Small Group: Sodium Handling Flashcards

1
Q

At the proximal tubule, there are many symporters. There is one antiporter, however. What is it?

A

The sodium/proton antiporter

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2
Q

What is acetazolamide?

A

A carbonic anhydrase inhibitor

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3
Q

How does the thick ascending loop of Henle generate a charge gradient?

A

The cotransporter pushes CL, K, and Na into the cell. Some potassium leaks back into the lumen, making the lumen positive.

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4
Q

Potassium is absorbed by the _______ cells.

A

principal

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5
Q

How does cirrhosis cause sodium retention?

A

Blood pools in the splanchnic veins (i.e., it can’t get through the liver) and the aortic and carotid bodies detect lower EABV–thus activating the RAAS system

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6
Q

What kind of diuretic is bumetanide?

A

Loop diuretic

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7
Q

Thiazides cause _______-calcemia.

A

hyper

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8
Q

What are three methods of aldosterone escape?

A

Decreased angiotensin II secretion
Increased pressure natriuresis (increased pressure in the tubules leading to decreased functioning of the NaH pump in the proximal tubule)
Increased secretion of ANP

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9
Q

Give __________ to people in hypovolemic shock.

A

saline

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10
Q

Spironolactone may induce __________.

A

metabolic alkalosis

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11
Q

In nephrotic syndrome, what is the effect on CVP, pulmonary pressure, and EABV?

A

CVP down
PP down
EABV down

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12
Q

What could be the cause of refractory edema in a patient taking multiple diuretics?

A

Diuretic resistance
Increased salt intake
Medication noncompliance

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13
Q

How does loop-diuretic resistance occur?

A

Sodium passes through the loop of Henle and goes to the distal convoluted tubule. The thiazide-sensitive channels are inducible; thus, after time the thiazides can reabsorb all of the extra sodium that passed by the loop of Henle.

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14
Q

What is the difference between primary and secondary hyperaldosteronism in terms of BP, EABV, and AngII levels?

A

Primary: BP high, EABV high, AngII levels low
Secondary: BP low, EABV low, AngII levels high

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