Lecture 8 - Regulation of K+

Question 1

What is the normal plasma K+ range?

What is the effect on raised and lowered EC K+ on the resting membrane potential?

Answer 1

• 3.5-5.5 mmol/L
• If Increased = resting membrane potential decreased (depolarised)
• If decreased = resting membrane potential increased (hyperpolarised)

Question 2

What are the ECG features of hypokalaemia (< 3.5 mmol/L) and hyperkalaemia ( > 5.5 mmol/L)

Answer 2

Hypokalaemia = prolonged PR interval, ST depression, shallow T-wave & prominent U wave

Hyperkalaemia = wide & flat P wave, widened QRS complex, ST depression, tall and peaked T-wave

Question 3

What are the normal IC and EC K+ values at rest?

Answer 3

IC = 130-140 mmol/L
EC = 3.5-5.5 mmol/L 

Therefore majority of K+ is intracellular, if cells burst/break, huge amount of K+ released into bloodstream (e.g.: rhabdomyolysis)

Question 4

In which 3 locations are K+ reabsorbed in the nephron & through which channels?
In which location is K+ secreted & through which channels?

Answer 4

Reabsorbed:

1) In PCT (67% of K+)
2) In thick ascending limb through NaK2Cl co-transporter
3) In DCT through ROM-K channels

Secreted:

1) In the collecting duct through ROM-K channels under influence of aldosterone

Question 5

How & why is plasma K+ increased during acidosis?

Answer 5

1) Alpha intercalated cells active during acidosis
2) H2O + CO2 combine via C.A and form H+ & HCO3-
3) These H+ ions secreted out in exchange for K+ via H/K exchanger
4) HCO3- ions put back into blood in exchange for Cl- ions coming in
5) K+ ions reabsorbed back into blood alongside Cl- ions
6) All cells also have H/K exchanger which increases K+ to be reabsorbed

Question 6

How & why is plasma K+ decreased during alkalosis?

Answer 6

1) Beta intercalated cells active in alkalosis
2) H2O + CO2 combine via C.A to form H+ & HCO3-
3) HCO3- ions move out via HCO3-/Cl- exchanger, Cl- moved into blood through Cl channel
4) H+ ions move into blood via H/K exchanger, K+ in plasma reduced

Question 7

What 3 things can cause hyperkalaemia?

What are the clinical features of hyperkalaemia?

Answer 7

1) Lack of excretions (e.g.: in CKD or AKI’s)
2) Release of K+ from cells (e.g.: in cell lysis, because patient is acidotic or in rhabdomyolysis)
3) Excess administration

• Can be asymptomatic but also will cause muscle weakness & cardiac arrhythmias

Question 8

What is the emergency treatment strategy for hyperkalaemia ( > 6.5 mmol/L)?

Answer 8

1) Calcium gluconate - Ca2+ stabilises myocardium to prevent arrhythmias but doesn’t treat hyperkalaemia.
2) Insulin + Glucose - drives K+ into cells to lower plasma K+ concentration, given with glucose to prevent hypoglycaemia. Doesn’t remove K+ from body
3) Calcium resonium - removed K+ from body by increasing excretion from bowels, but dialysis provides immediate removal.

Question 9

What are the 4 main causes of hypokalaemia?

Answer 9

1) Reduced dietary intake (prolonged starvation)
2) Increased entry into cells (patient is alkalotic)
3) Increased GI losses (diarrhoea/vomiting)
4) Increased urine losses (diuretics such as furosemide)

Question 10

What are the clinical effects of hypokalaemia?

How is hypokalaemia treated?

Answer 10

• Muscle cramps, weaknesses, tetany, vasoconstriction, arrhythmias, impaired ADH action causing thirst/polyuria and metabolic alkalosis due to increased IC H+ concentration.
• Treat the cause (e.g.: diuretics/diarrhoea), give potassium replacement (bananas, KCl in I.V bags or K+ sparing diuretics such as spironolactone)

Question 11

NB:

80% K+ removed by urine, 20% by bowels
Need to increase urinary excretion or dialysis to remove K+ from body

Answer 11

Yeah makes sense