L19.1 Potassium balance Flashcards
What is the normal distribution of Potassium: Extracellularly, intracellularly.
What is ratio of excretion via urine/faeces.
What is the dietary source
Highest cation in intracellular > EC.
90-95% excretion by kidneys (urine) over hours to days
5-10% excretion in faeces
Eaten in fruit, vegetables
What are the two substances responsible for initial K+ balance (short term) and how do they work
- Insulin: post prandial release shifts dietary K+ into cells. Also increases glucose transporter available.
- Catecholamines regulate internal K+ distribution
- a-adrenergic receptor impair cellular entry of K+
- b adrenergic receptors promote cellular entry of K+
For Both
- Binding to receptor triggering internal cascade to make ATP which stimulates NaKATPase which moves K+ out of blood into the skeletal muscle cells
How does EC K+ concentrations change around skeletal muscle during exercise and how is it balanced
- exercises causes increased movement of intracellular K+ into the interstitial space in skeletal muscle
- promotes local vasodilation, fatigue - Release of catecholamines (through B2 stimulation) limits the rise in EC [K+] that otherwise occurs as a result of normal K+ release by contracting muscle.
How can tonicity affect K+ concentrations across the EC/ IC compartment. Define tonicity
Tonicity: measure of osmotic pressure gradient and is influenced by solutes that cannot cross the membrane
- Hypertonicity (eg. hyperglycaemia) leads to water movement from the intracellular to extracellular compartment
- This water movement favours K+ efflux from the cell through the process of solvent drag = hyperkalaemia
- In addition cell shrinkage cause intracellular K+ concentration to increase, creating a more favourable concentration gradient for K+ efflux.
How can pH affect K+ concentrations across the EC/ IC compartment. What are the two pH states
Acidosis: (increase in EC H+ ions) drives K+ efflux as immediate buffering.
- Effective acidosis can also decouple/ lack of efficacy NaKATPase
- Alkalosis will cause K+ influx into cells.
Compare how much K+ is reabsorbed along the renal tubule (4)
- K+ freely filtered at the glomerulus
- K+ 60% reabsorped PCT
- K+ 30% reabsorbed thick ascending LoH.
- K+ variable reabsorption in collecting ducts
What are the main mechanisms of K+ movement in renal tubule (lumen blood) and where are they
- Paracellular solvent drag: PCT, TaL of LoH
- freely movement of Na+ and H2O drags K+.
- movement of Na+ changes lumen potential from more - to more + also which also forces K+ to be dragged - Transcellular
Thick ascending Limb (LoH)
a) N(a)KClCI2 co transporter into cell
- however recycling through ROMK which spits it back to the lumen which drives the + gradient for paracellular transport.
b) Chloride K co transporter taking K+ out of the cell into blood
- Aldosterone mediated K+ loss: DCT and collecting duct.
a) stimulates basolateral NaKATPase to get K+ back into cell from blood
b) direct increase of K+ permeability at luminal surface: promote K+ moving into lumen
c) stimulates ENac for Na+ absorption which increases (-) in lumen, favouring K+ excretion
What is the K range and symptoms of Hypokalaemia
Serum K <3.5 mmol/L severe, 3-3.5 mild
Severe symptoms:
- muscle weakness–>paralysis
- cardiac conduction abnormalities (arrhythmia)
- Cramps
- Constipation
What is a hereditary cause of hypokalaemic periodic paralysis (rare autosomal dominant) : mech, presentation, treatment
- Mutation of skeletal muscle ion channels (K+, Na, Ca2+)
- Causes recurrent episodes of muscle weakness/ stiffness.
Triggered by high carb meal (insulin) or SNS activation (b-agonist) - Treated by maintaining high K+ diet, K+ supplementation, K+ sparing diuretics,
carbonic anhydrase inhibitors (push up K+)
What are the potential causes of hypokalaemia due to losses and how to differentiate #1 causes
- Renal losses:
- hyperaldosteronism: Conns syndrome (adrenal adenoma). Also presents with hypertension, increased aldosterone: renin ratio.
confirmed by CT, MRI, adrenal sampling and removal of one adrenal gland
- licorice root candy: pseudohyperaldosteronism due to mineralocorticoid substance ,
- diuretics: Metolozone, thiazide at DCT, Frusemide at TAL
- renal tubular acidosis
- Gut losses:
- vomiting, diarrhoea, laxatives, ileostomy
How is hypokalaemia treated
- Treat the underlying problem : stop diuretic, find tumour, treat GE etc
- Mild: oral 1-2 slow K daily
- Severe: Iv replacement
How does TAL, DCT, Collecting duct diuretics work and give eg. Which is K sparing
PCT: mannitol only used in ICU
TAL: Frusemide: inhibit Na/K/2Cl co transporter so less K+ absorped, more in urine
DCT: Metolozone, thiazide: inihibit Na/Cl transporter which dysregulates K+ leading to hypokalaemia
Collecting duct: Spironolactone, Amiloride: K+ sparing diuretics
What is the K range and symptoms of Hyperkalaemia (5)
K>5.0 mmol/L
Symptoms:
- Fatigue or weakness
- Paresthesia,
- N and vomitting
- Dyspnoea,
- Palpitations
What are the potential causes for Hyperkalaemia (3)
- Pseudohyperkalaemia: on lab tests due to haemolysed sample.
- Increased dietary intake paired with
Decreased excretion
- Renal failure, Hypoalodosteronism
Acei/ ARB, other drugs
- Disruption of cell uptake:
- BB (block B agonist effect) , Acidosis, Rhabdomyolysis
What is the clinical disease of hypoaldosteronism, presentation, investigation, and treatment
Addisons disease: Deficient secretion of adrenocorticoid hormones: cortisol/aldosterone.
Presents
- hyperpigmented/tanned appearance due to excessive ACTH excretion stimulating melanocyte
- lethargy, weakness
- weight loss, low BP
Investigations
- on blood: high K+, low Na+. Short synacthen test which see if adrenal gland responds to ACTH.
- scan: structural disruption of adrenal gland due to TB, metastases (functional more likely)
- Treatment; dexammethosone, Fludrocortisone.
