Diabetes Mellitus is an endocrine condition characterised by chronic hyperglycaemia resulting from problems with the function of the insulin system.

There are different types resulting from different aberrations in the insulin system.

The two most common types are called Type 1 and Type 2.

Type 1 is caused by an autoimmune disease which destroys the insulin producing beta cells of the pancreas. This results in an absolute deficiency of Insulin and a deficiency of insulin leads to profound hyperglycaemia.

Type 2 is caused by a problem with insulin function. In type 2 the target tissues for Insulin become resistant to it and no longer respond as much as they should when its level goes up in the blood. This leads to a reduction in insulin activity and this leads to hyperglycaemia. The cause of insulin resistance is not understood. However it is usually seen in obese individuals, so obesity likely plays a pivotal role.

Contents:

In parts 1 to 2, we discuss the normal functioning of insulin in glucose homeostasis.

In part 3 we discuss type 1 Diabetes pathophysiology.

In part 4 we discuss type 2 diabetes pathophysiology.

In part 5 we discuss MODY (maturity onset diabetes of the young) which is a genetic form of diabetes and we also discuss gestational diabetes.

In parts 6 to 8 we move on to discuss complications of diabetes. In parts 6 and 7 we discuss diabetic emergencies, starting with diabetic ketoacidosis (DKA) in part 6 and then covering hyperosmolar hyperglycaemic state (HHS) and hypoglycaemia in part 7. In part 8 we look at chronic complications of diabetes, including vasculopathy, retinopathy, nephropathy and neuropathy.

In parts 9 to 11 we discuss the mechanism of action of oral antidiabetic drugs (also called oral hypoglycaemics). Drugs discussed include metformin, the sulphonylureas, the thiazolidinediones, the DPP4 inhibitors and the GLP1 analogues.

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