Diuretics pt. 2 (Exam III) Flashcards

1
Q

What does H₂O movement look like in the DCT?
How much Na⁺ absorption occurs in the DCT?

A
  • ↓H₂O movement
  • very little Na⁺ absorption
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2
Q

What ion gets reabsorbed in the DCT?
How does this occur?

A

Ca⁺⁺ is reabsorbed by PTH (Parathyroid hormone)

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3
Q

How do Thiazide diuretics elicit their effects?

Do they affect any other things?

A

Inhibition of NCC transporter (causing NaCl loss)

CA (Carbonic Anhydrase) inhibited slightly.

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3
Q

Combination of which two diuretic classes would cause a massive H₂O loss and require hospitalized monitoring?

A

Loop Diuretics + Thiazides

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4
Q

Which Thiazide diuretic is prototypical?

A

HCTZ (Hydrochlorothiazide)

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5
Q

Where is the final site of Na⁺ reabsorption?

Which site is the most important for K⁺ secretion?

A

Collecting Tubule

Collecting Tubule

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6
Q

Where do mineralcorticoids (like Aldosterone) elicit their effects?

A

Cortex portion of Collecting Tubule

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7
Q

Which channel is responsible for reabsorbing Na⁺ from the collecting tubule back into the blood?

A

ENaC (Epithelial Na⁺ Channel)

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8
Q

What potentiates the ENaC channel to increase Na⁺ retention?

A

Aldosterone

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9
Q

Where is Cl⁻ reabsorbed into the blood?
How is Cl⁻ reabsorbed into the blood?

A
  • Collecting Tubule
    1. ENaC retains Na⁺
    2. Less K⁺ driven out makes urinary lumen (-)
    3. (-) charge drives Cl⁻ through paracellular route into blood.
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10
Q

Which two diuretic classes are K⁺-wasting?

Which wastes more K⁺?

A

Loop Diuretics and CA Inhibitors (Acetazolamide)

Acetazolamide

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11
Q

Name two K⁺-sparing diuretics and their mechanism of action.

A

Spironolactone - blocks aldosterone receptors
Amiloride - Inhibits ENaC, blocking Na⁺ movement and thus K⁺ movement.

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12
Q

Rate of _____ secretion is positively correlated with aldosterone levels.

A

K⁺

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13
Q

What are the primary uses for K⁺-sparing diuretics?

A

States of excessive mineralcorticoids
- Conn’s Syndrome (excessive edema)
- Ectopic ACTH Production.

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14
Q

What are secondary uses for K-sparing diuretics?

A
  • CHF
  • Nephrotic Syndrome
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15
Q

What are 3 contraindications to K⁺-sparing diuretics?

A
  1. Patient takes K⁺ supplement
  2. Patient on drugs affecting K⁺ levels
  3. Liver Disease
16
Q

What is the most common result of K⁺-sparing diuretic toxicity?
What exacerbates this?
How can this be avoided?

A
  • Hyperkalemia
  • Renal Disease
  • Toxicity avoided by administering K⁺-sparing drug with a loop diuretic, balancing K⁺ levels.
17
Q

How does ADH increase H₂O reabsorption?

A
  1. ADH binds to receptor
  2. Aquaporin carrying vesicle merges with urinary cell membrane.
  3. H₂O has more aquaporins to move through
18
Q

What would osmolality be at the very apex of the thick ascending limb?

A

100 mOsm/L

19
Q

What drug directly inhibits ADH?

A

Conivaptan

20
Q

What is the primary use of mannitol?
What is a secondary use of mannitol?

A
  1. Reduction of ICP
  2. Removal of renal toxins (acute hemolysis or after radiocontrast)
21
Q

How does Mannitol elicit its effect?

A

Mannitol is essentially artificial osmolality, increasing urine volume by pulling H₂O towards it.

22
Q

What would the effects of mannitol toxicity be on serum Na⁺ specifically?

A
  1. Initial ↓ serum Na⁺
  2. Secondary ↑↑↑ serum Na⁺
23
Q

What would mannitol toxicity encompass?

Would this differ if the patient had renal failure?

A
  • Dehydration
  • ↑Na⁺
  • ↑K⁺

If the patient had renal failure then ↓Na⁺

24
Q

What diuretic can crystallize when given parenterally and must be given with an in-line filter?

A

Mannitol

25
Q

What is the most common reason for diuretic use?

A

Edema (peripheral or pulmonary)

26
Q

What syndrome is characterized by insufficient endogenous ADH?

What would the s/s be?

A

Diabetes Insipidous

Polydipsia & polyuria

27
Q

What is the treatment for Nephrogenic Diabetes Insipidous?

A

Thiazide Diuretics
- ↓ plasma volume, ↓ GFR, H₂O & NaCl reabsorption.

28
Q

Where does ADH elicit its effects?

A

Medulla portion of Collecting Duct