K+ Balance Flashcards

1
Q

Plasma K concentration is a function of what?

A

Internal and external K balance

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2
Q

Chronic changes in K concentration due to?

A

External balance issues

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3
Q

Acute changes in K concentration due to?

A

Could be both internal or external

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4
Q

How does the body handle acute K load?

A

Increase in cellular k uptake and enhanced renal k excretion
-About 75% is taken up into the cells followed by a relatively rapid excretion of K

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5
Q

Can urinary excretion exceed the filtered load of k?

A

Yes, due to tubular secretion

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6
Q

Primary defense against progressive K depletion and hypokalemia?

A

Renal K reabs. This is slow and can take days to develop so a substantial K deficit can occur in the meantime (unlike Na)

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7
Q

What is the major regulator of internal K balance?

A

Na-K ATPase

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8
Q

What factors affect internal K balance?

A
  • Plasma K concentration

- Hormones (insulin, catecholamines, aldosterone)

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9
Q

What factors stimulate Na-K-APTase activity?

A
  • High plasma [K]
  • Acute increase in plasma K stimulates insulin, aldosterone and catecholamine release which all favor K cellular uptake (also have passive diffusion into the cells)
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10
Q

Catecholamines effects on K

A

-Stimulate insulin
-Work on beta 2 to increase Na-K ATPase activity and lower plasma K concentration
-

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11
Q

Aldosterone effects on K

A

Stimulates Na-K ATPase activity and distal nephron K secretion and urinary excretion of K

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12
Q

Effect of exercise on plasma K

A

Increase

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13
Q

Effect of cell lysis on plasma k

A

Increase

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14
Q

Effect of alkalemia on plasma k

A

K+ enters the cell –exchanges with H+

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15
Q

Effect of acidemia on plasma K

A

K+ leaves the cell–exchanges with H+

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16
Q

Effect of intracellular acidosis on plasma K

A
  • Decreased intracellular pH inhibits K+ uptake, lowering intracellular K
  • This displaces K+ for exit from the cell (ie increase in K+ out of the cell)

Acidosis inhibits Na-K pump and N2CCK

17
Q

Effect of plasma tonicity on plasma K

A

Hypertonic plasma: K+ follows water via drag and K passively leaks out due to cell shrinkage

-glucose increases hypertonicity in diabetic patients causing K+ plasma to increase. In non diabetics, insulin causes uptake of K+ into cells (follows water and stim Na-K)

18
Q

How would you describe the filtration of k

A

it is freely filtered
-fractional abs of 80% in the PT and 10% in the TAL is constant regardless of K balance so reabs at these sites is not a major determinant of final renal k excretion

19
Q

How much of filtered K is delivered to distal nephron?

A

About 10%

20
Q

How is K reabs in the PT?

A

Through paracellular pathways in response to Na reabs-induced fluid movement

Late PT: positive transepithelial potential difference also drives this

Luminal K channels are only minimally conductive in the PT

21
Q

How is K reabs in the Thin descending limb?

A

-Deep juxtamedullary nephrons in the medulla passively secrete K into the lumen from the interstitium

22
Q

How is K reabs in the Thin ascending limb?

A

K passively moves from cell to interstitium

23
Q

How is K reabs in the TAL?

A
  • Passively due to luminal potential difference

- Actively with NKCC2 with ROMK recycling or BLM diffusion

24
Q

Alpha intercalated cells of the cortical collecting duct and outer medullary collecting duct?

A

Reabs K

  • Make up <30% of cells here
  • H-K ATPase actively reabs K across apical membrane and basolateral K channel for K efflux from the cell
25
Q

Principal cells of the cortical collecting duct and outer medullary collecting duct?

A

Secrete K

  • make up >70% of cells here
  • Apical K channels and Cl-K co transporter
  • Negative potential difference in this region favors Na reabs and tehrefore K transport
26
Q

Factors affecting distal nephron K secretion

A
  • K intake and plasma K concentration
  • Aldosterone
  • Distal tubule Na delivery and flow
  • Anions in tubular fluid
27
Q

Aldosterone effect on K

A

Stimulates principal cell transport processes

-note glucocorticoids dont directly affect renal K secretion