Rat 4

Describe the acute complications of diabetes mellitus with a focus on differential detection and treatment. -Dawn phenomenom

Early morning rise in blood glucose level related to release of growth hormone, cortisol, and catecholamines without preceding hypoglycemia.

Describe the acute complications of diabetes mellitus with a focus on differential detection and treatment. -Somoygi Effect

Low blood glucose levels during night that may lead to morning rise in blood glucose levels.

List the chronic complications of diabetes mellitus and discuss how good control of blood glucose limits the cellular degeneration in each instance. -microvascular retinopathy

Microvascular-damage to capillaries; retinopathies, nephropathies, and neuropathies Nonproliferative retinopathy=microaneurysms, capillary dilation, soft and hard exudates, may have no visual changes Proliferative retinopathy=formation of new blood vessels, scarring, retinal detachment. loss of visual acuity. Maculopathy=macular edema, loss of central vision Hyperglycemic lens edema=shunting of glucose to polyol pathyway, blurring of vision Cataract formation= chronic hyperglycemia, decreasing visual acuity

Describe the acute complications of diabetes mellitus with a focus on differential detection and treatment. -Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)

an uncommon but significant complication of type 2 diabetes mellitus with a high overall mortality occurs more often in elderly individuals who have other comorbidities, including infections or cardiovascular or renal disease differs from DKA in the degree of insulin deficiency (which is more profound in DKA) and the degree of fluid deficiency (which is more marked in HHNKS) clinical features of HHNKS include... a very high serum glucose concentration and osmolarity a near-normal serum bicarbonate level and pH clinical manifestations include... severe dehydration loss of electrolytes (including potassium) neurologic changes (such as stupor) management includes... fluid, insulin, electrolyte replacement

List the chronic complications of diabetes mellitus and discuss how good control of blood glucose limits the cellular degeneration in each instance. -nephropathy

glomerular basement membrane thickening, mesangial expansion, glomerulosclerosis, hyperfusion, and hyperfiltration. microalbuminemia, and htn slowly progressing to end stage kidney failure.

List the chronic complications of diabetes mellitus and discuss how good control of blood glucose limits the cellular degeneration in each instance. -skin and foot lesions (neuropathy)

loss of sensation, poor perfusion, suppressed immunity, and increased risk of infection. high risk for pressure ulcers, and delayed wound healing, abcess formation, development of necrosis and gangrene, particularly of toes and foot, infection, and osteomyelitis.

List the chronic complications of diabetes mellitus and discuss how good control of blood glucose limits the cellular degeneration in each instance. -neuropathy

oxidative stress, poor perfusion and ischemia, loss of nerve growth factor. nerve dysfunction, and degeneration.

Strict Control of blood glucose level

reduces some complications, particularly nonfatal myocardial infarction, but increases 5-year mortality. Strict control is not recommended for high-risk individuals with type 2 diabetes mellitus (DM), but the individual risk/benefit profile should be considered pg 478

Describe the acute complications of diabetes mellitus with a focus on differential detection and treatment. -Hypoglycemia

sometimes called insulin shock or insulin reaction. Type 2 diabetics are at less risk for hypoglycemia than those with type 1 because they retain relatively intact glucose counterregulatory mechanisms. However, hypoglycemia does occur in type 2 when treatment involves insulin Secretogogues or exogenous insulin. Treatment requires immediate replacement of glucose either orally or iv. Glucagon for home use can be prescribed for individuals who are at high risk.

DM Type 1

Diabetes Mellitus 1 Most common pediatric disease. Pathophysiology: (type iv hypersensitivity) has a strong genetic component and occurs mostly in people of Asian or African descent. Affected individuals have varying degrees of insulin deficiency. It's a slowly Progressive autoimmune T cell-mediated disease that destroys beta cells of the pancreas. Destruction of beta cells related to genetic susceptibility and environmental factors. The strongest genetic Association is with his the compatibility leukocyte antigen class II alleles HLA-DQ and HLA-DR. The destruction of beta cells result from lymphocytes and macrophages infiltration of the islets, resulting in release of inflammatory cytokines, activation of T Helper and T cytotoxic lymphocytes, and death of islets beta cells. Beta cell destruction is also mediated by the production of autoantibodies against islets cells, insulin, glutamic acid decarboxylase, and other cytoplasmic proteins. Insulin synthesis declines and hyperglycemia develops over time. 80% to 90% of the insulin-secreting beta cells of the islets of langerhans must be destroyed for insulin synthesis to decline enough. Clinical manifestations Affects the metabolism of fat, protein, and carbohydrates. Glucose accumulates in the blood and appears in the urine as the renal threshold for glucose is exceeded, producing an osmotic diuresis and symptoms of polyuria and thirst. Fluctuations in blood glucose levels occur. Protein fat breakdown occur because of the lack of insulin, resulting in weight loss. Increase metabolism of fats and proteins leads to a high level of circulating ketones, causing a condition known as diabetic ketoacidosis.

List the chronic complications of diabetes mellitus and discuss how good control of blood glucose limits the cellular degeneration in each instance. -Diabetic Retinopathy

Diabetic retinopathy-leading cause of blindness worldwide in adults less than 60 yrs of age. Results from relative hypoxemia, damage to the retinal blood vessels, rbc aggregation, and hypertension. Non-proliferative (stage I) - characterized by an increase in retinal capillary permeability, vein dilation, microaneurysm formation, and superficial (flame-shaped) and deep (blot) hemorrhages Pre-proliferative (stage II) - a progression of retinal ischemia with areas of poor perfusion that culminate in infarcts proliferative (stage III) - the result of neovascularization (angiogenesis) and fibrous tissue formation within the retina or optic disc Maculopathy Hyperglycemic lens edema Cataract formation

DM Type 2

Non-insulin dependent diabetes mellitus is highest among American Indians and Alaska natives. Risk factors are age, obesity, hypertension, physical inactivity, and family history. Genetic abnormalities combined with environmental influences, such as obesity, results and basic pathophysiologic mechanisms of type 2 diabetes, which are insulin resistance and decrease insulin secretion by beta cells. Insulin resistance is defined as a suboptimal response of insulin sensitive tissues to insulin and is associated with obesity. Several mechanisms are involved in abnormalities of the insulin signaling pathway and contribute to insulin resistance. These include an abnormality of the insulin molecule, high amounts of insulin antagonist, down regulation of the insulin receptor, and alteration of glucose transporter proteins. Diabetes is one of the most important contributors to insulin resistance and diabetes and acts of several important mechanisms -Adipokines are hormones produced in the adipose tissue. Obesity increases serum levels of leptin and decreased levels of adiponectin. These changes are associated with inflammation and decreased insulin sensitivity. -Elevated levels of serum free fatty acids and intracellular deposits of triglycerides and cholesterol are found in obese individuals. These changes interfere with intracellular insulin signaling, decreased tissue responses to insulin, altar incretin actions, and promote inflammation. -Inflammatory cytokines are released from intra-abdominal adipocytes or adipocyte associated mononuclear cells and induce insulin resistance and are cytotoxic to beta cells. -Obesity is correlated with hyperinsulinemia and decreased insulin receptor density. -Beta cell dysfunction develops and leads to a relative deficiency of insulin activity. Caused by a combination of the decrease in beta cell mass and a reduction in the normal beta cell function. -Glucagon concentration is increased because pancreatic alpha cells become less responsive to glucose inhibition, resulting in an increase in glucagon secretion. -Amylin is another beta cell hormone that is decreased in both type 1 and type 2 diabetes. It increases satiety and suppresses glucagon release from the alpha cells. Also contributes to islets cell destruction through the deposition of abnormal amyloid polypeptide in the pancreas. -Ghrelin is a peptide produced in the stomach and pancreatic islets that regulate food intake, energy balance, and hormonal secretion. Decreased levels have been associated with insulin resistance and increased fasting insulin levels. -Incretins Released from the GI tract in response to food intake and function to increase the secretion of insulin and have many other positive effects on metabolism. Clinical manifestations Are non-specific. Overweight, dyslipidemic, hyperinsulinemic, and hypertensive. Polyuria and polydipsia Fatigue, pruritus, recurring infections, visual changes, or symptoms of neuropathy

Define "HbA1c", including what "glycated hemoglobin" is, and identify the significance of this lab value.

When the body processes sugar, glucose in the bloodstream actually attaches to haemoglobin. The amount of glucose that combines with this protein is directly proportional to the total amount of sugar that is in your system at that time. Because blood cells in the human body survive for 8 to 12 weeks before renewal, measuring glycated haemoglobin (or HbA1c) can be used to reflect average glucose levels over that duration, providing a useful longer-term gauge of blood glucose control. If your blood sugar levels have been high in recent weeks, your hba1c will also be greater. Hba1c can indicate people with prediabetes or diabetes. Glycated hemoglobin: hemoglobin to which glucose is bound. Is tested to monitor the long-term control of diabetes mellitus. -4-7% normal (6.5% or higher is DM).

Describe the acute complications of diabetes mellitus with a focus on differential detection and treatment. -Diabetic Ketoacidosis

a serious complication related to a deficiency of insulin and increase in the level of insulin counter regulatory hormones. More common in type 1 diabetes because insulin is more deficient. Characterized by hyperglycemia, acidosis, and ketonuria. Insulin normally stimulates lipogenesis and inhibits lipolysis, thus preventing fat catabolism. With insulin deficiency, lipolysis is enhanced and there's an increase in the amount of nonesterified fatty acids delivered to the liver. The consequences increase glyconeogenesis contributing to hyperglycemia and production of Ketone bodies by the mitochondria of the liver at a rate that exceeds peripheral use. Accumulation of Ketone bodies causes a drop in PH, resulting in metabolic acidosis. Symptoms include Kussmaul respirations ( hyperventilation in an attempt to compensate for the acidosis)

List the chronic complications of diabetes mellitus and discuss how good control of blood glucose limits the cellular degeneration in each instance. -macrovascular

damage to larger vessels; coronary artery, peripheral vascular, and cerebral vascular Cardiovascular- endothelial dysfunction, hyperlipidemia, accelerated atherosclerosis, coagulopathies. symptoms include htn, CAD, cardiomyopathy and heart failure. ultimate cause of death in up to 68% of people with diabetes, with higher risk for women. Cerebrovascular-(same as cardiovascular) increased risk for ischemic and thrombotic stroke. Peripheral vascular-(same as cardiovascular), claudication, nonhealing ulcers, gangrene. Infection-impaired immunity, decreaesd perfusion, recurrent trauma, delayed wound healing, urinary retention. those w/ diabetes are at an increased risk because of... -Senses: impaired vision caused by retinal changes and impaired touch caused by neuropathy -hypoxia: once skin integrity is compromised, susceptibility to infection increases as a result of hypoxia glycosylated hemoglobin in the RBCs impedes the release of oxygen to tissues. -Pathogens: some proliferate rapidly because of increased glucose in body fluids, which provides an excellent source of energy -Blood supply: decrease results from vascular changes reduces the supply of white blood cells to the affected area -Suppressed immune response: chronic hyperglycemia impairs both innate and adaptive immune responses