Urinary: Control of Potassium

Question 1

What is the distribution of potassium in body fluids?

Answer 1

98% of K+ is in the ICF
(120-150 mmol/L)
Mainly in skeletal muscles, liver, RBCs and bone

2% of K+ is in the ECF
(3.5-5 mmol/L)

Question 2

Why is maintaining ECF K+ conc critical?

Answer 2

K+ affects the resting membrane potential and therefore the excitability of cardiac tissue.
Hypo and hyperkalaemia can cause life threatening arrhythmias.

Question 3

How many litres is the ECF?

Answer 3

14L

Question 4

How is ECF K+ regulated?

generally

Answer 4

Internal balance: immediate response to protect cardiac excitability. Moves K+ from ECF into cells via Na-K-ATPase, or moves K+ out of cells via K+ channels

External balance: Longer term response taking around 6-12 hours.
Regulates K+ secretion in late DT and CD.

Question 5

List the factors that promote K+ uptake into cells

internal balance

Answer 5

• increased K+ conc in the ECF
• hormones that act via Na-K-ATPase eg insulin, aldosterone and catecholamines
• alkalosis

Question 6

List the factors that promote K+ shift out of cells

internal balance

Answer 6

• exercise
• cell lysis
• increased ECF osmolarity
• decreased conc of K+ in ECF
• acidosis

Question 7

How does exercise affect ECF [K+]?

Answer 7

During the recovery phase of the action potential there is net release of K+, also skeletal muscle damage releases K+.

Non-contracting tissues (eg liver) uptake K+ to prevent hyperkalaemia, with the help of catecholamines

Question 8

Outline where along the nephron potassium is reabsorbed and secreted

Answer 8

Reabsorption:
PCT 67%
Thick AL 20%
Intercalated cells of the distal tubule and CD

Secreted: (varied and controlled)
By principal cells of the DT and CD.

Question 9

Outline the mechanism of k+ secretion in the DT and CD (eg ion channels)

Answer 9

Principle cells secrete K+:
Na-K-ATPase creates a chemical K+ gradient for secretion
And the low Na+ conc means Na+ travels across apical via ENaC into the the cell creating an electrical gradient.

K+ is therefore secreted across apical membrane

Question 10

How does aldosterone affect K+ secretion?

Answer 10

Aldosterone increases transcription of the relevant proteins needed for k+ secretion eg Na-K-ATPase, apical K+ channels and ENaC

Question 11

What is the mechanism for K+ absorption by intercalated cells?

Answer 11

It is an active process mediated by H-K-ATPase in the apical membrane

Question 12

What are some possible causes of hyperkalaemia?

Answer 12

• increased intake (very unlikely unless recieving inappropriate doses of IV K+)
• decreased renal excretion due to acute or chronic kidney injury
• drugs blocking potassium excretion eg ACE inhibitors, potassium sparing diuretics
• low aldosterone seen in addison’s disease
• diabetic ketoacidosis - no insulin
• tumour lysis

Question 13

What are the clinical features of hyperkalaemia?

Answer 13

• arrhythmias or heart block
• paralytic ileus in GI
• acidosis

Question 14

What is the treatment for hyperkalaemia?

Answer 14

Emergency treatment:

• give IV calcium gluconate which acts in 1 minute to reduce the effect of K+ on the heart
• give glucose and IV insulin to shift K+ into ICF
• remove excess K+ by dialysis

Longer term treatment:

• treat the cause
• reduce intake
• can give oral K+ binding resins which bind K+ into the gut so it is lost in faeces

Question 15

What are some possible causes of hypokalaemia?

Answer 15

• problems of external balance eg excessive loss due to diarrhoea or vomiting, renal loss due to diuretics or high aldosterone
• problems of internal balance eg metabolic alkalosis causing shift of K+ into ICF

Question 16

What are the clinical features of hypokalaemia?

Answer 16

• arrhythmias
• paralytic ileus
• muscle weakness
• unresponsive to ADH leading to polyuria

Question 17

What is the treatment for hypokalaemia?

Answer 17

• treat cause
• IV K+ (need to be v v careful)
• if due to high aldosterone give potassium sparing diuretics which block the action of aldosterone on principle cells