Urinary: Control of Potassium Flashcards Preview

ESA 3 > Urinary: Control of Potassium > Flashcards

Flashcards in Urinary: Control of Potassium Deck (17):

What is the distribution of potassium in body fluids?

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)


Why is maintaining ECF K+ conc critical?

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


How many litres is the ECF?



How is ECF K+ regulated?

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.


List the factors that promote K+ uptake into cells
(internal balance)

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


List the factors that promote K+ shift out of cells
(internal balance)

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


How does exercise affect ECF [K+]?

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


Outline where along the nephron potassium is reabsorbed and secreted

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.


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

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


How does aldosterone affect K+ secretion?

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


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

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


What are some possible causes of hyperkalaemia?

- 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


What are the clinical features of hyperkalaemia?

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


What is the treatment for hyperkalaemia?

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


What are some possible causes of hypokalaemia?

- 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


What are the clinical features of hypokalaemia?

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


What is the treatment for hypokalaemia?

- 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

Decks in ESA 3 Class (96):