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Pharmacology Exam 4 > Diuretics > Flashcards

Diuretics Flashcards

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1
Q

Carbonic anhydrase inhibitor

A

Acetazolamide

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2
Q

NaK 2Cl symport inhibitor

A

Furosemide

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3
Q

Na Cl symport inhibitors

A

Hydrochlorthiazide

Chlorothiazide

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4
Q

2 groups of K sparing diuretics

A

Epithelial Na channel inhibitors

Aldosterone antagonists

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5
Q

Epithelial Na channel inhibitors

A

Amiloride

Triamterene

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6
Q

Aldosterone antagonists

A

Spironolactone

Eplerenone

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7
Q

Osmotic diuretics

A

Mannitol

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8
Q

Vasopressin receptor antagonists

A

Demeclocycline

Tolvaptan

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9
Q

Endogenous OAT substrates (4

A

Urate
Bile acids
Oxalate
Prostaglandins

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10
Q

Exogenous OAT substrates (6)

A 
Hydrochlorothiazide
Furosemide
Acetazolamide
Probenecid
Pencillin
Aspirin
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11
Q

OCT endogenous substrates (3)

A

Creatinine
Epinephrine
Histamine

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12
Q

OCT exogenous substrates (5)

A 
Amiloride
Triamterene
Cimetidine
Atropine
Quinine
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13
Q

Site of action is in proximal tubule, where it competitively inhibits carbonic anhydrase

A

Acetazolamide

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14
Q

Carbonic anhydrase is responsible for ___ reabsorption and __ secretion

A

NaHCO3, acid (H+)

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15
Q 
Control vs. \_\_\_\_
Vol: 1 vs 3 (ml/min)
pH: 6 vs 8
Na+: 72 vs. 302
K+: 22 vs. 260
Cl-: 85 vs. 95
HCO3-: 1 vs. 120
A

Acetazolamide (CA inhibitor)

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16
Q

Acetazolamide effect on renal hemodynamics

A

Increases NaCl delivery to macula densa, reducing RBF (afferent arterioles constricted) and GFR

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17
Q

Uses=
Open-angle glaucoma
Altitude sickness
Epilepsy

A

Acetazolamide

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18
Q

ADEs=
Renal stone formation (urinary alkalinization)
Potassium wasting
Worsens hepatic encephalopathy (diversion of ammonia into systemic circulation)

A

Acetazolamide

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19
Q

Site of action is in thick ascending limb of the loop of Henle, inhibits Na+-K+-2Cl- symporters

A

Furosemide (also abolishes trans-epithelial potential difference that drives paracellular transport of Ca and Mg)

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20
Q 
Control vs. \_\_\_\_
Vol: 1 vs 8 (ml/min)
pH: 6 vs 6
Na+: 72 vs. 1615
K+: 22 vs. 115
Cl-: 85 vs. 990
HCO3-: 1 vs. 1
A

Furosemide

21
Q

Urinary effects:
Increase in Ca and Mg excretion
Decreased uric acid excretion (chronic effect, exacerbates gout)
Reduces ability of kidney to dilute urine when over-hydrated and concentrate urine during dehydration

A

Furosemide

22
Q

Furosemide renal hemodynamic effects:

A
  1. Increases RBF and redistributes it to cortex (prostaglandin-mediated)
  2. Stimulates release of renin (blocks TGF by inhibiting salt transport into the macula densa)
23
Q

Acutely increases systemic venous capacitance and decreases left ventricular filling pressure
May be beneficial to patients with pulmonary edema

A

Furosemide (prostaglandin mediated)

24
Q

PK= highly protein bound
Delivered to apical membrane by OAT
Short half-life
“Post-diuretic” sodium retention

A

Furosemide

25
Q

Uses=

  1. Hyponatremia + IV hypertonic saline
  2. Hypercalcemia + IV isotonic saline
  3. Edema of nephrotic syndrome
  4. Congestive heart failure
  5. Acute pulmonary edema
A

Furosemide

26
Q

ADEs= boxed warning for electrolyte and fluid loss
Hyponatremia, hypokalemia, hypocalcemia (cause in osteoporosis)
Hyperuricemia

A

Furosemide

27
Q

ADEs= ototoxicity (tinnitus, vertigo, deafness)
Hyperglycemia (caution in co-admin with sulfonylureas)
NSAIDs reduce diuretic effect

A

Furosemide

28
Q

Site of action is in distal convoluted tubule, where it inhibits Na+-Cl- symporter
ALSO weak inhibitor of carbonic anhydrase in PCT

A

Hydrochlorothiazide (chlorothiazide)

29
Q 
Moderate efficacy (5% of filtered load)
Shallow dose-response
Efficacy substantially reduced when GFR is low (<30-40 mL/min)
A

Hydrochlorothiazide

30
Q 
Control vs. \_\_\_\_
Vol: 1 vs 3 (ml/min)
pH: 6 vs 7.4
Na+: 72 vs. 650
K+: 22 vs. 110
Cl-: 85 vs. 650
HCO3-: 1 vs. 25
A

Hydrochlorothiazide

31
Q

DECREASES excretion of Ca
Decreases kidney’s ability to dilute urine during water diuresis (concentration ability is OK)
No effect on renal hemodynamics

A

Hydrochlorothiazide

32
Q

Protein bound and delivered by OAT

Longer half-lives

A

Hydrochlorothiazide

33
Q

Uses=

  1. Hypertension
  2. Mild edema
  3. Nephrogenic diabetes insipidus (paradoxical effect)
  4. Calcium nephrolithiasis and osteoporosis
A

Hydrochlorothiazide

34
Q 
ADEs= 
Hyponatremia, hypokalemia
Hyperuricemia
Hyperglycemia &amp; hyperlipidemia
Erectile dysfunction
A

Hydrochlorothiazide

35
Q

DDIs of HCT (2)

A
  1. NSAIDs reduce diuretic efficacy

2. Quinidine- hypokalemia increases risk of torsades de pointes (arrhythmia)

36
Q

Site of action is the late DCT and collecting duct, where they block epithelial Na+ channels on the apical membrane of principal cells

A

Triamterene and amiloride (ENaC inhibitors)

37
Q

Site of action is the late DCT and collecting duct, where they block CYTOSOLIC mineralocorticoid receptors in principal cells, reducing expression of some proteins

A

Spironolactone and eplerenone (Aldosterone antagonists)

38
Q

Abolish the trans-epithelial potential that drives tubular secretion of K+ and H+

A

ENaC inhibitors and aldosterone antagonists (ROMK channels and Type A intercalated cell H+-ATPase)

39
Q 
Control vs. \_\_\_\_
Vol: 1 vs 2 (ml/min)
pH: 6 vs 7.2
Na+: 72 vs. 375
K+: 22 vs. 15
Cl-: 85 vs. 345
HCO3-: 1 vs. 15
A

Triamterene (SOME ACTION ON CARBONIC ANHYDRASE)

40
Q

Potassium-sparing diuretics’ effect on renal hemodynamics

A

None

41
Q

Uses:
Prevent K+-wasting
Liddle syndrome
Cystic fibrosis

A

ENaC inhibitors (triamterene and amiloride, K-sparing diuretics)

42
Q 
Uses:
Prevent K+-wasting
Primary hyperaldosteronism
Hepatic cirrhosis
CHF
A

Aldosterone antagonists (spironolactone, eplerenone)

43
Q

ADEs= boxed warning for hyperkalemia (use cautiously with ACE inhibitors and NSAIDs)

A

Potassium sparing diuretics (triamterene, amiloride, spironolactone, eplerenone)

44
Q

ADEs= gynecomastia, impotence, hirsutism, decreased libido

A

Aldosterone antagonists (spironolactone > eplerenone)

45
Q

Site of action is entire tubule

Reduces renal medullary tonicity, which reduces the passive reabsorption of NaCl in the ascending limb

A

Mannitol (osmotic diuretic, increases the osmolarity of the tubular fluid)

46
Q

Expands ECF volume

Increases excretion of ALL electrolytes

A

Mannitol (osmotic diuretic)

47
Q

Increases RBF
GFR is unchanged
Inhibits release of renin

A

Mannitol

48
Q

Given IV for dialysis disequilibrium syndrome, reducing CSF and intra-ocular pressure, and minimizing acute tubular necrosis

A

Mannitol

49
Q

Contraindicated in heart failure (edema) and active cranial bleeding

A

Mannitol

Pharmacology Exam 4 (7 decks)

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