Diuretics Flashcards

(43 cards)

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
What are the osmotic diuertics?
Mannitol administrated systemically (orally -> osmotic diarrhea)
26
What are the MOA of Osmotic diuretics?
induce osmotic diuresis by preventing water reabsorption. extract water from intracellular compartment expands extracellular fluid volume (initially)
27
What are the therapeutic uses of osmotic diuretics?
increase urine volume in preference to Na+ excretion. reduction of intracranial pressure. reduction of intraocular pressure: acute glaucoma.
28
What are the side effects of osmotic diuretics?
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
What is the site of action forPotassium sparing: | Aldosterone antagonist?
CCT
30
What are the Potassium sparing: Aldosterone antagonist?
Spironolactone, Eplerenone
31
What is the MOAPotassium sparing: Aldosterone antagonist?
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
What is the therapeutic use of Potassium sparing: Aldosterone antagonist?
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
What are the side effects of Potassium sparing: Aldosterone antagonist?
hyperkalemia - metabolic acidosis in cirrhotic patients ataxia, confusion, drowsiness, headache, lethargy Spironolactone may cause gynecomastia, impotence, irregular menses, postmenopausal bleeding (less with Eplerenone).
34
What is the site of action forPotassium sparing: Na+ channel inhibitor?
CCT
35
What are the Potassium sparing: Na+ channel inhibitor?
Amiloride, Triamterene
36
What is the MOA for Potassium sparing: Na+ channel inhibitor?
Inhibits Na+ channel (ENaC) Increase renal excretion of: Sodium Calcium (moderate) Decrease renal excretion of: Potassium Hydrogen (acidosis)
37
What is the therapeutic use of Potassium sparing: Na+ channel inhibitor?
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
What are side effects and toxicity of Potassium sparing: Na+ channel inhibitor?
hyperkalemia. hyperchloremic metabolic acidosis. nausea, vomiting, headache.
39
What are the side effects of Potassium sparing: Na+ channel inhibitor: Triamterene?
reduce glucose tolerance | interstitial nephritis and renal stone (drug precipitate)
40
What does Triamterene do to uurine?
turns urine blue
41
What is the MOA for sodium polylstyrene sulfonate?
Cation-exchange resin used to reduce hyperkalemia Administered orally or as enema: -> not absorbed and chelate K+ ion in the large intestine
42
What is the the therapeutic use of Sodium polystyrene sulfonate?
severe) hyperkalemia | Correction may be long and emergency situation may require alternative approaches
43
What are the side effects of Sodium polystyrene sulfonate?
``` Hypokalemia, hypocalcemia, hypomagnesemia - hypernatremia - anorexia, constipation, diarrhea, fecal impaction (bezoar) ```