K+ and Ca2+ (Muster) - W2 Flashcards

1
Q

where is K+ primarily stored?

What could deplete those stores?

A
  • 98% intracellularly
  • burns
  • crush injuries
  • reperfusion injuries
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2
Q

How does insulin affect K+?

A
  • insulin increases Na-K ATPase
  • promotes skeletal and muscle uptake
  • eat –> insulin –> alleviates K+ serum
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3
Q

How do catecholamines affect K+?

A
  • bind to B2 receptors
  • stimulate the Na-K ATPase inducing cellular uptake
  • likely permissive at baseline
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4
Q

How does plasma concentration of K+ affect uptake?

A
  • serum K+ rises –> cellular uptake increased
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5
Q

How does exercise affect K+?

A
  • muscle cells release K+
    • related to degree of exercise
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6
Q

How does pH affect K+

A
  • K+ rises in serum.
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7
Q

What happens with tonicity and K+?

A
  • hyperglycemia
    • water and K+ leave the cell
    • more water than K+ leaves
  • K+ inside cell reduces Na-K ATPase
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8
Q

What do you give to prevent arhythmia and cardiac arrest with high potassium?

A
  • Ca2+

along w/insulin and glucose

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9
Q

What is the control of potassium:

proximal tubule

thick ascending limb

principle cell of collecting duct

A
  • proximal tubule = 55-65% via tight junctions
  • thick ascending limb = 25%
  • principle cell = 10%
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10
Q

What are the 4 stimuli for K+ secretion (and therefore excretion)

A
  1. sodium delivery to distal convoluted tubule
    1. more sodium = more K+ excretion
  2. increased flow rates
    1. higher flow = higher gradient stimulating movement into the lumen
  3. plasma levels of K+
    1. increased activity of ATPase w/higher levels
  4. aldosterone
    1. increases ENAC
    2. increases ROMK
    3. increases NA-K ATPase
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11
Q

What 2 things can stimulate aldosterone and what happens with each?

A
  1. Angiotensin II system
    1. used for NA+ retention
    2. stops ROMK channel
  2. serum potassium
    1. increases ROMK in membrane
    2. less stimulus for ang II
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12
Q

What are the stimuli for BK channel?

A
  1. increased FLOW
  2. increased EC potassium
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13
Q

How is K+ reabsorbed?

A
  • occurs in Alpha and beta intercalated cell
  • K+ is exchanged for H+
    • lots of H+ must be processed to reabsorb K+
  • active process!!
  • also requires reabsorption of bicarbonate
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14
Q

Describe the availability of calcium

A
  • 40-50% is bound to ALBUMIN
  • 10% BOUND to citrate, phosphate
  • 50% is available as ionized calcium
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15
Q

How much calicum is aborsbed in each part of the loop?

A
  • proximal tubule = 60-70%
  • thick segment = 20%
  • convoluted tubule = 10%
  • collecting duct = 5%
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16
Q

By which process is most of the calcium reabsorbed?

A
  • paracellular (85%)
17
Q

How is calcium reabsorbed in the thick ascending limb?

A
  • calcium sensing receptor
    • ​binds free calcium
    • when stuff isn’t bound, upregulates calcium reabsorption
    • bound = claudins can stop paracellular reabsorption of calcium
18
Q

How is calcium reabsorbed in the distal convoluted tubule and cortical collecting duct?

A
  • enters through TRPV5 channels
    • most is transcellular
  • binds to calbindin to carry it to the other side of the cell.
  • Na+/Ca2+ antiporter allows it into the capillary.
    • 3Na in to 1Ca out.
  • PTH can upregulate TRPV5 for increased uptake on luminal side and increased excretion on back side.
19
Q

When is PTH released?

A
  • PTH is released when all calcium receptors aren’t bound.
  • low ionized calcium stimulates PTH release.
20
Q

What does PTH do to bone?

A
  • stimulates IMMEDIATE release of stored skeletal calcium
  • LONG TERM
    • stimulates bone reabsorption
    • acts on cortical bone
    • also releases phosphorus
21
Q

What does PTH do to the gut?

A
  • increases calcium and phosphate reabsorption by increased 1,25 vitamin D
22
Q

What does PTH do to the kidney?

A
  • increases the production of vitamin D in the proximal tubule
  • increases renal Caclium reabsorption
  • stimulates renal phosphorus excretion - phosphorus wasting.