Diuretics Flashcards

1
Q

what are the carbonic anhydrase inhibitors (CAIs)

A

Acetazolamide,

Dorzolamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

MOA of Acetazolamide, Dorzolamide

A

inhibit C.A. IV on the
proximal convoluted tubule (PCT) brush border

inhibit cytoplasmic C.A. II
–> **Na+ reabsorption

–> *****↓ 85% PCT reabsorption of HCO3-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

clinical indications of acetazolamide and dorzolamide

A
  • glaucoma
  • **acute mountain sickness
  • to induce urinary alkalinization
  • edema: combined with NKCC or NCC inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

adverse effects of acetazolamide and dorzolamide

A
  • Bicarbonaturia
  • ***Hyperchloremic metabolic acidosis
  • Hypokalemia
  • Paresthesias
  • Renal stones
  • Sulfonamide hypersensitivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

contraindications of acetazolamide and dorzolamide

A

cirrhosis (increase plasma NH4+)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is an osmotic diuretic drug

A

mannitol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

MOA of mannitol

A

Osmotic Diuretics: freely filtered but poorly reabsorbed

increase tubular fluid osmotic pressure –>↓ tubular fluid reabsorption.

sites of action:
1. water-permeable
segments of the proximal tubule
2. **thin limbs of the loop of Henle (main site)
3. Increased distal flow stimulates K+ secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

clinical applications of mannitol (osmotic diuretic)

A

To decrease intracerebral pressure in cerebral edema

Oliguric state: Prophylaxis of acute renal failure (*increase tubular fluid flow)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

SE of mannitol

A

ECV expansion –> Risk of pulmonary edema in pts with heart failure

acute hypovolemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Contraindications of minnitol

A

*** Active cranial bleeding (mannitol & urea)

  • Anuria due to renal disease (kidney failure)
  • Impaired liver function (urea)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the NKCC inhibitors (loop diuretics)

A

Rx: Furosemide, Ethacrynic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

clinical indications for furosemide, ethacrynic acids (NKCC-I)

A
  1. Acute pulmonary edema
  2. Congestive heart failure
  3. Hypertension
  4. Refractory edema
  5. Acute renal failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Adverse effects of furosemide, ethacrynic acid

A

Hypokalemia & alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the NCC inhibitors (thiazides and sulfonamides)

A

Chlorthalidone,

Hydrochlorothiazide,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

MOA of chlorthalidone and hydrochlorothiazide

A

inhibit DCT Na+-Cl-
cotransporter (NCC) –> block coupled Na+ and Cl- reabsorption

  • increase luminal Na+ & Cl- in DCT
  • DIURESIS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

MOA of fursoemide and ethacrynic acid

A

Inhibit Na+-K+-2Cl-
cotransporter (NKCC) –>
inhibit reabsorption of solute
from thick ascending limb segments

Venodilation:↓ right atrial pressure & pulmonary capillary wedge pressure 
 within minutes (IV)

increase fractional Ca2+ excretion by 30% by decreasing the lumen-positive transepithelial potential that promotes paracellular Ca2+ reabsorption

increase fractional Mg2+ excretion > 60% by decreasing voltage-dependent paracellular transport

17
Q

Clinical indications for furosemide, Ethacrynic acid?

A

Acute pulmonary edema

Congestive heart failure

Hypertension

Refractory edema

Acute renal failure

18
Q

SE of furosemide and ethacrynic acid (NKCC inhibitors)

A

hypokalemia and alkalosis

19
Q

NCC inhibitors (thiazides and sulfonamides) MOA - chlorthalidone, hydrochlorothiazide

A

* inhibit DCT Na+-Cl-
cotransporter (NCC)

block coupled Na+ and Cl- reabsorption
- increase luminal Na+ & Cl- in DCT
- DIURESIS

decrease Ca2+ excretion

vasorelaxation
(increase Ca2+-activated K+ channels)

20
Q

clinical applications for NCC inhibitors (thiazides and sulfonamides) – chlorthalidone, hydrochlorothiazide

A

** Systemic Arterial Hypertension
- **most cost effective – mainstay of antihypertensive therapy
- less effective in patients with reduced renal function

  • **Congestive heart failure – control of edema
21
Q

hemodynamic and hormonal effects of NCC inhibitors (thiazides and sulfonamides) – chlorthalidone, hydrochlorothiazide

A

**Chronic antihypertensive effect: more related to decrease TPR than to dcrease BV

22
Q

SE of NCC inhibitors (thiazides and sulfonamides) – chlorthalidone, hydrochlorothiazide

A
  • hypokalemia
  • hyperglycemia
  • hyperlipidemia (except indapamide
23
Q

Drug interactions and precautions with NCC inhibitors (thiazides and sulfonamides) – chlorthalidone, hydrochlorothiazide

A

avoid in pts with DM

24
Q

MOA of amiloride?

A

inhibitor of renal epithelial Na+ channels

-Block epithelial Na+ channels on principal cells in the late DCT and initial connecting tubule and the cortical collecting ducts  modest natriuresis & prevention of K+ loss

25
Q

clinical indication for amiloride

A

used as K+-sparing agents in
hypokalemic alkalosis.

Used in combination with loop diuretics / thiazides to prevent
hypokalemia caused by these agents

26
Q

MOA of spirnolactone and eplerenone

A

Antagonize aldosterone receptors in the renal collecting tubules

Decrease Na+ reabsorption –> natriuresis

Decrease loss of K+ in exchange for Na+

27
Q

what drug does Prevention of LV remodeling and cardiac fibrosis

A

Spironolactone and eplerenone

28
Q

clinical application of spironolactone

A

adjunct to K+-wasting diuretics: used in edema and hypertension (coadministered with thiazide or loop diuretics)

*added to standard therapy of heart failure

  • *refractory edema associated with secondary aldosteronism**
  • cardiac failure
  • hepatic cirrhosis
  • nephrotic syndrome
  • severe ascites
29
Q

SE of spionolactone

A

hyperkalemia

30
Q

which drugs cause acidosis

A

Inhibition of carbonic anhydrase in PCT:
- acetazolamide

Block epithelial Na channels:
Amiloride
Triamterene

Block aldosterone receptor in collecting tubule:
Spironolactone
Eplerenone

31
Q

which drugs cuase alkalosis

A

Inhibition of Na+/K+/2Cl- cotransporter in TAL:
Ethacrynic acid
Furosemide
Torsemide

Inhibition of Na+/Cl- cotransporter in DCT:
Chlorthalidone
Hydrochlorothiazide
Indapamide

32
Q

Acetazolamide

effect on urinary electrolytes

A

incr. Na+
inc. K+
incr. HCO3-

33
Q

Ethacrynic acid
Furosemide
Torsemide

effect on urinary electrolytes

A
Na+
 K+
 Ca2+
 Mg2+
 Cl-

increase all

34
Q

Chlorthalidone
Hydrochlorothiazide
Indapamide

effect on urinary electrolytes

A

increase:
 Na+
 K+
 Cl-

decrease:
Ca2+

35
Q

Amiloride
Triamterene
Spironolactone
Eplerenone

effect on urinary electrolytes

A

incr. . Na+

decr. K+