ch 21 objective 8 ON FINAL
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13 terms
Terms | Definitions |
|---|---|
 diabetes mellitus | encompasses many etiologically unrelated diseases and includes many different causes of disturbed glucose tolerance..it is a syndrome that is characterized by chronic hyperglycemia and other disturbances of carbohydrate, fat, and protein metabolism. also a deficiency of amylin (a hormone co-secreted with insulin from the beta cells) in both types, causing altered glucagon control and assimilation of nutrients. (amyloid deposits may also be related to amylin loss) |
| Type 1 Diabetes mellitus, characterized by | a lack of insulin and relative excess glucose...mostly seen in whites, peaking at 12 years of age. can be immune or non-immune |
| Type 1 Diabetes mellitus, immune | beta cells are destroyed (likely by viral infections) and islet cell antibodies appear. disease seems to be caused by a gradual process of autoimmune destruction in genetically susceptible people. Macrophages T and B-lymphocytes and natural killer cells are often present. |
| Type 1 Diabetes mellitus, non-immune | genetic abnormalities or injury to the beta cells impairs or in ihibits insulin secretion. if the person is heterogeneous for HLA-DR3 and HLA-DR4 the risk is 20 to 40 times greater. |
| Type 1 Diabetes mellitus, results of | because of the decreased use of glucose, it accumulates in the blood and is released in the urine, causing polyuria (lots of pale pee) and polydipsia (excessive thirst) resulting from osmotic diuresis. ketoacidosis (increased ketones without the inhibiting effects of insulin)causes increased levels of circulating fatty acids, and weight loss. |
| Type 2 diabetes mellitus | more common. caused by genetic susceptibility, triggered by environmental factors. |
| Type 2 diabetes mellitus, characterized by | mostly found in people older than 30. the greatest risk factor is obesity. in the obese, insulin has a diminished ability to influence glucose uptake and metabolism. |
| Type 2 diabetes mellitus, results of | amyloid deposits in the islets, fatty atrophy of the pancreas and liver, and vaxcular sclerosis are generally present. some insulin production continues, but the mass and number of beta cells are decreased. insulin resistance in glucose and lipid metabolism and decreased insulin secretion are the major abnormalities in type 2. |
| Treatment for type 1 | Insulin injections (4/day). self monitoring of glucose. consume sufficient calories to maintain normal weight for age. caloric intake regulated with age, activity and severity of the diabetes. exercise can result in hypoglycemia, insulin dosage should be reduced before exercise. can be prevented using with immunizations using low doses of insulin and oral insulin agents. |
| Treatment for type 2 | appropriate meal planning as in type 1. only oral meds may be needed for management if the pancreas can still synthesize insulin (still some functioning beta cells) can use insulin injections. exercise (reduces after meal glucose levels and diminishes insulin requirements. |
| beta cell | a cell that produces insulin in the isles of Langerhans in the pancreas |
| see table pg 143 | ... |
| diagnosis of diabetes | more than one fasting glucose greater than 126 mg/dl, plasma glucose value in the 2 hour sample of 200 mg/dl or greater, random glucose level greater than 200 mg/dl with symptoms of polydipsia, polyphagia and polyuria, impaired fasting glucose as a fasting glucose greater than or equal to 110 mg/dl, but less than 126 mg/dl |
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