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Renal > Regulation of K, Ca, PO4, Mg > Flashcards

Regulation of K, Ca, PO4, Mg Flashcards

1
Q

Which ion has effects on membrane potential and muscle/nerve excitability when increased or decreased?

A

Potassium (K)

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2
Q

Hypokalemia on membrane potential

Hyperkalemia on membrane potential

A

Increased threshold needed to fire AP

Decreased threshold needed to fire AP

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3
Q

A patient is hyperkalemic. How might you tell from an EKG?

How to think about it?

A

High T wave
Low PR interval

Likes to re-polarize (high T)
Lower resting potential due to higher K (low PR)

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4
Q

A patient is hypokalemic. How might you tell from an EKG?

How to think about it?

A

Low T wave
High U wave

Likes to depolarize (smaller T wave)
U wave opposite of T wave (high U)

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5
Q

What situations will favor movement of K+ into ECF?

Why? (for each)

A

Hypokalemia - need to replenish plasma

Acidemia - buffering excess H+ moving INTO cells

Alpha-adrenergic agonists

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6
Q

What situations will favor movement of K+ into ICF?

Why? (for each)

A

Hyperkalemia - excess needs to go somewhere

Alkalemia - buffer H+ moving into plasma to replenish

Beta-adrenergic agonists

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7
Q

How is K+ reabsorbed in the:

PT
Loop
CD

A

PT - paracellular (+ lumen)

Loop - NaKCl2

CD - IC cells

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8
Q

Main physiologic control of K+ reabsorption/secretion is where?

How is K+ secreted?

A

CD

Principle cells and IC cells

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9
Q

A person is hypokalemic. What substance will be HIGH in the epithelial cells of the lumen?

Why?

A

Sodium (Na)

Less K+ to drive basolateral Na/K ATPase, so Na builds up in cell

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10
Q

Why does aldosterone cause up-regulations in K+ and H+ secretion?

A

Increases Na+ brought into cell (increases Na/K exchanger)

Increases negative lumen and need for electrochemical balancing

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11
Q

Reasoning for why high aldosterone causes alkalosis AND hypokalemia

A

Increased Na/H exchange = less H+ in body = H/K exchange = more K in cell = more Na/K exchange

OR just up-regulates both Na/H and Na/K exchangers

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12
Q

A patient is put on a diuretic for CHF. What is a potential side effect (potassium)?

What is the treatment? Why?

A

More Na+ delivery to CD –> more K+ secretion –> hypokalemia

Tx = Low-Na diet
Less excess delivery to CD = less K+ secretion

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13
Q

A patient is put on a low-sodium diet for health reasons. What is a potential side effect (potassium)?

Tx? Why?

A

Less Na+ delivered to CD –> Hyperkalemia

Tx = diuretic
More Na+ delivered to CD

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14
Q

Conn’s disease

Side effects?

A

Hyperaldosteronism

Hypokalemia (more Na/K exchange)
Alkalosis (more Na/H exchange)

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15
Q

Addison’s disease

Side effects?

A

Hypoaldosteronism

Hyperkalemia
Acidosis

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16
Q

Potential Tx for Conn’s disease?

A

Aldosterone antagonist

17
Q

Potential Tx for Addison’s disease?

A

Upstream diuretic (increase Na+ delivery to CD)

18
Q

A patient is on a loop diuretic. How will the RBF be affected?

A

Increased

More water excreted = volume depletion = compensation for low GFR by increasing RBF

19
Q

Main C.A. inhibitor drug

Main osmotic diuretic

A

Acetazolamide

Mannitol

20
Q

Main loop diuretics

A

Furosemide (Lasix)

Bumetanide (Bumex)

21
Q

Main thiazide diuretic

A

Hydrochlorothiazide

22
Q

Main aldosterone antagonist

Main K+ - sparing diuretics

A

Spironolactone

Amiloride, Triamterene

23
Q

How do K+-sparing diuretics work?

A

Block Na+ channels in the CD

24
Q

A patient comes in with rigid muscles. ABG values show high pH. What is the cause?

A

Low H+ = low free Ca++

Hypocalcemic tetany

25
Q

A patient is alkalemic and hypocalcemic. What is the body’s response to fix the calcium problem?

A

Upregulate PTH

Increases Ca++ absorption
Increases bone reabsorption
Increases vitamin D activation for Ca++ absorption

26
Q

Other name for activated vitamin D

A

Calcitriol

27
Q

How is Ca++ reabsorbed in the:

PT
Loop
DT

A

PT - paracellular (bulk flow)

TAL - (+) lumen pushes it paracellular

DT - calbindin, TRPV5 channels

28
Q

How exactly does the body regulate Ca++ reabsorption?

A

Vit. D and PTH regulate the TRPV5 channels in the DCT

29
Q

How does the body respond to high Ca++?

A

Increase calcitonin

30
Q

How does the plasma phosphate (PO4) level compare to reabsorption capacity?

A

Plasma PO4 is such that reabsorption is always maximized

31
Q

How is PO4 reabsorbed?

A

Na/PO4 co-transporter

Basolateral P/anion antiporter

32
Q

How does the body regulate PO4 reabsorption?

A

PTH - decreases Tm of Na/PO4 transporter, so some is excreted

33
Q

How does regulation of Ca++ compare to that of PO4?

A

Opposite - both use PTH but in opposite directions

34
Q

3 forms of Mg in the blood

A

Free
Complexed w/ anions
Bound to plasma proteins

35
Q

Where does the majority of Mg reabsorption occur?

A

thick ascending loop (pushed by positive lumen) by paracellular movement

Renal (11 decks)

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