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Physiology 1 : renal > Potassium Balance > Flashcards

Potassium Balance Flashcards

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1
Q

What are the most prevalent cations in body fluids?

A

→ Na+ and K+

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2
Q

Where is potassium found?

A

→ in leafy vegetables
→ Most fruit and juice
→ potatoes

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3
Q

What is the intra and extracellular concentration of potassium?

A

→ I : 150mmol/L

→E : 4.5 mmmol/L

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4
Q

What cell types have the most potassium?

A

→ Muscle cells

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5
Q

What is the internal potassium balance maintained by?

A

→ Insulin
→ Adrenaline
→ pH
→ Aldosterone

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6
Q

What is the external potassium balance maintained by?

A

Input
→Diet

Output
→ urine & stools
→ sweat

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7
Q

What is acute regulation of K+?

A

→The distribution of K+ through ICF and ECF compartments

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8
Q

What is chronic regulation of K+?

A

→ Kidney adjusting K+ excretion + reabsorption

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9
Q

What are the 2 functions of K+?

A
  1. Determines ICF osmolality
  2. Determines resting membrane potential
  3. Affects vascular resistance
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10
Q

What does the sodium/potassium pump do?

A

→ Na+ ions are pumped out of the cell
→ K+ pumped into the cell
→ energy driving the pump is released by ATP hydrolysis

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11
Q

What happens to K+ concentration after a meal?

A

→ Increase in plasma K+

→ shifted into ICF compartment

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12
Q

What hormones is the ICF K+ shift due to?

A

→ insulin
→ adrenaline
→ aldosterone
→ pH changes

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13
Q

What is hyperkalaemia defined as?

A

→ plasma K+ is above 5.5 mM

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14
Q

What is hypokalaemia defined as?

A

→ plasma K+ is below 3.5 mM

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15
Q

What is resting potential formed from?

A

→ ionic gradients

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16
Q

What is the normal distribution between IC and EC K+?

A

→ External - 3.5 mM

→ Internal - 140 mM

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17
Q

What happens to the equilibrium potential when you have hyperkalaemia?

A

→ Less negative

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18
Q

What happens to the equilibrium potential when you have hypokalaemia?

A

→ More negative

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19
Q

What happens during hyperpolarization (less K+) ?

A

→ more negative voltage across the membrane
→ Decreased excitability of neurons
→Longer to reach threshold
→ Longer to reach action potential

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20
Q

What happens during depolarization (more K+)?

A

→ Less negative voltage
→ Threshold is approached quicker
→ Increased excitability

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21
Q

What is hypokalaemia caused by?

A

→ Renal or extra renal loss of K+

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22
Q

What are causes of hypokalaemia?

A

→ Diuretics without KCl
→ Hyperaldosteronism ( Conn’s syndrome)
→ Prolonged vomiting (Increased aldosterone secretion)
→ Profuse diarrhoea

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23
Q

What does hypokalaemia result in?

A

→ Decrease adrenaline, aldosterone and insulin

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24
Q

What is hyperkalaemia caused by?

A

→ Prolonged exercise

→ Kidneys excrete K+ easily

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25
Q

What are disease states that cause hyperkalaemia?

A

→ Insufficient renal excretion
→ Increased release from damage body cells
→ Long term use of potassium sparing diuretics
→ Addisons disease

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26
Q

What happens if plasma K+ is above 6.5 mM?

A

→ Systolic cardiac arrest

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27
Q

What is used to drive K+ into the cells?

A

→ Insulin/glucose infusion

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28
Q

What hormones stimulate the Na+-K+ pump?

A

→ Aldosterone

→ Adrenaline

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29
Q

What is external balance of K+ regulated by?

A

→ the kidneys

30
Q

What are human kidneys designed to do?

A

→ Conserve Na+ and excrete K+

31
Q

What drugs raise serum K+ levels?

A

→ B blockers

→ ACE inhibitoris

32
Q

What drug causes hypokalaemia?

A

→ loop diuretics

33
Q

Why do the plasma and glomerular fluid have the same concentration?

A

→ Na+ and K+ are freely filtered at the glomeruli

34
Q

How is K+ maintained at high levels within the kidney cells?

A

→ Sodium travels from the tubular lumen to the ECF bringing glucose and AA with it
→the Na+ and K+ pump maintains this on the basolateral side
→ Maintains K+ at high levels in the kidney cells

35
Q

How do Na+ and K+ move in the loop of henle?

A

→Active reabsorption/pumping of Na+ & Cl- out of the fluid into the medulla

→done via a Na+/2Cl-/K+ symporter on the luminal membrane

→driven by the [Na+] gradient from lumen-cell.

→You also have entry of Na+ from Na+-H+ antiporter

→On the basolateral side you have a Na+/K+ ATPase pump and co-transport of Cl- & K+ out of the cell (especially in the thick ascending limb).

36
Q

Where is 90% of the potassium reabsorbed?

A

→ PCT and loop of henle

37
Q

What is excretion of K+ into urine controlled by?

A

→ secretion in principal cells of late DCT and CD

38
Q

How do you get the K+ to go into the urine in the DCT?

A

→ eNAC channels are present on the luminal side
→ activated by aldosterone
→ as Na+ enters the cell it changes the electrical potential on the luminal side
→ allow K+ to be secreted out
→ there are K+/Cl- symporters that pump K+ out

39
Q

What inhibits eNAC channels?

A

→ diuretics

40
Q

What determines K+ secretion in the DCT?

A

→ Increased K+ intake

→ Changes in blood pH

41
Q

What happens to K+ during alkalosis?

A

→ Increased excretion of K+

→ Decreased serum K+

42
Q

What happens to K+ during acidosis?

A

→ Decreased excretion of K+

→ Increased serum K+

43
Q

What causes the switch between secretion and absorption?

A

→ Activity of Na+ / K+ pump
→ Electrochemical gradient
→ Permeability of luminal membrane channel

44
Q

What effect does aldosterone have on the Na+/ K+ pump?

A

→ Increase K+ influx
→ Increase intracellular potassium
→ increase cell-lumen concentration gradient

45
Q

What is the major regulator of K+ balance?

A

→ aldosterone

46
Q

What effect does aldosterone have on the eNAC channels?

A 
→ More eNAC channels 
→ Increased Na+ reabsorption 
→ Decreased cell negativity 
→ Increased lumen negativity 
→ Increase voltage gradient
47
Q

What does aldosterone do to the luminal membrane?

A

→ Makes it more permeable to K+

48
Q

How does an increase in plasma K+ increase K+ secretion?

A

→ Slows exit from basolateral membrane
→ Increases concentration gradient towards urine
→ Increases activity of Na+/K+ ATPase
→ Stimulates aldosterone secretion

49
Q

Flow chart for what happens during increased K+ intake

A 
Increased K+ intake 
↓ 
Increased plasma K+ 
↓
Increased aldosterone secretion from adrenal cortex
↓
Increased plasma aldosterone 
↓ 
Increased K+ secretion from cortical collecting ducts
↓
Increased K+ secretion
50
Q

How is K+ secreted during alkalosis?

A

→ Increased activity of Na+/K+ pump and increased K+ in the cell
→ Favours the concentration gradient for K+ secretion
→ Increase in tubular fluid pH
→ increases permeability of luminal membrane

51
Q

How is K+ secreted during acute acidosis?

A

→ increase in H+ of ECF reduces the activity of the Na+/K+ ATPase pump
→ Decreases intracellular K+
→ reduces passive diffusion of K+

52
Q

What does an increase in tubule fluid flow rate result from?

A

→ increased GFR or inhibition of reabsorption upstream or diuretics

53
Q

What does an increase in tubule fluid flow rate result in?

A

→ sweeping away of K+
→ makes tubular K+ low
→ more rapid rate of net secretion

54
Q

What does anti diuretic hormone do?

A

→ Stimulates K+ secretion by increasing the conductance of the luminal membrane

55
Q

Where does reabsorption of K+ occur in severe hypokalaemia?

A

→ alpha intercalated cells of late DCT

→ K+/H+ pump

56
Q

Flow chart for when ECFV decreases

A

Adrenal cortex increases aldosterone secretion and proximal tubule increases Na+ reabsorption
↓
tubules decrease flow rate
↓
cortical collecting ducts increase K+ secretion (aldosterone) and decrease K+ secretion (flow rate)
↓
K+ unchanged

57
Q

How does the RAAS system regulate sodium and BP?

A

→ JGA senses a fall in BP
→ Macula densa detects low Na+ in the DCT
→ Renin is released from JGA → Angiotensin II
→ Causes vasoconstriction and stimulates adrenal cortex

58
Q

How does aldosterone restore BP?

A

→ Acts on DCT to increase Na+ reabsorption
→ Increases activity and inserts more Na+/K+ ATPase pumps
→ Na+ ions bring water with them via osmosis

59
Q

How is renin release suppressed?

A

→ suppressed by -ve feedback with angiotensin II

60
Q

How does aldosterone increase serum pH?

A

→ Acts on intercalated cells
→ Increase activity of Na+, H+ antiporter and influences acid- base status
→ Increases H+ secretion

61
Q

What factors shift K+ into cells?

A

→ Insulin
→ Aldosterone
→ Beta adrenergic stimulation
→ Alkalosis

62
Q

What factors shift K+ out of cells?

A 
→ Insulin deficiency 
→ Aldosterone deficiency 
→ Beta adrenergic blockade
→ Acidosis 
→ Cell lysis 
→ Strenuous exercise 
→ Increased ECF osmolarity
63
Q

What does the adrenal cortex produce?

A

→ Gluco corticoid hormones
→ Mineralocorticoud hormones
→Sex hormones

64
Q

What is primary adrenal insufficiency / Addisons?

A

→ Damage to cortex
→ Decreased hormone production
→ numerous symptoms

65
Q

What is a result of a deficiency in aldosterone?

A

→ Secretion of large amounts of Na+
→ Low serum Na+ levels
→ Body retains K+

66
Q

What is the treatment of addisons?

A

→ Treatment usually involves corticosteroid replacement for life

67
Q

What is secondary adrenal insufficiency?

A

→ pituitary secretes less ACTH
→ Decrease cortisol
→ Adrenal glands shrink

68
Q

What is hyperaldersteronism/Conns syndrome?

A

→ excess release of aldosterone
→ due to tumor
→ Aldosterone release without angiotensin II

69
Q

What does an increase in plasma aldosterone mean?

A

→ Kidneys to stimulate Na+ reabsorption and K+ excretion
→ increase BP and Na delivery to macula densa
→ decrease release of renin
→ Increase fluid volume
→ Hypokalaemia, hypernatremia and alkalosis

70
Q

What is the treatment for Conns syndrome?

A

→ surgical removal of tumor containing adrenal gland

→ Hypertension and hyperkalaemia

Physiology 1 : renal (13 decks)

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