Diuretics Flashcards

1
Q

Osmotic Diuretic drugs

A

Mannitol
Urea
Glycerin
Isosorbide

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2
Q

Site of action of Osmotic diuretics

A

Acts on both the Loop of Henle, which is the primary site, and in the Proximal Tubule, which is the secondary site

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3
Q

Therapeutic uses of Osmotic diuretics

A
Treatment of cerebral edema (Mannitol is contraindicated in generalized edema)
Treatment of glaucoma
Treatment of acute renal failure
Mobilization of edema fluid
Used in patients with drug overdose
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4
Q

Osmotic diuretics pharmacokinetics

A

Mannitol and Urea are administered IV
Glycerin and Isosorbide are administered orally
Mannitol is not metabolized and is eliminated rapidly by the kidneys

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5
Q

Loop or High Ceiling Diuretic drugs

A

Furosemide
Bumetanide
Ethacrynic acid

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6
Q

Site of action of Loop Diuretics

A

Thick ascending limb of the Loop of Henle

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7
Q

MOA of Loop Diuretics at site of action

A

Inhibit the Na+-K-2Cl symporter at the luminal membrane in the thick ascending limb of the Loop of Henle
Also results in inhibiting the paracellular reabsorption of Na+, Ca2+, and Mg2+
Loop diuretics are the most efficacious because about 25% of filtered Na+ is reabsorbed in the thick ascending limb

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8
Q

MOA of Loop Diuretics at the Distal Tubule and Collecting Duct

A

Increase Na+ delivery to the distal tubule and collecting duct which increases depolarization of the luminal membrane, creating a negative lumen
This facilitates K+ excretion in principal cells and H+ secretion in type A intercalated cells into the lumen
This results in hypokalemia and systemic alkalosis

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9
Q

MOA of Loop Diuretics elsewhere

A

Stimulates the Renin-Angiotensin-Aldosterone system, contributing to hypokalemia and systemic alkalosis
Increase total renal blood flow by a mechanism which may involve prostaglandins
Increase systemic venous capacitance which may be mediated by prostaglandins

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10
Q

Edema therapeutic uses of Loop Diuretics

A

Treatment of acute pulmonary edema and pulmonary congestion
Treatment of generalized edema associated with congestive heart failure, chronic renal failure, and liver cirrhosis
Treatment of increased intracranial pressure and udder edema
Treatment of edema of nephrotic syndrome which is usually refractory to other diuretics

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11
Q

Therapeutic use of Furosemide

A

Loop Diuretic

Used for treatment of exercise-induced pulmonary hemorrhage in horses

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12
Q

Therapeutic uses of Loop Diuretics combined with saline

A

Combined with isotonic saline to treat hypercalcemia and to prevent volume depletion
Combined with hypertonic saline for the treatment of life-threatening hyponatremia because loop diuretics inhibit the kidney from producing concentrated urine

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13
Q

Pharmacokinetics of Furosemide

A

Loop Diuretic
Administered intravenously and orally
Onset of action is rapid and duration is short
Partly metabolized by conjugation and partly excreted unchanged in urine, and actively secreted in urine by the organic acid secretory mechanism

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14
Q

Adverse effects of Loop Diuretics

A
Ototoicity
Hypokalemia
Hypomagnesemia
Acute hypovolemia
Hypotension
Hyperglycemia
Systemic alkalosis
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15
Q

Thiazide Diuretic drugs

A

Hydrochlorothiazide

Chlorothiazade

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16
Q

Site of action of Thiazide Diuretics

A

Distal convoluted tubule

17
Q

MOA of Thiazide Diuretics

A

Inhibit the Na+-Cl symporter in the distal convoluted tubule resulting in inhibition of tubular reabsorption of Na+,Cl, and diuresis
Diuretic efficacy is moderate because 5% of Na+ occurs in the early distal tubule
Inhibit K+ and Mg2+ reabsorption but increase reabsorption of Ca2+
This causes hypokalemia and systemic alkalosis by mechanisms similar to Loop Diuretics

18
Q

Therapeutic uses of Thiazide Diuretics

A

Treatment of edema of CHF, liver cirrhosis, nephrotic syndrome, and acute glomerular nephritis
Treatment of nephrogeni diabetes insipidus
Treatment of calcium nephrolithiasis
Treatment of udder edema in cows
Treatment of hypertension alone or combined with other antihypertensive drugs

19
Q

Adverse effects of Thiazide Diuretics

A

Electrolyte imbalanes (hyponatremia, hypokalemia, hypomagnesemia) are less than with Loop Diuretis
Hyperglycemia
Hypersensitivity reactions in patients allergic to sulfonamides
Hyperlipidemia

20
Q

Pharmacokinetics of Thiazide Diuretics

A

Administered orally
Bind extensively to plasma proteins
Excreted mainly by the kidneys and actively secreted in urine by the organic acid secretory mechanism
Decreased renal blood flow decreases their effectiveness

21
Q

Potassium-sparing Diuretic drugs

A

Spironolactone
Triamterene
Amiloride

22
Q

Site of action of Potassium-sparing Diuretics

A

Late distal tubule and collecting duct

23
Q

MOA of Potassium-sparing Diuretics

A

Competitively blocks aldosterone by binding to aldosterone receptor in the late distal tubule and collecting duct (=aldosterone antagonist)
This results in excretion of NaCl and diuresis, as well as retention of K+ adn H+
Diuretic efficacy depends on the levels of endogenous aldosterone
Diuretic efficacy is mild because only 2% of Na+ reabsorption occurs in the late distal tubule and collecting duct

24
Q

Therapeutic uses of Spironolactone

A

Potassium-sparing Diuretic
Diuretic
Treatment of primary and secondary hyperaldosteronism

25
Q

Adverse effects of Spironolactone

A

Potassium-sparing Diuretic
Hyperkalemia
Systemic acidosis
Adverse effects on reproduction because it acts on progesterone and androgen receptors

26
Q

Pharmacokinetics of Spironolactone

A

Potassium-sparing diuretic
Administered orally
Readily absorbed and highly bound to plasma proteins
Extensively metabolized by liver and converted to an active metabolite
Onset of action is slow (2-3 days) and duration is long

27
Q

MOA of Trimterene and Amiloride

A

Potassium-sparing diuretics
Block epithelial Na+ channels in the luminal membrane of the principal cells in the late distal tubule and collecting duct
This results in excretion of Na+ and diuresis, as well as retention of K+ and H+
The diuretic efficacy is mild, similar to Spironolactone

28
Q

Therapeutic uses of Trimterene and Amiloride

A

Potassium-sparing diuretics
Treatment of hypokalemia and hypomagnesemia
Occasionally used in edematous disorders and hypertensions (very weak diuretics)

29
Q

Adverse effects of Trimterene and Amiloride

A

Potassium-sparing diuretics
Hyperkalemia
Systemic acidosis

30
Q

Pharmacokinetics of trimterene and AMiloride

A

Potassium-sparing diuretics
Administered orally
Amiloride is excreted by the kidneys
Trimeterene is converted to an active metabolite int he liver which is actively secreted in the urine

31
Q

Carbonic Anhydrase Inhibitor drugs

A

Acetazolamide
Methazolamide
Dorzolamide and Brinzolamide (topical ophthalmic)

32
Q

Site of action of Carbonic Anhydrase Inhibitors

A

Proximal Tubule (primary site) and collecting duct (secondary site)

33
Q

MOA of Carbonic Anhydrase Inhibitors

A

Reversible inhibition of carbonic anhydrase which inhibits the exchange for Na+ in the proximal tubule
Carbonic anhydrase inhibitors lower intraocular pressure (IOP) by inhibition of CCA in the eye, decreasing formation of aqueous humor

34
Q

Therapeutic uses of Carbonic Anhydrase Inhibitors

A

Treatment of open angle glaucoma

Acetazolamide has been used in udder edema

35
Q

Adverse effects of Carbonic Anhydrase Inhibitors

A
Mild systemic acidosis
Hypokalemia
Hyperglycemia
Signs in dogs - vomiting, diarrhea, hyperventilation
Polyuria and polydipsia
Behavior changes pruritus of paws
36
Q

Pharmacokinetics of Carbonic Andhydrase Inhibitors

A

Acetazolamide is administered orally
Onset of action about 30 minutes and duration about 4-6 hours in small animals
Acetazolamide is eliminated mainly by the kidneys and is actively secreted in urine by the organic acid secretory mechanism
Dorzolamide and Brinzolamide are administered topically on the eye