Chapter 19 Diabetes Type 1
Insulin-Dependent
PATHOPHYSIOLOGY
Type 1 diabetes, previously called insulin-dependent diabetes mellitus (IDDM), or juvenile-onset diabetes, is an autoimmune disease that destroys the beta cells of the pancreas, which results in insulin deficiency. Complete insulin deficiency necessitates the use of exogenous insulin to promote appropriate glucose use and to prevent complications related to elevated glucose levels, such as diabetic ketoacidosis and death.
Insulin is necessary for the following physiologic functions: (1) to promote the use and storage of glucose for energy in the liver, muscles, and adipose tissue; (2) to inhibit and stimulate glycogenolysis or gluconeogenesis, depending on the body’s requirements; and (3) to promote the use of fatty acids and ketones in cardiac and skeletal muscles. Insulin deficiency results in unrestricted glucose production without appropriate use, which leads to hyperglycemia and increased lipolysis and production of ketones and, in turn, to hyperlipidemia, ketonemia, and ketonuria. The insulin deficiency also heightens the effects of the counterregulatory hormones—epinephrine, glucagon, cortisol, and growth hormone (see Box 19-1 for these hormones’ functions).
INCIDENCE
1. Type 1 diabetes accounts for the majority of new diabetes cases in youth.
2. The onset most commonly occurs around puberty (ages 10–14 years).
3. Among preschool-aged children, the disease is more commonly diagnosed in boys.
4. Among children 5 to 10 years of age, the disease is more commonly diagnosed in girls.
5. The disease is diagnosed more often in winter than in summer.
6. Diabetic ketoacidosis is a frequent cause of morbidity and sometimes of death.
CLINICAL MANIFESTATIONS
Initial Effects
4. Recent weight loss (during a period of less than 3 weeks)
9. Dehydration (usually 10% dehydrated)
10. Diabetic ketoacidosis (Box 19-2)—hyperglycemia, ketonemia, ketonuria, metabolic acidosis, Kussmaul respirations
12. Change in level of consciousness (due to progressive dehydration, acidosis, and hyperosmolality, which results in decreased cerebral oxygenation)
Box 19-2 Signs of Diabetic Ketoacidosis
• Kussmaul respirations (deep, sighing respirations)
• Hyperglycemia (serum glucose level higher than 300 mg/dl)
• Ketonuria (moderate to large amounts; positive Ketostix result)
• Metabolic acidosis (pH <7.3; increased partial pressure of carbon dioxide [PCO2]; decreased partial pressure of oxygen [PO2]; sodium bicarbonate [NaHCO3] <15 mEq/L)
• Dehydration (as a result of polyuria and polydipsia)
• Electrolyte imbalance (falsely elevated potassium and sodium levels)
• Potential for life-threatening cardiac arrhythmias (as a result of electrolyte imbalance)
• Cerebral edema (caused by overzealous infusion of fluids)
Diagnosis is confirmed by the presence of symptoms combined with an elevated blood glucose level (higher than 200 mg/dl) and glycosuria.
