Ch41 Diabetes Mellitus

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Ch41 Diabetes Mellitus
2015-03-15 18:40:47
diabetes mellitus
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  1. Where is insulin synthesized?
    pancreas by the β cells of the islets of Langerhans
  2. B cells produce
  3. α cells produce
  4. δ cells produce
  5. F cells produce
    pancreatic polypeptide
  6. Hormonal regulation
    • ingestion of nutrients stimulates release of glucose dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) from cells in the gut;
    • these stimulate the production of insulin and inhibit glucagon
    • insulin stimulates diffusion of glucose into adipose and muscle tissue 
    • glucose oxidized in the cell (glycolysis) and used primarily for glycogenesis
  7. In a fasting state, what is glucose's role?
    • glucose produced by glycogenolysis and gluconeogenesis while insulin secretion falls to basal level 
    • glucagon responsible for glucose production in fasting state 
    • other counterregulatory hormones help (ex: corticosteroids, GH, catechlamines)
  8. What is responsible for glucose production in fasting state?
  9. What happens to glucose while exercising
    • initially insulin drops and glucagon and catecholamine rise; increasing production of FFAs and stimulating glycogenolysis 
    • rise in glucose to meet energy demands 
    • muscle tissue increases metabolism of glucose as exercise cont; increasing insulin sensitivity and maintaining normal blood glucose levels in presence of lower insulin levels
  10. Glucose when Stress?
    • stress hormones (corticosteroids and catecholamines) increase production of glucose in liver and glucagon in pancreas, & decrease use of glucose 
    • catecholamines increase production of FFAs and inhibits glucose uptake in periphery 
    • all this leads to hyperglycemia
  11. Type 1 DM
    characterized by destruction of B cells of pancreas
  12. Type I DM 
    etiology may be immune-mediated or idiopathic

    diagnosed between 5-20 yrs of age
  13. What happens in Type I DM
    • absolute insulin deficieny 
    • overproduction of glucagon stimulates glycogenolysis and gluconeogenesis
    • glucose lvl rise, leads to polyuria, polydipsia, and polyphagia 
    • FFAs are turned into ketones --> ketoacidosis
  14. Type 2 DM
    • most common form;
    • non-caucasian and elderly
    • insulin resistance and B cell dysfunction lead to a relative lack of insulin
  15. Type 2 DM 
    [risk factors]
    common factors: obesity, aging, and sedentary lifestyle
  16. Type 2 DM
    • polyuria, polydipsia, polyphagia - subtle 
    • ketoacidosis is uncommon 
    • HHNK - hyperglycemic hypersmolar nonketotic coma can develop due to severe dehydration (more common in older adults)
  17. Gestational DM
    • onset during pregnancy
    • precipitated by the presence of placental hormones 
    • manage thru dietary counseling, exercise, and blood glucose/ketone monitoring
  18. Pre-diabetes
    impaired glucose tolerance and impaired fasting glucose tolerance
  19. Acute hyperglycemia
    by alterations in nutrition, inactivity, or inadequate use of antidiabetic meds

    prone to infections
  20. Acute hyperglycemia 
    polyuria, polydipsia, polyphagia, nausea, fatigue, blurred vision
  21. Chronic hyperglycemia 
    what it can lead to 
    • systemic changes over time and increase the risk of other diseases, including metabolic syndrome, hypertension, cardiovascular disease, and stroke 
    • complications: vascular and neuropathic
  22. Vascular complications
    Macrovascular: damage to large blood vessels; leads to CVD and stroke 

    Microvascular: retinopathy and nephropathy fr. abnormal thickening of basement membrane in capillaries; may lead to blindness and renal failure
  23. macrovascular complications
    MD - independent risk factor for CAD (coronary artery disease)
  24. Microvascular complications
    • hyperglycemia disrupts platelet function and growth of basement membrane 
    • thickening of basement membrane may improve with glycemic control 
    • risk factors: +hypertension and smoking
  25. Neuropathic complications 
    [autonomic dysfunction]
    • GI disturbances
    • bladder dysfunction, 
    • tachycardia
    • postural hypotension
    • sexual dysfunction
  26. Neuropathic complications 
    [sensory disturbances]
    • carpal tunnel syndrome, paresthesias
    • or dysesthesias in extremities
  27. Neuropathic complications
    • excessive glucose thought to interfere with myoinositol in neurons and reduced myoinositol in peripheral nerves 
    • glycemic control may prevent/improve symptoms of diabetic neuropathy
  28. complications in pregnancy
    • Type 1: higher risk of perinatal infant mortality and congenital abnormalities 
    • glycemic control before and during reduce risks
  29. Protein
    • used to repair and growth of tissue 
    • stimulates secretion of insulin w/o increasing plasma blood glucose 
    • excessive protein may cause nephropathy
  30. Fat
    • sat, monounsaturated, unsat. 
    • dietary saturated fat and cholesterol lead to ypercholesterolemia 
    • limit sat fat to less than 7% of total intake and <200 mg of cholesterol daily
  31. Carbohydrates
    • categorized as monosaccharides and polysaccharides 
    • monitored with carbohydrate counting 
    • glycemic load and index may also be of benefit
  32. Obesity and eating disorders
    • obesity: a body mass index (BMI) >30kg/m2
    • bulimia and anorexia more common in type 1 DM
  33. Exercise
    • lowers cardiovascular risk factors 
    • may be beneficial toward wt reduction or maintenance 
    • may lower meds requirements 
    • Type 1 DM at risk of hypoglycemia and ketoacidosis
  34. Oral antidiabetic agents
    • Sulfonylureas
    • biguanides
  35. sulfonylureas
    induce insulin release by B cells, augment the action of insulin in glucose disposal, diminish insulin clearance by liver, and reduce hepatic glucose production
  36. Biguanides
    suppress hepatic gluconegogenesis and enhance glucose uptake by peripheral tissues
  37. Oral antidiabetic agents
    • α-Glucosidase inhibitors
    • Thiazolidinediones
  38. α-Glucosidase inhibitors
    diminish postprandial hyperglycemia by delaying carbohydrate absorption
  39. Thiazolidinediones
    increase tissue sensitivity to insulin and inhibit hepatic gluconeogenesis
  40. Incretins
    inhibit enzymatic breakdown of the incretin hormones, GLP-1 and GIP
  41. Amylins
    amylin-mimetic agents used in conjunction with insulin for the management of glycemia
  42. Complication of insulin therapy
  43. Testing for glucose
    • glycosylated hemoglobin (glycemic control)
    • vlues of less than 7%
    • capillary glucose testing 
    • test for glucosuria and ketones