1. Diuretics and Angiotensin Drugs Flashcards

1
Q

Mannitol - MOA

A

Osmotic diuretic - Increase tubular osmolarity –> increased urine flow

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2
Q

Mannitol - Clinical Use

A
  • Shock
  • Drug overdose
  • Increased intracranial or intraocular pressure
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3
Q

Mannitol - Toxicities

A
  • Pulmonary edema
  • Dehydration
  • CI in anuria and CHF
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4
Q

Acetazolamide - MOA

A

Carbonic anhydrase inhibitor

  • Self-limited NaHCO3 diuresis and reduction of total body HCO3 stores
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5
Q

Acetazolamide - Clinical Use

A
  • Glaucoma
  • Urinary alkalinization
  • Metabolic alkalosis
  • Altitude sickness
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6
Q

Acetazolamide - Toxicities

A
  • Hyperchloremic metabolic acidosis
  • Neuopathy
  • NH3 toxicity
  • Sulfa allergy

“ACIDazolamide causes ACIDosis”

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7
Q

Loop Diuretics - Available Drugs

A
  • Furosemide
  • Ethacrynic acid
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8
Q

Furosemide - MOA

A

Sulfonamide loop diuretic

  • Inhibit Na, K, Cl cotransport of thick ascending loop
  • Abolishes hypertonicity of medulla –> prevents concentration of urine
  • Stimulates PGE release –> vasodilation of afferent arteriole: inhibited by NSAIDs
  • Increase Ca excretion

“loops lose Ca”

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9
Q

Furosemide - Clinical Use

A
  • Edematous states - CHF, cirrhosis, nephrotic syndrome, pulmonary edema
  • HTN
  • Hypercalcemia
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10
Q

Furosemide - Toxicities

A

“OH DANG”

  • Ototoxicity
  • Hypokalemia
  • Dehydration
  • Allergy (Sulfa)
  • Nephritis (interstitial)
  • Gout
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11
Q

Ethacrynic Acid - MOA

A

Non-sulfa loop diuretic

  • Inhibit Na, K, Cl cotransport of thick ascending loop
  • Abolishes hypertonicity of medulla –> prevents concentration of urine
  • Stimulates PGE release –> vasodilation of afferent arteriole: inhibited by NSAIDs
  • Increase Ca excretion

“loops lose Ca”

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12
Q

Ethacrynic Acid - Clinical Use

A
  • Diuresis in patients allergic to sulfa drugs
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13
Q

Ethacrynic Acid - Toxicities

A
  • Ototoxicity
  • Hypokalemia
  • Dehydration
  • Interstitial nephritis
  • Hyperuricemia
  • Acute gout - never use to treat gout
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14
Q

Thiazide Diuretics - Available Drugs

A
  • Hydrochlorothiazide
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15
Q

Hydrochlorothiazide - MOA

A

Inhibit NaCl reabsorption in early distal tubule –> reduce concentrating capacity of nephron

  • Decrease Ca excretion
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16
Q

Hydrochlorothiazide - Clinical Use

A
  • HTN
  • CHF
  • Idiopathic Hypercalciuria
  • Nephrogenic diabetes insipidus
  • May potentially be used for prevention of kidney stones that are secondary to hypercalciuria
17
Q

Hydrochlorothiazide - Toxicities

A

“HyperGLUC

  • HyperGlycemia
  • HyperLipidemia
  • HyperUricemia
  • HyperCalcemia
  • Hypokalemic metabolic alkalosis
  • Hyponatremia
  • Sulfa allergy
18
Q

K Sparing Diuretics - Available Drugs

A
  • Spironolactone
  • Triamterene
  • Amiloride
  • eplerenone

“The K STAys”

19
Q

Spironolactone - MOA

A

K sparing diuretic

  • Competitive aldosterone receptor antagonist in cortical collecting tubule
20
Q

Spironolactone - Clinical Use

A
  • Hyperaldosteronism
  • K depletion
  • CHF
21
Q

Spironolactone - Toxicities

A
  • Hyperkalemia - can cause arrhythmias
  • Endocrine effects –> gynecomastia, antiandrogen effects
22
Q

Triamterene - MOA

A

K sparing diuretic

  • Block Na channels in cortical collecting tubule
23
Q

Triamterene - Clinical Use

A
  • Hyperaldosteronism
  • K depletion
  • CHF
24
Q

Triamterene - Toxicities

A
  • Hyperkalemia - can cause arrhythmias
25
Q

Amiloride - MOA

A

K sparing diuretic

  • Block Na channels in cortical collecting tubule
26
Q

Amiloride - Clinical Use

A
  • Hyperaldosteronism
  • K depletion
  • CHF
27
Q

Amiloride - Toxicities

A
  • Hyperkalemia - can cause arrhythmias
28
Q

Effects of Diuretics on NaCl

A

All diuretics Increase urine NaCl nad may thus decrease serum NaCl

29
Q

Effect of Diuretics on K

A

Most diuretics increase urine K and may decrease serum K

  • K sparing diuretics do not increase urine K
30
Q

Effect of Diuretics on Serum pH

A

Acidemia

  • Carbonic anhydrase inhibitors (Acetazolamide) - Decrease HCO3 reabsorption
  • K sparing - Aldosterone blockade prevents K secretion and H secretion. Also, hyperkalemia leads to K entering cells at cost of H exiting cells

Alkalemia

  • Loop diuretics and Thiazide diuretics via several mechanisms
    1. Volume contraction –> increased AT II –> Increased Na/H exchange in proximal tubule –> increased HCO3 (Contraction alkalosis)
    1. K loss leads to K exiting all cells in exchange for H entering cells
    1. In low K state, H is exchanged for Na in cortical collecting tubule instead of K –> alkalosis and paradoxical aciduria
31
Q

Effect of Diuretics on Ca

A
  • Loop diuretics - Decrease paracellular Ca reabsorption –> hypocalcemia
  • Thiazides - Increase paracellular Ca reabsorption in proximal tubule and loop of Henle
32
Q

ACE Inhibitors - Available Drugs

A
  • Captopril
  • Enalapril
  • Lisinopril
33
Q

ACE Inhibitors - MOA

A

Inhibit Angiotensin Converting Enzyme –> reduce levels of AT II and prevent inactivation of bradykinin (a potent vasodilator)

Renin release will be increased due to loss of feedback inhibition

34
Q

ACE Inhibitors - Clinical Use

A
  • HTN
  • CHF
  • Diabetic renal disease
  • Prevent unfavorable heart remodeling as a result of chronic HTN
35
Q

ACE Inhibitors - Toxicities

A

“CApTOPRIL”

  • Cough
  • Angioedema
  • Taste changes
  • hypOtension
  • Pregnancy problems (fetal renal damage)
  • Rash
  • Increasd Renin
  • Lower AT II
  • Also, Hyperkalemia

Avoid in bilateral renal artery stenosis - Significantly reduce GFR by preventing constriction of the efferent arteriole - Increase serum creatinine

36
Q

ARB’s - Available Drugs

A

“-sartans”

37
Q

ARB’s - MOA

A

Competitive inhibitors of Angiotensin receptors

38
Q

ARB’s - Clinical Use

A
  • HTN
  • CHF
  • Diabetic renal disease
  • Prevent unfavorable heart remodeling as a result of chronic HTN
39
Q

ARB’s - Toxicities

A
  • Angioedema
  • Taste changes
  • hypOtension
  • Pregnancy problems (fetal renal damage)
  • Rash
  • Increasd Renin
  • Also, Hyperkalemia
  • NO Cough