Flashcards in Urinary: Control of Potassium Deck (17):
What is the distribution of potassium in body fluids?
98% of K+ is in the ICF
Mainly in skeletal muscles, liver, RBCs and bone
2% of K+ is in the ECF
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
- increased K+ conc in the ECF
- hormones that act via Na-K-ATPase eg insulin, aldosterone and catecholamines
List the factors that promote K+ shift out of cells
- cell lysis
- increased ECF osmolarity
- decreased conc of K+ in ECF
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
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
What is the treatment for hyperkalaemia?
- 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?
- paralytic ileus
- muscle weakness
- unresponsive to ADH leading to polyuria