Chapter 20 Health Alt Flashcards

Question

Acute Complications of Diabetes Mellitus

Answer 1

-Hypoglycemia ->Hypoglycemia in diabetes is sometimes called insulin shock or insulin reaction. Individuals with type 1 diabetes require insulin to manage their diabetes and are at more risk for hypoglycemia than those with type 2 diabetes because they have more severe deficits in their ability to control serum glucose levels. Significant drops in blood sugar most often occur when there is an unexpected change in caloric intake or exercise without appropriate modification of insulin dosing. Hypoglycemia sometimes occurs in type 2 diabetes during treatment with oral hypoglycemic medications. Symptoms include pallor, tremor, anxiety, tachycardia, palpitations, diaphoresis, headache, dizziness, irritability, fatigue, poor judgment, confusion, visual disturbances, hunger, seizures, and coma. -Diabetic ketoacidosis (DKA) ->Diabetic ketoacidosis (DKA) is a serious complication related to a deficiency of insulin and an increase in the levels of insulin counterregulatory hormones (catecholamines, cortisol, glucagon, GH). DKA is much more common in type 1 diabetes because insulin is more deficient. It is characterized by hyperglycemia, acidosis, and ketonuria. Insulin normally stimulates lipogenesis and inhibits lipolysis, thus preventing fat catabolism. Symptoms of DKA include Kussmaul respirations (hyperventilation in an attempt to compensate for the acidosis), postural dizziness, central nervous system depression, ketonuria, anorexia, nausea, abdominal pain, thirst, and polyuria. DKA is managed with a combination of fluids, insulin, and electrolyte replacement. -Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS) ->Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS) is an uncommon but significant complication of type 2 diabetes mellitus with a high overall mortality. It occurs more often in elderly individuals who have other comorbidities, including infections or cardiovascular or renal disease. HHNKS differs from DKA because type 2 diabetes is characterized by a lesser degree of insulin deficiency, which therefore prevents lipolysis and the production of ketones. However, hyperglycemia is usually more profound in HHNKS leading to more polyuria and fluid deficiency. Therefore the clinical features of HHNKS include a very high serum glucose concentration and osmolarity without metabolic acidosis. Clinical manifestations include severe dehydration; loss of electrolytes (especially potassium); and neurologic changes, such as stupor. Management includes fluid, insulin, and electrolyte replacement

Answer 2

-Microvascular disease: Diabetic microvascular complications are characterized by occlusion of capillaries, with associated ischemia of tissues. It is a leading cause of blindness, end-stage kidney failure, and various neuropathies. ->Diabetic retinopathy: Diabetic retinopathy is a leading cause of blindness worldwide and is a common complication of type 2 diabetes because of the likelihood of long-standing hyperglycemia before diagnosis. Diabetic retinopathy results from relative hypoxemia, damage to retinal blood vessels, red blood cell (RBC) aggregation, and hypertension. Macular edema is the leading cause of blurred vision among persons with diabetes. ->Diabetic nephropathy: Diabetes is the most common cause of chronic kidney disease and end-stage kidney disease, and nearly half of individuals with diabetes mellitus develop diabetic kidney disease. Renal glomerular changes occur early in diabetes mellitus, occasionally preceding the overt manifestation of the disease. There is progressive glomerulosclerosis and decreased glomerular blood flow and glomerular filtration that can progress to renal failure. Microalbuminuria is the first manifestation of diabetic kidney dysfunction and signals the onset of systemic diabetic complications. ->Diabetic neuropathies: Diabetic neuropathy is the most common complication of diabetes. The underlying pathologic mechanism includes metabolic and vascular factors related to chronic hyperglycemia with ischemia and demyelination contributing to neural changes and delayed conduction. Loss of pain, temperature, and vibration sensation is more common than motor involvement and often involves the extremities first in the hands and feet. -Macrovascular disease: Macrovascular disease (lesions in large- and medium-sized arteries) increases morbidity and mortality and increases the risk for hypertension, accelerated atherosclerosis, cardiovascular disease, stroke, and peripheral vascular disease, particularly among individuals with type 2 diabetes mellitus. ->Cardiovascular disease: Cardiovascular disease is the primary cause of death of people with diabetes, with higher risk for women. Hypertension often coexists with diabetes mellitus. Diabetes also is associated with deleterious changes in serum lipids, including high levels of low-density lipoproteins (LDLs), and low levels of high-density lipoproteins (HDLs). The incidence of congestive heart failure is higher in individuals with diabetes, even without myocardial infarction. ->Stroke: Stroke is twice as common in those with diabetes (particularly type 2 diabetes) as in the nondiabetic population. As in CAD, accelerated atherosclerosis of the cerebral vessels results from insulin resistance and hyperglycemia, especially when associated with hypertension and hyperlipidemia. ->Peripheral vascular disease: Diabetes mellitus increases the incidence of peripheral vascular disease (PVD). Age, duration of diabetes, genetics, and additional risk factors (smoking, hyperlipidemia, hypertension) influence the development and management of PVD. PVD in those with diabetes is more diffuse and often involves arteries below the knee. Occlusions of the small arteries and arterioles can lead to claudication (pain from reduced blood flow during exercise), ulcers, gangrene, and amputation. The lesions begin as ulcers and progress to osteomyelitis or gangrene, requiring amputation. -Infection

Answer 3

-Hypercortical function (inc cortisol secretion) ->Cushing syndrome ->Manifestations resulting from chronic excess cortisol, regardless of cause ->Cushing disease ->Excessive anterior pituitary secretion of ACTH; excess endogenous secretion ->Manifestations ->Weight gain in trunk (“truncal obesity”), facial (“moon face”), cervical areas (“buffalo hump”) ->Glucose intolerance and protein wasting: Glucose intolerance occurs because of cortisol-induced insulin resistance and increased gluconeogenesis and glycogen storage by the liver. Protein wasting is caused by the catabolic effects of cortisol on peripheral tissues. Muscle wasting leads to muscle weakness. In the skin, loss of collagen leads to thin, weakened integumentary tissues through which capillaries are more visible and are easily stretched by adipose deposits.

Answer 4

-Congenital adrenal hyperplasia (Congenital adrenal hyperplasia results from an inherited deficiency of an enzyme that is critical in cortisol biosynthesis. Because cortisol is not produced efficiently, the concentration of ACTH increases and causes adrenal hyperplasia, which results in the overproduction of mineralocorticoids or androgens, or both.) ->Deficiency in cortisol production causing increase in ACTH concentration -Hyperaldosteronism ->Primary hyperaldosteronism (Conn syndrome) ->Increased aldosterone secretion from abnormality in adrenal cortex ->Secondary hyperaldosteronism ->Extra-adrenal stimulus of aldosterone secretion ->Manifestations ->Hypertension, hypokalemia, and hypervolemia

Answer 5

-Hypersecretion of adrenal androgens ->Feminization (female secondary sex characteristics) -Hypersecretion of adrenal estrogens ->Virilization (male secondary sex characteristics) -hypersecretion of adrenal androgens and estrogens may be as a result of adrenal tumors.

Answer 6

-Adrenocortical hypofunction (hypocortisolism): low levels of cortisol secretion ->Addison disease (Addison disease is characterized by inadequate corticosteroid and mineralocorticoid synthesis and elevated levels of serum ACTH (loss of negative feedback).) ->Primary adrenal insufficiency ->Autoimmune mechanisms destroy adrenal cortical cells ->Addisonian crisis—hypotension leading to vascular collapse and shock ->Secondary hypocortisolism ->Decreased ACTH, adrenal atrophy ->Often results from prolonged exposure to exogenous glucocorticoids