S6.2 Potassium Control

Question 1

K+ is high inside the cell and low outside. What are the effects on either side of the membrane?

Answer 1

Inside: maintaining cell volume and pH, cell growth
Outside: regulate membrane potential

Question 2

Majority of K+ is absorbed in the proximal tubule, by what method?

Answer 2

Paracellular solvent drag

The change in lumen from – to + created by ROMK allowed for further paracellular reabsorption

Question 3

How is K+ absorbed in the thick ascending limb?

Answer 3

Via NaK2Cl driven by NaKATPase

Question 4

How is K+ reabsorbed in the DT and CD?

Answer 4

Via K+ channels on the basolateral membrane

Question 5

What is liddle’s syndrome?

Answer 5

In the collecting duct, the activity of ENaC is increased, making the lumen negative and favouring K+ secretion.
This leads to hypertension and hypokalaemia

Question 6

What tubular factors affect K+ secretion?

Answer 6

ECF [K+] - increases permeability of apical k+ channels and stimulates aldosterone

Aldosterone - increases transcription of proteins for pump, K+ channels and ENaC

Acid base status - acidosis decreases secretion (vv for alkalosis)

Question 7

What luminal factors affect K+ secretion?

Answer 7

Increased DT flow rate increases K+ loss

Increased Na+ delivery to DT means more Na+ absorbed so more K+ loss

Question 8

What affect does acidosis have on [K+]?

Answer 8

Causes hyperkalaemia
Acidosis causes shift of H+ into cells, so there is K+ shift out of cells and more K+ reabsorption in the DT leading to hyperkalaemia.

Question 9

What affect does alkalosis have on [K+]?

Answer 9

Causes hypokalaemia

Alkalosis causes shift of H+ out of cells, so shift of K+ into cells and less K+ reabsorption, causing hypokalaemia.

Question 10

Define hyperkalaemia

Answer 10

[K+] > 5.0 mmol/L

Question 11

What are some causes of hyperkalaemia?

Answer 11

Decreased renal excretion (drugs like ACEi, K+sparing diuretics)
Diabetic ketoacidosis
Cell lysis (muscle crush injuries, tumour lysis)
Metabolic acidosis

Question 12

What are the clinical features of hyperkalaemia?

Answer 12

Arrhythmia, heart block.
ECG shows high T wave, ST depression
Acidosis

Question 13

What is the treatment for hyperkalaemia?

Answer 13

Emergency: IV Ca2+ gluconate, remove excess K+ by dialysis

Long term: reduce intake, remove excess K+ (dialysis in AKI/CKI)

Question 14

Summarise the aldosterone paradox

Answer 14

During volume depletion - Aldosterone stimulates NaCl and inhibits ROMK

In hyperkalemia - Aldosterone stimulates ROMK and inhibits NaCl

Question 15

Define hypokalaemia

Answer 15

[K+] < 3.5 mmol/L

Question 16

What are some causes of hypokalaemia?

Answer 16

Excess loss (diarrhoea/vomiting) increased urine loss (diuretics, high aldosterone)
Reduced dietary intake

Question 17

What are the clinical features of hypokalaemia?

Answer 17

Heart – arrhythmias, on ECG get U wave, low ST segment
Skeletal muscle - neuromuscular dysfunction then muscle weakness
Polyuria

Question 18

What is the treatment for hypokalaemia?

Answer 18

K+ replacement (IV/oral), K+ sparing diuretics if due to increased aldosterone (block action of aldosterone on principle cells).

Question 19

What affect on acid-base status does vomiting or diarrhoea have?

Answer 19

Vomiting: metabolic alkalosis (loss of H+)
Diarrhoea: metabolic acidosis (loss of HCO3-)

Question 20

Why is calcium important in cells?

Answer 20

For nerve and muscle function

Question 21

What is the active from of Vit d called?

Answer 21

Calcitriol