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Pharm Block 2 > Diuretics > Flashcards

Diuretics Flashcards

1
Q

What are side effects of loop diuretics?

A 
Hypovolemia
Hypokalemia
Hyperuricemia
Hyperglycemia
Alkalosis
Ototoxicity
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2
Q

Hyperuricemia is a side effect of which diuretics? How?

A

Loop
Thiazide/Thiazide-like
*They increase urate reabsorption in the PT

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3
Q

What are loop diuretics used to treat?

A

Hypertension
Edema - cardiac, hepatic, renal in origin
Acute pulmonary edema

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4
Q

What are thiazide/thiazide-like diuretics used to treat?

A

Hypertension
Edema from CHF
Hypercalciuria/Ca salt - Renal caliculi

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5
Q

What effect do loop and thiazide diuretics have on GFR?

A

Loop: increase GFR and RBF
Thiazide: decrease GFR

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6
Q

Which diuretic causes gynecomastia?

A

Spironolactone&raquo_space;> Eplerenone

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7
Q

What side effect is specific to sodium channel blockers?

A

Mild azotemia

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8
Q

Which diuretic decreases both GFR and RBF?

A

High doses of Triamterene (Na channel blocker)

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9
Q

Which class of diuretics causes hyperkalemia?

A

K-sparing diuretics

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10
Q

What are the therapeutic uses of K-sparing diuretics?

A

Hypertension

Edema

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11
Q

What considerations are taken into account when using K-sparing diuretics?

A

Prescribe WITH a loop or thiazide diuretic.

If you used JUST a loop or thiazide, you LOSE potassium but with a K-sparing diuretic, you promote diuresis/natriuresis without potassium loss.

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12
Q

Which class of diuretics have the highest intrinsic activity? Highest cost?

A

Activity: Loop > Thiazide > K-sparing
Cost: K- sparing > Loop > Thiazide

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13
Q

What are the K-sparing diuretics?

A

Aldosterone antagonists: Spironolactone, Eplerenone

Na-channel blockers: Amiloride, Triamterene

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14
Q

What are the thiazide/thiazide-like diuretics?

A

Hydrochlorothiazide, Metolazone

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15
Q

What are the loop diuretics?

A

Furosemide
Bumetadine
Ethacrynic acid

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16
Q

What are the therapeutic uses of Carbonic anhydrase inhibitors?

A

“GAMA”
Glaucoma - reduce intraocular pressure, decrease aqueous humor production
Alkalinize the urine - decrease drug toxicity
Mountain or altitude sickness
Anticonvulsant

17
Q

What are the side effects of carbonic anhydrase inhibitors?

A 
Metabolic acidosis (since you block HCO3- absorption)
Hypokalemia
18
Q

Carbonic anhydrase inhibitors increase the excretion of

A

Sodium
Potassium
Bicarbonate
Water

19
Q

Loop diuretics help excrete:

A

Na, Cl, K, water AND CALCIUM! (enhances calcium excretion)

20
Q

What percentage of the filtered sodium load is excreted by the different diuretics?

A

Loop: High 20-30%
Thiazides: Intermediate 8-10%
K-sparing: Low 2-3%

21
Q

The kidney reabsorbs what percentage of Na and Cl of the filtered load in the different parts of the nephron?

A

PT: 50-70% absorbed
Ascending limb: 20-30%
Distal tubule/Collecting Duct: 8-9%

22
Q

What ions are absorbed/secreted in the PT?

A 
Sodium
Chloride
Potassium
Bicarbonate
Water
23
Q

What ions are absorbed in the distal tubule/collecting duct?

A

Sodium
Potassium SECRETED
Water permeability regulated by ADH

24
Q

What are the renal vasodilators?

A

Fenoldapam, dopamine, atriopeptins

25
Q

Which diuretics are secreted by OAT?

A

Acetazolamide (CAI) - PT (major) and distal tubule
Furosemide, ethacrynic acid, bumetanide (Loop) - cortical and medullary ascending limb
Hydrochlorothiazide, metolazone (Thiazides) - cortical distal tubule

26
Q

Which diuretics increase urate reabsorption?

A

Loops and thiazides -> hyperuricemia

27
Q

What is a ceiling diuretic dose? What does it depend on?

A

Dose at which you get your maximum or ceiling effect

Depends on DIURETIC (loop > thiazide > K-sparing) and DISEASE (cirrhosis, heart failure, etc)

28
Q

What happens if you exceed ceiling dose?

A

No additional effect

Possible adverse effect

29
Q

What compartmentalization of fluids?

A

*Diuresis derives fluid from intravascular space first, then ECF, then body

Intravascular space, edematous tissues (ECF), body compartment (peritoneal or pleural)

Quick equilibration between intravascular and ECF
Slow equilibration between body compartment and ECF and intravascular

30
Q

At what rate is fluid mobilized between body compartment and vascular space?

A

No faster than 0.5kg/day

31
Q

What is the importance of compartmentalization of fluids?

A

Dictates rate of fluid mobilization

Determines volume status

32
Q

What is the ultimate goal of diuretic therapy?

A

Correct a disturbance in the ECF, balance input/output

  • Potassium
  • Acid and base
33
Q

What are the prototypic drugs used in hypertension therapy? What is the basis?

A

Furosemide
Hydrochlorothiazide
- Reduce renal tubular sodium and water reabsorption -> increase their excretion -> reduce ECF volume -> venous return falls -> CO decreases -> lower blood pressure

34
Q

What is the proposed mechanism for how diuretics treat hypertension/create a fall in peripheral resistance

A
  1. lower sodium level, lower plasma, less CO, hypotensive effect
  2. Decreased Na/H2O in vessel wall -> PGI2 and NO release -> vascular K-channel activation -> decreased sensitivity to NE -> increased Na-Ca exchange
35
Q

How do diuretics treat CHF?

A

Use prototypic drugs like furosemide and hydrochlorothiazide -> reduce fluid volume -> reduce preload -> reduction in heart size -> improve efficiency -> reduce edema/symptoms

36
Q

What role do aldosterone antagonists have on CHF?

A

They improve survival from CHF, even WITH ACE INHIBITORS (compared to standard therapy, which is ACE inhibitor + loop diuretic)

37
Q

How do aldosterone antagonists work to improve CHF mortality rates?

A
  • Inhibits renal and cardiac effects of aldosterone
  • Weak diuretic so it has a small effect on salt/water excretion and CHF symptoms
  • Inhibits cardiac hypertrophy and fibrosis caused by aldosterone
38
Q

What is the foundation of edema therapy?

A

Reduce intravascular volume
Reduce ECF and edema

*increase salt and water excretion by reducing their absorption!

Pharm Block 2 (7 decks)

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