Quick bit of physiological background:
- ADH is made in the magnocellular neurones in the supraoptic and paraventricular nuclei of the hypothalmus
- ADH is stored in the posterior pituitary
- it is released in response to raised plasma osmolality (osmoreceptors in hypothalamus) or decreased volume (baroreceptors in carotids, atria)
- its effect is to increase the insertion of aquaporin 2 channels in the collecting ducts of the kidney, hence increasing water reabsorption.
- it also increases peripheral vascular resistance
SIADH is diagnosed in the presence of:
- concentrated urine ( sodium >20mmol/l and osmolality >500mosmol/kg) AND
- hyponaturaemia (<125) or low plasma osmolality (<260mosmol/kg) AND
- the absence of hypovolaemia, oedema or diuretics.
Causes of SIADH include:
- malignancy: small cell lung cancer, pancreas, prostate, lymphoma
- lung pathology: TB, pneumonia, aspergillosis
- CNS pathology: injury, GBS, fits, subarachnoid/subdural haemorrhage, abscess, stroke
- metabolic: porphyria
- drugs: opiates, carbamazepine, SSRIs, TCA
So lets now finish todays battles by widening this topic out to hyponatraemia...