuresis; 2. Increased excretion of Na, Cl, and K and decreased excretion of Ca2+ (stimulated reabsorption)
  2. No tubuloglomerular feedback (after macula densa) or RBF
23
Q

Hydrochlorothiazide, Chlorothiazide, Methyclothiazide , Bendroflumethiazide, Hydroflumethiazide, Polythiazide, Trichlormethiazide, Indapamide, Chlorthalidone, Quinethazone, Metolazone - Potency

A

Chlorothiazide-> lowest potency
Polythiazide/Trichlormethiazide-> highest potency

Chlorthalidone-> longest 1/2-life (47hrs)

24
Q

Hydrochlorothiazide, Chlorothiazide, Methyclothiazide , Bendroflumethiazide, Hydroflumethiazide, Polythiazide, Trichlormethiazide, Indapamide, Chlorthalidone, Quinethazone, Metolazone - Uses (3)

A

HTN, mild edema, calcium nephrolithiasis

25
Q

Hydrochlorothiazide, Chlorothiazide, Methyclothiazide , Bendroflumethiazide, Hydroflumethiazide, Polythiazide, Trichlormethiazide, Indapamide, Chlorthalidone, Quinethazone, Metolazone - SE/Toxicity

A

Hyponatremia, hypokalemia, hypercalcemia, metabolic alkalosis, allergic sulfur rxn, hyperglycemia (diabetes mellitus)

26
Q

Hydrochlorothiazide, Chlorothiazide, Methyclothiazide , Bendroflumethiazide, Hydroflumethiazide, Polythiazide, Trichlormethiazide, Indapamide, Chlorthalidone, Quinethazone, Metolazone - D/I

A

Quinidine –> hypokalemia increases risk of torsades de pointes (ventricular tachycardia)

27
Q

Triamterene, Amiloride - MOA

A
  1. K+ sparing diuretic-> inhibition of ENaC Na channels in late distal tubule/collecting ducts => decreased Na reabsorption (i.e. increased urinary excretion of Na+) = decreased water reabsorption and decreased K and H excretion
  2. Do not affect TGF or RBF
28
Q

Triamterene, Amiloride - Potency (2)

A

Amiloride -> longer 1/2-life, more potent, renal excretion

Triamterene-> metabolized for excretion

29
Q

Triamterene, Amiloride - Uses (2)

A

Used in combo w/ other diuretics to treat HTN, mild edema

30
Q

Triamterene, Amiloride - SE (2)

A

Hyperkalemia; metabolic acidosis

31
Q

Triamterene, Amiloride - D/I

A

Pentamide/trimethoprim (used to treat Pneumocystis infxn in AIDS pts) –> also ENaC inhibitors

32
Q

Spironolactone, Eplerenone - Class and MOA (3)

A
  1. Steroid K+ sparing diuretic
  2. Mineralocorticoid receptor (MR) (aka aldosterone receptor antagonist) –> inhibits aldosterone induced expression of Na channels (ENaC) and Na/K ATPase=> reduced Na/water retention (increased urinary excretion of Na+) and decreased K, H+ urinary excretion
  3. Also inhibits androgen synthesis (use in prostate cancer)
33
Q

Spironolactone, Eplerenone - Tx

A

Hyperaldosteronism (and endocrine diseases), HTN

34
Q

Spironolactone, Eplerenone - Toxicity

A

Cross rxn w/ androgen receptor (gynecomastia, impotence) –> less w/ eplerenone
Hyperkalemia; metabolic acidosis

35
Q

Spironolactone, Eplerenone - D/I

A

ACE inhibitor/angiotensin receptor blocker –> hyperkalemia

36
Q

Nesiritide - Class and MOA

A
  1. Brain natriuretic peptide (BNP)
  2. Binds to specific receptors and via c-GMP signaling inhibits Na+ reabsorption in the inner medullary collecting duct and thus increase Na+ excretion
  3. Also inhibits renin-angiotensin II-aldosterone pathway
37
Q

Nesiritide - Formation

A

Peptide –> given IV

38
Q

Nesiritide - Uses

A

Currently limited Tx use

Acutely decompensated CHF

39
Q

What type of diuretics are thiazide diuretics?

A

Na+-Cl- symport inhibitors

40
Q

What type of diuretics are loop diuretics?

A

Na+-K+-2Cl symport inhibitors

41
Q

What type of diuretics are K+ sparing diuretics?

A

Na+ channel inhibitors

Renal Pharmacology (17 decks)

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