Diabetes Mellitus: Types and Pathophysiology

Study Notes

Diabetes mellitus is a group of metabolic disorders characterized by high blood sugar levels (hyperglycemia) due to defects in insulin secretion, insulin action, or both.
Classified into two main types:
- Type 1 diabetes (T1D): beta-cell destruction, usually leading to absolute insulin deficiency
- Type 2 diabetes (T2D): insulin resistance, impaired insulin secretion, and increased glucose production

Normal glucose metabolism:
- Insulin stimulates glucose uptake in cells
- Glucagon stimulates glucose release from storage
In diabetes:
- Insulin deficiency or resistance leads to hyperglycemia
- Increased glucose production in the liver
- Impaired glucose uptake in peripheral tissues

Type 1 diabetes:
- Genetic predisposition
- Autoimmune destruction of beta-cells
Type 2 diabetes:
- Obesity and physical inactivity
- Insulin resistance
- Family history
- Age (>45 years)
- Ethnicity (African American, Hispanic, American Indian)

Diagnostic criteria:
- Fasting plasma glucose ≥ 126 mg/dL
- 2-hour plasma glucose ≥ 200 mg/dL during an oral glucose tolerance test
- Hemoglobin A1c (HbA1c) ≥ 6.5%
Additional tests:
- Urine test for ketones (in T1D)
- Autoantibody tests (in T1D)

Lifestyle modifications:
- Healthy diet
- Regular physical activity
- Weight loss (if overweight)
Pharmacological interventions:
- Insulin therapy (in T1D and some T2D cases)
- Oral antidiabetic agents (in T2D)
- Injectable medications (in T2D)
Monitoring and surveillance:
- Regular blood glucose monitoring
- HbA1c monitoring
- Screening for complications

Diabetes mellitus is a group of metabolic disorders characterized by high blood sugar levels (hyperglycemia) due to defects in insulin secretion, insulin action, or both.
Classified into two main types: Type 1 diabetes (T1D) and Type 2 diabetes (T2D).

In normal glucose metabolism, insulin stimulates glucose uptake in cells, and glucagon stimulates glucose release from storage.
In diabetes, insulin deficiency or resistance leads to hyperglycemia, increased glucose production in the liver, and impaired glucose uptake in peripheral tissues.

Type 1 diabetes is caused by genetic predisposition and autoimmune destruction of beta-cells.
Type 2 diabetes is caused by obesity and physical inactivity, insulin resistance, family history, age (>45 years), and ethnicity (African American, Hispanic, American Indian).

Common symptoms of diabetes include polyuria (excessive urination), polydipsia (excessive thirst), polyphagia (excessive hunger), fatigue, blurred vision, and slow healing of cuts and wounds.
Diabetes may be asymptomatic in early stages.

Diagnostic criteria for diabetes include fasting plasma glucose ≥ 126 mg/dL, 2-hour plasma glucose ≥ 200 mg/dL during an oral glucose tolerance test, and hemoglobin A1c (HbA1c) ≥ 6.5%.
Additional tests for diabetes diagnosis include urine test for ketones (in T1D) and autoantibody tests (in T1D).

Acute complications of diabetes include diabetic ketoacidosis (DKA) and hypoglycemia.
Chronic complications of diabetes include microvascular complications (retinopathy, nephropathy, neuropathy) and macrovascular complications (cardiovascular disease, peripheral artery disease, stroke).

Lifestyle modifications for diabetes management include healthy diet, regular physical activity, and weight loss (if overweight).
Pharmacological interventions for diabetes management include insulin therapy (in T1D and some T2D cases), oral antidiabetic agents (in T2D), and injectable medications (in T2D).
Monitoring and surveillance for diabetes management include regular blood glucose monitoring, HbA1c monitoring, and screening for complications.