55 Pathophysiology of DM (Henry) Flashcards
. Identify the distinguishing features between Type I and Type II diabetes mellitus as they relate to: b-cell function, insulin sensitivity, blood glucose levels, Hb1Ac measurements, and ketone production.
Type I: B cell destruction by infiltration of activated T-lymphocytes, absolute insulin deficiency, Progression is very dif from type II, takes some time before sx are experienced. High blood glucose. Can lead to ketone production.
Type II: Insulin resistance and insulin secretory defect. Increase in B cell mass. Normal blood glucose levels.
Describe the relative significance of obesity, genetics, environment, and the immune system in the development of Type I and Type II diabetes.
Type I: Genetic predisposition (key genes related to MHC locus). Immune mediated. Environmental factors (viruses/toxins that have molecular mimicry to B cells?)
Type II: Genetic predisposition (if twin has type II, 90% chance you’ll get it, Type I is 25-50%), obesity (huge correlation btwn visceral adiposity and resistance to insulin), and environmental factors
.
List the signs and symptoms, as well as the cause of the signs and symptoms, of Type I and Type II diabetes.
Type I: Can detect autoantibodies many years before onset of disease. Polyuria, thirst, blurred vision, wt loss, weakness, dizzy, sensory nerve dysfunction (paresthiasis), level of consciousness
Type II: High insulin and normal plasma glucose. Metabolic syndrome (see below). Asympto initially. Infections (from elevated glucose), neuropathy (retinal, peripheral), polyuria, thirst, etc, obesity and metabolic syndrome.
Compare and contrast the metabolic changes that occur in patients with Type I or Type II diabetes.
Type I: Increase in gluconeogenesis, increase in glycogenolysis, decreased glycolysis, promote ketogenesis.
Type II: Metabolic syndrome (hyperinsulinemia, dyslipidemia, hypertension) – can result in coronary artery disease and stroke. Insulin increases Na retention, thus high BP.
Predict common therapeutic strategies employed and the rationale for these strategies in treating Type I and Type II diabetes mellitus.
Type I: Diet, patient education, and INSULIN.
Type II: Diet, pt. education, lots of pharmacological strategies (increase insulin secretion/action by mimicking GLP1, inhibit degradation of GLP1. Inhibit K secretion, etc. etc.) Insulin can be used when other strategies don’t work well.
Recognize the acute complications potentially experienced by patients with diabetes mellitus and the general therapeutic approach to addressing these complications.
Hypoglycemia – sx from ANS (tachycardia, sweating, tremors, nausea, hunger), Neurologic sx (confusion, irritable, blurred vision, tired)
Treat w/ glucose or glucagon.
Diabetic Ketoacidosis – insulin deficiency causes mobilization of energy stores which includes ketogenesis and thus metabolic acidosis. More common in Type I. Treat by restoring plasma vol., reduce glucose, correct acidosis, replenish
Be familiar with common measurements used to monitor glycemic control.
Cap blood testing, urine ketone testing, cap ketone testing, glycated hemoglobin testing.