Diabetes/Biliary Disorders

1. Diabetes/Biliary Disorders By Diana Blum MSN Metropolitan Community College

2. Definition • Disorder of carbohydrate, protein, and fat metabolism resulting from an imbalance between insulin availability and need. • Group of metabolic diseases characterized by increased levels of glucose in the blood (hyperglycemia) resulting from defects in insulin secretion, insulin action, or both

3. Statistics • Third leading cause of death • Becoming more common • 285 million people globally currently have • 1/3 of which are undiagnosed • By 2030 it will exceed 438 million • More elderly have (ages 65-74) • Prevalent in Caucasians, African Americans, Native Americans, and Hispanics • Leading cause of : • Non traumatic amputations, blindness, and ESRD

4. Why is this happening? • Obesity • Inactivity • Aging • urabanization

5. Risk Factors • Family history • Obesity • Ethnicity • Age >45 • HTN • Lipid profile abnormalities • Gestational diabetes

6. Insulin • Anabolic Hormone produced by beta cells in the islets of langerhans in the pancreas • Transports and metabolizes glucose for energy • Signals the liver to stop the release of glucose • Prevents fat and glycogen breakdown • Enhances dietary fat storage in adipose • Increases protein synthesis • Controls level of glucose in blood • Regulates production of • Regulates storage of glucagon

7. Diabetes • Cells stop responding to insulin • Pancreas may stop producing Both lead to Hyperglycemia and complications like DKA and HHNS

8. Diabetes

9. Type 1 AKA juvenile onset • Insulin dependent(natural level low or absent) • Needed to prevent ketosis and to normalize lipid and protein metabolism. • Autoimmune process that destroys beta cells of the pancreas • Decreasing insulin production, unchecked glucose production by the liver, and fasting hyperglycemia • Can not store glucose from food • Contributes to fat breakdown, increased ketones (byproducts of fat breakdown) • Genetics play role • Can occur at any age but typically less then 3o • Usually have a thin stature and abrupt symptom onset • Prone to DKA • May be triggered by virus or toxins

11. Type 2 • Non insulin dependent Diabetes • Pancreas retains some function but resistance to insulin is a major cause • Insulin becomes less effective at stimulating glucose uptake by tissues and regulating glucose release by liver • Genetics may play role • Obesity also plays a role • Usually onset after 30 • Can take oral nasal or sq insulin

13. GOAL: • Euglycemia and to prevent complications Treatment: wt reduction, exercise, diet modification, oral hypoglycemic agents, insulin shots

14. Gestational • Glucose intolerance associated with pregnancy • 2-10% women annually • Related to secretion of placental hormones which cause insulin resistance • At risk: obese, history of gestational diabetes, glycosuria, stillbirth or abortion, and fam history • TX: diet modifications, insulin

15. PreDiabetes • Normal glucose metabolism • Obesity • Previous personal history of hyperglycemia

16. Chronic complications to diabetes • Retinopathy • Diabetic nephropathy • Neuropathy • Macrovascular complications

19. Nephropathy

20. Pancreas

21. Pancreas • Exocrine: produces digestive enzymes, functions carried out by acinar tissue (grape like clusters that contain pancreatic fluid) • Excretions are alkaline in nature- high sodium bicarb • Amylase, trypsin, lipase • Secretin is a major stimulus to increase bicarb secretion in pancreas • Vagus nerve is also influential

22. Pancreas • Anatomy • Fish shaped in ULQ behind stomach • Endocrine and exocrine functions • Endocrine: secretes blood hormones to regulate blood sugar • Islets of langerhans are collection of alpha, beta, and delta cells • Beta cells produce insulin (lowers sugar) • Alpha cells secrete glucagon (raises sugar) • Delta cells secrete somatostatin (increases sugar)

23. Glucose • Circulates in the blood • Major sources of: • Ingested food absorption in GI tract • Production in liver from food substances

24. Glucagon • Secreted by alpha cells in islets of Langerhans • Stimulates conversion of glycogen to glucose in the liver • GOAL: protect the brain and heart • Mobilize glucose stores from the liver

25. Glucose Metabolism • Liver helps maintain blood glucose and serves to store it. • Liver takes up excess glucose after meal • Glycogenesis} glucose molecules taken up combined, and then stored as glycogen • Glycogenolysis} when glucose levels in blood falls • Gluconeogenesis} fats and protein broken down in response to low serum glucose levels and molecules used to make e glucose

26. What are signs/ symptoms of hyperglycemia?

27. 3 P’s} polyuria, polydipsia, polyphagia • Fatigue • Weakness • Sudden vision changes • Tingling/numbness of hands or feet • Dry skin • Slow to heal wounds • Recurrent infections

31. Diagnosis criteria • Random glucose test >200mg/dL • 3 P’s • Fasting glucose >126mg/dL • Glucose tolerance test>200mg/dL 2 hours post • Begin screen at age 45 • Screen <45 if: obese, sedentary, close relative with diabetes, high risk ethnic, babies born >9 pounds, HTN, cholesterol issues

32. Assessment • BP • BMI • Foot exam • Skin exam • Neuro exam • Oral exam

33. Diagnostics • HGBA1C • Fasting Lipid Profile • Urinalysis • EKG • CMP

34. American Diabetes Association Glycemic Goals: • HbA1C goal: <7 % (6% is upper limit for normal) without signif. Hypoglycemia • Preprandial glucose: 90-130 mg/dL • Postprandial (peak 11/2 hour) 180 mg/dL • 50% of the blood glucose values within target (70 to 140 mg/dL) • No more than 30% of readings above 200 • No more than 1 or 2 mild hypoglycemic episodes per 1 to 2 weeks

35. ADA glycemic goals (continued): • LDL <100 mg/dL • Triglycerides <150 mg/dL • HDL >40 for males, >50 for females • Blood pressure: <130/80 with no signs of orthostatic hypotension • Minimal to no peripheral edema • Urinary albumin excretion <30 • Retention of recognition of hypoglycemia

37. MEDS • Insulin used to be from pork or bovine • Now it is synthetic

38. An infusion of 50 Units of regular insulin in 100 ml of NS is running at 3 ml/hr for a patient with diabetes. This infusion is delivering how many units per hour? • A. 1.5 Unit/hr • B. 2.5 Unit/hr • C. 3 Unit/hr • D. 4 Unit/hr

39. IV contains 125 units of regular insulin in 250 ml of NS infusing at 8 ml/hr for a pt with diabetes and pancreatitis. This delivers a dose of how many units per hour? • A. 2 unit/hr • B. 4 unit/hr • C. 6 unit/hr • D. 8 unit/hr

40. Insulin • A polypeptide (so would degrade in GI tract) • Human insulin is produced by DNA technology through strains of EColi or Yeast • By modifying amino acid sequence gives Insulin different properties • Concentration: • 100 Units/ml • 500 Units/ml Regular Insulin for insulin resistance (but due to conc. Mimics intermed acting)

42. What is the most serious adverse reaction to insulin? ________________ Insulin preparations vary in their times of onset and duration of activity. - - this is due to the size & composition of insulin crystals in the preparations and the amino acid sequence of the polypeptides. (the less soluble the insulin is, the LONGER is it’s action)

43. Insulin types • Rapid acting • Short acting • Intermediate acting • Long acting • Insulin combinations

47. What can affect the absorption of Insulin? • a. _____________ • b.______________ • c.______________ • d.______________ • Insulin is inactivated by, insulinase, an enzyme in the liver.

48. causes of increased needs for Insulin • Infection • Wt gain • Puberty • Inactivity • Hyperthyroidism

49. What can cause reduced insulin needs? renal failure adrenal insufficiency wt loss increased exercise

50. Route of Insulin admin. (continued) • Regular insulin for drip • used to treat acute hyperglycemia, ketoacidosis, HHS • Continuous subcutaneous infusion pumps: • used with rapid acting insulin infused at low dose to deliver basal insulin and get deliver bolus for postprandial blood glucose control • requires MUCH TRAINING