Diabetes type 1

Diabetes type 1

1. Risk Factors

   • Environment
     • Viral infection
       • Enteroviruses, coxsackie virus B
         • Trigger autoimmune responses via structural homology between viral structures and B-cells antigens
           • β-cell destruction
             • Lack of insulin production
         • Direct cytolytic effect
   • Genetic
     • Risk genetic loci
       • Lymphocyte-defined HLA-D antigens
         • HLA-DRB1
       • HLA-DR4
         • DQB1*0302
         • HLA-DRB1*04
       • HLA class II DR3
         • HLA-DRB1*0301
         • DQB1*0201
     • Family History
   • Birth Weight
     • >4500 g

2. Complications

   • Short term
     • Hypoglycemia
       • Low blood glucose (< 60 mg/dl) due to high insulin intake or use of certain oral medications
         • Sweaty, confuse, dizzy, light headedness, double vision
           • Fruit juice, dextrose, hard candies, honey or IV D50 (If unconscious)
     • Ketoacidosis (DKA)
       • Lack of insulin production causes liver to break down fat for energy
         • Ketones accumulation and acid-base imbalance
           • Nausa & vomit, excessive thirst, hyperglycemia, & Kussmaul breathing (deep long rapid breath)
   • Long term
     • Microvascular complications
       • Induce by chronic hyperglycemia via production of advance glycation end products (AGEs), creation of a proinflammatory microenvironment, & induction of oxidative stress
         • Retinopathy
           • Regular comprehensive eye examination and dilation
           • Retina blood vessels are damaged
             • Blindness, Cataracts, Glucoma
         • 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
         • Neuropathy
           • Excess sugar injures the wall of capillaries that nourish nerves
             • Tingling, numbness, burning or pain in limbs
           • Annual screening for distal symmetric polyneuropathy
     • Macrovascular complications
       • Atherosclerosis
         • 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)

3. Pathogenesis

   • Islet cell autoantibodies attack pancreatic β-cells
     • β-cells destruction
       • Little or no insulin production
         • No glucose entering cells
           • Blood glucose control is lost
             • Increase glucose in blood and urine
               • Hyperglycemia

4. Diagnosis

   • Fasting plasma glucose (FPG)
     • >126 mg/dL (7.0 mmol/L)
   • Glycated hemoglobin (A1C) test
     • greater preanalytical stability, no fasting required
     • Limited availability in certain regions
     • A1C level >6.5%
   • 2-h plasma glucose (2-h PG) value after a 75-g oral glucose tolerance test (OGTT)
     • >200mg/dL(11.1mmol/L)
   • Random blood sugar test
     • Blood sugar level >11.1mmol/L)

5. Treatments

   • Insulin pump
     • It is a device to deliver rapid acting insulin to the body through the catheter
       • Advantages: Increase blood sugar control- reduction of hypoglycemia- ease of adjusting insulin doses with exercise or travel
       • Disadvantages: skin infection, ketoacidosis (due to pump dysfunction), expense, weight gain
   • Insulin injection
     • Rapid acting (Lispro)
       • Onset 15 Mins, peak at 30-60 mins, last for 5 hrs
     • Short acting (Regular)
       • Onset 60 mins, Peak at 2-3 hrs, last for 6 hrs
     • Intermediate acting (NPH)
       • Onset 1-4 hrs, peak at 8-12 h, last for 18-24 hrs
     • long acting (Glargine)
       • Onset 6 hrs, peak at 14- 24 hrs, last for 36 hrs
     • Side effect
       • Allergic respond to animal derived insulin
       • Somogyi phenomenon
         • 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
       • Hypoglycemia
       • Dawn phenomenon
         • 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
       • Lipodystrophy
         • Atrophy of subcutaneous tissue which may result in poor absorption of insulin
           • Rotation of insulin injection site
   • Nutritional therapy
     • Fat intake less than 7% & sugar intake less than 10%
     • Plate Method
       • Helps patient see the proportion of vegetable, starch and meat that should fill a 9” inch plate
         • 25% protein + 25% grain and starchy food + 50% non starchy vegetable
     • Higher intake of fruit & vegetable > 5 serving a day decrease the risk of CV
   • Exercise
     • Increase insulin receptor site
     • Decrease blood sugar level
     • Help loss weight
     • Best done after meal, small carb snack can be eaten every 30 mins, monitor blood glucose before, during and after exercise
   • Self monitoring of blood glucose
     • Early detection on episodic hyperglycemia and hypoglycemia
     • 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

6. Clinical manifestations

   • Polyuria
   • High risk of infection
     • Hyperglycemic environment favors immune dysfunction and encourage bacterial survival
   • Unexplained weight loss
   • Polydipsia
   • Fatigue/weakness
   • Blurred vision
   • Polyphagia
   • Slow healing of cuts and grazes
   • Ketoacidosis- first manifestation of the disease in some patients

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