Potassium balance Flashcards
Explain distribution of potassium
Intracellular [K+] ~ 150mmol/L
Extracellular [K+] ~ 4.5mmol/L
How is day to day/minute to minute regulation controlled?
Through insulin, aldosterone, pH, adrenaline etc. (internal balance)
How is external balance controlled?
Diet
What is acute regulation?
Distribution of K+ through ICF and ECF compartments
What is chronic regulation?
Achieved by the kidney adjusting K+ excretion and reabsorption
What are the functions of potassium?
- Determines ICF osmolality → cell volume
- Determines resting membrane potential (RMP) → very important for normal functioning of excitable cells
i. e. repolarisation of cell myocardial, skeletal muscle & nerve cells - Affects vascular resistance
What is Hyperkalaemia?
Plasma [K+] > 5.5mM
What is Hypokalaemia?
Plasma [K+] < 3.5mM
What normally determines resting membrane potential?
The dynamic balance between membrane conductance to Na+ and K+. Can be measured using Nernst equation.
What causes hypokalaemia?
Hypokalaemia caused by renal or extra-renal loss of K+ or by restricted intake
e.g
Long-standing use of diuretics w/out KCl compensation
Hyperaldosteronism/Conn’s Syndrome
( aldosterone secretion)
Prolonged vomiting → Na+ loss → aldosterone secretion → K+ excretion in kidneys
Profuse diarrhoea (diarrhoea fluid contains 50mM K+)
How does hypokalaemia affect hormones?
Hypokalaemia results in ↓release of adrenaline, aldosterone & insulin
What causes hyperkalaemia?
Acute hyperkalaemia normal following prolonged exercise → normal kidneys excrete K+ easily
Disease states:
Insufficient renal excretion
Increased release from damaged body cells eg. during chemotherapy, long-lasting hunger, prolonged exercise or severe burns
Long-term use of Potassium-sparing diuretics
Addison’s disease (adrenal insufficiency)
What can result from hyperkalaemia?
Plasma [K+] > 7mM life-threatening → asystolic cardiac arrest
How to treat Hyperkalaemia?
Insulin/Glucose infusion used to drive K+ back into cells Other hormones (aldosterone, adrenaline) stimulate Na+-K+ pump = increase in cellular K+ influx
How is normal K homeostasis a limiting factor in the therapy of CVD?
Drugs like β-blockers, ACE inhibitors etc raise serum [K] →risk of hyperkalaemia
Conversely, loop diuretics used to treat heart failure, enhance the risk of hypokalaemia
Where does most K get reabsorbed?
PCT and loop of Henle. 90%
Explain K movement in PCT
- Sodium-potassium pump between tubular cells and ECF
- K can diffuse out into ECF through conc gradient
- Ions can leave from the tubular lumen to ECF through passive and paracellular movements.
Explain Na/K movement in LoH
- Sodium-potassium pump between tubular cells and ECF
- K can diffuse out into ECF through conc gradient
- Sodium clacum potassium pump.
What happens which lots of K in diet?
Excretion of K into urine by overload is controlled by secretion in principal cells of late DCT & CD.
ENaC=epithelial Na channel (sodium from lumen to cell )(aldosterone sensitive) causes k to move from cell to lumen
What determines K+ secretion in DCT?
Increased K+ intake
Changes in blood pH
Alkalosis ⇒ ↑excretion of K+ ⇒ ↓serum [K+]
*Acute Acidosis ⇒ ↓excretion of K+ ⇒ ↑serum [K+]
How is K secretion in DCT achieved?
activity of Na-K-ATPase pump
electrochemical gradient
permeability of luminal membrane channel
Aldosterone is a major regulator of K balance in the body. How does it work?
- ↑activity of Na+/K+ pump ↑K+ influx ↑[K+]i cell-lumen concentration gradient
- ↑ENaC channels ↑Na+ reabsorption ↓cell negativity and ↑lumen negativity voltage gradient
- Redistributes ENaC from intracellular localization to membrane
- ↑permeability of luminal membrane to K+
How does High potassium conc cause increase in potassiums secretion?
slows exit from basolateral membrane ↑[K+]i cell-lumen concentration gradient
↑activity of Na+/K+ ATPase ↑[K+] within the cell
↑Plasma [K] stimulates aldosterone secretion
How does Addison’s disease affect potassium?
Deficiency in aldosterone means body secrets lots of Na, low serum Na levels. Causes body to retain K - hyperkalaemia.
What is Conn’s syndrome?
↑↑↑ Plasma Aldosterone kidneys to stimulate Na+ reabsorption & K+ excretion. develop hypertension* and ↑fluid volume and hypokalaemia (↓[K+]), hypernatremia and alkalosis
*↑bp & Na delivery to macula densa leads to ↓↓release of renin renin-independent cause of hypertension (very difficult to control)
