Regulation of K balance Flashcards

(21 cards)

1
Q

Counterion of K

A

phosphate or sulfate, not chloride. Phosphate and sulfate are poorly resorbed in distal tubule and collecting duct. Some organic ions can be turned into HCO3-, and HCO3- in collecting duct facilitates potassium excretion.

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2
Q

[K plasma]

A

3.5-5.0 meq/L

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3
Q

Functions of intracellular K

A
Maintenance of cell volume (direct relationship)
Necessary for RNA/protein synthesis (deficiency = stunted growth)
Regulates acid/base balance (loss = acidosis, gain = alkalosis)
Maintains membrane potential
Cofactor for some enzymes 
Vascular function (low K = vasoconstriction, and opposite)
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4
Q

Insulin

A

Brings glucose into cells,
Increases Na uptake bc it needs phosphate from Na/phosphate symporter
Pulls K out of blood
Can cause hyperkalemia right after starvation

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5
Q

Epinephrine via B2-receptors

A

B-receptors increase Na-K ATPase activity, pulling more K into the cell and possible producing hypokalemia, limits K going out

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6
Q

Norepinephrine via alpha-receptor

A

Causes K to shift out of cells, minimizes hypokalemia after exercise, limits K coming in

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7
Q

Hypertonicity

A

Causes K to exit cell

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8
Q

Exercise

A

Shifts K out of cells, where it functions as vasodilator

Someone treated with B-adrenergic antagonists can experience hyperkalemia after exercise

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9
Q

External K intake

A

Low K diet reduces transcription of Na/K ATPase (less K going into cells)
High K diet increases transcription of Na/K ATPase
All intake of K is excreted by kidney

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10
Q

Regulation of K absorption

A

85% is resorbed in proximal tubule. This is also primary site of regulation.

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11
Q

Effects of Acid/Base balance on K

A

Mineral acids cause K to shift out of cells

Organic acids have minimal effect

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12
Q

Effect of intracellular K on action potential

A

hypokalemia makes threshold potential more negative

hyperkalemia makes threshold potential less negative

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13
Q

Effect of Ca+2 on excitability

A

Hypercalcemia raises threshold potential

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14
Q

K secretion in nephron

A

K is secreted predominantly in proximal collecting duct but also in distal tubule

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15
Q

Ion transport In TALH

A

K is taken up by Na/Cl/K transport on lumen side and ejected into lumen again via K channel. K also comes into the cell by Na/K ATPase on basolateral membrane

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16
Q

Ion transport in collecting duct

A

Principal cells take in Na and secrete K via different channels, but Na/K ATPase on basolateral side connects the two events. Increasing Na resorption/K secretion also increase paracellular diffusion of Cl

17
Q

Effect of flow rate on K secretion in collecting duct

A

High flow means more K secretion

Higher sodium delivery = more K secretion

18
Q

Effect of ADH on K secretion

A

With no ADH, CD is impermeable to water and has high flow, maintaining high K secretion
ADH slows passage of water but also stimulates K secretion so there is no net change

19
Q

Acid-Base effects on K secretion

A

Acidosis in CD causes principal cells to decrease K secretion.
Alkalosis in causes principal cells to increase K secretion

20
Q

alpha-intercalated cell

A

Cell in CD that secretes H+ in exchange for K resorption

If Principal cell secretes more K, alpha-intercalated cell will pick up the extra K and secrete H

21
Q

Aldosterone

A

Hyperkalemia directly cause Aldosterone secretion, which increases K secretion
If aldosterone release is prompted by Na deficiency, Na resorption in nephron segments proximal to CD, leaving K secretion unchanged