Please enable JavaScript.
Coggle requires JavaScript to display documents.
HYPOKALAEMIA (Increased entry into cells (increased insulin (Aetiologies…
HYPOKALAEMIA
Decreased intake
rare to cause significant hypokalaemia
Increased entry into cells
increased insulin
Pathophysiology
increased activity of Na/K ATPase
Aetiologies
refeeding syndrome (endogenous insulin release due to high carbohydrate load)
treating DKA
increased beta-adrenergic activity
Pathophysiology
increase activity of Na/K ATPase and Ka-K-2Cl cotransporter (and by increasing insulin)
Aetiologies
stress-induced release of epinephrine
alcohol withdrawal
acute MI
head injury
theophylline intoxication
exogenous administration (asthma/HF)
Increased extracellular pH
Pathophysiology
H+ ions leave cells, K goes in
**hypokalaemia NB to maintain metabolic acidosis as it promotes bicarb reabsorption
hypokalaemic periodic paralysis (rare)
neuromuscular disorder, K suddenly moves into cells (exercise, stress, carbohydrate meal); normal K in between
increased RBC production
Pathophysiology
new cells take up K
Aetiology
giving B12/folate in megaloblastic anaemia
Hypothermia
can drive K into cells
Increased GIT losses
Upper GI losses
Actually urinary losses due to metabolic alkalosis
increased bicarb gets to distal K secretory site + increased aldosterone --> potassium secretion
Lower GI losses
diarrhoea
Increased urinary losses
Increased mineralocorticoid activity
aldosterone mainly stimulates Na reabsorption via ENaC --> passive K movement into the lumen
Increased distal delivery of sodium and water
Aetiology
diuretics that act proximal to potassium secretory site
carbonic anhydrase inhibitors
loop diuretics
thiazide-type
primary aldosteronism
nonreabsorbable anions (not Cl) in distal nephron
vomiting, proximal RTA --> bicarbonate
DKA --> beta-hydroxibutyrate