Sodium Balance and Transport Flashcards

1
Q

Where in the nephron does the hormonal fine tuning of Na+ reabsorption happen?

A

The collecting duct.

The PT and medullary thick ascending limb are going to reabsorb the vast majority of it no matter what.

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2
Q

In the first 3rd of the proximal tubule (PT), sodium is preferentially reabsorbed with which solutes?

A

Exchange with H+, and cotransport with glucose and amino acids.
(Bicarb happens further along, and Cl- not as much in the PT)

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3
Q

Where in the PT is most Cl- reabsorbed?

How does absorption in the early PT contrast from that in late PT?

A

More Cl- absorbed in the late PT.
Early PT: paracellular.
Late PT: transcellular

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4
Q

Review: What ion channel is the major player in Na+ reabsorption in the thick ascending limb?
What drug inhibits this?

A

NKCC2

Furosemide.

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5
Q

Review: What ion channel is the major player in Na+ reabsorption in the DCT?
What drugs inhibits this?

A

Na+/Cl- cotransporter.

Thiazide diuretics inhibit this.

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6
Q

Review: What molecule is the major player in Na+ reabsorption in the collecting duct?
What’s a drug inhibits this?

A

ENaC

Amelioride inhibits it.

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7
Q

How does Cl- reabsorption vary between areas of the collecting tubule with Principal Cells and areas with Intercalated Cells?

A

It’s paracellular between Principals Cells.

Intercalated cells have Cl-/HCO3- exchangers that bring Cl- in transcellularly.

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8
Q

4 responses to low effective circulating volume?

A

Activation of RAAS.
Sympathetic activation (including increased Na+ reabsorption).
Vasopressin release.
Shutting of atrial natriuretic peptide (ANP).

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9
Q

If GFR goes up, does enough Na+ get absorbed?

A

Yes… the Na+ absorption goes up to compensate.

“glomerulotubular balance”

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10
Q

How is “glomerulotubular balance” achieved?

A

Basically through pressure changes - with greater GFR, less hydrostatic pressure and more osmolality remains in the efferent arteriole / vasa recta, facilitating absorption.

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11
Q

What effect does AVP have on the thick ascending limb?

A

It stimulates NKCC2 (the opposite effect of a loop diuretic).

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12
Q

What affect does hypercalcemia have on the thick ascending limb?

A

High Ca++ hits CaSR (Ca++ sensing receptor)… inhibits NKCC2 (acting like a loop diuretic).

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13
Q

What effects do prostaglandins have on ENaC?

Thus what side effect can NSAIDs have?

A

Prostaglandins inhibit ENaC.

NSAIDs can thus increase ENaC activity, and in rare cases, cause edema/hyponatremia.

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14
Q

2 things that must be true for you to call something hypovolemia?

A

Low total body Na+.

Decreased effective circulating blood volume.

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15
Q

3 types of clinical finding seen in hypovolemia?

A

Orthostasis.
Reduced skin turgor.
Reduced organ perfusion / shock.
(Other things too… like reduced JVP)

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16
Q

Can hyperglycemia cause hypovolemia?

A

Yes - at really high levels, it will act as a diuretic.

17
Q

Treatment for hypovolemia?

A

Salt and water. (Saline!)

18
Q

Does hypervolemia mean increased effective vascular volume?

A

Not necessarily. For example, in heart failure, it can be stuck in the venous or pulmonary circulation.

19
Q

Treatment for hypervolemia?

A

Depends on cause…

usually diuretics and salt restriction would be indicated though