Disorders of Fluid & Electrolyte Balance

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  • Created by: Becca
  • Created on: 27-12-13 21:57
What causes hyponatraemia?
H2O retention secondary to defect in excretion (advanced renal failure, effective circulating volume depletion, SIADH, hormonal changes), primary polydipsia (often schizophrenic, psychological desire to drink, uses thirst mechanism) & reset osmostat
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What is the consequence & treatment for hyponatraemia?
Consequence: H2O moves into cells -> cerebral oedema -> lightheadedness, N+V, lethary, seizures, coma. Treatment: depends on severity/cause - water restriction, increase salt intake/diuretics
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What is pseudohyponatraemia?
Volume displacement caused by a hyperosmolar state e.g in patients with hyperproteinaemia/glycaemia/lipidaemia. Plasma [Na+] in blood sample appears to be low as some osmolality is contributed by increased protein/glucose/lipid. No treatment needed!
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What causes hypernatraemia?
Water loss when thirst (main defence) can't be normally expressed e.g. babies/elderly who can't express their desire to drink or patients with altered mental status
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What causes hypernatraemia? What is the consequence & treatment for hypernatraemia?
Causes: mainly H2O loss e.g. diabetes insipidus, fever, impaired thirst or Na+ retention. Consequence: H2O moves out of cells -> decrease brain volume, lethargy, seizure, coma. Treatment: decrease Na+ & increase H2O
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How is internal & external K+ balance maintained?
Internal: after meal, K+ moves from ECF->ICF (buys time for kidney). External: between dietary K+ in & excreted K+ out in urine/stool/sweat (secretion of K in principal cells of LDT/CD, where almost all K excretion happens)
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What happens when there is an increase in extracellular [K+]?
Most K+ intracellular, markedly affected by small changes in extracellular K+. Increase [K+]: depolarise membrane -> more excitable but persistent depolarisation inactivates Na channels -> decrease membrane excitability -> impaired cardiac conduction
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What happens when there is an decrease in extracellular [K+]?
Decrease [K+] -> hyperpolarise membrane -> less excitable but more excitable in cardiac myocytes due to removal of normal inactivation of Na channgels. Dietary K+ intake can't be rapidly excreted. Decrease extracellular K+ decreases ADH sensitivity
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What does intracellular [K+] affect?
Protein & glycogen synthesis
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What physiological factors influence transcellular distribution of K+?
Na/K-ATPase (promotes K+ uptake), insulin (glucagon) & catecholamines (B2 receptors, both increase K+ uptake into cells & activate ATPase), plasma [K+] and exercise
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What pathological factors influence transcellular distribution of K+?
Chronic diseases (especially renal), extracellular pH (lowered pH: H+ in, K+ out & raised pH: H+ out, K+ in), hyperosmolality (solvent drag) & rate of cell breakdown (severe trauma e.g. burns)
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What causes hypokalaemia? (part 1)
K+ depletion by abnormal losses: decreased net intake (may contribute but rarely solely responsible for hypokalaemia), increased entry into cells (transient decrease plasma [K+], alkalosis/insulin/B2-adrenoceptor activation), increased GI losses
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What causes hypokalaemia? (part 2)
Increased urinary losses: loop/thiazide diuretics, vomiting (metabiolic alkalosis), mineralocorticoid excess, renal tubular acidosis (type 1 classic distal, type 2 proximal) & hereditary disorder. Also increased sweat loss, replaced with H2O
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What are the symptoms of hypokalaemia?
No symptoms in mild disorder. Non-specific symptoms in severe: muscle weakness (change in resting membrane potential), arrhythmia, constipation, renal dysfunction (poluria/dipsia, resistance to ADH). Hypokalaemia can help maintain metabolic alkalosis
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What causes hyperkalaemia?
Increased intake, movement from cells to ECF (metabolic acidosis, insulin deficiency, tissue catabolism, severe exercise, B-adrenoceptor antagonism, pseudohyperkalaemia) & decreased urinary excretion (renal failure, hypovolaemia, hypoaldosteronism)
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What are the symptoms & treatments for hyperkalaemia?
Muscle weakness/paralysis (sustained depolarisation inactivates Na+ channels, decrease excitability) & arrhythmias. Treatment: antagonism of membrane action (Ca restores excitability), increase K entry into cells (insulin + glucose) & remove excess K
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What is the relationship between acid-base balance & K+ balance?
Acidosis -> hyperkalaemia. Alkalosis -> hypokalaemia. Renal tubular acidosis (metabolic acidosis): type 1 -> hypokalaemia, type 2 -> hypokalaemia, type 4 (hypoaldosteronism) -> hyperkalaemia. Hypokalaemia -> metabolic alkalosis
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What is the consequence & treatment for hyponatraemia?

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Consequence: H2O moves into cells -> cerebral oedema -> lightheadedness, N+V, lethary, seizures, coma. Treatment: depends on severity/cause - water restriction, increase salt intake/diuretics

Card 3

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What is pseudohyponatraemia?

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Card 4

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What causes hypernatraemia?

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Card 5

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What causes hypernatraemia? What is the consequence & treatment for hypernatraemia?

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