TYPE 2 DIABETES [T2D]

1. Pathophysiology

1.1. Impaired insulin secretion in the pancreas, B cells unable to keep up with insulin demand causing them to fail

1.1.1. Insulin resistance contributes to increased glucose production in the liver

1.1.1.1. Increased glucose

1.1.1.1.1. Malfunction in feedback loops leads to receptor and post receptor defects

1.2. If insulin resistance and B cell dysfunction are both present hyperglycaemia is escalated

2. Signs and Symptoms

2.1. Insulin resistance

2.1.1. Hirsutism

2.1.2. Central obesity

2.1.3. Skin tags

2.1.4. Acanthosis nigricans

2.2. Blurred vision

2.3. Lethargy, polyuria, polydipsia

2.4. Weight loss

2.5. Fequent fungal or bacterial infections

2.6. Loss of sensation (ie touch, vibration, cold)

2.7. Poor wound healing

2.8. High BP

2.9. Mood swings

2.10. Excessive thirst

2.11. Frequent urination

3. Epidemiology

3.1. Lower socioeconomic backgrounds

3.2. Gender distribution is equal

3.3. Global

3.3.1. Burden of suffering is 751 DALY's per 100,000

3.3.2. Prevalence to increase 6059 to 7079 individuals per 100,000 by 2030

3.3.3. Affects 6.28 of world population

3.3.3.1. 4.4% of those aged 15–49 years,

3.3.3.2. 15% of those aged 50–69

3.3.3.3. 22% of those aged 70+

3.4. Australia

3.4.1. Aboriginal and Torres Strait Islander people

3.4.1.1. 4 times more likely to have diabetes than non-Indigenous Australians

3.4.1.2. Direct or indirect cause of 20% of death

3.4.1.3. Children and adolescents rates are 6–20 times higher than non-Indigenous youth

4. History/Progression

4.1. History/people at high risk

4.1.1. Lack of PA

4.1.2. Poor diet

4.1.2.1. High calorie diet with large amounts of fats and carbohydrates

4.1.3. Genetic predisposition

4.1.3.1. Family hx of T2D due to genetic mutations

4.1.4. Ethnicity

4.1.4.1. Black African, African Caribbean and South Asian have a higher risk of developing T2D

4.1.5. Overweight

4.1.6. Gastrointestinal diabetes

4.1.6.1. Women with hx have a seven-fold elevated risk of developing T2D in the future

4.1.7. Age

4.1.7.1. Over 55

4.2. Progression

4.2.1. High risk people

4.2.1.1. 5-10% develop diabetes anually

4.2.1.1.1. 3/4 of people with impaired fasting glucose or impaired glucose tolerance will develop T2D over their lifetime

4.2.1.2. If glucose metabolism can return to normal due to interventions or spontaneously, they have half the risk of developing T2D

4.2.2. Insulin resistance/pre diabetes

4.2.2.1. Increase amounts of insulin produced

4.2.2.2. Decline in B cell function as early as 12 years before diagnosis

4.2.2.3. Unable to maintain glucose homeostasis

4.2.3. T2D

4.2.3.1. Progressive loss of B cell function

4.2.3.2. No complications

4.2.3.3. Possible hyperglycaemia

4.2.4. T2D with vascular complications

4.2.4.1. Cardiovascular disease

4.2.4.2. Atherosclerosis

4.2.4.3. Dyslipidaemia

4.2.4.4. Endothelial disease

4.2.4.5. Hyperglycaemia

5. Diagnostics

5.1. T2D

5.1.1. Conventional

5.1.1.1. Examinations/tests

5.1.1.1.1. Symptomatic patients

5.1.1.1.2. Asymptomatic patients

5.1.1.2. Treatment/Management

5.1.1.2.1. Create goals of

5.1.1.2.2. Pharmacotherapy

5.1.1.2.3. Surgical interventions

5.1.2. Osteopathic

5.1.2.1. Physical examinations/tests

5.1.2.1.1. Case Hx

5.1.2.1.2. Medical Hx

5.1.2.1.3. Systems

5.1.2.1.4. Examinations

5.1.2.2. Treatment/management

5.1.2.2.1. Treatment

5.1.2.2.2. Management

5.2. Osteoarthritis (OA)

5.2.1. Conventional

5.2.1.1. Examinations/tests

5.2.1.1.1. Diagnosis without further investigation

5.2.1.1.2. Case history

5.2.1.1.3. Outcome measures

5.2.1.1.4. Tests

5.2.1.1.5. Examination

5.2.1.2. Treatment/management

5.2.1.2.1. Non-pharmacological

5.2.1.2.2. Pharmacological

5.2.2. Osteopathic

5.2.2.1. Examinations

5.2.2.1.1. Same as T2D

5.2.2.2. Management

5.2.2.2.1. Create SMART goals

5.2.2.2.2. Same as conventional management

5.2.2.3. Treatment

5.2.2.3.1. Lymphatic drainage to whole body

5.2.2.3.2. Muscle energy techniques (MET)