EPIDEMIOLOGY, PATHOPHYSIOLOGY, AND CLINICAL PRESENTATION OF DIABETES


I. Risk factors for NIDDM:

  1. NIDDM has more of a genetic component than IDDM
  1. RR 2.0 with one first-degree relative, 4.0 with two
  2. More common in African-Americans and Native Americans
  1. Obesity, esp. upper-body, and sedentary lifestyle
  2. Age
  3. High progesterone states, e.g. pregnancy
  4. Diet: low fiber and high "dietary glycemic index" (higher with simpler carbohydrates and refined starches) associated with RR 1.47 of developing NIDDM after adjustment for age, MDI, smoking, exercise, family hx, alcohol and total caloric intake in 65,000 prospectively studied female RN's age 40-65 over 6y of f/u (branch of Nurses' Health Study, JAMA 277:472, 1997; comparing lowest to highest quintiles)

II. Pathophysiology of NIDDM

  1. Peripheral insulin resistance (either due entirely to excess fat tissue and hyperglycemia or to intrinsic insulin resistance in muscle and liver) with relative insulinopenia, though may have actually high insulin levels at some point; in late disease, can get absolute insulinopenia ("burnt-out" pancreas)
  2. Some complications may be due to hyperglycemia (neuropathy, retinopathy); some to hyperinsulinemia (cardiovascular complications)
  3. Glucose intolerance gradually progresses to full-blown diabetes over years

III. Secondary causes

  1. Pancreatic disease
  2. Curhing's sd.
  3. Acromegaly
  4. Pheo
  5. Hemochromatosis
  6. Drugs worsening NIDDM:
  1. B-blockers (decrease insulin secretion)
  2. Thiazides (decrease insulin secretion)
  3. H2-blockers
  4. Niacin
  5. OCPs
  6. Ca-blockers
  7. Pentamidine
  8. Phenytoin
  9. Corticosteroids

IV. Clinical presentation

  1. Weight loss/failure to grow normally
  2. Loss of appetite
  3. Polyuria
  4. Fatigue
  5. Polydipsia
  6. Emot'l disturbance
  7. Abd. cramps
  8. Leg cramps
  9. In kids: enuresis, behavioral disturbance