Here is the list of competencies from the exam again- https://www.cdecb.ca/wp-content/uploads/Appendix-A-Competency-Profile-With-Weightings.pdf

Pathophysiology

1.A Describes the pathophysiology and progression of all types of diabetes.

Type 1 diabetes

Type 1 diabetes is an autoimmune disease where the person’s own immune system starts attacking their own beta cells. Beta cells are the only cells in the body that secrete insulin and are located in the pancreas, in the islets of Langerhans. In the early stages, the immune system hasn’t completely destroyed all the beta cells there is some insulin production but there is still hyperglycemia. This is called the honeymoon phase in type 1 diabetes. Often patients have lower insulin requirements at this stage as their own pancreas is still producing insulin. However, as the disease progresses patients will completely lose all their beta cells. Since insulin is necessary for glucose intake into many tissues, type 1 diabetes before the invention of insulin was a slow death sentence. Once the beta cells are totally destroyed endogenous insulin is necessary. Type 1 diabetes is a disease of insulin deficiency.

Another type of cell that is affected in type 1 diabetes, along with the beta cells, are the alpha cells. The alpha cells secretes glucagon which reverses the effect of insulin. Glucagon causes blood sugars to go up. If a person skips a meal or fasts, the alpha cells produce glucagon to prevent the sugars from falling too low. Since the brain runs on sugar, hypoglycemia can cause symptoms such as confusion, weakness and dizziness. The alpha cells work with beta cells to keep sugars in a narrow range. Without the beta cells, the alpha cells become dysfunctional. This is why people with type 1 diabetes are more susceptible to hypoglycemia and sometimes have worse episodes of hypoglycemia than people with type 2.

LADA can be viewed as slow type 1 diabetes. The beta cells will eventually get destroyed by the immune system but it just happens later in life and the process is slower.

Type 2 diabetes

With type 2 diabetes, the beta cells slowly become dysfunctional from a variety of factors such as insulin resistance, glucose toxicity, inflammation, and others factors that are not understood. Obesity is present in 80-90% of people with type 2 diabetes. Obesity causes insulin resistance. At first the beta cells overproduce insulin to overcome the insulin resistance. At this stage there is significant hyperinsulinemia (insulin overproduction) but there is no hyperglycemia (you could test a person’s sugars at this point and it would be normal) as the beta cells are producing enough insulin to overcome the insulin resistance. The beta cells eventually tire out leading to beta cell dysfunction. At first, sugars gradually go up leading to pre-diabetes. Some studies show that beta cell dysfunction can pre-date the diagnosis by years, perhaps even a decade or more. Eventually beta cell dysfunction progresses and medications are needed. Given enough time, patients will eventually need insulin once all their beta cells stop working. However, in real life practice, with the advent of GLP-1 analogs, which preserve beta cells, I have started less and less people on insulin in my practice.

Gestational Diabetes

Any form of diabetes plus pregnancy = gestational diabetes. When the pregnancy is over then the type of diabetes is no gestational diabetes and the type goes back to whatever they had before. The placenta produces a number of counter-regulatory hormones that cause insulin resistance. If the beta cells are not functional enough to produce enough insulin to overcome the insulin resistance, then hyperglycemia occurs. Insulin resistance drops rapidly once the placenta is gone.

Monogenic Diabetes

Monogenic diabetes is a name for many forms of diabetes which are all caused by genetic defects. The defects leads to impaired ß cell development, impaired ß cell glucose sensing, or defects in the ATP K+ channels in ß cells. The classic signs of MODY are young age of diagnosis, family history of diabetes in an autosomal dominant pattern of transmission, and insulin independence.