Changes

===Pathophysiology===

===Pathophysiology===

The glucococorticoid hormone '''cortisol''' enables animals to cope with stress while the minerlaocorticoid '''aldosterone''' plays a critical role in the regulation of sodium and potassium concentrations and of extracellular fluid volume. Aldosterone normally acts to increase sodium excretion and potassium reabsorption in the kidney so deficient aldosterone secretion will result in '''hyponatraemia''', '''hypochloraemia''' and '''hyperkalaemia'''.  Since they are unable to regulate their body sodium concentration, Addisonian animals become severely dehydrated and hypovolaemic, reducing the perfusion of peripheral tissues. During an Addisonian crisis, this can result in gastro-intestinal haemorrhage and allow translocation of bacteria across the gut barrier.

The glucococorticoid hormone '''cortisol''' enables animals to cope with stress while the minerlaocorticoid '''aldosterone''' plays a critical role in the regulation of sodium and potassium concentrations and of extracellular fluid volume. Aldosterone normally acts to increase sodium reabsorption and potassium excretion in the kidney so deficient aldosterone secretion will result in '''hyponatraemia''', '''hypochloraemia''' and '''hyperkalaemia'''.  Since they are unable to regulate their body sodium concentration, Addisonian animals become severely dehydrated and hypovolaemic, reducing the perfusion of peripheral tissues. During an Addisonian crisis, this can result in gastro-intestinal haemorrhage and allow translocation of bacteria across the gut barrier.

Deficiency of cortisol results in '''hypoglycaemia''' (as cortisol usually antagonises the action of insulin), increased circulating levels of [[Lymphocytosis|lymphocytes]] and [[Eosinophilia|eosinophils]] and increased skin pigmentation. This latter syndrome occurs as low levels of glucocorticoids allow increased ACTH production as negative feedback on the pituitary is removed or decreased. As ACTH is released, so is MSH (Melanocyte Stimulating Hormone), increasing the pigmentation of the skin in chronic cases of hypoadrenocorticism.

Deficiency of cortisol results in '''hypoglycaemia''' (as cortisol usually antagonises the action of insulin), increased circulating levels of [[Lymphocytosis|lymphocytes]] and [[Eosinophilia|eosinophils]] and increased skin pigmentation. This latter syndrome occurs as low levels of glucocorticoids allow increased ACTH production as negative feedback on the pituitary is removed or decreased. As ACTH is released, so is MSH (Melanocyte Stimulating Hormone), increasing the pigmentation of the skin in chronic cases of hypoadrenocorticism.