S5: regulation of potassium & fluid replacement therapy

Question 1

Describe potassium handling in the proximal convoluted tubule

Answer 1

K+ reabsorption occurs passively in the PCT & around 2/3 is reabsorbed here
Occurs via a paracellular mechanism (solvent drag) and is directly proportional to water and Na+ movement

Question 2

Describe potassium handling in the thick ascending limb of the loop of Henle

Answer 2

Roughly 20% of K+ is reabsorbed through transcellular and paracellular pathways
Transcellular: Na+/K+/ATPase creates a gradient for sodium-potassium-chloride cotransporter (NKCC2) on the apical membrane
NKCC2 pumps Na+, K+ and 2Cl- into the cell from the lumen
Intracellular K+ can enter the bloodstream via the K+/Cl- symporter or through the K+ uniporter
Paracellular: movement of K+ through apical ROMK channels

Question 3

Describe potassium reabsorption in the DCT and cortical collecting duct

Answer 3

Around 10% of filtered potassium is reabsorbed here, via alpha and beta intercalated cells
The apical H+/K+/ATPase mediates the movement of H+ into the lumen, driving K+ into the intercalated cell
Then, the basolateral K+ channel allows the K+ inside the cell to leak out into the bloodstream
Alpha intercalated cell (acidosis) – reabsorb H+ & secrete K+ + HCO3-
Beta intercalated cell (alkalosis) – secrete H+ & reabsorb K+ + HCO3-

Question 4

Describe potassium secretion in the DCT and collecting duct

Answer 4

Mediated via the principal cells
Contain ENaC on the apical membrane and Na+/K+/ATPase on the basolateral membrane
Accumulation of intracellular K+ (high intracellular K+ compared to luminal concentration) creates a chemical gradient
Na+ moves from the lumen into the cell down the concentration gradient through ENaC
Creates a favourable electrochemical gradient which allows for K+ secretion via K+ channels on the apical membrane (into the urine)

Question 5

Describe the causes of hyperkalaemia

Answer 5

Lack of excretion
Release from cells
Excess administration

Question 6

Describe the treatment of hyperkalaemia

Answer 6

Calcium gluconate – Ca2+ stabilises the myocardium, preventing arrythmias
Insulin – drives K+ into cells to lower plasma concentrations (given with glucose to avoid hypoglycaemia)
Calcium resonium – removes K+ by increasing excretion from the bowels (only way to remove K+ without renal replacement therapy)

Question 7

Describe the causes of hypokalaemia

Answer 7

Reduced dietary intake
Increased entry into cells
Increased GI losses
Increased urine loss

Question 8

Describe the treatment of hypokalaemia

Answer 8

Treat the cause
Give potassium replacement 
-oral: bananas, oranges, sando-K
-IV: add KCL to IV bags
-potassium sparing diuretics: spironolactone & amiloride

Question 9

Explain why the percentage of body weight is different in different sexes and ages

Answer 9

Fluid proportion depends on muscle mass – therefore men have more fluid 
60% - males 
50% - females 
45% - elderly 
75% - infants

Question 10

Describe what happens if dextrose is given to a patient

Answer 10

Glucose taken up by cells rapidly – hyperglycaemia if infusion rate quicker than uptake and metabolism
H20 reduces osmolality of all compartments

Question 11

Describe what happens if 0.9% saline is given to a patient

Answer 11

Na+ remains in the ECF

No change in osmolality

Question 12

Describe what happens if Hartman’s is given to a patient

Answer 12

Retained in the ECF as osmolarity maintained with effective osmoles sodium, potassium & calcium

Question 13

Describe what happens if 1000ml 4% dextrose/0.18% saline is given to a patient

Answer 13

800ml H20 reduces osmolarity of all compartments

200ml 0.9% saline remains in ECF

Question 14

Why do patients need fluids and which fluids should be given?

Answer 14

Nil by mouth, malfunctioning GI tract, dehydration, fluid losses & abnormal electrolytes
Give maintenance fluids if unable to take orally & replace as close to fluid lost as possible

Question 15

Describe why hospitalised patients have increased risk of hyponatraemia and volume overload

Answer 15

Increased ADH – non-osmotic stimuli: drugs, pain, nausea, low effective circulating volume
Generally, don’t sweat excessively
Stress response: RAAS, catecholamines & reduced caloric expenditure
Reduced free water excretion = hyponatraemia
Increased water & salt retention = volume overload

Question 16

Describe how trimethoprim causes drug-induced hyperkalaemia

Answer 16

Trimethoprim acts as a competitive inhibitor of the epithelial sodium channel
Blocks ENaC channel, therefore decreasing the concentration gradient, resulting in impaired potassium secretion