Electrolytes Flashcards
What is the normal reference range for sodium?
135-145mmols/L
Values less than 120 or more than 150 are potentially dangerous
What can contribute to sodium abnormalities?
Intake
Loss or retention (gut, sweat, renal)
Water intake/loss/retention
What are the clinical features of hypernatraemia?
H2O depletion (Vol decrease): Unconscious/confused pts Infants Thirst centre damage Dehydration
Conn’s/Cushings (Aldo increase)
DI (ADH Deacrease):
Cranial – no ADH
Nephrogenic – ADH ineffective
Addison’s (Adrenal insufficiency) (Aldo )
What are the clinical features of hyponatraemia?
H2O excess (vol increase):
infusion of hypotonic fluid
psychogenic DI
Na+ depletion (Na+ decrease from gut/skin/sweat)
Heart failure (Renal blood flow decrease)
SIADH (ADH increase)
Diuretics (Vol decrease)
Loss of Na+ and H2O (Vol decrease): Osmotic diuresis (eg diabetes)
What are the common causes of hyponatraemia?
Iatrogenic eg fluid mismanagement Drugs especially diuretics Renal failure Addison’s disease Hypothyroidism Liver failure Heart failure SIADH
What is the reference range for potassium?
3.5-5mmol/L
Values less than 3 or more than 6 are potentially dangerous
What are the normal intracellular and extracellular concentrations of potassium?
Intra- 150mmol/L
Extra- 5mmol/L
Describe acidosis
ATPase slows
Less potassium into cells
Hyperkalaemia
Describe alkalosis
ATPase speeds up
More potassium into cells
Hypokalaemia
How is ATPase usually regulated in the red blood cells?
Catecholamines (e.g. Adrenaline)
Insulin
How is ATPase usually regulated in the kidney?
Mineralocorticoid activity:
Aldosterone
(Cortisol)
Diuretics:
Spironolactone
Amiloride
What are some of the common causes of potassium abnormalities?
Intake
Distribution
Loss/Retention:
Renal
Gut
Oral
What are the clinical features of hyperkalaemia?
Spurious (common): Haemolysis – release from cells Delay – release from cells EDTA contamination – direct from K+ salt of EDTA Drip arm – K+ drip
Mineralocorticoid deficiency – decreased Na+ K+/H+ exchange: Addison’s disease RTA IV (hyporeninaemic hypoaldosteronism)
Acidosis – Distribution:
Diabetic ketoacidosis
Lactic acidosis
Chronic respiratory acidosis
Hypoxia & related – ineffective pumps:
Hypoxia
Renal failure
Potassium sparing diuretics:
Spironolactone – aldosterone inhibitor
Amiloride - Na+ K+/H+ pump inhibitor
What are the clinical features of hypokalaemia?
Mineralocorticoid excess – increased Na+ K+/H+ exchange: Conn’s syndrome Cushing’s syndrome Licorice Secondary hyperaldosteronism
Increased cellular uptake:
Insulin excess
Alkalosis: plus increased renal loss
Increased catecholamines
Renal tubular acidosis (RTA):
Type I – H+ excretion impaired
Type II – HCO3- reabsorption impaired
Excess Na+ for exchange:
Prolonged saline infusion – more Na+ to reabsorb in exchange for K+
Loop/thiazide diuretics – inhibit Na reabsorption earlier in tubule
Extra-renal causes – may also cause secondary hyperadosteronism due to fluid loss: Diarrhoea Laxative abuse GI infection Prolonged vomiting
How do you avoid leaky red cells giving a spurious potassium result in the lab?
Check using heparinised sample & arrange for rapid analysis by the laboratory.