|
?:definition
|
-
Diagnosis based on elevated levels of fasting plasma glucose or random plasma glucose plus symptoms. Hyperglycemia in diabetes mellitus (DM) occurs as a result of reduced insulin secretion, decreased glucose usage, or increased glucose production. Type I DM: About 10% of all cases; Insulin deficiency resulting from autoimmune beta cell destruction (type IA) or idiopathic (type IB). Type II DM: About 90% of all cases; Heterogeneous disorder of glucose metabolism characterized by variable degrees of insulin resistance, impaired insulin secretion, and increased hepatic glucose production. Drugs have been associated with hyperglycemia that can progress to new onset DM: Can mimic type I or II; Mechanisms: Diminished insulin production, inhibited insulin secretion, and reduced beta cell volume (e.g., cyclosporine); Autoimmune destruction of beta cells and increased insulin antibody titers (e.g., interleukin-2); Hormone stimulated gluconeogenesis and decreased insulin sensitivity (e.g., glucocorticosteroids); Decreased insulin sensitivity (e.g. protease inhibitors); Often reversible by discontinuation of drug, or can be controlled with oral antidiabetic agents and/or insulin. Common findings/symptoms: polydipsia, polyphagia, polyuria, weight loss, hypercholesterolemia, and hypertriglyceridemia. Acute complications: Diabetic ketoacidosis (DKA) particularly type I; Nonketotic hyperosmolar state (NKHS) particularly type II diabetes; Both can result in neurologic symptoms including coma. Long term complications are microvascular (e.g., retinopathy), macrovascular (e.g., coronary artery disease), neuropathic (e.g., paresthesias).
|
![[This page as RDF]](https://research.tib.eu/covid-19/static/rdf-icon.gif){kind=icon}