Читать книгу The Diabetes Ready Reference for Health Professionals - Kathryn Mulcahy - Страница 6

PATHOPHYSIOLOGY OF DIABETES

I. DEFINITION OF DIABETES

A. Diabetes is a chronic metabolic disorder in which the body cannot metabolize carbohydrates, fats, and proteins because of defects in insulin secretion and/or action. B. The chronic hyperglycemia of diabetes is associated with long-term damage, dysfunction, and failure of various organs, especially the eyes, kidneys, nerves, heart, and blood vessels.

C. Diabetes is classified into three primary types, which are different disease entities but share the symptoms and complications of hyperglycemia (high blood glucose).

D. Pre-diabetes, once called “borderline diabetes,” is a degree of hyperglycemia that may precede type 2 diabetes and increases risk for future diabetes and cardiovascular disease.

II. TYPE 1 DIABETES

A. Causes

1. Genetic predisposition

2. Environmental exposure: virus, toxin, stress

3. Autoimmune reaction: beta cells that produce insulin in the pancreas are destroyed. When 80–90% of the β-cells are destroyed, overt symptoms occur.

B. Characteristics

1. Usually occurs before 30 years of age, but can occur at any age

2. Abrupt onset of signs and symptoms of hyperglycemia: increased thirst and hunger, frequent urination, weight loss, and fatigue

3. Ketosis prone

C. Treatment

1. Insulin by injection with syringes or pump

2. Medical nutrition therapy

3. Physical activity

4. Diabetes self-management education

5. Self-monitoring of blood glucose and ketones

III. TYPE 2 DIABETES

A. Causes

1. Insulin resistance: unable to utilize insulin that the body makes because of cell-receptor defect; glucose is unable to be absorbed into cells for fuel.

2. Decreased insulin secretion: pancreas does not secrete enough insulin in response to glucose levels.

3. Excess production of glucose from the liver: result of defective insulin secretory response; dawn phenomenon (see Glossary) is an example.

B. Characteristics

1. Usually occurs after 30 years of age, but can occur in children and adolescents

2. Increased prevalence in some ethnic groups, e.g., African Americans, Latinos, Native Americans, Asian Americans, and Pacific Islanders

3. Strong genetic predisposition

4. Frequently obese

5. Not prone to ketoacidosis until late in course or with prolonged hyperglycemia

6. May or may not have symptoms of hyperglycemia

7. May also have blurred vision, delayed healing, numb-ness and tingling of the hands and feet, recurring yeast infection

C. Treatment

1. Diet/weight management

2. Exercise/increased physical activity

3. Oral hypoglycemic/antihyperglycemic agents, insulin sensitizers, and/or insulin

4. Diabetes self-management education

5. Self-monitoring of blood glucose

6. Treatment of comorbid conditions (e.g., hypertension, lipid abnormalities)

IV. GESTATIONAL DIABETES MELLITUS (GDM)

A. Causes

1. Insulin resistance due to pregnancy

2. Genetic predisposition

B. Characteristics

1. Carbohydrate intolerance identified by screening those at risk during pregnancy (see page 5)

2. Usually asymptomatic condition

C. Treatment

1. Diet: provide adequate calories without hyperglycemia or ketonemia

2. Exercise: program that does not cause fetal distress, contractions, or hypertension (>130/80 mmHg)

3. Insulin: if unable to consistently maintain plasma glucose ≤90 mg/dl (≤5.0 mmol/l) fasting and ≤120 mg/dl (≤6.7 mmol/l) 1 hour postprandial

4. Self-monitoring

a. Blood glucose: required to determine effectiveness of treatment and possible need for insulin. Glucose should be checked fasting and 1–2 hours postprandially.

b. Ketones: test for ketones using first morning urine sample. Presence of ketones may indicate starvation rather than hyperglycemic ketosis.