Diabetes type 1

Risk Factors
1. Environment
  1. Viral infection
    1. Enteroviruses, coxsackie virus B
      1. Trigger autoimmune responses via structural homology between viral structures and B-cells antigens
        β-cell destruction
        Lack of insulin production
      2. Direct cytolytic effect
2. Genetic
  1. Risk genetic loci
    1. Lymphocyte-defined HLA-D antigens
      1. HLA-DRB1
    2. HLA-DR4
      1. DQB1*0302
      2. HLA-DRB1*04
    3. HLA class II DR3
      1. HLA-DRB1*0301
      2. DQB1*0201
  2. Family History
3. Birth Weight
  1. >4500 g
Complications
1. Short term
  1. Hypoglycemia
    1. Low blood glucose (< 60 mg/dl) due to high insulin intake or use of certain oral medications
      1. Sweaty, confuse, dizzy, light headedness, double vision
        Fruit juice, dextrose, hard candies, honey or IV D50 (If unconscious)
  2. Ketoacidosis (DKA)
    1. Lack of insulin production causes liver to break down fat for energy
      1. Ketones accumulation and acid-base imbalance
        Nausa & vomit, excessive thirst, hyperglycemia, & Kussmaul breathing (deep long rapid breath)
2. Long term
  1. Microvascular complications
    1. Induce by chronic hyperglycemia via production of advance glycation end products (AGEs), creation of a proinflammatory microenvironment, & induction of oxidative stress
      1. Retinopathy
        Regular comprehensive eye examination and dilation
        Retina blood vessels are damaged
        Blindness, Cataracts, Glucoma
      2. Nephropathy
        Annual screening for microalbuminuria Treatment: ACE inhibitor or ARB (Antiotensin II receptor blocker)
        Damage of tiny blood vessels that filter waste from blood
        Dialysis and/or kidney transplant
      3. Neuropathy
        Excess sugar injures the wall of capillaries that nourish nerves
        Tingling, numbness, burning or pain in limbs
        Annual screening for distal symmetric polyneuropathy
  2. Macrovascular complications
    1. Atherosclerosis
      1. Narrowing of arterial walls via large blood vesseles plaque build up
        Cardiovascular disease, Stroke
        Regular blood pressure monitoring (goal <130/80 mmHg), Lipid testing annually (goal LDL < 100 mg/dl, HDL < 50 mg/dl, fasting triglycerides < 150 mg/dl ) , Asprin therapy (75-162 mg/day)
Pathogenesis
1. Islet cell autoantibodies attack pancreatic β-cells
  1. β-cells destruction
    1. Little or no insulin production
      1. No glucose entering cells
        Blood glucose control is lost
        Increase glucose in blood and urine
        Hyperglycemia
Diagnosis
1. Fasting plasma glucose (FPG)
  1. >126 mg/dL (7.0 mmol/L)
2. Glycated hemoglobin (A1C) test
  1. greater preanalytical stability, no fasting required
  2. Limited availability in certain regions
  3. A1C level >6.5%
3. 2-h plasma glucose (2-h PG) value after a 75-g oral glucose tolerance test (OGTT)
  1. >200mg/dL(11.1mmol/L)
4. Random blood sugar test
  1. Blood sugar level >11.1mmol/L)
Treatments
1. Insulin pump
  1. It is a device to deliver rapid acting insulin to the body through the catheter
    1. Advantages: Increase blood sugar control- reduction of hypoglycemia- ease of adjusting insulin doses with exercise or travel
    2. Disadvantages: skin infection, ketoacidosis (due to pump dysfunction), expense, weight gain
2. Insulin injection
  1. Rapid acting (Lispro)
    1. Onset 15 Mins, peak at 30-60 mins, last for 5 hrs
  2. Short acting (Regular)
    1. Onset 60 mins, Peak at 2-3 hrs, last for 6 hrs
  3. Intermediate acting (NPH)
    1. Onset 1-4 hrs, peak at 8-12 h, last for 18-24 hrs
  4. long acting (Glargine)
    1. Onset 6 hrs, peak at 14- 24 hrs, last for 36 hrs
  5. Side effect
    1. Allergic respond to animal derived insulin
    2. Somogyi phenomenon
      1. Taking too much insulin before bed leads to hypoglycemia
        In the early morning Hyperglycemia may occur due to hormonal secretion such as glucocorticoid according to circadian rhythms
        More food intake in the evening, less insulin dose at bedtime
    3. Hypoglycemia
    4. Dawn phenomenon
      1. Abnormally early morning (2 am-8 am) increases in blood glucose due to the random release of cortisol & growth hormones
        Less carb intake at bedtime, adjust insulin dose or medication
    5. Lipodystrophy
      1. Atrophy of subcutaneous tissue which may result in poor absorption of insulin
        Rotation of insulin injection site
3. Nutritional therapy
  1. Fat intake less than 7% & sugar intake less than 10%
  2. Plate Method
    1. Helps patient see the proportion of vegetable, starch and meat that should fill a 9” inch plate
      1. 25% protein + 25% grain and starchy food + 50% non starchy vegetable
  3. Higher intake of fruit & vegetable > 5 serving a day decrease the risk of CV
4. Exercise
  1. Increase insulin receptor site
  2. Decrease blood sugar level
  3. Help loss weight
  4. Best done after meal, small carb snack can be eaten every 30 mins, monitor blood glucose before, during and after exercise
5. Self monitoring of blood glucose
  1. Early detection on episodic hyperglycemia and hypoglycemia
  2. Adjustment of a therapeutic regimen in respond to blood glucose level ( between 4 to 6 mmol/L) by altering dietary intake, physical activity & insulin doses intake
Clinical manifestations
1. Polyuria
2. High risk of infection
  1. Hyperglycemic environment favors immune dysfunction and encourage bacterial survival
3. Unexplained weight loss
4. Polydipsia
5. Fatigue/weakness
6. Blurred vision
7. Polyphagia
8. Slow healing of cuts and grazes
9. Ketoacidosis- first manifestation of the disease in some patients

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Diabetes type 1

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