potassium balance Flashcards
describe the distribution of potassium
what are acute and chronic potassium regulation ?
Acute regulation:
Distribution of K+ between intra- and extra-cellular fluid compartments
i.e. largely internal K+ balance
Chronic regulation:
Achieved by the kidney adjusting K+ excretion & reabsorption
i.e. largely “output part” of external K+ balance
what are some functions of potassium ?
- Determines intracellular fluid osmolality → cell volume
- Determines resting membrane potential (RMP) → very important for normal functioning of excitable cells
i.e. repolarisation of myocytes, cardiomyocytes & neurons - Affects vascular resistance
how is sodium - potassium balance maintained ?
Na+-K+-ATPase pump maintains:
HIGH intracellular [K+] & LOW intracellular [Na+]
what is hypo and hyperkalemia ?
Hyperkalaemia = plasma [K+] > 5.5mM
Hypokalaemia = plasma [K+] < 3.5mM
how are ECGs changed due to hypo and hyperkalemia ?
Hypokalaemia: ↓ amplitude T-wave, prolong Q-U interval, prolong P-wave
Hyperkalaemia: ↑ QRS complex, ↑ amplitude T-wave, eventual loss P-wave
how does increased plasma potassium affect resting membrane potential ?
causes depolarisation, which raises the resting membrane potential making cells more excitable.
how does lowered plasma potassium affect resting membrane potential ?
causes hyperpolarisation, which lowers the resting membrane potential making cells less excitable.
describe 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 50 mM K+)
Hypokalaemia results in:
↓ Resting membrane potential
↓ Release of adrenaline, aldosterone & insulin
describe hyperkalaemia
Acute hyperkalemia is normal during prolonged exercise.
Causes of Hyperkalemia:
Insufficient renal excretion (e.g., kidney disease).
Increased K⁺ release from damaged cells (e.g., chemotherapy, prolonged fasting, severe burns, prolonged exercise).
Long-term use of potassium-sparing diuretics.
Addison’s disease (adrenal insufficiency) → reduced aldosterone → impaired K⁺ excretion.
Severe Hyperkalemia (>7mM):
Can be life-threatening, leading to asystolic cardiac arrest.
Treatment & Regulation:
Insulin/glucose infusion drives K⁺ back into cells.
Insulin plays a crucial role, possibly by stimulating Na⁺/K⁺ ATPase.
Other hormones (aldosterone, adrenaline) also stimulate the Na⁺/K⁺ pump, promoting cellular K⁺ uptake.
what drugs increase the chance of hypo and hyperkalaemia ?
- Drugs like β-blockers, ACE inhibitors etc ↑ serum [K +]⇒ ↑ risk of hyperkalaemia
- loop diuretics, used to treat heart failure ⇒ ↑ risk of hypokalaemia
what has the kidney evolved to do ?
Conserve Na+
Excrete K+
what determines potassium secretion in the DCT and how is this achieved ?
determined by:
* Increased K+ intake
* Changes in blood pH
* Alkalosis ⇒ ↑ excretion of K+ ⇒ ↓ serum [K+]
* Acute Acidosis ⇒ ↓ excretion of K+ ⇒ ↑ serum [K+]
achieved by:
* activity of Na-K-ATPase pump
* electrochemical gradient
* permeability of luminal membrane channel
how does increased plasma potassium lead to increased loss in potassium via urination ?
- Slows exit from basolateral membrane
↑ [K+]i
cell-lumen concentration gradient - ↑ activity of Na+/K+ ATPase
↑ [K+] I - Stimulates aldosterone secretion
what does aldosterone do ?
what is the mechanism of action for aldosterone ?
- ↑ Na⁺/K⁺ ATPase activity → ↑ K⁺ influx → ↑ intracellular [K⁺] → Favors K⁺ secretion due to cell-lumen concentration gradient.
- ↑ ENaC channels → ↑ Na⁺ reabsorption → ↓ intracellular negativity & ↑ lumen negativity → Creates a voltage gradient favoring K⁺ secretion.
- Redistributes ENaC to the membrane → Increases luminal membrane permeability to K⁺, enhancing K⁺ secretion.
how acidosis and alkalosis affect potassium secretion ?
Alkalosis:
Increased plasma pH enhances Na⁺/K⁺ ATPase activity, increasing intracellular K⁺.
This creates a stronger concentration gradient for K⁺ secretion.
Tubular fluid pH increases due to decreased H⁺ secretion in the proximal tubule, leading to increased HCO₃⁻ in the fluid.
Higher tubular pH enhances luminal membrane permeability to K⁺.
Acute Acidosis:
Increased [H⁺] in ECF reduces Na⁺/K⁺ ATPase activity.
This lowers intracellular [K⁺], reducing the passive diffusion of K⁺.
As a result, K⁺ excretion decreases.
how does tubular flow rate affect potassium secretion ?
increase in Tubular Fluid Flow Rate:
Caused by ↑GFR, inhibition of upstream reabsorption, or K⁺-wasting diuretics.
Sweeps away secreted K⁺, keeping tubular fluid [K⁺] low.
Maintains a favorable K⁺ gradient for continued secretion.
Anti-Diuretic Hormone (ADH):
Stimulates K⁺ secretion by increasing K⁺ conductance of the luminal membrane.
Effect is weaker than aldosterone in promoting K⁺ secretion.
describe potassium reabsorption in DCT and CT
Limited role under normal conditions since most K⁺ reabsorption occurs in the PCT & Loop of Henle.
Mechanism not fully understood, but H⁺/K⁺ ATPase may be involved → H⁺ excretion coupled with K⁺ reabsorption.
Becomes active in severe hypokalemia, helping conserve K⁺.
Final urinary K⁺ excretion can be <15 mmol/day.
K⁺ Conservation in Low K⁺ Conditions (Dietary Deficiency or Diarrhea):
Proximal tubule & Loop of Henle function as usual.
Distal tubule, connecting tubule, & cortical collecting duct stop secreting K⁺ and may even reabsorb it.
Medullary collecting duct reabsorbs remaining K⁺, leading to minimal K⁺ excretion in urine.
what happens when extracellular fluid volume decreases ?
give a summary of factors that alter K distribution between ICF and ECF
describe Addisons disease
- Primary Adrenal Insufficiency
- Rare compared to secondary adrenal insufficiency
- Damage to cortex ↓↓ hormone production numerous symptoms
- Deficiency in aldosterone
body secreting large amounts Na
low serum Na levels
body retaining K
hyperkalaemia - Treatment usually involves corticosteroid (steroid) replacement therapy for life.
describe secondary adrenal insufficiency
describe Conns syndrome
- ↑↑↑ Plasma Aldosterone → Kidneys stimulate Na⁺ reabsorption & K⁺ excretion.
Results in:
* Hypertension due to ↑ fluid volume.
* Hypokalemia, hypernatremia, and alkalosis (↓K⁺, ↑Na⁺, ↑pH).
* Renin-Independent Hypertension:
* ↑ BP & Na⁺ delivery to macula densa → ↓↓ Renin release.
* Hypertension is difficult to control.
Treatment:
Surgical removal of tumor-containing adrenal gland.
Hypertension & hypokalemia controlled with K⁺-sparing agents (e.g., spironolactone).
