Show Menu

Diabetes Mellitus Cheat Sheet (DRAFT) by

Diseases and their pathophysiology

This is a draft cheat sheet. It is a work in progress and is not finished yet.


Insulin is produced in the Islet of Langerhans of the pancreas
Normal blood glucose: 4 to 6 mmol/L
Release of insulin leads to the transp­ort­ation of glucose from the bloods­tream into the cell.
Rise of insulin leads to storage of glycogen in the liver and inhibits glucon­eog­enesis


A disorder of glucose metabolism related to absence or deficient insulin supply or poor utiliz­ation of insulin.


Type 1
Type 2
Primary defect
Absent or minimal insulin production due to autoimmune process
Insulin resist­ance, decreased insulin production and alteration in production of adipokines
Common in young people but can occur at any age
Greater than 35 but can occur at any age
Type of onset
Abrupt signs and symptoms
Insidious and can go undiag­nosed for years
Nutrit­ional Status
Thin, normal and Obese
Obese oe normal
Thirst, Polyuria, Polyph­agia, Fatigue, Weight loss
Frequently none, fatigue, recurrent infections
Required for all
Summary of Diabetes Mellitus


AKA Impaired glucose tolerance or impaired fasting glucose
Noted when fasting glucose is higher than normal but lower than DM.
Usually do not have symptoms however, the A1c should be tested regularly
Reducing risk by eating healthy, mainta­ining a healthy weight and exercising regularly

Secondary Diabetes

DM caused by another medical condition or a treatment of a medical condition.

Type 1 Diabetes Mellitus

This occurs from the gradual destru­ction of pancreatic beta cells by an autoimmune process either directly or indire­ctly.
It can either be Type 1a (immune) or Type 1b (idiop­athic)
Manife­sta­tions occur when the pancreas can no longer produce insulin which justifies the abrupt onset.
The classic symptoms are polydi­psia, polyuria and polyphagia
Outside supply of insulin is required or diabetic ketoac­idosis can be developed
Other symptoms include weakness and fatigue and change in visual acuity.
Polydipsia is as a result of osmotic concen­tration of glucose in the body.
Polyphagia is caused by cellular malnou­ris­hment from lack of energy which means the cells do not get glucose to convert to ATP.
Weight loss occurs the body turns to other sources such as fat and protein for strength.
Weakness and fatigue from energy loss

Diagno­stics Studies

Glycalated Hemoglobin A1c greater than or equals to 6.5%
Fasting blood glucose level greater than or equals to 7.0 mmol/L
Random plasma glucose greater than or equal to 11.1 mmol/L
Two hour plasma glucose in a 75G OGTT greater than or equal to 11.1mmol/L
*A1c test indicates the level of glucose over a particular time. It should be done every 3-6 months.

Gestat­ional Diabetes

Occurs during pregnancy.
Detected between 24 and 28 weeks of pregnancy,

Type 2 DM

Most powerful risk factor is obesity.
Endogenous insulin is still produced by the body. However, the insulin is either insuff­icient, poorly utilized or both.
There are four major factors that play a role in the develo­pment of DM2.
1. Insulin resistance as a result of unrece­ptive receptors, insuff­icient receptors or both. Both hyperg­lyc­aemia and hyperi­nsu­linemia occurs as the body tries to decrease glucose by increasing insulin produc­tion,
2. A signif­icant decrease in the ability of the pancreas to produce insulin.
3. Inappr­opriate glucose production by the liver which leads to increased glucagon production which stimulates the glucose production in liver. In total increasing sugar level.
4. Alteration hormones and cytokines production by adipose tissues.
Onset of disease is gradual.
Diabetic ketoac­idosis compli­cation can be prevented with a sufficient endogenous supply. However osmotic and electr­olyte loss can become severe and cause hypero­smolar and hyperg­lyc­aemic state.
Manife­sta­tions Nonspe­cific and not limited to fatigue, recurrent infect­ions, prolonged wound healing, visual acuity changes, and painful neuropathy of the feet.

Diabetic ranges