Regulation of K Balance Flashcards

1
Q

Role of Epinephrine in extrarenal regulation of plasma K+

A

Lowers serum K by uptake into cells of extrarenal tissues even while stimulating K+ excretion by kidney

differing responses for alpha and b receptor stimulation

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2
Q

Role of Insulin in extrarenal regulation of plasma K+

A

Stimulate Na/K ATPase causing flux of K+ into cells and efflux of Na+ from cellls

Insulin & Glucose administration can treat hyperkalemia

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3
Q

Role of Aldosterone in extrarenal regulation of plasma K+

  • Renal
  • Extrarenal
A

Renal: increase K+ excretion by kidney

Extrarenal: increase K+ secretion into intestinal fluids & saliva

Enhances acid excretion via production of systemic alkalosis (K is low)

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4
Q

Which factors enhance K+ uptake? how?

A

-Insulin and Beta- Catecholamines

both by activating Na/K ATPase (catecholamine is via cAMP)

  • Alkalosis
    “k is lo”
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5
Q

Which factors impairs K+ uptake? how?

A

-alpha catecholamines
opposite of beta

  • acidosis
    donnan effect; inhibit Na/K ATPase
  • Cell damage
    release of intracellular contents
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6
Q

Which factors enhance K+ cell efflux? how?

A

-hyperosmolality
due to contraction of ICF volume and increased intracellular K+

  • strenuous exercise
    activating alpha catecholamines
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7
Q

Which factor has loose correlation/ effect on potassium?

A

external potassium balance

ration vs total body K+ until severe state

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8
Q

Filtered load equation

A

GFR * plasma concentration * % filterability

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9
Q

Plasma protein characteristics

A
  • not filterable under normal circumstances

- any substance bound to plasma protein will not be filtered

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10
Q

PCT and PST

  • what is always reabsorbed?
  • what is mostly reabsorbed?
  • what is secreted?
  • major mechanism/ form of transport?
A

Always reabsorbed

  • glucose
  • amino acids

Most reabsorbed

  • Na
  • K
  • Cl
  • HCO3
  • Ca
  • P

Secreted

  • cations and anions
  • drugs, metabolites, creatinine, urate

Major mechanism
Na/K ATPase pump in basolateral membrane

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11
Q

K+ reabsorption in Proximal Tubule

  • what does it effect
  • locations
A
  • similar to Na reabsorption
  • does NOT play a direct role in regulation of K+ balance
  • INDIRECT ROLE
  • changing NaCl reabsorption has considerable effects on distal tubular flow and distal tubular Na+ delivery, which impacts K+ later on

PCT: S1 &S2
PST : S2 & S3

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12
Q

How does K+ get reabsorbed in PT? (8)

- driven by what?

A

1) Early PT, Na reabsorbed with HCO3
2) Cl gets let behind
3) Negative TEPD builds up
4) Cl is repelled and reabsorbed
5) Continued NaCL reabsorption drags water along (solvent drag)
6) Positive TEPD builds up as Cl- reabsorbs
7) Postive TEPD repels K
8) K reabsorbed paracellularly

driven by lumen-positive transepithelial potential difference (TEPD) - found in late proximal tubule

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13
Q

Early PCT reabsorbs a lot of sodium! Explain the effects of it?

A

Creates lumen-negative potential difference

pushes paracellular Cl- to get reabsorbed in the straight PT

reversal of the PD to a positive value will help push NA and K via paracellular reabsorption

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14
Q

Loop of Henle transport and medullary recycling steps (4)

A

1) K secreted in cortical CD
2) K reabsorbed by outer medulla CD and inner medulla CD
3) K+ floats in interstitium
4) K secreted into Late PT/descending thin limbs of LoH

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15
Q

Goal of Loop of Henle transport and medullary recycling

A

increase presence of medullary K

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16
Q

Purpose of Loop of Henle transport and medullary recycling

A

large K presence decreases NKCC2 reabsorption by TAL
-> enhanced Na-delivery to distal tubule-> stimulates NA reabsorption and K secretion-> helps you excrete K during dietary loading

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17
Q

Where is K+ secreted? reabsorbed?

A

BOTH in late DT and cortical CD

-according to needs of the body

18
Q

What secretes K?

A

principal cells and beta-intercalated cells

19
Q

Most important factors that stimulate potassium secretion

  • by which channels
A

1) increased ECF (K)
2) aldosterone
3) increased tubular flow rate

potassium channels, epithelial sodium channels (EnaC), renal outer medullary potassium (ROMK)

20
Q

What reabsorbs K?

A

alpha intercalated cells

21
Q

Most important factors that stimulate potassium reabsoprtion

A

1) K deficiency, low K diet, hypokalemia

2) K loss through severe diarrhea

22
Q

What is reabsorbed in these cells? What is secreted?

1) principal cells
2) alpha intercalated cells
3) beta intercalated cells

A

1) Principal cells
Reabsorbed: Na, H2O
Secretes: K

2) alpha intercalated cells
Reabsorbed: K+, HCO3
Secretes: H

3) beta intercalated cells
Reabsorbed: H, Cl
Secretes: K, HCO3

23
Q

Factors that regulate K+ secretion (5)

A

Buildup of extracellular K

1) activate Na/K ATPase pump in basolateral membrane of principal cells
2) Reduced back-leakage of K+ from ICF to renal interstitium
3) activate synthesis of K channels and insertion into luminal membrane
4) activate aldosterone secretion
5) increased DT flow rate

24
Q

How does increased flow rate enhance K secretion (2)?

A

dilutes K secreted in lumen -> increasing the K concentration gradient

Delivers more Na to DT for reabsorption-> gradient across the tubular cell rises-> K secretion is promoted

25
Q

How does decreased flow rate slow K secretion

A

K concentrations build up earlier in the tubule-> decreasing concentration gradient between cell and tubular fluid-> secretion slows

26
Q

Why is relationship between distal tubular flow rate and potassium secretion important? ( think aldosterone, sodium, potassium)

A

prevents physiological conflict between the role for aldosterone in regulation of potassium and sodium excretion

  • increased flow rate in DT PRESERVE normal potassium excretion during changes in sodium intake and aldosterone levels
  • high sodium/decreased aldosterone and high tubular flow rates counterbalance each other
27
Q

Acute alkalosis

- effects

A
  • acute process that decreases in H+ ion concentration in extracellular fluid

alkalemia ( high blood ph)

everything increases!!
- increase Na/K atpase pump activity 
- increase k concentration 
- increase passive diffusion of K into tubule lumen
- increase K channels
- increase K secretion 
End result: hypokalemia ( K is lo)
28
Q

Acute acidosis

- effects

A
  • acute process that increases in H+ ion concentration in extracellular fluid

acidemia ( low blood ph)

everything decreases!!
- decrease Na/K atpase pump activity 
- decrease k concentration 
- decrease passive diffusion of K into tubule lumen
- decrease K channels
- decrease K secretion 
End result: hyperkalemia ( K is lo)
29
Q

Acute vs chronic acidosis

- elaborate on chronic acidosis ( 3)

A

TIME DEPENDENT

chronic acidosis stimulates K secretion

Chronic

1) decreases reabsorption of water and solutes in PT
- by inhibiting Na/K ATPase
2) increase tubular flow to DT and CD
3) RAAS stimulated bc of lack of water reabsorption and decrease of ECF volume
- Result: K secretion rises

30
Q

Acidosis on stabilizing K secretion

A

acidosis-> decrease proximal reabsorption -> increase distal flow -> activate distal K secretion

acidosis -> decrease intracellular K content-> inhibit distal K secretion

31
Q

Volume expansion on stabilizing K secretion

A

Volume expansion-> decrease proximal reabsorption -> increase distal flow -> activate distal K secretion

Volume expansion -> decrease aldosterone-> inhibit distal K secretion

32
Q

High water intake (water diuresis) on stabilizing K secretion

A

high water intake-> decrease water reabsorption -> increase distal flow -> activate distal K secretion

high water intake -> decrease ADH-> inhibit distal K secretion

33
Q

Volume Contraction on stabilizing K secretion

A

volume contraction-> decrease GFR -> decrease distal flow -> inhibit distal K secretion

volume contraction -> increase renin-> increase angiotensin II -> increase aldosterone -> activate distal K secretion

34
Q

ADH on K+

A

increase K+ secretion

- via Na resorption and stimulation of K+ channels

35
Q

Luminal flow rate on K+

A

increase K+ secretion

36
Q

Acidosis on K+

A

decrease K+ secretion

37
Q

Alkalosis on K+

A

increase K+ secretion

38
Q

Glucocorticoids on K+

A

increase K secretion

  • via binding of mineralocorticoid receptor
  • increase GFR
  • increase fluid flow rate
39
Q

Anion delivery on K+

A

increase K secretion

  • acts as osmotic diuretic
  • increases tubular fluid flow rate
  • impact electrochemical differences
40
Q

What are some effect on Na Cl reabsorption in PT? (3)

A
  • reduce Na+ delivery to the CNT and CCD
  • decrease the lumen-negative potential
  • decrease K + secretion
41
Q

Aldosterone characteristics on K+

A
  • akaliuretic hormone, induced by hyperkalemia

However, under certain circumstances associated with marked induction of aldosterone, such as dietary sodium restriction, sodium
balance is maintained without effects on K + homeostasis
- aldosterone-paradox

42
Q

Effects of diuretics on K

A

inhibit Na reabsorption

  • will promote K+

( exceptions are K sparing drugs)