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LIVER and PANCREAS DYSFUNCTION Zelne Zamora, DNP, RN PANCREAS Exocrine Secretes digestive enzymes into the small intestines Breakdown of CHO, protein, and fats Endocrine Produces hormones Insulin Glucagon EXOCRINE FUNCTION CCK: Cholecystokinin Secretin Stimulus for enzyme secretion Secretion of bicarb and water Lipase: Fats Amylase: Carbohydrates Trypsin: Proteins EXOCRINE FUNCTION 90% of pancreatic digestive enzymes are proteolytic Trypsin Chymotrypsin splits proteins into peptones Elastase Breakdown elastic tissue EXOCRINE FUNCTION Amylolytic Breakdown of carbohydrates Amylase Lipolytic Breakdown of fats Lipase Phospholipase A ENDOCRINE FUNCTION Islet of Langerhans Alpha cells Beta cells Glucagon: ↑ blood glucose Insulin: ↓ blood glucose Delta cells Somatostatin PANCREATITIS Inflammation of the pancreas Autodigestion of the pancreas by pancreatic enzymes Cellular destruction and organ damage ACUTE PANCREATITS Acute Mild or Nonhemorrhagic Severe or Hemorrhagic Fulminant EPIDEMIOLOGY 185,000 cases each year 150,000 cholelithiasis or sustained alcohol abuse African-Americans are at ↑ risk CAUSES Alcohol consumption Gallstones Pancreatic obstruction Drugs and toxins Hyperlipidemia Family history Trauma and iatrogenic factors SIGNS and SYMPTOMS Severe abdominal pain Epigastrium radiating to midback Not relieved by vomiting Fever, malaise Nausea, vomiting Rigid and distended Rebound tenderness Absent or diminished bowel sounds SIGNS and SYMPTOMS Dyspnea and Tachypnea Grey Turner’s sign Large ecchymosis appearing in the flanks Cullen’s sign Pulmonary infiltrates Ecchymosis in umbilical area Hypovolemic Shock DIAGNOSTIC FINDINGS Serum Amylase Serum Lipase Normal (23-85 u/L) Normal (0-160 u/L) Serum trypsinogen: elevated Urinary amylase: elevated DIAGNOSTIC FINDINGS Hematocrit: initially elevated then later decreased WBC: elevated C-reactive protein: elevated Liver function tests: elevated DIAGNOSTIC FINDINGS Sodium and Potassium: decreased Blood glucose: elevated Serum Calcium: decreased Albumin and Magnesium: decreased DIAGNOSTIC FINDINGS Abdominal and Chest X-ray CT scan, Ultrasound, MRI Endoscopic Retrograde Cholangiopancreatography (ERCP) Aspiration biopsy Stool studies: steatorrhea COMPLICATIONS Hypovolemic shock 3rd spacing Hemorrhage Vomiting Decreased protein intake COMPLICATIONS Pulmonary complications Atelectasis Acute lung injury Pleural effusion ARDS COMPLICATIONS Cardiovascular Release of myocardial depressant factor Pancreatic pseudocyst Cavity next to pancreas Filled with necrotic products COMPLICATIONS Pancreatic abscess 2-4 weeks after episode Necrosis of tissue Relocation of bacteria Hypocalcaemia can occur with severe disease COMPLICATIONS Fluid and electrolytes Vomiting NG suction Redistribution of fluids TREATMENT Pain Management IV opioid analgesics Dilaudid IV PCA Demerol and Morphine IV GI rest Decrease stimulation of pancreas Nasogastric tube insertion TREATMENT Fluid and Electrolyte replacement Cessation of alcohol consumption Nutrition: enteral versus parenteral Surgery if there is biliary obstruction TREATMENT Respiratory Oxygen Monitor oxygen saturation Arterial blood gas Ventilator support TREATMENT Fluid volume deficit IV fluids Plasma expanders Vasopressors Blood replacement Strict intake and output TREATMENT Fluid and electrolyte imbalance LR or IV maintenance fluid containing K+ Calcium gluconate Hypocalcemia Chvostek’s sign Trousseau’s sign TREATMENT Pseudocyst, abscess or fistula Monitor for signs and symptoms of shock Prepare patient for surgery Watch for infections post-operatively TREATMENT Biliary drainage tube Surgical debridement ERCP Sphinceterotomy Gallstone removal Stent placement Balloon dilatation Laparoscopic cholecystectomy with CBDE MEDICATIONS Viokase Pancrease Replace pancreatic enzymes Replace pancreatic enzymes Glucagon Treat hypoglycemia NURSING IMPLICATIONS Vital signs Laboratory values Hypovolemic shock Sepsis Amylase, Lipase BMP Fluid and electrolytes NPO NGT Nutrition NURSING IMPLICATIONS Administer pain medication Monitor blood glucose Monitor intake and output Daily weight CHRONIC PANCREATITIS Persistent inflammation of the pancreas Scarring and calcification of the pancreatic ducts CAUSES 70% is caused by alcohol abuse 20% is caused by obstruction, trauma, metabolic disturbances SIGNS & SYMPTOMS 80% of pancreatic destruction causes Malabsorption resulting in nutritional deficits Diarrhea and steatorrhea Impaired glucose regulation DIAGNOSTIC FINDINGS LFT, CMP, CBC, ESR Stool studies Abdominal CT scan Abdominal US Images organ, detect inflammation Detect inflammation and calcifications ERCP looks for stones TREATMENT GI rest Pain control No Alcohol Daily weight TREATMENT Low fat, protein, and high carbohydrate diet Oral pancreatic enzymes Monitor blood glucose TREATMENT Replacement of fat soluble vitamins Octreotide (Sandostatin) Celiac plexus block LIVER FUNCTION Glucose metabolism Ammonia conversion Glycogenolysis Gluconeogenesis Ammonia to urea Urea excreted in the urine Protein metabolism Synthesis of plasma proteins LIVER FUNCTION Fat metabolism Vitamin and iron storage Fatty acids broken down for energy Vitamin A,B,D, and Bcomplex vitamins Bile formation Bilirubin excretion Drug metabolism LIVER FUNCTION TESTS ALT: Alanine aminotransferase ALP: Alkaline phosphotase AST: Aspartate aminotransferase Bilirubin Albumin LIVER PANEL Total Protein GGT: Gammaglutamyl transferase LDH: Lactic acid dehydrogenase Prothrombin time HEPATIC DYSFUNCTION Primary liver disease Obstruction of bile flow Altered hepatic circulation Acute or chronic CAUSES Toxicities: Chemicals, Plants, Drugs Bacterial invasion Nutritional deficiency Autoimmune Hepatitis Viruses Hepatitis A,B,C,D,E CHRONIC LIVER DISEASE 12th leading cause of death in the United states among young and middle-aged adults 40% associated with alcohol use Cirrhosis SIGNS & SYMPTOMS Jaundice Portal hypertension Ascites and varices Nutritional deficiencies Hepatic encephalopathy Coma JAUNDICE Bilirubin level >2.5 mg/dL All body tissue become tinged yellow Hepatocellular jaundice Obstructive jaundice PORTAL HYPERTENSION Increased pressure through portal venous system Obstructed blood flow through damaged liver Commonly associated with liver cirrhosis PORTAL HYPERTENSION GI bleeding Black tarry stool Hematemesis Encephalopathy Coagulopathy Ascites ASCITES Backup of venous blood flow from portal HTN Failure to metabolize aldosterone Movement of fluid from vessels to peritoneal space Accumulation of albumin-rich fluid HEPATIC ENCEPHALOPATHY Life-threatening complication of liver disease Liver unable to detoxify toxic byproducts of metabolism Ammonia is the major etiologic factor of encephalopathy HEPATIC ENCEPHALOPATHY Mental changes Motor disturbances Altered mood and sleep patterns Asterixis “liver flap” Flapping tremor of the hands Constructional apraxia VIRAL HEPATITIS Systemic, viral infection Necrosis and inflammation of liver cells Altered liver function 5 definitive types of viral hepatitis Hepatitis A, B, C, D, E HEPATITIS A Hepatitis A Virus Fecal-oral transmission Poor sanitation Person-person contact Water and food borne Incubation 15-50 days SIGNS and SYMPTOMS Hepatitis A Phases Preicteric Flu-like symptoms Fatigue Loss of appetite Nausea Cough Joint pain SIGNS and SYMPTOMS Icteric Jaundice Dark colored urine RUQ pain Itchy skin Clay-colored stools Poor appetite Some preicteric symptoms subside SIGNS and SYMPTOMS Post icteric phase Things start to return to normal Fatigue can remain HEPATITIS A Mild with recovery No carrier state Spread from person to person – poor hand washing, intimate kissing (fecal oral) Spread by food or water Doesn’t usually lead to chronic state HEPATITIS A Prevention Hand washing Safe water supplies Proper sanitation Sewage disposal HAV vaccination Medical Management Bed rest during acute stage Small frequent meals Supplemental IV with glucose Gradual progressive ambulation HEPATITIS B Hepatitis B Virus Parenteral transmission – serum or blood Intimate contact with carriers Transfer of blood or serum through shared needles Perinatal: mother to baby Occupational hazard to health care workers HEPATITIS B Hemodialysis Tattooing or body piercing Perinatal: mother to baby Occupational hazard to health care workers Can lead to chronic state Can develop cirrhosis later HEPATITIS B Incubation: 28-160 days Symptoms: rash and arthralgias Outcome: may be severe Carrier state possible Increased risk of chronic hepatitis HEPATITIS B Prevention Hand washing Wear gloves when handling body fluids safe sex HBV vaccination Hepatitis B Immunoglobulin Medical management Alpha-interferon Lamivudine (Epivir) and adefovir (Hepsera) Bed rest until s/s subside Restrict activities Adequate nutrition HEPATITIS B PANEL HBsAg: Hepatitis B surface antigen HBsAb or Anti-HBs: Hepatitis B surface antibody HBcAb: Hepatitis B core antibody HEPATITIS C Hepatitis C Virus Non-A, Non-B virus Blood transfusion transmission Exposure to contaminated blood HEPATITIS C Shared needles of drug abusers Intimate contact with infected partner [Rare] Increased risk for STDs 90% of transfusion – associated hepatitis Can lead to chronic hepatitis, liver failure and liver cancer HEPATITIS C Incubation: 15-160 days Symptoms: similar to HBV. Less severe and anicteric Chronic carrier state Can lead to chronic liver disease Increased risk for cancer HEPATITIS C No benefit from rest, diet, or vitamin supplements Antiviral agents Interferon (Intron-A) Ribavirin (Rebetol) Side effect: hemolytic anemia HEPATITIS D Delta agent HBV surface antigen required for replication Incubation: 21-140 days Symptoms: similar to HBV Can lead to carrier state, chronic active hepatitis, and cirrhosis HEPATITIS E Hepatitis E Virus Fecal-oral transmission – esp. contaminated water Low risk for person to person contact Incubation: 15-65 days Symptoms: Similar to HAV Severe in pregnant women Seen commonly in Asia HEPATITIS G and GB VIRUS C Non A-E virus Incubation: 14-145 days 2 isolates of same virus Resembles HCV – similar transmissions Autoantibodies are absent Co-infection with other viruses Persistent infection – up to 9 years No Tx TOXIC HEPATITIS Resembles viral hepatitis Exposure to toxic chemicals Medications Botanicals Alcohol Industrial chemicals Remove causative agent TOXIC HEPATITIS Anorexia, nausea, vomiting Jaundice Hepatomegaly No effective antidotes Delay in treatment can result in increased severity DRUG INDUCED HEPATITIS Most common cause of acute liver failure 50% of all cases in the U.S. Acetaminophen has been identified as the leading cause of acute liver failure DRUG INDUCED HEPATITIS Onset is abrupt Early symptoms Late symptoms Fever, chills, rash, arthralgia, pruritus, anorexia Jaundice, dark urine, enlarged and tender liver Treatment Short course of highdose corticosteroids TREATMENT Rest Small, frequent meals Low protein, fat, and high carbohydrate IV fluid containing dextrose as needed Monitor labs