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Drugs > Diuretics and Anti-diuretics > Flashcards

Diuretics and Anti-diuretics Flashcards

1
Q

What are Furosemide and Bumetanide?

A

Loop diuretics

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2
Q

What are examples of thiazide diuretics?

A

Chlorthalidone
Hydrochlorothiazide
Metalazone

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3
Q

Which diuretics are potassium sparing?

A

Spironolactone

Amiloride and Triamterene

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4
Q

What are Vasopressin, desmopressin, and demecocycline?

A

ADH agents

Demecocycline is an antagonist

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5
Q

What is an example of an osmotic diuretic?

A

Mannitol

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6
Q

What is acetazolamide?

A

Carbonic Anhydrase inhibitor

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7
Q

What is the mechanism of action of loop diuretics?

A

Inhibit Na+/K+/2Cl- pump in thick ascending limb –> increased excretion of Na+, Cl-, K+, and water

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8
Q

What is the mechanism of action of Chlorthalidone, hydrochlorothiazide, and metalazone? What is the effect?

A

Block the Na+/Cl- transporter in the distal convoluted tubule
–> increased excretion of Na+, Cl-, K+, and water

Also, binds to SUR–>open K+ channel–> hyperpolarization of smooth muscle cells–> vasodilation

Reduces HR and TPR–> decreased BP

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9
Q

How is potassium lost if it is an Na+/Cl- symporter that is blocked?

A

K+ is exchanged for the increased Na+ in the cortical collecting tubule

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10
Q

What is the mechanism of action of spironolactone?

A

Inhibition of aldosterone receptors

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11
Q

What does aldosterone usually do? Why is it beneficial to antagonize it?

A

Aldosterone activates the tsx/synthesis of Enac, activates Na+/K+ exchangers, that normally cause retention of Na+ and excretion of K+

Inhibition–>increased excretion of Na+ and water, and increased retention of K+

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12
Q

What is the mechanism of action of amiloride and triamterene? What is the effect?

A

Inhibition of Na+/K+,H+ exchangers and Enac (Na+ channel)

–> increased excretion of Na+ and water, increased retention of K+

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13
Q

What is the effect of ADH agonists?

A

Bind to V2 receptors–> stimulate GPCR–>cAMP

–>aquaporin recruitment–>increased water retention

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14
Q

What is the mechanism/effect of mannitol?

A

Mannitol increases osmolarity–>increased water excretion

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15
Q

What is the mechanism/effect of carbonic anhydrase inhibitors?

A

Inhibit HCO3- reabsorption–>increased water excretion

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16
Q

Is acetazolamide generally used long term?

A

No…leads to increased NaCl reabsorption after a few days, also many side effects

17
Q

When are loop diuretics used?

A 
Pulmonary edema
Other edematous conditions
Hyperkalemia
Acute renal failure
Anion overdose
18
Q

What are thiazide diuretics used for?

A

HTN
CHF
Nephrolithiasis caused by hypercalcemia
Nephrogenic diabetes insipidus

19
Q

What causes nephrogenic diabetes insipidus?

A

No ADH receptors in kidneys

20
Q

What are the side effects of thiazide diuretics?

A 
Hyperglycemia
Hyperuricemia
Hypokalemia
Hyperlipidemia
Hyponatremia
Allergic reactions
21
Q

What causes thiazide diuretics to produce hyperglycemia?

A

They bind to SUR (sulfonyl urea receptor) on K+ channel controlling insulin release→opens the channel and hyperpolarizes the β cell→suppression of insulin release

22
Q

What conditions are thiazide diuretics used to treat? (according to JNC VII)

A

Risk of stroke
CAD
CHF
DM

23
Q

What conditions should thiazide diuretics NOT be used?

A

Post MI

Chronic kidney disease

24
Q

Why is it beneficial for an ACE inhibitor to be added to a thiazide regimen?

A

Thiazides increase tubular Na+–>increased renin
–>increased aldosterone–>increased Na+ reabsorption

ACE inhibitors inhibit the renin–>aldosterone

25
Q

Besides preventing potassium wasting, when else are potassium sparing diuretics used?

A

Hyperaldosteronism
Post MI
CHF

26
Q

What are the side effects of potassium sparing diuretics?

A 
Hyperkalemia
Hyperchloremic metabolic acidosis
Gynectomastia (spironolactone)
Acute renal failure (triamterene)
Kidney stones
27
Q

When are ADH agonists used? (Vasopressin, Desmopressin)

A

Diabetes insipidus

Bedwetting

28
Q

When is mannitol used?

A

To reduce body water

To reduce intracranial/intraocular pressure

29
Q

What toxicities does mannitol have?

A 
Extracellular volume expansion
Dehydration
Hyperkalemia
Hypernatremia
Hyponatremia when renal function is impaired
30
Q

When are carbonic anhydrase inhibitors used?

A

Glaucoma
To produce urinary alkalinization
Metabolic alkalosis (treated with volume and Cl-)
Acute mountain sickness

31
Q

What are the side effects of carbonic anhydrase inhibitors?

A

Hyperchloremic metabolic acidosis
Renal stones
Renal potassium wasting

32
Q

What causes the hyperuricemia associated with loop diuretics and thiazides?

A

Hypovolemia-associated uric acid reabsorption

33
Q

Where does ADH originate?

A

Posterior pituitary

34
Q

What stimulates ADH release?

A

Changes in plasma volume

Cholestcystokinin (from small intestine)

Drugs (6 decks)

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