6a.) Potassium Flashcards
What % of total body potassium is intracellular?
98%
State intracellular and extracellular K+ concentration (in healthy patient)
- Intracellular: 140- 150mmol/L
- Extracellular: 3.5 - 5.5mmol/L
Why is a high [K+] necessary inside cells and mitochondria?
- Regulating cell volume
- Regulating pH
- Controlling enzyme function
- DNA & protein synthesis
- Cell growth
Why is a low extracellular [K+] essential?
- Maintain steep [K+] gradient across cell membranes as this gradient is largely responsible for membrane potential of excitable and non-excitable cells
Summarise how potassium is regulated/handled in the nephron
- Most (67%) of it absorbed in PCT
- Some more (20%) absorbed in thick ascending limb of Loop of Henle
- Potassium secretion in cortical collectin ducts via ROMK (the amount secreted varies)
Describe consequeces on cardiovascular and musculoskeletal system if extracellular [potassium] is too low (hypokalaemia)
Cardiovascular
- Increase K+ gradient across cell membrane
- Slows repolarisation of cardiac cells
- Keeps cells nearer to their threshold for firing for longer than usual
- During slower repolarisation they are easily excited which can lead to early after depolarisations- tachycardia- ventricular fibrillation
Musculoskeletal
Low extracellular K+ increases resting membrane potential which decreases excitablity:
- Muscle cramps
- Constipation
- Muscle weakness
Describe consequences of hyperkalaemia on cardiovascular and musculoskeletal systme
Cardiovascular
Reduce potassium gradient which inactivates some of sodium channels:
- Slows upstroke
- Bradycardia
- Asystole
Musculoskeletal
- Early: increase in irritabilty
- Late: weakness
Describe fluid distribution in male and female adult
State what happens to Na+/K+ ATPase transporters in basolateral membrane of principal cells in cortical collecting duct when:
- Hyperkalaemia
- Hypokalaemia
- Hyperkalaemia: increase activity of Na+/K+ ATPase in basolateral membrane of cortical collecting ducts
- Hypokalaemia: decrease activity of Na+/K+ ATPase in basolateral membrane of cortical collecting ducts
Describe the effect of sodium reabsorption of potassium excretion
- ROMK channels in cortical collectind cuts are freely open for K+ to move
- BUT need -ve lumen for K+ to move into filtrate
- Movement of Na+ out of lumen via ENaC channels creates -ve lumen
- Therefore greater sodium reabsorption promotes pottasium excretion
Describe effects of aldosterone on kidneys in hyperkalaemia
Increase in extracellular [K+] stimulates aldosterone release. Aldosterone then:
- Promotes synthesis of Na+/K+ ATPase and insertion of these channels into basolateral membane in cortical collecting ducts
- Increases Na+ reabsorption and therefore K+ excretion
Describe how pH changes can affect renal potassium excretion
- Potassium secretion reduced in acute acidosis
- Potassium secretion increased in acute alkalosis
A higher pH increases apical K+ channel activity and basolateral Na+/K+ activity
Describe the effect of increased flow rates on renal K+ handling
Increased flow rates in lumen:
- Reduce [K+] in lumen, increase conc gradient, enhance potassium secretion
- Activate BK potassium channels- increase secretion
- Activate ENaC channels which promotes Na+ reaborption and therefore makes lumen more -ve and so promotes K+ secretion
Describe the effect of reduced Na+ delivery to cortical collecting duct on K+ secretion
Reduced Na+ delivery leads to reduced Na+ reabsorption in collecting ducts which in turn:
- Decreases activity of Na+/K+ ATPase which lowers intracellular potassium concentration which then decreases K+ secretion
- Lumen isn’t made as -ve hence decreases K+ secretion
Describe the effects of vasopressin on renal potassium excretion
- Vasopressin reduces urinary flow rates (which should decrease K+ secretion)
- HOWEVER, also stimulates apical K+ channel activity to help maintain K+ secretion
Describe how magnesium deficiency can cause hypokalaemia
- Magnesium can bind to and block pore of ROMK channel
- Reduce K+ secretion into lumen
- If have magnesium deficiency, decrease this inhibitory effect henc more K+ can be excreted leading to hypokalaemia
State normal urine potassium values
60 - 80 mmol/L
What proportion of K+ is excreted by kidneys and by bowels?
- Kidney: 80%
- Bowel: 20%
State some possible causes of hyperkalaemia
- Lack of excretion
- AKI
- CKD
- Potassium sparing diuretics e.g. spironalactone, amiloride
- Aldosterone deficiency
- Release from cells
- Acidosis (H+ move into cell so K+ move out)
- Cellular breakdown e.g. from ischaemia, toxins, chemo
- Excess administration e.g. potassium containing fluids, blood transfusion (as cells start to break down)
Describe the immediate treatment for hyperkalaemia
- Insulin & glucose: insulin shifts K+ into cells- lasts 6 hours
- Calcium gluconate: stabilised cardiac membrane potential
- Salbutamol: shifts K+ into cells- lasts 6 hours
Describe long term treatment of hyperkalaemia
- Low K+ diet
- Calcium resonium to bind K+ in gut
- Stop offending medications
- Furosemide: enhances K+ loss in urine
- Dialysis
State some possible causes of hypokalaemia
- Potassium entering cells
- Insulin
- Alkalosis
- Beta 2 agonists
- Extra renal losses
- Diarrhoea
- Laxatives
- Vomitting
- Decreased intake
- Renal losses
- Diuretics
- Renal tubular acidosis
- Increased aldosterone
- Increased urine flow
- Magnesium deficiency
- DKA
How do you treat hypokalaemia?
Treat the cause, so if the following are the cause:
- Diuretics: change to K+ sparing
- Diarrhoea: stop
- Poor oral intake: increase intake (bananas, oranges, sando-k, IV fluids)
State some factors that increase and inhibit:
a. ) Na+/K+ ATPase
b. ) K+ excretion
