Chapter 41: Diabetes Mellitus Flashcards Preview

Patho Final Exam > Chapter 41: Diabetes Mellitus > Flashcards

Flashcards in Chapter 41: Diabetes Mellitus Deck (10):

Classification of Glucose Intolerance Disorders

- 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)


Diabetes Mellitus

- 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


Type 1 Diabetes Mellitus

- 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


Type 2 Diabetes Mellitus

- 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


Acute Hyperglycemia

- 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


Chronic Hyperglycemia

- 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


Macrovascular Complications

- 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)


Microvascular Complications

- 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


Diabetic Neuropathy

- 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


Hypoglycemia Complications

- 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