Diabetes Mellitus Flashcards
What is Normal insulin metabolism
Produced by B -cells in islets of Langerhans of Pancreas
Released continuously into bloodstream in small increments with larger amounts released after food
Stabilizes glucose level in range of 70 to 120 mg/dL
Normal Insulin Secretion
Type 1 Diabetes Mellitus Etiology and Pathophysiology
Autoimmune destruction of β-cells
Total absence of insulin
Genetic predisposition and viral exposure
Idiopathic diabetes
Latent autoimmune diabetes in adults (LADA)- Older adult who are not obese
Type 1 Diabetes Mellitus Onset of Disease
Autoantibodies are present for months to years before symptoms occur
Manifestations develop when pancreas can no longer produce insulin—then rapid onset with ketoacidosis
Necessitates insulin
Patient may have temporary remission after initial treatment
Type 2 Diabetes Mellitus
Formerly known as adult-onset diabetes (AODM) or non–insulin-dependent diabetes (IDDM)
Most prevalent type (90% to 95%)
Risk factors: overweight, obesity, advancing age, family history
Type 2 Diabetes Mellitus Etiology and Pathophysiology
Pancreas continues to produce some endogenous insulin
Insulin insufficient or poorly utilized
Multiple etiologic factors
Obesity is greatest risk factor
Genetic component increases insulin resistance and obesity
Four major metabolic abnormalities
Insulin resistance
Decreased insulin production by pancreas
Inappropriate hepatic glucose production
Altered production of hormones and cytokines by adipose tissue (adipokines- They interfere with absorption of glucose)
Type 2 Diabetes Mellitus Onset of Disease
Gradual onset
Hyperglycemia may go many years without being detected
Many times discovered with routine laboratory testing
Altered Mechanisms in Type 1 and Type 2 Diabetes
Type 2 Classic symptoms
Polyuria (frequent urination)
Polydipsia (excessive thirst)
Polyphagia (excessive hunger)
Weight loss
Weakness
Fatigue
Type 2 Nonspecific symptoms
Classic symptoms of type 1 may manifest
Fatigue
Recurrent infection
Recurrent vaginal yeast or candidal infection
Prolonged wound healing
Visual changes
Diagnostic Studies
Hemoglobin A1C level: 6.5% or higher
Fasting plasma glucose level: higher than 126 mg/dL
Two-hour plasma glucose level during OGTT: 200 mg/dL (with glucose load of 75 g)
Classic symptoms of hyperglycemia with random plasma glucose level of 200 mg/dL or higher
Fructosamine
Reflects glucose levels past 1-3 weeks
Autoantibodies
Hemoglobin A1C test
Glycosylated hemoglobin: reflects glucose levels over past 2 to 3 months
Used to diagnose, monitor response to therapy, and screen patients with prediabetes
Goal: less than 6.5%
Goals of diabetes management
Decrease symptoms
Promote well-being
Prevent acute complications
Delay onset and progression of long-term complications
Need to maintain blood glucose levels as near to normal as possible
Patient teaching
Nutritional therapy
Drug therapy
Exercise
Self-monitoring of blood glucose
Diet, exercise, and weight loss may be sufficient for patients with type 2 diabetes
All patients with type 1 require insulin
Insulin Categorized according to onset, peak action, and duration
Rapid-acting
Short-acting
Intermediate-acting
Long-acting
Examples of rapid acting
Humalog
Novalog
Apidra
Examples of short acting
Humalin R
Novalin R
Examples of Intermediate Acting
NPH
Humulin N
Novolin N
Examples of long acting
Lantus
Levemir
Rapid acting onset, peak, duration
onset: 10-30 minutes
peak: 30 minutes- 3 hours
duration: 3-5 hours
Short acting onset, peak, duration
Onset: 30 min- 1 hour
Peak: 2-5 hours
Duration: 5-8 hours
Intermediate acting onset, peak, duration
Onset: 1.5-4 hours
Peak: 4-12 hours
Duration: 12-18 hours
Long acting onset, peak, duration
Onset: 0.8-4 hours
Peak: No pronounced peak
Duration: 24+ hours
Rapid-acting (bolus)
Lispro, aspart, glulisine
Onset of action 15 minutes
Injected within 15 minutes of mealtime
Short-acting (bolus)
Regular with onset of action 30 to 60 minutes
Injected 30 to 45 minutes before meal
Onset of action 30 to 60 minutes