-Increased loss of sodium, chloride and water and decreased secretion of potassium (mineral corticoid deficiency/aldosterone) resulting in hyponatremia, hyperkalemia, dehydration, weakness and fatigue, orthostatic hypotension/decreased CO.
-Hyperpigmentation (elevated levels of ACTH)
-Poor tolerance to stress (decrease in glucocorticoids) as well as hypoglycemia, fatigue, weakness, fever, anorexia, nausea, vomiting, weight loss.
-Decrease in androgens (sparse axillary and pubic hair in women)
-Beta cells are able to secrete insulin initially, but the beta cell response may be diminished.
-Insulin resistance: inability of cells (particularly muscle, liver, fat) to take up and metabolize glucose because of a slower cycling of glucose carriers to the cell membrane surface and defective utilization of the glucose that is able to get into cells. This causes an increase in insulin secretion by beta cells and increased production of glucose by the liver.
-Occurs gradually and is often asymptomatic in the beginningType II much more common than type I
-Much stronger genetic component than type I, probably a combination of environmental factors and genetics
-Less prone to ketoacidosis than type I
Insulin resistance related to metabolic syndrome: obesity (particular upper body, waist/hip ratio), high levels of plasma triglycerides, low levels of HDLs, hypertension, systemic inflammation, cardiovascular disease, abnormal vascular endothelium, abnormal thrombolysis