Diabetes Mellitus Type I

Diabetes Mellitus Type I

1. Etiology and Pathophysiology

   • Most often occurs in people under 30. Peak onset usually occurs between ages 11 and 13
     • Accounts for 5-10% of those with diabetes
   • Mainly a disorder of glucose metabolism
     • Absent or insufficient supply of endogenous insulin
       • Insulin promotes glucose transport from blood stra to cytoplasm of cells
         • Insulin stimulates storage of glucose as glycogen in liver and muscle
           • Anabolic hormone
           • Increases protein synthesis
           • Enhances fat deposition
           • Skeletal muscle & Adipose tissue have specific receptors for insulin and are considered insulin dependent
       • Pancreatic beta-cells release proinsulin
         • Proinsulin is made up of two polypeptide chains; A & B. Chain C links chains A & B, insulin forms when chain C is cleaved off
           • Serum levels of C are good indicators of pancreatic function
         • Pancreatic beta-cells are progressively destroyed, becoming reduced to 80-90% of normal function.
   • Causes
     • Beta cell destruction usually leading to absolute insulin deficiency
       • Type 1A Immune mediated
         • Immune mediated destruction of beta cells. occurs more commonly in children and adolescents.
           • Genetic predisposition; an environmental triggerring event, such as an infection and a T-lymphocyte-mediated hypersensitivity reaction against beta-cell antigens.
           • Research
             • MHC genes on chromosome 6 that encode human leukocyte antigen (HLA)-DQ and HLA-DR
               • MHC susceptibility genes regulating beta cell replication and function has been identified on chromosome 11
                 • Type 1A diabetes-associated antibodies may exist for years before onset of hyperglycemia
                   • Antibody Types
                     • Insulin autoantibodies (IAAs)
                     • Islet Cell autoantibodies
                       • including antibodies directed at other islet autoantigens
                       • Glutamic acid decarboxylase
                       • Tyrosine phosphatase IA-2
             • Results from an interaction between the environment and genetics.
               • Led to research methods directed at prevention and early control of the disease.
       • Type 1B Idiopathic
         • Cases of beta cell destruction with no evidnce of autoimmunity present. Only a small number of people fall into this category; most are of Asian and Africa descent
           • Individuals have episodic DKA due to varying degrees of insulin deficiency with periods of absolute insulin deficiency that may come and go.

2. Management

   • Exogenous Insulin
     • Always a necessity for type 1 diabetes. Clients develop diabetic ketoacidosis without insulin
     • Honeymoon period; when a client first starts insulin treatment, little is required because the beta-cell mass remains sufficient for glucose control. Beta-cell degradation continues and eventually more insulin is required.
     • Rapid,short-acting (bolus), taken before meals.
     • Intermediate, or long-acting (basal), released over 24 hours.
     • Subcutaneous Injection
       • Abdomen is preferred site (fastest absorption)
       • Rotate area on injection site
     • Problems: Somogyi effect, Dan phenomenon, Hypoglycemia, Allergic reaction, Lipodystrophy
   • Goals: Decrease symptoms, promote well-being, prevent acute complications, delay onset and progression of long-term complications
   • Insulin Pump
     • Continuous subcutaneous infusion
     • Battery-operated device
   • Nutritional Therapy
     • Equal distribution of carbs through meals
     • Intermeal/bedtime snacks often necessary
     • Supplement 20g/h carbs for moderate physical activity
     • Usual food intake balanced with insulin
   • Exercise
     • Important for overall health and wellness
     • Balance exercise with diet and insulin
       • Prevents glucose imbalance
   • Patient Teaching
     • Self-monitor blood glucose
     • Self-inject insulin
     • Obtain A1C test every 3-6 months
     • Know signs and symptoms of hypo- and hyperglycemia
     • Carry some form of glucose at all times
     • Instruct family member on how to give injections
     • Learn how to exercise and food affect blood glucose

3. Onset

   • Long pre-clinical period
     • Manifestations develop when pancreas can no longer produce insulin
       • Signs and Symptoms
         • Impending/actual ketoacidosis
         • Recent and sudden weight loss
         • Polydipsia, polyphagia, polyuria

4. Diagnostics

   • Fasting plasma glucose test
     • No caloric intake for at least 8 hours.
     • Confirmed with repeated testing on different days
     • High day-to-day variability
     • Mean normal glucose level is 5.5 mmol/L. Greater than or equal to 7 mmol/L indicates diabetes
   • Casual blood glucose
     • Non-fasting
     • Assumes recent meal, therefore higher diagnostic levels of plasma glucose
     • Normal range is 4.4-7.8 mmol/L. Greater than or equal to 11 mmol/L & one or more classic symptoms indicates diabetes
     • Affected by: Food, stress, medications, exercise.
   • Testing for antibodies to GAD or IA-2 and for IAAs using sensitive assays can be used to identify new cases of type 1 diabetes.
   • Hemoglobin A1C
     • CDA Recommended
     • Convenient (no fasting required)
     • Tests for amount of glucose attached to hemoglobin molecules
     • Tests overall glucose over 120 days
     • Normal range is under 6%. Greater than or equal to 6.5% is an indication of diabetes.
   • Oral Glucose Tolerance Test
     • Fasting blood glucose is taken first as baseline
     • Patient drinks solution containing 75g-100g glucose
     • Blood sample redrawn after 2 hours
     • Tests speed at which glucose is cleared from blood
     • Greater than or equal to 11mmol/L after 2 hours indicates diabetes

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