NUR355 Module 8 Hepatic & Biliary Disorders PDF

Acute & Chronic Health Disruptions in Adults l Module 8 – Gastrointestinal Coordinating Care for Patients with Hepatic Disorders and Biliary & Pancreatic Disorders Chapter 59 & 60 Liver Hepatocytes, the major parenchymal cells in the liver, play pivotal roles i...

Acute & Chronic Health Disruptions in Adults l Module 8 – Gastrointestinal Coordinating Care for Patients with Hepatic Disorders and Biliary & Pancreatic Disorders Chapter 59 & 60 Liver Hepatocytes, the major parenchymal cells in the liver, play pivotal roles in metabolism, detoxification, and protein synthesis 500+ Functions of the Liver  Hepatitis Epidemiology Prevalent worldwide Risk is generally based on individual behavior and exposure Pathophysiology Inflammation of liver cells = dysfunction Limits the liver’s ability to  Detoxify substances  Produce proteins and clotting factors  Store vitamins, fats and sugars Mild to severe Acute or chronic Causes Viral (most common): A, B, C, D, E, Alcohol Medications Chemicals Autoimmune diseases Metabolic problems  Hepatitis Clinical Manifestations Complications: Severe hepatic failure Mild: flu-like symptoms Abd pain, N/V, anorexia Hepatic Encephalopathy – Liver is unable Irritability to detoxify blood; Unable to convert ↑ bilirubin ammonia into urea.  Pruritus (from bile salt accumulation) Impaired mentation  Jaundice – aka icterus (liver is unable Altered LOC to metabolize and excrete bilirubin) Confusion  Clay-colored stools (lack of bile acids Somnolence secreted by liver) Insomnia  Dark amber urine Malaise Fever Ascites – ↑ liver enzymes accumulation of fluid ↑ serum ammonia in the peritoneal cavity ↓ albumin secondary to low serum albumin levels  Hepatitis A Virus (HAV) Most common type Fecal-oral route Acute infection (up to 8 weeks) Educate: Self-limiting Vaccinate Vaccine available Hand washing Clinical Manifestations Sources of infection Contaminated food, milk, water, shellfish May be asymptomatic or mild Crowded conditions (e.g., day care, nursing home) Abrupt onset of fever with anorexia, nausea, vomiting, Persons with subclinical infections, infected food malaise, abdominal pain, myalgia, diarrhea, urticaria, handlers, sexual contact, IV drug users cough, and hepatosplenomegaly Poor personal hygiene Later: clay-colored stools, jaundice Poor sanitation Isolation precautions: standard Diagnosis of hepatitis A = presence of anti–hepatitis A immunoglobulin M If incontinent  contact isolation (IgM anti-HAV), which can be elevated for as long as 6 months.  Hepatitis B Virus (HBV) Transmission by blood, bodily fluids or secretions Acute or chronic infection Vaccine available Risk Factors Unprotected sex Household contact of chronically infected Hemodialysis Occupational exposure Injection drug users Recipients of blood products Treatment Interferon and antivirals (ex. tenofovir)  Hepatitis B surface antigen (HBsAg): acute or chronic hepatitis B virus infection or within 30 days of hep B vaccine  Hepatitis B surface antibody (anti-HBs): recovery and immunity from hepatitis B virus infection Isolation precautions: standard  Hepatitis C Virus (HCV) Transmission by blood, bodily fluids or secretions Acute or chronic infection Most common indication for liver transplantation Vaccine NOT available Risk Factors IV drug use High-risk sexual behaviors Occupational exposure Perinatal exposure Blood and blood products Clinical Manifestations Acute: asymptomatic Chronic: liver damage  15- to 20-year delay between infection and the Treatment manifestations of liver damage Interferon and antivirals Isolation precautions: standard  Hepatitis D Virus (HDV) Also called delta virus Cannot survive on its own Requires HBV to replicate Transmitted percutaneously No vaccine Hepatitis E Virus (HEV) Similar to hepatitis A Transmitted via fecal-oral route Most common mode of transmission: drinking contaminated water Occurs primarily in developing countries Few cases in United States No vaccine  Viral Hepatitis Stages of viral hepatitis: Preicteric/Prodromal (flu- Acute infection: Large numbers of hepatocytes are destroyed; Liver cells can like symptoms) regenerate in normal form after resolution of infection (acute = 6 months) Post-icteric/Convalescent (Recovery) Antigen-antibody complexes activate complement system  Hepatitis - Diagnostics Review Table 59.2 Diagnostic Testing for Liver Disorders H&P Alanine transaminase (ALT): enzyme found in the liver that helps convert proteins into Labs: AST, ALT, albumin energy for the liver cells. When the liver is damaged, ALT is released into the Specific antigen and/or antibody bloodstream and levels increase. for each type of viral hepatitis Aspartate transaminase (AST): enzyme that helps metabolize amino acids. Like ALT, Viral genotype testing AST is normally present in blood at low levels. An increase in AST levels may indicate liver damage, disease or muscle damage. Liver biopsy Alkaline phosphatase (ALP): enzyme found in the liver and bone and is important for FibroScan breaking down proteins. Higher-than-normal levels of ALP may indicate liver damage or FibroSure (FibroTest) disease Albumin and total protein: albumin is one of several proteins made in the liver. Lower- than-normal levels of albumin and total protein may indicate liver damage or disease. Bilirubin: product of hemolysis. Bilirubin passes through the liver and is excreted in stool. Elevated levels of bilirubin (jaundice) might indicate liver damage or disease or certain types of anemia. Gamma-glutamyltransferase (GGT): enzyme in the blood. Higher-than-normal levels may indicate liver or bile duct damage. L-lactate dehydrogenase (LD): enzyme found in the liver. Elevated levels may indicate liver damage but can be elevated in many other disorders. Prothrombin time (PT): the time it takes your blood to clot. Increased PT may indicate liver damage.  Hepatitis – Management Nutrition: Teaching Emphasis on well-balanced diet that patient Hand hygiene can tolerate Avoid high risk behaviors Adequate fluid intake Vaccinate (A & B) Adequate calories are important during Safe public water supply, sewage acute phase (hepatocytes need nutrients to Avoid alcohol and hepatoxic medications regenerate) Fat content may need to be reduced temporarily Vitamin supplements Small, frequent meals Sharps & Needle Stick Injuries! Pancreas Pancreas Amylase – breaks down carbohydrates Protease – breaks down protein into amino acids (alanine, lysine, histidine, glutamine) Lipase – breaks down fat  Acute Pancreatitis Acute inflammation of pancreas Spillage of pancreatic enzymes into surrounding pancreatic tissue causing autodigestion and severe pain Varies from mild edema to severe necrosis Causes Gallstones (women) Alcohol (men) Other less common causes  Drug reactions  Pancreatic cancer  Hypertriglyceridemia  Trauma (ex. ERCP)  Acute Pancreatitis Clinical Manifestations Abdominal pain predominant  Sudden onset Abdominal fullness (gas/bloating)  LUQ or mid-epigastric Hiccups  Radiates to back Indigestion  Deep, piercing, continuous, or steady Nausea/vomiting  Rebound tenderness Fever  Eating worsens pain Tachycardia  Starts when recumbent Hypotension  Not relieved with vomiting Acute pancreatitis with necrosis: Grey Turner’s or Cullen’s sign  Acute Pancreatitis Diagnostics Labs  ↑↑ Amylase  ↑ Lipase  ↑ Liver enzymes  ↑ Glucose  ↑ Bilirubin  ↓ Calcium Abdominal ultrasound Chest X-ray CT with contrast ERCP – Endoscopic retrograde cholangiopancreatography EUS – Endoscopic ultrasonography MRCP – Magnetic resonance cholangiopancreatography  Acute Pancreatitis - Management Objectives include:  Aggressive hydration – lactated ringers Relief of pain Prevention or alleviation of shock  Pain management – IV opioids, may be paired with antispasmodic; side-lying Decreased pancreatic secretions position with the head elevated 45 degrees Correction of fluid/electrolyte  Decrease pancreas stimulation – NPO, NGT (if vomiting &/or ileus present); imbalances pain/restlessness can increase metabolic rate and stimulate pancreas Prevention/treatment of infections  Decrease acid formation – antacids, histamine H2-receptor antagonists, PPIs Removal of precipitating cause  Metabolic problems – oxygen, glucose levels  Monitor fluid & electrolyte balance: If gallstones are cause – may need cholecystectomy Frequent vomiting, along with gastric If pseudocyst is present – will need drain Resume oral intake when pancreatitis resolves & bowel sounds present suction, may result in: Inflamed & necrotic pancreatic tissue can harbor/grow bacteria – start ↓chloride, ↓sodium, ↓potassium antibiotics early Education: No smoking (nicotine stimulates pancreas) Fat restriction (fat stimulates the secretion of cholecystokinin, which then stimulates the pancreas); Carbs preferred. Avoid crash and binge dieting, which can precipitate attacks S/S infection, diabetes, or steatorrhea (foul-smelling, frothy stools). May need exogenous enzyme supplementation  No Morphine  Chronic Pancreatitis Continuous, prolonged inflammatory, and fibrosing process of the pancreas  Incurable disease Diagnostics – may be difficult to confirm. Based on signs/symptoms, labs, imaging Labs: Amylase/lipase, ↑bilirubin, ↑alkaline phosphatase, mild leukocytosis, ↑ESR CT, US, ERCP Stool samples for fat content Decreased fat-soluble vitamin and cobalamin levels Glucose intolerance/diabetes Clinical Manifestations Upper abdominal pain (same Surgery (not curative) as acute) Treatment Risky, not always appropriate  Recurrent/constant Pain management Peustow procedure – Diverts bile flow or relieves ductal  Worse with overeating IV fluid replacement obstruction and alcohol Laparoscopic draining – for abscesses or pseudocysts Electrolyte management Diarrhea, N/V Nutritional support Steatorrhea/oily stools Insulin Education Pale, or clay colored stool Avoid alcohol, caffeine & coffee Pancreatic enzyme Malabsorption with weight Do not chew pancreatic enzymes replacement Limit fat in diet loss Refer to support groups  Pancreatic Cancer Treatment: Surgery, chemotherapy, radiation Cause unknown Risk factors Whipple procedure Smoking (pancreaticoduodenectomy) – a Diets high in fat, meat, fried complex surgery to remove the food, refined sugars, nitrates head of the pancreas, the first Diabetes, chronic pancreatitis part of the small intestine Family hx (duodenum), the gallbladder Age (>60) Diagnostics and the bile duct. US, MRI, ERCP Used to treat tumors and other Biopsy disorders of the pancreas, Clinical Manifestations intestine and bile duct. Depends on tumor growth Early: may be asymptomatic Jaundice Poor Prognosis. Dull pain (epigastric and back) Most patients die within 5 to 12 months of diagnosis. Anorexia, weight loss The 5-year survival rate is only 8% Fatigue Biliary System  Gallbladder & Bile Ducts Primary purpose of the biliary system – transports bile from the liver, where it is produced, to the gallbladder, where it is stored, and then to the duodenum, where it aids in the digestion of fat Bile – a digestive enzyme that helps break down fats; Bile is a mixture of mainly cholesterol, bilirubin and bile salts  Cholecystitis Inflammation of the gallbladder caused by an obstruction of bile flow  Calculous (with gallstones)  Acalculous (without gallstones) Risk factors Causes: abd sx, long-term IV nutrition, prolonged fasting, Obesity Sickle Cell Disease, DM, AIDS Rapid weight loss Weight loss surgery Gallstones (Cholelithiasis) – High fat diet hard deposits formed from bile Pregnancy Genetics Medications (estrogen, octreotide, and cholesterol- lowering medications) Gallstones classification: cholesterol stones (the most common type), pigmented (formed from excess bilirubin), and mixed stones (combination of both types)  Cholecystitis Clinical Manifestations Cholecystokinin is activated when eating RUQ pain and causes the Rebound tenderness or guarding gallbladder to contract Fever, tachycardia and release bile, + Murphy’s sign leading to pain in Impaired bile flow: jaundice, dark cholecystitis. amber urine, clay-colored stools Tachycardia Diagnostics Treatment Abd x-ray Lithotripsy (small stones) Abd US Medications Laparoscopic surgery CT, HIDA scan NPO Dissolution medication ERCP IV hydration Cholecystography Correct electrolyte/fluid imbalances Cholangiogram Pain management WBC IV antibiotics, if needed ↑ Liver enzymes (AST, ALT, LDH, ALP) Teaching ↑ Bilirubin Postop instructions T-Tube management Avoid diet high in saturated fats