Gen Path Exam 2 - Pathology of Diabetes Flashcards
Syndrome with disordered carbohydrate metabolism and inappropriate hyperglycemia due to either a deficiency of insulin secretion or to a combo of insulin resistance and inadequate insulin secretion to compensate
Diabetes mellitus
Leading cause of end-stage renal disease, adult-onset blindness, and nontraumatic lower extremity amputations resulting from atherosclerosis of arteries
Diabetes
Due to pancreatic islet beta cell destruction predominantly by an autoimmune process, and these pts are prone to ketoacidosis
Type 1 diabetes mellitus
Most prevalent form of diabetes mellitus
Type 2 diabetes mellitus
Due to insulin resistance, mainly caused by visceral obesity, with a defect in compensatory insulin secretion
Type 2 diabetes mellitus
Used to be termed juvenile-onset diabetes mellitus, or ketosis-prone diabetes mellitus, or insulin-dependent diabetes mellitus
Type 1 diabetes mellitus
Used to be termed adult-onset diabetes mellitus,
ketoacidosis-resistant diabetes mellitus or non-insulin-dependent diabetes mellitus
Type 2 diabetes mellitus
Known as latent autoimmune diabetes in adults
Type 1.5 diabetes
Autoimmune diabetes that begins in adulthood and does not need insulin for glycemic control at least in the first 6 months after diagnosis
Type 1.5 diabetes
Shares genetic, immunologic, and metabolic features with both Type 1 and Type 2 diabetes mellitus
Type 1.5 diabetes
Some consider it to be a slowly progressive form of Type 1 diabetes mellitus, while others consider it a separate distinct form of diabetes
Type 1.5 diabetes
Refers to disorders due to monogenic defects in beta-cell function, with little or no defect in insulin action that was observed in non-obese children, adolescents, and young adults
Maturity-onset diabetes of the young
Characterized by carbohydrate intolerance during pregnancy usually resolving after delivery
Gestational diabetes mellitus
Diabetes that develop secondary to some other identifiable etiology or acquired disease
Secondary diabetes
Pt has hyperglycemia with little or no endogenous insulin secretion
Type 1 diabetes mellitus
Onset of disease is abrupt with marked polyuria, polydipsia, polyphagia, weight loss, fatigue
Type 1 diabetes mellitus
Highly prone to ketosis; pts frequently present for tx in an intial episode of diabetic ketoacidosis
Type 1 diabetes mellitus
Marked sensitivity/brittleness to exogenous insulin administration, particularly with regular insulin
Type 1 diabetes mellitus
In Type 1 diabetes mellitus, a prodromal phase of polyuria, polydispia, and weight loss may precede the development of what?
Diabetic ketoacidosis
Type 1 diabetes mellitus incidence most commonly peaks during what times in a person’s life?
Middle of first decade
Time of growth acceleration of adolescence
Pts maintain some endogenous insulin secretory capability by pancreatic beta-cells despite the overt abnormalities of glucose homeostasis, including fasting hyperglycemia and/or carbohydrate intolerance
Type 2 diabetes mellitus
Pts are NOT absolutely dependent on insulin for life
Type 2 diabetes mellitus
Why are pts with Type 2 diabetes mellitus relatively resistant to development of ketosis in the basal state?
They have retention of endogenous insulin secretory capabilities
Generally demonstrate marked resistance or insensitivity to the metabolic actions of endogenous as well as exogenous insulin, in part as the result of decreased insulin receptors
Type 2 diabetes mellitus