Overview

• Typically older in onset but increasingly affecting children and teenagers due to rising obesity.
• Onset is insidious (gradual) rather than sudden.
• More common than Type I, accounting for about 90% of diabetes cases.
• Often leads to chronic complications, and sometimes acute complications, if blood glucose is not well-controlled.

Causes and Risk Factors:

• Cells become less sensitive to insulin, meaning that:
  • Cells become insulin-resistant, and
  • Insulin can no longer stimulate cells to insert GLUT4 glucose transporters into cell membranes, leading to low glucose uptake by cells
  • Cells become starved for glucose.
  • Glucose builds up in blood leading to hyperglycemia

• Thought to be triggered by several possible factors:
  • Family history.
  • Obesity.
  • Sedentary lifestyle.
  • Other environmental factors.

Typical Onset:

• Typically older in onset but increasingly affecting children and teenagers due to rising obesity.
• Onset is insidious (gradual) rather than sudden.

Pathophysiology:

• Lack of insulin prevents glucose entry into cells,
  • as cell’s require insulin to insert GLUT4 glucose transporters into their cell membranes.
  • leading to high blood glucose levels (hyperglycemia).
• Cells become starved for glucose, impairing ATP production.
• Excess glucose diffuses into urine, drawing water and causing polyuria, causing
• Dehydration triggers thirst (polydipsia).
• The body responds by breaking down proteins and fats for energy:
  • Gluconeogenesis: Produces glucose from proteins and fats.
  • Lipolysis: Leads to high lipid levels (lipidemia).

Effects on the Body

• Muscle wasting due to protein breakdown.
• High blood lipids increase risk of atherosclerosis.
• Ketone production causes ketosis and potentially ketoacidosis:
  • Blood becomes acidic.
  • Ketones and glucose are excreted in urine (ketonuria and glucosuria).

Signs and Symptoms:

• Polydipsia:  Increased thirst (due to dehydration)
• Polyphagia:  Increased hunger
• Polyuria:  Increased urine volume (due to glucosuria and osmotic diuresis)
  • Electrolyte loss (sodium, potassium) follows water loss.
• Fatigue (due to cell’s reduced ability to uptake glucose)
• Blurred vision (due to retinopathies and diabetic cataracts)
• Slowed healing of wounds (due to cell’s reduced ability to uptake glucose)
• Irritability, slowed reaction, and cognitive impairment (due to neuronal energy deficiency)

Diagnostic Blood Tests:

1. Glycated hemoglobin (A1c) test
   • Measures the percentage of hemoglobin with blood sugar attached.
   • Reflects blood glucose control over 2-3 months.
   • Levels above 6.5% suggest diabetes.
2. Random blood sugar test
   • Blood sample taken randomly, regardless of fasting.
   • Blood glucose above 110 mg/dL indicates abnormality.
3. Fasting blood sugar test
   • Fasting for 12 hours before testing.
   • Normal: <110 mg/dL.
   • Diabetic: >125 mg/dL.
4. Glucose tolerance test:
   • Drink 75g glucose, measure levels at 1 and 2 hours.

Urinalysis:

• Urine tests:
  • Glucosuria: Glucose in urine.
  • Ketonuria: Ketones in urine.
  • Useful for detecting diabetic ketoacidosis.

Treatments:

1. Lifestyle modifications:  Can reverse some issues by improving insulin sensitivity.
   • Healthy diet.
     • • Avoid high-glycemic foods (candies, sugary drinks).
       • Favor complex carbohydrates (fibers, polysaccharides).
   • Regular exercise.
     • • Helps reduce blood glucose by increasing skeletal muscle uptake.
       • Monitor blood sugars during activity.
       • Have carbohydrate snacks available to prevent hypoglycemia.
   • Stress reduction:
     • Stress increases cortisol and glucocorticoids, which raise blood glucose levels.
     • Managing stress helps control glucose.
   • Weight control:
     • Reducing body mass index (BMI) decreases insulin resistance.
2. Oral hypoglycemic agents: Lower high blood glucose by increasing cellular responsiveness or insulin secretion.
   • Oral hypoglycemic agents for type 2
     1. Metformin:
        • • Reduces hepatic gluconeogenesis.
          • Decreases the liver’s production of excess glucose.
     2. Medications to enhance insulin sensitivity:
        • • Improve tissue response to insulin.
3. Insulin injections: Necessary for Type I and often Type II or gestational when beta cells are dysfunctional or destroyed.
   • Administered via injections or continuous insulin pumps.
     • • New technology allows for precise, continual insulin delivery to stabilize blood glucose levels.
     • Note: Insulin cannot be taken orally because stomach acids degrade it.

Complications of Uncontrolled Diabetes and Risk of Long-Term Damage:

• Blood vessel damage leads to:
  • Atheromas formation.
  • Vascular damage affecting organs. and putting person at risk for:
    • Cardiovascular disease: Stroke, heart attack, peripheral vascular disease.
    • Kidney failure (due to nephropathy).
    • Nerve damage: Neuropathy
    • Pregnancy complications: Stillbirths and miscarriages.
    • Increased risk of amputations due to ischemia and gangrene.
    • Eye damage: Leading to blindness due to retinal damage (diabetic retinopathy).
      • Damage to tiny retinal blood vessels produces:
        • Microaneurysms: Weakening and bulging of vessel walls.
        • Hemorrhages: Bleeding into the retina.
        • Neovascularization: Formation of new, fragile blood vessels that can rupture and cause scarring and distortion of retina.
          • Blood and debris can float in the vitreous humor, impairing vision.
        • Macular edema causes swelling in the central retina, resulting in distorted vision.

• Blurred Vision or Vision Loss: 
  • also due to development of diabetic (sugar) cataracts results from hyperglycemia

Summary

• Monitoring and controlling blood glucose minimizes complications.
• Lifestyle modifications and medication optimize management.
• Avoid extremes of hypoglycemia and hyperglycemia during daily activities and exercise.
• Proper diet and regular activity help prevent vascular damage and improve quality of life.