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? _________ _________ __________ __________ W H AT A R E T H E R I S K FAC T O R S ? 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 DIABETES PREDIABETES Normal glucose metabolism Obesity Previous personal history of hyperglycemia TYPE 1: JUVENILE 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 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 W H AT I S T H E OV E R A L L G OA L ? C H R O N I C C O M P L I C AT I O N S TO DIABETES 15 NEPHROPATHY 16 SIGNS AND SYMPTOMS • 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 DIAGNOSIS CRITERIA AMERICAN DIABETES A S S O C I AT I O N G LYC E M I C G OA L S : 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 23 A DA G LYC EMI C G OA L S ( C O N T I N U ED) : 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 24 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 Increases Needs Infection Wt gain Puberty Inactivity Hyperthyroidism Decreases Needs Exercise Renal Failure Weight Loss Adrenal Insufficiency 29 O R A L H Y P O G LYC E M I C AG E N TS : 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. 33 ORAL HYPOGLYCEMIC AGENTS NEVER GIVEN TO PREGNANT WOMEN AS CAN D E P L E T E I N S U L I N F R O M T H E F E T A L PA N C R E A S 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 34 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 37 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 !! 38 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 39 ORA L HYPOG LYCEMIC AG EN TS: Α - G LU C O S DA S E I N H I B I T O R S - 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 40 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 42 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 45 TEACHING OPPORTUNITY Nutrition management Exercise Exams P R O B L E M S WI T H E X E R C I S E 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 48 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 49 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 50 Anaerobic activity: - wt lifting (avoided) unless approved by cardiologist and ophthalmologist - if approved: - 3x/week, targeting all major muscle groups 51 ELECTROLYTE MANAGEMENT Phosphate is not recommended to be replaced Calcium and Magnesium may be Potassium shifts from intracellular to extracellular placing them at risk for ____? _HYPOKALEMIA_. Bicarb is only replaced in life threatening situations( acidosis <6.9) • HYPOGLYCEMIA/INSULIN SHOCK • 1) The person will be sweating, clammy, pale, trembling and feel weak. • 2) Ask the person what he needs and get it for him or her. • 3) Feed the person a quickly absorbed sugar such as fruit juice, honey or a soft drink. Do not attempt to feed a person who has lost consciousness. W H AT D O YO U D O I F T H E Y BECOME UNCONSCIOUS BEFORE ABLE TO FEED A CARB/JUICE, ETC.? • Dextrose 50% • (D 50) • 25gm/50ml - 1 ampule • Usual Dose: 1 amp Action: Provides glucose calories for metabolic needs Indications: Hypoglycemia, Use with insulin for hyperkalemia Precautions: Monitor blood glucose, can cause thrombosis in small veins. BILIARY TRACT ASSESSMENT Present illness: digestive disturbance, pain, meals, aggravating and relieving factors PMH: GB dx, pregnancy, surgery, meds Fam Hx: GB dx System: pruritis, indigestion, fat intolerance, dyspepsia, n/v, light colored stools, dark urine HEPATITIS JAUNDICE Hepatitis A (HAV) Hepatitis B (HBV) Hepatitis C (HCV) Hepatitis D (HDV) Hepatitis E (HEV) What is it? HAV is a virus that causes inflammation of the liver. It does not lead to chronic disease. HBV is a HCV is a virus HDV is a virus that causes HEV is a virus that causes virus that that causes inflammation of the liver. inflammation of the liver. It is causes inflammation of It only infects people with rare in the United States. There is inflammationthe liver. This HBV. no chronic state. of the liver. infection can lead The virus to cirrhosis and can cause cancer. liver cell damage, leading to cirrhosis (scarring of the liver) and cancer. Incubation period 15 to 50 days. 45 to 2 to 25 2 to 8 2 to 9 weeks. Average 40 days. Average 30 days. 160 weeks. weeks. days. Average Average 7 to 9 120 weeks. days. Hepatitis A Hepatitis B Hepatitis C Hepatitis D (HAV) (HBV) (HCV) (HDV) How is it spread? Transmitted by Contact with Contact with Contact with infected fecal/oral route, infected infected blood, contaminated through close blood, seminal blood, needles. Sexual contact person-to-person fluid, vaginal contaminated with HDV-infected contact or ingestion secretions, IV needles, person. of contaminated contaminated razors and food and water. needles, tattoo/body including piercing tattoo/body tools. piercing tools. Infected Infected mother to mother to newborn. newborn. NOT easily Human bite. spread Sexual through sex. contact. Hepatitis E (HEV) Transmitted through fecal/oral route. Outbreaks associated with contaminated water supply in other countries. Hepatitis A (HAV) Symptoms May have none. Adults may have light stools, dark urine, fatigue, fever and jaundice (yellowing of the skin). Hepatitis B (HBV) Hepatitis C (HCV) Hepatitis D (HDV) May have none. Even fewer acute Same as HBV. Some people have cases seen than any mild flu-like other hepatitis. symptoms, dark Otherwise same as urine, light stools, HBV. jaundice, fatigue and fever. Hepatitis E (HEV) Same as HBV. Treatment of chronic disease No specific treatment. Interferon and anti- Interferon Interferon. virals. (peginteferon) along with the antiviral ribavirin. Supportive. Hepatitis A (HAV) Hepatitis B (HBV) Hepatitis C (HCV) Hepatitis D (HDV) Hepatitis E (HEV) Who is at risk? Household or sexual contact with an nfected person or iving in an area with HAV outbreak. Travelers to developing countries, men who have sex with men and IV and non-IV drug users. Infant born to Anyone who had a blood IV drug users, men Travelers to infected mother,transfusion or organ transplantwho have sex with developing countries, having sex with before 1992, health care men, dialysis patients, especially pregnant infected person workers, IV drug users, dialysis healthcare workers, women. or multiple patients, infants born to infants born to partners, IV infected mother and having infected mothers and drug users, multiple sex partners. those having sex with a emergency HDV infected person. responders, health care workers, men who have sex with men, household contacts of chronically infected persons and dialysis patients. Hepatitis A (HAV) Hepatitis B (HBV) Hepatitis C (HCV) Hepatitis D (HDV) Hepatitis E (HEV) Prevention Get a hepatitis A vaccine. Get a hepatitis B vaccine. Take immune globulin within two weeks of Take immune exposure. globulin within two weeks of exposure. Wash hands with soap and water after going to the Practice safe sex. toilet. Clean up infected Use household bleach to blood with bleach clean surfaces and wear protective contaminated with feces, gloves. such as changing tables. Don't share razors, Practice safe sex. toothbrushes or needles. Don't inject street drugs. Don't get a tattoo or body piercing. Practice safe sex. Clean up spilled blood with bleach. Wear gloves when touching blood. Don't share razors or toothbrushes. Don't inject street drugs. Don't get a tattoo or body piercing. Get a hepatitis B vaccine Avoid drinking or using to prevent HBV infection. potentially contaminated water. Practice safe sex. Wash your hands with soap and water after going to the toilet. CIRRHOSIS 12th leading cause of death Irreversible Causes: hepatitis, rt heart failure, ETOH Alcohol is most common in USA S/S: gradual, fatigue, weakness, anorexia, wt loss, VIT D deficiency PORTAL HTN Result of scarring of liver Normal is 3mmHG increases to 10mmHG Portal veins carry blood from GI tract Causes varices or thin walled veins being prone to rupture and ascites CHOLELITHIASIS Gallstones in biliary tract If stone can’t pass it causes obstruction 2 stone types: cholesterol and pigmented s/s: fever, N/V, abd pain, right shoulder pain, back pain, restlessness after meals, jaundice, pruritis, clay colored stools, dark urine, deficiencies in vitamin A, E, D, K Diagnostics: abd x-ray, US, MRI, FLP, ERCP, TX: LAP- Chole, provide rest, IVF, NG Sxn, Antibx, low fat liquid diet immediately after episode avoiding eggs, cream, pork, fried foods, cheese, rich dressings, gas forming veggies, and alcohol. BILIARY DYSKINESIA • Motility disorder of the GB • Uncommon • S/S: episodic epigastric or RUQ pain, N/V • Pain occurs after fatty meal • Dx: serum bilirubin amylase, lipase, AST, ALT,CBC • Tx: surgery, low fat diet, meds (ursodial or chenodiol), lithotripsy, herbal goldenseal ASSESSMENT Present illness: general well being, digestive problems, pain PMH: abd trauma, abd disorders, surgery, metabolic disorders, meds FAM HX: pancreatic disorders System: pruritis, resp distress, n/v, abd pain Functional: diet, ETOH use Exam: restlessness, flushing, diaphoresis, low grade fever, tachycardia, tachypnea, hypotension, jaundice, dryness, scratches, abd distention, tenderness, hypoactive bowel tones, abd discoloration PANCREATITIS • Inflamed pancreas from activation of potent pancreatic enzymes within the pancreas, mainly trypsin – Acute or chronic • Causes: ETOH, viral infections, peptic ulcer dx, cysts, renal fx, hyperparathyroidism, trauma, surgery, etc • S/S: abd pain, severe vomiting, flushing, cyanosis, dyspnea, low grade fever, tachycardia and tachypnea, hypotension, distended abd, absent bowel tones = ileus, shock PANCREATIC CANCER Spreads quickly • 75% are adenocarcinomas at head of pancreas 43920 new cases each yr in USA • Many cases are men in 60s Risk factors: smoking, pancreatitis, high fat diet Dx: Spiral CT is the most accurate tool S/S:pain, jaundice, liver enlargement, wt loss, glucose intolerance, anorexia, vomiting, weakness, diarrhea • The most common sign is painless progressive jaundice Tx: surgery, pain meds, tube feedings, post op radiation, chemo NSG DX: pain, fear, skin integrity, disturbed body image THE END Questions