Diuretics Flashcards

1
Q

Osmotic Diuretics act on which part(s) of the nephron?

A

PT & DLH

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2
Q

acetazolamide acts on which part of the nephron?

A

PT

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3
Q

Furosemide acts on which part of the nephron?

A

TAL

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4
Q

hydrochlorothiazide acts on which part of the nephron?

A

DCT

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5
Q

amiloride & spironolactone act on which part of the nephron?

A

CD

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6
Q

Tolvaptan acts on which part of the nephron?

A

CD

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7
Q

how does mannitol reduce H20 & sodium reabsorption?

A

it increase the capillary oncotic pressure which will drive water & sodium out of the ICF and into the tubular lumen

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8
Q

What is the MOA of acetazolamide?

A

directly inhibits carbonic anhydrase

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9
Q

What is the MOA of furosemide?

A

blocks NKCC channels in TAL

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10
Q

What is the MOA of amiloride?

A

blocks ENaC channels in CD

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11
Q

What is the MOA of hydrochlorothiazide?

A

blocks NCC channels in DCT

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12
Q

What is the MOA of spironolactone?

A

MR receptor antagonist

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13
Q

What is the MOA of Tolvaptan?

A

acts on V2 receptors in CD to decrease sensitivity to aldosterone

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14
Q

What are the main clinical uses of mannitol?

A

decreases intracranial & intraocular pressure

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15
Q

How does acetazolamide decrease formation of uric acid stones?

A

It alkalizes the urine

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16
Q

How does inhibition of carbonic anhydrase affect the action of NHE channels in the PT?

A

It decreases Na+ & bicarbonate reabsorption and decreases H+ excretion

17
Q

What are some of the AEs of acetazolamide?

A

exacerbation of calcium phosphate kidney stones; hyperchloremic metabolic acidosis; Type II Renal Tubular Acidosis

18
Q

In addition to blocking NKCC channels, furosemide also activates what and how does this affect Na+ reabsorption?

A

Furosemide also activates PG synthesis which further decreases Na+ reabsorption in the kidneys

19
Q

What is a major downstream effect of blocking NKCC channels in the TAL?

A

activation of RAAS system due to increased Na+ concentration in the tubular lumen

20
Q

What are some of the main AEs of furosemide?

A

hypokalemia; hyponatremia; hypocalcemia; hypomagnesemia w/ chronic use; hypochloremia; metabolic alkalosis (caused by activation of RAAS); hyperuricemia

21
Q

Explain how hydrochlorothiazide can be used to treat calcium phosphate kidney stones?

A

It increases Ca2+ reabsorption in PT & DCT thus reducing tubular Ca2+ concentration

22
Q

Thiazides can also be used to treat which type of diabetes? Be specific.

A

Nephrogenic DI

23
Q

What are relative contraindications for thiazide use?

A

hypochloremic metabolic alkalosis; Diabetes mellitus (thiazides can cause hyperglycemic & hyperlipidemia); Pts. on Li+ based antipsychotics (thiazides reduce Li+ excretion increasing risk for Li+ poisoning; can precipitate gout

24
Q

How does amiloride prevent potassium wasting?

A

blockage of ENaC channels in CD disrupts Na+/K+ gradient that drives K+ secretion

25
Q

What are the main clinical uses for amiloride?

A

Li+ induced DI (decreases Li+ reabsorption in CD); hyperaldosteronism

26
Q

What are the main AEs of amiloride?

A

hyperkalemia; normal anion gap metabolic acidosis; Type IV renal tubular acidosis

27
Q

What are the main clinical uses of Tolvaptan?

A

polycystic kidney disease; SIADH; hyponatremia