3.1 Regulation Of Potassium And Magnesium Flashcards
(37 cards)
what ion determines the resting membrane potential?
potassium
what is the extracellular concentration of potassium?
4-5mmol/L
what happens to the membrane potential if the extracellular fluid concentration of potassium rises/falls?
rises : the resting membrane potential is depolarised (becomes less negative)
falls: the resting membrane potential is hyper polarised ( becomes more negative)
describe the movement of potassium in the kidney?
PCT: reabsorbs 65%. passive reabsorption by paracellular transport via concentration gradient/ solvent drag
TAL: reabsorbs 20% of potassium through trans cellular and paracellular transport mechanisms
DCT: reabsorption and leakage is equal
late DCT and CD: secretion by principle cells. reabsorption by intercalated cells if plasma levels are too low
describe the channels used in transcellular transport of potassium in the TAL?
Apical surface -Na/K/2Cl cotransporter for reabsorption - ROMK for secretion basolateral surface - NA/K ATPase - ROMK - Cl/K cotransporter all reabsorbing potassium
how does activation of the RAAS system affect potassium handling in the kidney ?
activation of RAAS increases the secretion of aldosterone by the adrenal glands.
Aldosterone acts a the principle cells to increase the expression of ENAC and ROMK channels. This increases the amount of potassium secreted into the tubular filtrate
How would acidosis affect potassium handling in the kidney?
would have greater activation of H+/K+ ATPase in the alpha intercalated cells of the collecting duct. This exchanges H+ ions for K+ ions and therefore we would have increase reabsorption of potassium
what are some of the common causes of hypokalaemia?
excess insulin alkalosis certain catecholamines insufficient intake ( anorexia nervosa/ prolonged fasting) too much aldosterone loop and thiazide diuretics vomiting diarrhoea (leading to metabolic alkalosis) diuretics sweat - excessive exercise, hot climate
what are some of the causes for too much aldosterone?
primary aldosteronism
compensated heart failure
cirrhosis
why can alkalosis cause hypokalaemia?
as K+ is moved into cells in exchange for H+ in an effort to decrease the pH
what does hypokalaemia become symptomatic
when the potassium concentration falls below 2-2.5mmol/L
what is hypokalaemia?
when plasma concentration of potassium falls below 3.5mmol/L
how does hypokalaemia affect the resting membrane potential?
as the potassium will tend to move down its concentration gradient, the concentration within the cell will fall, therefore the cell will become hyper polarised and the resting membrane potential will increase
what are the clinical effects of hypokalaemia?
- muscle weakness, cramps, tetany (starts in lower extremities)
- Impaired liver conversion of glucose to glycogen (raised blood sugar) as insulin requires potassium to work
- Vasoconstriction and cardiac
arrythmias - Impaired ADH action causing thirst, polyuria and no concentration of urine
- Metabolic alkalosis due to increase in intracellular H+ concentration
what is the treatment of hypokalaemia?
treating the underlying cause
oral or intravenous K+
what commonly causes hyperkalaemia?
- Reduced renal excretion due to AKI or CKD
- mineralcorticoid deficiency (e.g. Addison’s disease) resulting in less aldosterone and less potassium secretion
- K+ sparing diuretics or renal tubular defects
- Increased plasma load
- Insulin deficiency – Type 1
diabetes • Transcellular shift of K+ out of cells: due to metabolic acidosis, insulin
deficiency, exercise or drugs
(digoxin) - Pseudohyperkalemia
- Certain catecholamines
- Hypoaldosteronism and drugs
which reduce effect of aldosterone (renin inhibitors, ACE inhibitors etc.)
what might increase the plasma load of potassium?
dietary changes
IV infusion
cellular tissue breakdown
what is pseudohyperkalaemia?
an artifact, not true hyperkalaemia:
due to hemolysis during
venipuncture or storage of the sample, a high white cell or platelet count
what are the clinical features of hyperkalaemia?
muscle weakness
cardiac arrhythmias
fatigue
- can be asymptomatic
why might hyperkalaemia be a medical emergency?
due to the effects on the heart
slightly depolarised membrane inactivated some of the voltage gated sodium channels of the heart slowing the upstroke of an AP
- mild hyperkalaemia = increased excitation
- moderate hyperkalaemia = slowed conduction due to inactivation of sodium channels. lengthening of ECG
- severe hyperkalaemia = heart can stop - asystole
what is severe hyperkalaemia?
a plasma concentration of potassium of greater than 6.5mmol/L
what is the emergency treatment for hyperkalaemia?
• Calcium gluconate – Ca 2+ stabilises the myocardium, preventing arrythmias
• Insulin – drives K+ into cells to lower plasma concentrations. Given with
glucose to avoid hypoglycemia
• Calcium resonium - Removes K+ by
increasing excretion from the bowels. Only way to remove K+ without renal replacement therapy
what ECG changes are seen during hyperkalaemia?
peaked T wave P wave flatten / disappear PR interval lengthening Widening of the QRS complex bradycardia sine wave pattern (cardiac arrest)
what are treatments that may help hyperkalaemia but aren’t first line?
- Salbutamol – Drives K+ into cells when given nebulized or IV. Should not be used in patients with ischemic heart disease or arrythmias
- Sodium bicarbonate – Correction of acidosis, would also drive K+ into cells. Not used in patients at risk of fluid overload
- Renal replacement therapy – Dialysis or hemofiltration are used if medical therapies fail to correct hyperkalemia
