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Pancreatic endocrine function (Chronic complications (Microvascular…
Pancreatic endocrine function
Diabetes Mellitus
Type I: autoimmune destruction of insulin-producing beta cells in Islets
Decreased insulin production -> increased glucagon -> increased glucose and hyperglycemia
Polyuria (excessive urination) from osmotic diuresis
Onset peaks at age 12
Polydipsia (excessive thirst) from intracellular dehydration as water osmotically pulled out of cell
Polyphagia (excessive hunger) from altered use of depletion of carb, fat and protein stores
Increase glycosylated hemoglobin (HbA1c) from permanent attachmentof glucose to Hb
Type II: insulin resistant
Insulin resistance -> hyperinsulinemia (early) -> "exhaustion" of beta cells over time -> decreased insulin secretion (late) -> hyperglycemia
Insulin resistance
Sub-optimal response to insulin by liver, muscle, and adipose
Down-regulation of insulin receptors and altered insulin signaling
Altered function of GLUT (glucose transporter) -> decreased glucose uptake by cell
Change also associated with inflammatory cytokines released from adipose tissue and increased glucagon
Risk factors: age, obesity, family history, inactivity, hypertension
Chronic complications
Microvascular disease: chronic hyperglycemia -> capillary endothelial damage, occlusion and ischemi
Neuropathy -> pain and tissue injury
Vascular damage -> ischemia and demyelination -> nerve damage and slowed conduction
Signs and symptoms range from tingling and burning to muscle atrophy to loss of pain sensation
Nephropathy -> chronic kidney disease
Hyperglycemic damage and inflammation -> renal glomerular damage and renal fibrosis
Signs and symptoms include microalbuminuria (protein loss in urine) and fluid overload and hypertension
Retinopathy -> blindness
Vascular damage -> retinal and macular damage
Infarcts, neovascularization and fibrous tissue formation -> further damage and blindess
Macrovascular disease: lesions in medium and larger arteries
Infection
Insulin production and function
Production
Secretion from Islet of Langerhans beta cells driven by blood glucose
Increased blood glucose -> increased nsulin secretion -> decreased blood glucose
Insulin receptor binding on target cell -> glucose transporter to cell surface -> glucose uptake
Function
Blood glucose homeostasis
Increased fatty acid and protein synthesis
Promote cell growth and differentiation
Increased cellular uptake of glucose (especially in liver), skeletal muscle and adipose tissue
Acute complications
Hypoglycemia (insulin shock)
Too much insulin with respect to diet and metabolic need -> hypoglycemia
Diaphoresis, irritability, confusion, tachycardia, tremor, headache, hunger, seizures, coma, death
Diabetic ketoacidosis (DKA)
More likely in Type I
Have enough insulin to prevent lipolysis but not enough to prevent hyperglycemia
Precipitated by stressors (infection, trauma, failure to treat)
Decreased insulin and increased stress hormones (cortisol, catecholamines) -> hyperglycemia
Osmotic diuresis -> dehydration -> hyperosmolality and volume depletion
Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)
More like in Type II
Have enough insulin to prevent lypolysis, but not enough to prevent hyperglycemia
Without insulin, high rates of lipolysis (fat breakdown) -> increased free fatty acids (FFA) -> goes to liver -> liver converts FFA -> glucose (gluconeogenesis) -> excess FFA are converted to ketoacids
Clinical presentation: deep, rapid breathing (Kussmaul), ketonuria, polyuria