Sandbox:Vindhya

Medical and Neurologic causes

Neurologic disorders	Cerebral neoplasms, cerebral trauma and post concussive syndromes ,Cerebrovascular disease, subarachnoid hemorrhage, Migraine, encephalitis,cerebral syphilis, Multiple sclerosis,Wilsons disease,Huntington disease,Epilepsy
Endocrine disorder	Pituitary dysfunction, Thyroid dysfunction, parathyroid dysfunction, Adrenal dysfunction,pheochromocytoma
Systemic conditions	Hypoxia, Cardiovascular disease, pulmonary insufficiency, anemia
Inflammatory disorders	Lupus erythematosus, rheumatoid arthritis, polyarteritis nodosa, temporal arteritis
Deficiency states	Vitamin B12 deficiency, pellagra
Miscellaneous	hypoglycemia, carcinoid syndrome, uremia, premenstrual syndrome, porphyria
Substances	Caffeine,cannabis,Hallucinogens, theophylline, amphetamines,yohimbine,sympathomimetics, mercury, Arsenic,organophosphates,benzene
Withdrawal	alcohol,caffeine, opiods,antihypertensives

siadh classification

Classification

SIADH may be classified in to several sub-types based on the pattern of AVP secretion across a range of plasma osmolalities:

• Type A : is the commonest form of SIADH responsible for a much higher proportion of SIADH, at around 60–70%. Characteristically, type A patients exhibit excessive, random secretion of AVP, with loss of the close linear relationship between plasma osmolality and plasmaAVP. Type A is common in lung cancer; invitro studies have demonstrated that some lung tumours synthesize AVP, and that tumour tissue stains positive for AVPmRNA.Plasma AVP concentrations in type A SIADH are not suppressed physiologically by drinking , which makes patients vulnerable to the development of severe hyponatremia. Studies have also demonstrated a lowerosmotic threshold for thirst appreciation in this type of SIADH. This type of SIADH is also characteristic of nasopharyngeal tumours, which also stain positive for AVP mRNA.

• Type B: is also common (20–40%). The osmoticthreshold for AVP release is lowered – a reset osmostat – such that secretion of AVP occurs at lower plasma osmolalities than normal. Because AVP is suppressed at plasma osmolalities below the lower, reset threshold, further over-hydration leads to suppression of AVP release, which protects against the progression to severehyponatraemia. Although most tumours manifest type ASIADH, some also present with type B SIADH, so thepattern of abnormal AVP secretion cannot be utilized to predict the causation of SIADH.

• Type C :is a rare condition characterized by failure to suppress AVP secretion at plasma osmolalities below the osmotic threshold. Plasma AVP concentrations are thus inappropriately high at low plasma osmolalities, but there is a normal relationship between plasma osmolality and plasma AVP at physiological plasma osmolalities. This variant may be due to dysfunction of inhibitory neurons in the hypothalamus, leading to persistent low-grade basal AVP secretion.

• Type D: is a rare clinical picture of SIADH with low or undetectable AVP levels and no detectable abnormality in circulating AVP response . It is thought that a nephrogenic SIADH (NSIAD) may be responsible for this picture . Gain-of-function mutations in the V2 receptor leading to a clinical picture of SIADH, with undetectable AVP levels, have been described. The identified mutations had different nucleotide substitutions causing different levels of V2 receptor activation. This syndrome appears to be inherited in an X-linked manner,although heterozygous females may have varying degrees of inappropriate antidiuresis. Owing to variable expressivity of the gene involved, NSIAD may be clinically undetectable for years, until other contributing factors in later life lead to clinically significant hyponatraemia .