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Pharmacology > Diuretics > Flashcards

Diuretics Flashcards

1
Q

Thiazide and related diuretics

A

Hydrochlorothiazide
Chlorthalidone
Indapamide
Metolazone

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2
Q

Thiazide and related diuretics - MoA

A

Acts on early portion of the distal tubule to inhibit the Na+, Cl- symporter that participates in the reabsorption of sodium and chloride from this segment of the nephron. This action leads to the delivery of a greater volume of sodium and chloride-enriched tubular fluid to the late distal tubule and collecting duct, which in turn stimulates the exchange of sodium and potassium at these sites. In this process a small amount of potassium is secreted into urine in the tubules –> kaliuretic effect; can cause hypokalemia. Thiazide also increase magnesium excretion, but decrease calcium excretion in the urine.
Decrease Ca excretion result from decreased expression of Ca transport proteins (epithelial Ca channel calbindin, sodium-calcium exchanger protein) in renal tubules after thiazide adm.

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3
Q

Thiazide and related diuretic - Clinical use

A

Hypertension
Edema associated with heart failure, cirrhosis, corticosteroid therapy, estrogen therapy.
Renal disorders such as nephrotic syndrome
Nephrogenic diabetes insipidus (decrease excessive urine V dramatically, reduction in plasma V –> increase Na&water reabsorption from proximal tubule –> less water delivered to diluting segments of nephron)
Nephrolithiasis (kidney stones) –> reduces Ca excretion

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4
Q

Thiazide and related diuretic - Adverse effects

A

Hypokalemia –> hypokalemic metabolic alkalosis
Hyponatermia
Hypomagnesemia
Hyperglycemia
Hyperlipidemia
Hyperuricemia –> can lead to gout
Hypercalcemia
Decreases the insulin sensitivity –> can cause diabetes in some pat.
Thiazide-induced hypokalemia can decrease insulin secretion.
Blood cell deficiencies

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5
Q

Thiazide and related diuretic - Interactions and Contraindication

A

Interactions:
Potentiated the diuretic effect of loop diuretics

Contraindications:
Hypotension
Sulfa-allergy
Gout
Renal failure
Lithium therapy
Hypokalemia
May worsen diabetes
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6
Q

Which is the most frequently used thiazide diuretic?

A

Hydrochlorothiazide

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7
Q

Loop diuretics

A

Furosemide
Bumetanide
Torsemide
Ethacrynic acid

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8
Q

Loop diuretics - MoA

A

Inhibit the Na+, K+, 2Cl- symporter in the ascending limb of loop of Henle and thereby exert a powerful natriuretic effect. Inhibit the reabsorption of a greater percentage of filtered sodium and produce a dose dependent diuresis throughout their clinical dosage range.
They produce kaliuresis by increasing the exchange of sodium and potassium in the late distal tubule and collecting duct.
They increase magnesium and calcium excretion by reducing the reabsorption of these ions in the ascending limb by way of inh Na+K+2Cl- symporter. They cause a reduction of potassium back diffusion, and this increases magnesium and calcium excretion.

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9
Q

Loop diuretics - Clinical use

A

Pulmonary edema(iv)
Preferred diuretics in the treatment of persons with renal impairment (creatinine clearance <30mL/min)
Edema caused by heart failure, cirrhosis.
Hypertension(but thiazide drugs are more preferred)
Hypercalcemia

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10
Q

Loop diuretics - Adverse effects

A 
Hypokalemia --> metabolic alkalosis
Hypocalcemia
hypomagnesemia
Hyponatremia
Hyperuricemia
Hyperglycemia
Hyperlipidemia
Ototoxicity; tinnitus, ear pain, vertigo and hearing deficits.
Blood cell deficiencies 
Hypersensitivity reactions
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11
Q

Loop diuretics - Interactions

A

Diuretic effect decreased by NSAIDs. Adm with ACE inh may cause excessive hypotension

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12
Q

Which loop diuretic has the highest incidence of ototoxicity?

A

Ethacrynic acid

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13
Q

Potassium-Sparing Diuretics

A

Amiloride
Triamterene
Spironolactone
Eplerenone

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14
Q

Potassium-Sparing Diuretics - Interactions

A

Adm with ACE inh or potassium –> hyperkalemia

Adm with NSAIDs –> renal failure

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15
Q

Amiloride - MoA

A

Blocking the entry of sodium into the principal tubular cells of the late distal tubule and collecting duct, these drugs prevent sodium reabsorption at this site and indirectly reduce the secretion of potassium into the tubular filtrate and urine. They produce a modest amount of natriuresis but decrease kaliuresis.

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16
Q

Amiloride - Clinical use

A

Treat hypokalemia induced by thiazide and loop diuretics

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17
Q

Amiloride - Adverse effects

A

Hyperkalemia
Blood cell deficiencies
GI distress

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18
Q

Spironolactone - MoA

A

Block aldosterone binding to the mineralocorticoid receptor in epithelial cells of the late distal tubule and collecting duct. When activated they interact with DNA to promote expression of genes for sodium channels and the sodium pump that enable sodium reabsorption and potassium secretion.
Reduces sodium reabsorption and accompanies secretion of potassium

19
Q

Spironolactone - Clinical use

A

Hyperaldosteronism
Reduce mortality in pat with heart failure
Prevent hypokalemia
Polycystic ovary disease and hirsutism (becayse of antiandrogenic effect)

20
Q

Spironolactone - Adverse effects

A

Gynecomastia
Impotence in men
Hyperkalemia

21
Q

Eplerenone - Clinical use

A

Counteract the effects of excessive aldosterone in pt with heart failure

22
Q

Osmotic Diuretics

A

Glycerol

Mannitol

23
Q

Osmotic Diuretics - MoA

A

Increased osmotic pressure of the plasma –> attract water from interstitial and transcellular fluids
decreased intraocular V & pressure by attracting water from ocular fluids into the circulation

24
Q

Osmotic Diuretics - Adverse effects

A

Excessive plasma V expansion –> heart failure and pulmonary congestion and edema
Nausea
Vomiting

25
Q

Osmotic Diuretics - Interactions

A

Potentiates effects of other diuretics

26
Q

Glycerol - Clinical use

A

Acute glaucoma

27
Q

Mannitol - MoA

A

After IV adm, it is filteres at the glomerulus but not reabsorbed from the renal tubules. Osmotically attracts and retains water as it moves through the nephron and into the urine –> decreased tubular sodium conc and conc gradient between tubular fluid and cells –> retards the reabsorption of sodium

28
Q

Mannitol - Clinical use

A

Cerebral edema and reduce intracranial pressure
Acute glaucoma
Diuretic –> improve renal function in the oliguric phase of acute renal failure
Maintain renal function and decreased renal toxicity of antineoplastic platinum compounds (cisplatin)
Promote renal excretion of toxic substances in cases of drug overdose or poisoning.

29
Q

Carbonic Anhydrase Inhibitors

A

Acetazolamide

Dorzolamide

30
Q

Carbonic Anhydrase Inhibitors - MoA

A

Inh CA throughout the body. This enzyme catalyzes the conversion of CO2 and water to carbonic acid which spontaneously decomposes to bicarbonate and hydrogen ions.
CA catalyzes the formation of bicarbonates and participates in this way in aqueous humor formation; bicarbonate is secreted into the posterior chamber of the eye along with water and other substances that make up the aqueous humor secretion and intraocular pressure.

CA is required for the reabsorption of sodium bicarbonate from the prox tubule and for secretion of hydrogen ions in the collecting duct. In the reabsorption of sodium bicarbonate, bicarbonate must be converted to CO2 and water by CA, because apical cell membrane of tubular epithelial cells is impermeable to bicarbonate. CO2 and water can diffuse into the tubular cells, where CA converts them back into bicarbonate –> transported into the interstitial fluid for diffusion into the circulation. Inh of this –> decrease reabsorption of sodium bicarbonate and increase in its renal excretion –> alkalinization of urine –> hyperchloremic metabolic acidosis. Hyperchloremia due to increased reabsorption of chloride as a compensation for decreased bicarbonate reabsorption.

Counteract fluid retention –> decrease in CSF pressure + prevent fall in CSF pH.
Inhibition in CNS: increase seizure threshold

31
Q

Carbonic Anhydrase Inhibitors - Clinical use

A

Glaucoma (acute&chronic)
Used to alkalinize the urine
Prevention and treatment of high-altitude sickness (mountain sickness) (counteract respiratory alkalosis)
Epilepsy

32
Q

Carbonic Anhydrase Inhibitors - Adverse effects

A 
Drowsiness
Paresthesia
Hypokalemia
Hyperglycemia
Hypersensitivity 
Blood cell deficiencies
Hepatic insufficiency 
Metabolic acidosis
Uremia
33
Q

Carbonic Anhydrase Inhibitors - Interactions

A

Decrease excretion of weak bases (amphetamine, pseudoephedrine, quinidine) –> increased serum levels and cause toxicity

Serum levels increased by salicylates

34
Q

Dorzolamide - Clinical use

A

Glaucoma

Ocular hypertension

35
Q

Dorzolamide - Adverse effects

A

Bitter taste
Blurred vision
Ocular discomfort
Allergic reactions

36
Q

Antidiuretic Hormone Antagonist

A

Conivaptan

Tolvaptan

37
Q

Antidiuretic Hormone Antagonist - MoA

A

V2: coupled with insertion of aquaporin channels in the apical membranes of renal collecting ducts –> reabsorption of water.
–> Help maintain plasma osmolality
Antagonism of V2: free water excretion –> aquaresis

38
Q

Antidiuretic Hormone Antagonist - Clinical use

A

Euvolemic and hypervolemic hyponatremia

39
Q

Antidiuretic Hormone Antagonist - Adverse effects

A

Hypernatremia

40
Q

Antidiuretic Hormone Antagonist - Contraindications

A

hypovolemic hyponatremia

Pt taking 3A4 inhibitors

41
Q

Antidiuretic Hormone Antagonist - Interactions

A

Increase serum levels of midazolam, simvastatin + drugs metabolized by 3A4.

42
Q

Conivaptan - MoA

A

Blocks V1A and V2 receptors

43
Q

Tolvaptan - MoA

A

Blocks V2 receptors

Pharmacology (55 decks)

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