03b: PCKD, DI Flashcards Preview

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Flashcards in 03b: PCKD, DI Deck (23)
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1
Q

Which mutation(s) can result in congenital nephrogenic diabetes insipidus? Star the one seen in females.

A
  1. Mutation in V2 receptor (X-linked)

2. Mutation in AQP (non-X-linked)*

2
Q

Patient with HT, hypokalemia, and metabolic alkalosis. (High/low) levels of (X) is classic for these findings.

A

High

X = aldosterone (via upregulation of ENaC)

3
Q

Liddle’s syndrome: what’s the key mutation?

A

ENaC channel gain-of-function mutation that decreases its internalization (thus higher cell surface expression of channel)

4
Q

Liddle’s syndrome presents with (high/low) BP, (hypo/hyper)-kalemia, and metabolic (acidosis/alkalosis). Aldosterone levels are (high/low).

A

High; hypo-kalemia; alkalosis

Low

5
Q

Liddle’s follows which inheritance pattern?

A

AD

6
Q

(X) syndrome is referred to as “pseudo-hyperaldosteronism” because (Y) levels are (low/high).

A
X = Liddle's
Y = aldosterone and renin

Low (though presents with Sx of high aldosterone level due to up-regulated ENaC)

7
Q

Treatment of Liddle’s syndrome includes:

A
  1. Low Na diet

2. ENaC channel inhibitors (amiloride, triamterene)

8
Q

T/F: Liddle’s syndrome can be treated with spironolactone.

A

False - aldosterone inhibitors don’t work

9
Q

Patients with Alport syndrome present with (proteinuria/hematuria) and (rapidly/slowly) progressive renal failure.

A

Hematuria (may have some proteinuria as podocytes become compromised);
Slowly

10
Q

Majority of patients with Alport syndrome inherited mutation via (X) pattern of inheritance. This mutation is in (Y).

A
X = X-linked dominant (85%)
Y = Collagen alpha-5
11
Q

First-line Rx for uncomplicated cystitis

A

Trimethoprim/sulfamethoxazole

12
Q

Second-line Rx for uncomplicated cystitis

A
  1. Fluoroquinolones

2. Beta-lactams

13
Q

(X) diuretics ONLY block urinary diluting capacity by blocking (Y) at site where (Z) (reabsorption/secretion) makes urine hypo-osmotic.

A

X = thiazide
Y = NCC (Na/Cl cotransporter)
Z = Na
Reabsorption (Cortical diluting site of DCT)

14
Q

(X) diuretics block BOTH urinary diluting capacity by blocking (Y) at which site?

A
X = loops
Y = Na-K-2Cl cotransport

Thick ascending limb

15
Q

(X) diuretics (increase/decrease) renin/aldosterone levels by messing with tubuloglomerular feedback.

A

X = loop

Increase

16
Q

(X) diuretics are antagonized by NSAIDs. Why?

A

X = loops

Prostaglandin synthesis contributes to diuretic effect of these agents

17
Q

List some drugs that reduce efficacy of loop diuretics by (stimulating/inhibiting) (X)-mediated tubular secretion.

A

Inhibiting;
X = oatp

  1. Probenecid (gout- blocks urate reabs)
  2. Penicillins
18
Q

Which characteristic of a drug’s metabolite would allow it to antagonize effect of loop diuretic?

A

Anionic (decreases loops secretion by oatp)

19
Q

How does chronic renal insufficiency affect efficacy of diuretics?

A

Decreased renal blood flow and increased anionic metabolites reduce diuretic renal excretion and efficacy

20
Q

How does nephrotic syndrome affect efficacy of diuretics?

A

Hypoalbuminemia increases Vd of diuretics thus decreasing renal excretion and their efficacy

21
Q

(X) diuretic is used in combo with Li to prevent development of Li-induced (Y). How does the drug do this?

A
X = amiloride
Y = DI

Blocks Li uptake into principal cells via ENaC

22
Q

Spironolactone is (agonist/antagonist) to (X) and affects which channels/transporters?

A

Antagonist
X = mineralocorticoid R

Decrease expression of ENaC, ser/thr kinase (activates ENaC), and NaK ATPase

23
Q

T/F: spironolactone typically used in hyperaldosteronism.

A

True - antagonizes both renal and non-renal actions of aldosterone