NURS 282 Lecture Notes - Lecture 4: Nateglinide, Basal Metabolic Rate, Muscle Weakness
Document Summary
Part one: pancreas & dm: glucose metabolism. Insulin deficiency puts the body into catabolic mode. In the absence of insulin: glycogen converted into glucose, proteins degraded into amino acids. Fats converted to glycerol & free fatty acids. Increased glycogenolysis (breakdown of glycogen: breakdown of glycogen into free glucose. Increased gluconeogenesis (generation of glucose: due to amino acids & fatty acids produced from metabolic breakdown of proteins & fats, reduced glucose utilization, due to, decreased cellular uptake of glucose, decreased conversion of glucose to glycogen. Typically develops during childhood or adolescence: destruction of pancreatic beta cells (autoimmune, dka. Insulin still produced: reduced binding, reduced # of receptors, reduced receptor responsiveness, may initially be managed w/ lifestyle modification, po meds, progression to insulin, at risk for hhns. Long term: htn - hypertension, hd heart disease, nephropathy, retinopathy, neuropathy, amputation. Gestational dm: placenta produces hormones that antagonize the actions of insulin.
