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Sodium Concentration Disorders - Coggle Diagram
Sodium Concentration Disorders
Hyponatraemia with Hypovolaemia
Extrarenal (urinary sodium <20 mmol/L)
Vomiting
Diarrhoea
Haemorrhage
Burns
Pancreatitis
Renal (urinary sodium >20 mmol/L)
Osmotic diuresis
Diuretics
Adrenocortical insufficiency
Tubulointerstitial renal disease
Recovery phase of acute tubular necrosis
Salt loss>water loss
ADH secretion is initially suppressed (via the hypothalamic osmoreceptors) but, as fluid volume is lost, volume receptors override the osmoreceptors and stimulate both thirst and the release of ADH. This is an attempt by the body to defend circulating volume at the expense of osmolality.
With extrarenal losses and normal kidneys, the urinary excretion of sodium falls in response to the volume depletion, as does water excretion, leading to concentrated urine containing <10 mmol/L of sodium. However, in salt-wasting kidney disease, renal compensation cannot occur and the only physiological protection is increased water intake in response to thirst.
Hyponatraemia + Euvolaemia
Abnormal ADH release
SIADH
Psychiatric
Increased ADH sensitivity
ADH-like substances
Unmeasured osmotically active substances stimulating osmotic ADH release
Hyponatraemia with euvolaemia results from an intake of water in excess of the kidneys’ ability to excrete it (dilutional hyponatraemia); there is no change in body sodium content but the plasma osmolality is low. With normal kidney function, dilutional hyponatraemia is uncommon even if a patient drinks approximately 1L per hour.
Hyponatraemia + Hypervolaemia
Heart failure
Liver failure
Oliguric kidney injury
Hypoalbuminaemia
Pseudohyponatraemia