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Diabetes/Biliary. MCC NURSING Diana Blum MSN. Definition. Disorder of carbohydrate, protein, and fat metabolism resulting from an imbalance between insulin availability and need.
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Diabetes/Biliary MCC NURSING Diana Blum MSN
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
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
Why is this happening? • _________ • _________ • __________ • __________
InsulinHormone • 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
Diabetes • Cells stop responding to insulin • Pancreas may stop producing Both lead to Hyperglycemia and complications like DKA and HHNS
PreDiabetes • Normal glucose metabolism • Obesity • Previous personal history of hyperglycemia
Insulin dependent(natural level low or absent) • Autoimmune process that destroys beta cells of the pancreas • Genetics play role • May be triggered by virus or toxins Type 1: Juvenile
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
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
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
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
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
MEDS • Insulin • What is it’s most serious side effect?_______ • What can affect the absorption of Insulin? a. _____________ b.______________ c.______________ d.______________ • Insulin is inactivated by, insulinase, an enzyme in the liver.
needs for Insulin Decreases Needs Increases Needs • Infection • Wt gain • Puberty • Inactivity • Hyperthyroidism • Exercise • Renal Failure • Weight Loss • Adrenal Insufficiency
Oral hypoglycemic agents:NEVER GIVEN TO TYPE I • First modify diet, exercise • Second modify diet, exercise, hypoglycemic • agents • Third: Insulin added to treatment as B-cells have declined over time • HOWEVER, those that respond BEST to oral agents are >40 years and have had diabetes Type II less than 5 years.
Oral hypoglycemic agentsNEVER GIVEN TO PREGNANT WOMEN AS CAN DEPLETE INSULIN FROM THE FETAL PANCREAS • 1. Sulfonylureas: • promote insulin release from Bcells • tolbutamide • glyburide • glipizide • gluimepiride • Adverse effects: • wt gain, hyperinsulinemia, hypoglycemia • NOT to be admin. To those with hepatic/renal insufficiency as causes delayed excretion resulting in • hypoglycemia
2. Meglitinide “postprandial glucose regulator” • repaglinide • nateglinide • Work like sulfonylurea but rapid onset and short duration • Very effective in early release of insulin following a meal • Very effective with metformin • Take 1 to 30 minutes AC • Caution with hepatic impairment • Causes wt gain • Hypoglycemia a factor but less than sulfonylureas
Oral hypoglycemic agents:INSULIN SENSITIZERS • Biguanides • METFORMIN (increases glucose uptake thereby decreasing insulin resistance) • Does NOT promote Insulin secretion • hypoglycemia is way less than sulfonylureas (only occurs if caloric intake not enough) • IT CAN REDUCE HYPERLIPIDEMIA • THE ONLY ORAL AGENT PROVEN TO DECREASE CV MORTALITY !!
Metformin: • - pt usually loses wt due to loss of appetite • - needs to be discontinued for pt needing IV contrast for diagnostic study • - should not be used with pts on heart failure meds causes increased risk of lactic acidosis
Oral hypoglycemic agents:α-glucosdase inhibitors • - take at beginning of the meal • - delays digestion of carbohydrates thereby decreasing glucose absorption • Acarbose • Miglitol • - do not stimulate insulin release • - do not cause hypoglycemia • Major side effects: • - flatulence, diarrhea, abd cramping • DO NOT USE WITH PT WITH INFLAMMATORY BOWEL • DISEASE, COLONIC ULCERATION, INTESTINAL OBSTUCTION
Complications • DAWN PHENOMENON: • early-morning hyperglycemia caused by decreased effectiveness of insulin & increased secretion of growth hormone & other hormones overnight. What can be changed in the insulin dosing to prevent this?? • Somogyi Effect • Hypoglycemia occurs in the middle of the nite • Glucose is released from liver • Sugar level increases while sleeping. • Pg 1681
Acute Complications Diabetic Ketoacidosis (DKA): - hyperglycemia induced crisis - precipitated by stress, infections, MI trauma, alcohol, dehydration, electrolyte loss - non-compliance - S/S: abd pain, vomiting, Kussmaul respirations, acetone breath, - severely dehydrated - may be alert, lethargic, comatose TREATMENT: fluids, K+, regular Insulin, treatment of cause, ICU
Hyperosmolar Hyperglycemic State (HHS)nonketotic - less common than DKA - insulin level is too low to prevent hyperglycemia but high enough to prevent fat breakdown - Profound dehydration - mental status changes, hyperosmolarity, - extreme hyperglycemia (>600 mg/dL) - no ketoacidosis -precipitated by: acute stress (dehydration, infections) OFTEN FATAL -hypotension, tachycardia, seizures DX: BMP, CBC, ABG
Complications of HHS: • Cerebral infarct & MI • Mesenteric thrombosis • Pulmonary embolism • DIC • Cerebral edema • CHF • ARDS • rhabdomyolysis
Teaching Opportunity • Nutrition management • Exercise • Exams
Problems with exercise for Diabetics: • Screen for retinopathy first since strenuous exercise may precipitate vitreous hemorrhage or retinal detachment • Pts with eye involvement must avoid physical activity that involves straining, jarring, valsalva-like maneuvers • Those with CVD, >35 yrs, autonomic neuropathy, PVD, microvascular disease need cardiovascular evaluation and stress test before exercise program
Exercise (continued) • Repetitive exercises on insensitive feet will cause ulcerations • NO to treadmill, jogging, prolonged walking, step exercise • Recommend: swimming, bicycling, rowing, chair exercises, arm exercises, other non-wt-bearing
Exercise (continued) • Aerobic activity: • - swim, walk, run as this promotes utilization of glucose as the fuel, desirable for CV health, hypertension, lipid profiles, circulation, wt loss • Recommended: • - 150 minutes/week of moderate (50 to 70 % of max heart rate) • - 90 min/week of vigorous (70% of max heart rate) • EXERCISE 3 days/week with no more than 2 consecutive days without exercise