Diuretics Flashcards

1
Q

What is a diuretic?

A

: diuretic are agents that increase renal excretion of water and salts (mostly sodium).

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2
Q

What are the therapeutic use of diuretics?

A

: reduces the fluid volume in the body

edema, congestive heart failure, hypertension.

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3
Q

What are the classes of diuretics?

A
Thiazides 
K+ sparing 
Carbonic anhydrase 
osmotic diuretics
loop diuretic
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4
Q

What is the site of action for thizade/

A

DCT

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5
Q

What are the name of all the thiazides?

A
Hydrochlorothiazide,
 Chlorothiazide, 
Chlorthalidone, 
Bendroflumethiazide, 
Indapamide, 
Metolazone
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6
Q

What are thiazides derivatives of?

A

Sulfanamide

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7
Q

What is the mechanism of action of Thiazides?

A

Inhibits sodium-chloride cotransporterm - NCC

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8
Q

What is the result of thiazide MOA?

A

Increase renal excretion of:
Sodium and chloride
Potassium
Hydrogen (causing metabolic alkalosis)

Decrease renal excretion of:
calcium

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9
Q

What are the therapeutic uses of Thiazides?

A

Hypertension.

Edema associated with congestive heart failure, hepatic cirrhosis and renal diseases.

Nephrolithiasis (calcium stones).

Nephrogenic diabetes insipidus.

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10
Q

What are the SE of thiazides?

A
  • Water and electrolyte imbalance: hypokalemic metabolic alkalosis, and hyperuricemia.

Hypercalcemia.

Hyponatremia.

Hyperglycemia associated to hypokalemia.

Allergic reaction (sulfonamide).

Weakness, paresthesia, impotence.

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11
Q

What are advers reactions of sulfas?

A

Skin reactions, from benign rash to potentially lethal toxidermias, are adverse drug reactions to sulfonamides

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12
Q

What is the site of action of Loop diuretics?

A

TALH

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13
Q

What are the classes of Loop diuretics?

A

Sulfonamide derivative:
- Furosemide, Bumetanide, Torsemide

Non-sulfonamide loop diuretic:
- Ethacrynic acid

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14
Q

What is the MOA of loop diuretics?

A

inhibit Na/K/2Cl co-transporter on TALH

inhibit the reabsorption of Ca2+ and Mg2+, Na, K, Cl, H+(causing metabolic alkalosis)

direct effect on vasculature (prostaglandins)
increase renal blood flow
increase systemic venous capacitance

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15
Q

What are the therapeutic uses of loop diuretics?

A
acute pulmonary edema and other edema
 chronic congestive heart failure
 hypertension
 acute hypercalcemia
 hyperkalemia (in combination with NaCl)
 intoxication with anion: bromide, fluoride, iodide
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16
Q

What are the side effects and toxicity of loop diuretics?

A
hypokalemic metabolic alkalosis
 ototoxicity
 hyperuricemia (gout)
 hypomagnesemia
 allergic reactions to sulfonamides
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17
Q

What is the site of action of carbonic anhydrase inhibitors?

A

PCT

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18
Q

What are the cabonic anhydrase inhibitors?

A

Acetazolamide, Methazolamide – sulfonamide derivatives

19
Q

What is the MOA of Carbonic anhydrase inhibitors?

A

Inhibits carbonic anhydrase at PCT

acidifies the urine
alkalizes the blood.

20
Q

What is the result of the MOA of carbonic anhydrase inhibitors?

A

Inhibits carbonic anhydrase

Increase renal excretion of:
Sodium (mild)
Potassium
Bicarbonate (alkalinization of urine)

Decrease renal excretion of:
Hydrogen (acidosis)

21
Q

What are the therapeutic uses of carbonic anhydrase inhibitors?

A

glaucoma (open angle).

cystinuria by enhancing the excretion of uric acid and organic acid.

metabolic alkalosis.
acute mountain sickness.

22
Q

What is the side effects and toxcity of carbonic anhydraes inhibitors?

A
hyperchloremic metabolic acidosis. 
 stones: phosphate and calcium.
 drowsiness and paresthesias.
 potassium wasting.
 allergic reactions to sulfonamides.
23
Q

What is the mechanism of K+ loss?

A

Enhanced Na+ delivery results in K+ loss in the collecting duct

24
Q

What is the site of action of Osmotic diuretics?

A

PCT

Descending limb

25
Q

What are the osmotic diuertics?

A

Mannitol

administrated systemically (orally -> osmotic diarrhea)

26
Q

What are the MOA of Osmotic diuretics?

A

induce osmotic diuresis by preventing water reabsorption.

extract water from intracellular compartment

expands extracellular fluid volume (initially)

27
Q

What are the therapeutic uses of osmotic diuretics?

A

increase urine volume in preference to Na+ excretion.

reduction of intracranial pressure.

reduction of intraocular pressure: acute glaucoma.

28
Q

What are the side effects of osmotic diuretics?

A

excessive loss of more water relative to sodium:
-> dehydration and hypernatremia (hyperkalemia)

initial expansion of extracellular fluid volume may result in hyponatremia:
-> pulmonary edema and heart failure

29
Q

What is the site of action forPotassium sparing:

Aldosterone antagonist?

A

CCT

30
Q

What are the Potassium sparing: Aldosterone antagonist?

A

Spironolactone, Eplerenone

31
Q

What is the MOAPotassium sparing: Aldosterone antagonist?

A

inhibit the mineralocorticoid receptor in the principal cells of the collecting tubule and collecting duct. :
repress the expression of EnaC and Na+/K+ ATPase.

increase sodium, calcium secretion

inhibit potassium, hydrogen secretion

32
Q

What is the therapeutic use of Potassium sparing: Aldosterone antagonist?

A

edema and hypertension.
enhance Na+ excretion and reduce K+ wasting.

primary hyperaldosteronism.

edema associated with secondary hyperaldosteronism.

off label use of spironolactone to treat androgen-dependent hirsutism.

drug-resistant hypertension

33
Q

What are the side effects of Potassium sparing: Aldosterone antagonist?

A

metabolic acidosis in cirrhotic patients

ataxia, confusion, drowsiness, headache, lethargy

Spironolactone may cause gynecomastia, impotence,

irregular menses, postmenopausal bleeding (less with Eplerenone).

34
Q

What is the site of action forPotassium sparing: Na+ channel inhibitor?

A

CCT

35
Q

What are the Potassium sparing: Na+ channel inhibitor?

A

Amiloride, Triamterene

36
Q

What is the MOA for Potassium sparing: Na+ channel inhibitor?

A

Inhibits Na+ channel (ENaC)

Increase renal excretion of:
Sodium
Calcium (moderate)

Decrease renal excretion of:
Potassium
Hydrogen (acidosis)

37
Q

What is the therapeutic use of Potassium sparing: Na+ channel inhibitor?

A

counteract the loss of potassium induced by loop diuretics or thiazides.
pseudo-hyperaldosteronism (Liddle’s syndrome).
lithium-induced nephrogenic diabetes insipidus (can induce Li+ toxicity)
improve mucociliary clearance in patients with cystic fibrosis.

38
Q

What are side effects and toxicity of Potassium sparing: Na+ channel inhibitor?

A

hyperkalemia.
hyperchloremic metabolic acidosis.
nausea, vomiting, headache.

39
Q

What are the side effects of Potassium sparing: Na+ channel inhibitor: Triamterene?

A

reduce glucose tolerance

interstitial nephritis and renal stone (drug precipitate)

40
Q

What does Triamterene do to uurine?

A

turns urine blue

41
Q

What is the MOA for sodium polylstyrene sulfonate?

A

Cation-exchange resin used to reduce hyperkalemia
Administered orally or as enema:
-> not absorbed and chelate K+ ion in the large intestine

42
Q

What is the the therapeutic use of Sodium polystyrene sulfonate?

A

severe) hyperkalemia

Correction may be long and emergency situation may require alternative approaches

43
Q

What are the side effects of Sodium polystyrene sulfonate?

A
Hypokalemia, 
hypocalcemia,
 hypomagnesemia
- hypernatremia
- 
anorexia, constipation, diarrhea, fecal impaction (bezoar)