Chapter 41: Diabetes Mellitus

Question 1

Classification of Glucose Intolerance Disorders

Answer 1

• Type 1 diabetes mellitus (DM)
• Type 2 diabetes mellitus
• Other specific types of diabetes mellitus
• Gestational diabetes mellitus
• Pre-diabetes classes: Impaired glucose tolerance (2-hour post–glucose value of 140 to 200 mg/dl) and impaired fasting glucose tolerance (Fasting plasma glucose value of 100 to 125 mg/dl)

Question 2

Diabetes Mellitus

Answer 2

• endocrine disorder diagnosed by the presence of chronic hyperglycemia
• Diagnosis: if any two of the following conditions occurs:
• Random sampling of blood glucose above 200 mg/dl with classic signs and symptoms
• Fasting blood glucose level of greater than 126 mg/dl
• Blood glucose concentration greater than 200 mg/dl 2 hours after a 75-g oral glucose load
• HgbA1c level above 6.5

Question 3

Type 1 Diabetes Mellitus

Answer 3

• Characterized by destruction of the β cells of the pancreas
• Usually diagnosed between 5 and 20 years of age
• Etiology may be immune-mediated or idiopathic (without autoimmune markers or HLA association)(Autoimmune markers: chromosome 6)
  (HLA: DR3 and DR4 MHC genes)
• Results in absolute insulin deficiency
• Overproduction of glucagon stimulates glycogenolysis and gluconeogenesis
• Glucose levels rise, leading to polyuria (increased urination), polydipsia (thirst), and polyphagia (hunger): classic signs
• FFAs are transformed into ketones, leading to ketoacidosis (Deep, labored respirations that are “fruity” in odor (Kussmaul respirations) occur)
• Ketoacidosis occurs as a result of increased lipolysis and conversion to ketone bodies
• Excessive ketones result in metabolic acidosis
• Ketoacidosis may occur with type 2 DM under severe stress, sepsis, stroke, or myocardial infarction
• Acidosis-induced hyperkalemia may occur

Question 4

Type 2 Diabetes Mellitus

Answer 4

• Most common form of DM
• Non-Caucasian and elderly disproportionately affected
• Insulin resistance and β cell dysfunction lead to a relative lack of insulin (Suspect decreased number of insulin receptors or abnormal translocation of glucose transporters) (As disease progresses, insulin production may be impaired)
• Risk factors: female sex, obesity, aging, and sedentary lifestyle
• Polyuria, polydipsia, and polyphagia may be more subtle
• Ketoacidosis is uncommon
• Nonketotic hyperglycemic hyperosmolar coma can develop, more common in older adults (Severe hyperglycemia with no or slight ketosis and striking dehydration)
• Hyperosmolar coma occurs because endogenous insulin suppresses ketone formation and thus prevents ketoacidosis
• Hyperglycemia may go untreated for a time and result in persistent glycosuria with osmotic diuresis
• Dehydration develops with high osmolality and hemoconcentration of erythrocytes, proteins, and creatinine

Question 5

Acute Hyperglycemia

Answer 5

• Commonly caused by alterations in nutrition, inactivity, or inadequate use of antidiabetic medications
• Dawn phenomenon: rise in glucose in early morning hours from growth hormone, cortisol, glucagon, and epinephrine release
• Somogyi Effect: Rebound hyperglycemia
• Symptoms: polyuria, polydipsia, polyphagia, nausea, fatigue, blurred vision
• More prone to infections

Question 6

Chronic Hyperglycemia

Answer 6

• May lead to systemic changes over time and increase the risk of other diseases, including metabolic syndrome, hypertension, cardiovascular disease, and stroke
• Complications are categorized as vascular and neuropathic

Question 7

Macrovascular Complications

Answer 7

• damage to large blood vessels; leads to cardiovascular disease, peripheral vascular disease, and stroke
• Preventive: caloric restriction, exercise, possibly drugs, control dyslipidemia, and hypertension
• DM is an independent risk factor for coronary artery disease (CAD) (Dyslipidemia, hypertension, and impaired fibrinolysis are present in uncontrolled DM; improve with blood glucose control)

Question 8

Microvascular Complications

Answer 8

• retinopathy and nephropathy from abnormal thickening of the basement membrane in capillaries; may lead to blindness and renal failure
• Hyperglycemia disrupts platelet function and growth of the basement membrane
• Thickening of basement membrane may improve with glycemic control
• Urine protein loss occurs in nephropathy
• Preventive: control blood glucose, hypertension; stop smoking

Question 9

Diabetic Neuropathy

Answer 9

• Autonomic dysfunction: GI disturbances, bladder dysfunction, tachycardia, postural hypotension, and sexual dysfunction
• Sensory dysfunction includes carpal tunnel syndrome, paresthesias in extremities, especially feet (Amputation 15 to 40 times higher than in nondiabetic individuals)
• Excessive glucose is thought to interfere with myoinositol in neurons and reduced myoinositol in peripheral nerves
• Hypertriglyceridemia, obesity, smoking, and hypertension enhance development of neuropathy
• Glycemic control may prevent or improve symptoms of diabetic neuropathy

Question 10

Hypoglycemia Complications

Answer 10

• Causes include Insufficient food intake, unplanned activity, or an inappropriate insulin or sulfonylurea dose
• Counterregulatory mechanisms symptoms include Pallor, tremor, diaphoresis, palpitations, and anxiety
• Neuroglycopenic symptoms include Hunger, visual disturbance, weakness, paresthesias, confusion, agitation, coma, death
• Can have hypoglycemia unawareness