Potassium Control Flashcards
What maintains the ICF and ECF [K]
N-K-ATPase
How does the internal balance control [K] in ECF
Movement of K into cells - N-K-ATPase
Movement of K out of cells into ECF - K channels
What increases K uptake by cells
Hormones - act via N-K-ATPase
Increased [K] in ECF
Alkalosis - low ECF [H+] drives K into cells
What hormones increase cellular K uptake and how
Insulin - increases N-K-ATPase in muscle and liver cells
Aldosterone - stimulates N-K-ATPase in nephrons
Catecholamines - act via beta-2-adenoreceptors to stimulate N-K-ATPase
How is hyperkalaemia treated
IV insulin and dextrose
What factors increase K shift out of cells
Exercise - net release of K during recovery phase of AP. This increases plasma [K] -> taken up by non-contractile tissues to prevent high hyperkalaemia
Cell lysis
Increased ECF osmolarity
Low ECF [K]
Acidosis - high [H+] drives K out of cells
How does external balance control ECF [K]
External controls total body K over long term by regulating K excretion in DCT and cortical CD
Where is K reabsorbed
PCT
Thick AL
DCT - intercalated cells
Cortical CD - intercalated cells
Medullary CD - intercalated cells
Where is K secreted
DCT
Cortical CD - principal cells
How is K secretion achieved
N-K-ATPase creates chemical gradient for K secretion into lumen
Na moves from lumen into the cell in the DCT and CD, creating a -ve lumen potential which promotes K secretion
Both of these create a electro-chemical gradient that promotes K secretion
What tubular factors affect K secretion
ECF [K] - stimulates N-K-ATPase, changes permeablity of apical K channels and affects aldosterone release
Aldosterone - increased transcription of relavent proteins that promotes K secretion, increased N-K-APTase, increased K channels and increased ENaC
Acid base status:
- Acidosis inhibits N-K-ATPase -> decreases K channel permeability
- Alkalosis stimulate N-K-ATPase -> increases K channel permeability
What luminal factors affect K secretion
Increased distal tubular flow - washes away luminal K to maintain concentration gradient
Increased Na delivery to distal tubule -> increased Na absorbed -> increased K loss
How is K absorbed in DCT and cortical CD and what cells absorb it
K is absorbed in intercalated cells via H-K-ATPase
What might cause hyperkalaemia
Increased intake - unlikely. Only if renal dysfunction present or if inappropriate dose of IV K
Decreased renal excretion - AKI, CKI, drugs, low aldosterone (Addisons)
Internal shifts - diabetic ketoacidosis, cell lysis (muscle injuries), metabolic acidosis, exercise
What clinical features would hyperkalaemia cause
Heart - altered excitability -> arrhythmias and heart block
Gastrointestinal - neuromuscular dysfunction
Acidosis
