Gastrointestinal Laboratory Testing and Accessory System Disorders Cathy Gibbs BSN, RN

Laboratory and Diagnostic Examinations Serum bilirubin test Direct & Indirect bilirubin Elevated with alcoholism, biliary obstruction, anemia, hepatitis, malaria, pancreatitis, cirrhosis Liver enzyme tests-(SGOT, AST) An enzyme found primarily in the heart and liver Elevated in liver necrosis and CA, alcoholism and pancreatitis Serum protein test Measures total protein in the blood. Decreased with cirrhosis Measure of nutrition-decreased intake Bilirubin=a by-product of hemoglobin metabolism Direct bilirubin-excreted by the GI tract Indirect circulates in the bloodstream

Laboratory and Diagnostic Examinations Oral cholecystography (gallbladder series) Using oral dye the gallbladder is viewed via x-ray to view obstruction of ducts Intravenous cholangiography (IV cholangiogram) Using IV dye the ducts are viewed by taking x-rays every 20 minutes until the ducts are viewed to rule out blockage Patient is NPO and receives a cleansing laxative the morning of the test Operative cholangiography Done in the OR during a cholesystectomy

Laboratory and Diagnostic Examinations Ultrasound of the liver, gallbladder, and biliary system Gallbladder scanning Liver biopsy Invasive procedure performed in a surgical setting Using a needle or punch a sample if tissue is taken using sterile technique Patient NPO, watch for bleeding Liver scanning

Laboratory and Diagnostic Examinations Blood ammonia Hepatitis virus studies Check for the Hepatitis antigen Serum amylase test Cardinal test elevated in pancreatitis Urine amylase test Elevated in pancreatitis and cholelithiasis Ultrasound of pancreas CT scan of the abdomen Blood ammonia- Produced by the breakdown of proteins by bacteria in the intestine, ammonia is then detoxified by the liver into urea and excreted circulating levels should be very low, levels monitor liver function Serum amylase test Enzyme breaks down starch to sugar

Laboratory and Diagnostic Examinations Endoscopic retrograde cholangiopancreatography of the pancreatic duct (ERCP) Patient NPO Views the liver, gallbladder and pancreas Gold standard to diagnose stones in the common bile duct

Disorders of the Liver Cirrhosis Jaundice Hepatitis Liver abscess Cholecystitis Cholelithiasis Pancreatitis

Cirrhosis Etiology/Pathophysiology Chronic, degenerative disease of the liver Fibrous scar tissue restricts the flow of blood to the liver Parenchyma degenerates and the liver lobules are filled with fat Alteration of liver function Reduced ability to metabolize albumin The liver has the potential for regeneration but with repeated insults and continued diminished blood flow the scar tissue increases and the organ atrophies

Cirrhosis Complications Clotting dysfunction Portal hypertension The liver has a reduced capacity to produce RBC’s, decreased or absent ability to absorb VIT K, and the inability to produce the clotting factors 7,9,10 Portal hypertension Obstruction of the portal vein as it enters the liver, leads to increased pressure in the veins that drain the GI tract Ascites Because the damaged liver cannot metabolize protein effectively protein levels are high in the vascular space, thus fluid begins to leak from the vessels into the extravascular space

Cirrhosis Complications Esophageal varices Enlarged veins at the lower end of the esophagus that are prone to bleeding Treatment Beta blockers to reduce pressure Sengstaken/blakemore tube Hepatic encephalopathy Decreased protein metabolism = increased blood ammonia levels Asterixis-hand flapping tremor from increased ammonia. Lactulose Neomycin Lactulose traps the ammonia in the gut and has a laxative effect and the ammonia is expelled in stool. Neomycin is given to reduce the bacterial flora in the colon, because bacterial action on protein in the colon produces ammonia

Cirrhosis Types of cirrhosis Alcoholic cirrhosis-portal-most common Postnecrotic cirrhosis-caused by viral hepatitis, exposure to hepatotoxic chemicals, or infection Primary biliary cirrhosis-destruction of bile ducts, more often in women Secondary biliary cirrhosis-from prolonged biliary tract obstruction from gall stones or tumor or inflammation Cardiac cirrhosis-from long standing right sided heart failure

Cirrhosis Clinical manifestations/Assessment Early stages Abdominal pain Liver is firm and easy to palpate hepatomegaly

Cirrhosis Clinical manifestations/Assessment Nausea and vomiting Late stages Dyspepsia Changes in bowel habits Nausea and vomiting Gradual weight loss Ascites Enlarged spleen Spider angiomas Anemia Bleeding tendencies, epistaxis, bleeding gums Purpura Hematuria Jaundice Disorientation Dark amber urine Clay colored stools

Systemic clinical manifestations of liver cirrhosis.

Hepatomegaly and Ascites

Jaundice

Jaundice

Urine bilirubin

Cirrhosis Medical management/Nursing interventions Eliminate the cause Alcohol Hepatotoxins Environmental exposure to harmful chemicals Antiemetics Benadryl and Dramamine Contraindicated: Vistaril, compazine, and Atarax Diet Well-balanced High calorie Moderate protein Low fat Low sodium Supplemental vitamins and folic acid

Cirrhosis Ascites Bedrest Strict I&O Restrict fluids and sodium Medical management/Nursing interventions (continued) Ascites Bedrest Strict I&O Restrict fluids and sodium Diuretics: aldactone, Lasix, HCTZ Vitamins K, C, and folic acid supplements Paracentisis-draining the fluid from the abdomen Pt sits up and fluid is drained LeVeen peritoneal-jugular shunt-shunts ascites in the superior vena cava Pt must be monitored for symptoms of CHF, leakage of fluid, infection (peritonitis) and shunt occlusion

Cirrhosis Medical management/Nursing interventions (continued) Ruptured esophageal varices Maintain airway; establish IV Vasopressin drip to control bleeding Sengstaken-Blakemore tube Endoscopic sclerotherapy Portacaval shunt-shunts the blood from portal circulation to the inferior vena cave to decrease portal pressure Blood transfusion

Cirrhosis Medical management/Nursing interventions Hepatic encephalopathy Decrease protein in diet Avoid drugs which are detoxified by the liver Lactulose Neomycin

Cirrhosis Vitamin/Supplements Vitamin A-increased mobilization Liver alteration and enhanced cardiogenesis Vitamin D-less converted to active form Altered Ca++ metabolism, increased bone fractures Thiamin- decreased absorption, increased destruction and excretion Nerve damage, psychosis related to Wernicke-Korsakoff syndrome (loss of short term memory, inability to learn new skills, confabulation to hide deficits, double vision, rapid eye movements, lack of muscular coordination, decreased mental function) Folate-decreased absorption Megaloblastic anemia

Cirrhosis Vitamin/Supplements Vitamin C-decreased absorption Decreased protection from ethanol toxicity Iron-increased absorption Increased damage to the liver Magnesium-increased excretion EKG changes (bradycardia or heartblock) DT’s Zinc-increased excretion Slow wound healing Potassium-increased excretion Muscle weakness, EKG changes (>7 peaked t waves, >10 cardiac function can cease)

LaVeen Continuous Peritoneal Shunt

Hepatitis Etiology/Pathophysiology Inflammation of the liver resulting from several types of viral agents or exposure to toxic substances Other modes of exposure- tattoos, body piercing and nail salons

Hepatitis Etiology/Pathophysiology (continued) Hepatitis A Most common Oral-fecal transmission Hepatitis B Transmission by contaminated serum; blood transfusion, contaminated needles, dialysis, or direct contact with infected body fluids Hepatitis C Transmitted through contaminated needles and blood transfusions

Hepatitis Etiology/Pathophysiology (continued) Hepatitis D Co-infection with hepatitis B Hepatitis E Fecal contamination of water Rare in the U.S.; usually in developing countries Hepatitis G Co-infection with hepatitis C related to blood exposure

Hepatitis Clinical manifestations/Assessment General malaise Aching muscles Photophobia Headaches Chills Abdominal pain Dyspepsia Nausea

Hepatitis Clinical manifestations/Assessment (continued) Diarrhea/constipation Pruritus Hepatomegaly Enlarged lymph nodes Weight loss

Hepatitis Medical management/Nursing interventions Treat symptoms Small, frequent meals Low fat, high carbohydrate IV fluids for dehydration Avoid unnecessary medications, especially sedatives and alcohol

Hepatitis Medical management/Nursing interventions (continued) Vitamin C-healing Vitamin B-complex-assists in the absorption of fat soluable vitamins Vitamin K-increase coagulation

Disorders of the Liver, Biliary Tract, Gallbladder, and Pancreas Medical management/Nursing interventions (continued) Antivirals-used to decrease the viral load thus altering the progression of the disease Gamma globulin or immune serum globulin Hepatitis B immune globulin (HBIG) Should be given to anyone exposed to hepatitis B Hepatitis B vaccine Should be given to people identified as high risk for developing hepatitis B

Hepatitis Medical management/Nursing interventions (continued) Liver transplantation Has less chance for rejection than most transplants However if done for hepatitis B/C there is a greater the 50% chance for reinfection within 5 years

Liver Abcess Etiology/Pathophysiology An accumulation of living and dead WBC’s, bacteria and liquified liver cells Related to the bodies inability to fight off the disease Clinical manifestations/Assessments Fever Chills RUQ pain and tenderness Hepatomegly Jaundice Anemia

Liver Abcess Medical management/Nursing interventions Ultrasound, CT, liver scan IV antibiotics Percutaneous drainage of liver abscess Open surgical drainage

Cholecystitis & Cholelithiasis Etiology/Pathophysiology An obstruction, gallstone, or tumor prevents bile from leaving the gallbladder and the trapped bile acts as an irritant causing inflammation Risk factors Female; 40; American Indian or white; obesity; pregnancy; diabetes; multiparous women; use of birth control

Path of Bile Flow

Common sites of gallstones (From Phipps, W.J., Monahan, F.D., Sands, J.K., Marek, J.F., Neighbors, M. [2003]. Medical-surgical nursing: health and illness perspectives. [7th ed.]. St. Louis: Mosby.) Common sites of gallstones

Cholelithiasis-Gallstones Most common gallbladder disease May remain in gallbladder or lodge in bile ducts Gall bladder can become necrotic What does necrotic mean?

Cholecystitis and Cholelithiasis Clinical manifestations/Assessment Indigestion after eating foods high in fat Severe, colicky pain in the right upper quadrant Anorexia Nausea and vomiting Flatulence Increased heart and respiratory rates Diaphoresis

Cholecystitis and Cholelithiasis Clinical manifestations/Assessment (continued) Low-grade fever Elevated WBC Mild jaundice Steatorrhea-fatty stool, clay colored stools related to lack of bile in the intestinal tract Dark amber urine Increased urobilinogin as kidneys try to remove excess bilirubin from kidneys

Palpable gallbladder

Cholecystitis and Cholelithiasis Medical management/Nursing interventions Bedrest NG tube to suction NPO IV fluids Antispasmodic/analgesic Antibiotics Avoid spicy foods when allowed PO intake Lithotripsy-shockwaves thru water to break the stones into fragments that are removed by the flow of bile out of the gallbladder and into the intestine Cholecystectomy Laparoscopic Open

Pancreatitis Etiology/Pathophysiology Inflammation of the pancreas where pancreatic enzymes autodigest the gland Edematous-causes fluid accumulation and swelling but is usually self limiting Necrotizing-causes cell death, tissue damage and systemic complications The acinar cells which are the secreting cells of the pancreas atrophy and are replaced by fibrotic tissue that results in necrosis results from seeding of bacteria into the inflammation Enzymes cannot flow out of the pancreas related to occlusion of the pancreatic duct by edema, stones, scar tissue As the enzymes build up the duct ruptures releasing the enzymes that begin digesting the pancreas Predisposing factors Alcohol Trauma Infectious disease Certain drugs

Pancreatitis Mortality/Morbidity: Although acute pancreatitis should be noted, chronic pancreatitis has a more severe presentation as episodes recur Acute respiratory distress syndrome (ARDS), acute renal failure, cardiac depression, hemorrhage, and hypotensive shock all may be systemic manifestations of acute pancreatitis in its most severe form

Pancreatitis Clinical manifestations/Assessment Abdominal pain, epigastric pain or right upper quadrant pain radiating to the back Distension, guarding, and rigidity Anorexia; nausea and vomiting Malaise Low-grade fever Jaundice-if the common bile duct is obstructed Weight loss Steatorrhea Tachycardia, tachypnea, hypotension Diminished or absent bowel sounds

Pancreatitis Clinical manifestations/Assessment Lung auscultation may reveal basilar rales, especially in the left lung Muscular spasm may be noted secondary to hypocalcemia Family history of hypertriglyceridemia Previous biliary colic Binge alcohol consumption Severe cases may have a Grey Turner sign (ie, bluish discoloration of the flanks) and Cullen sign (ie, bluish discoloration of the periumbilical area) caused by the retroperitoneal leak of blood from the pancreas in hemorrhagic pancreatitis

Pancreatitis Clinical manifestations/Assessment An acute pseudocyst is an effusion of pancreatic juice that is walled off by granulation tissue after an episode of acute pancreatitis Hemorrhage into the GI tract retroperitoneum or the peritoneal cavity is possible because of erosion of large vessels Common bile duct obstruction may be caused by a pancreatic abscess, pseudocyst, or biliary stone that caused the pancreatitis An internal pancreatic fistula from pancreatic duct disruption or a leaking pancreatic pseudocyst may occur

Pancreatitis Clinical manifestations/Assessment A complete blood count (CBC) demonstrates leukocytosis (WBC >12000) with the differential being shifted towards the segmented polymorphs If blood transfusion is necessary, as in cases of hemorrhagic pancreatitis, obtain type and crossmatch Measure blood glucose level because it may be elevated from B cell injury in the pancreas Obtain measurements for BUN, creatine (Cr), and electrolytes (Na, K, Cl, CO2, P, Mg); a great disturbance in the electrolyte balance is usually found, secondary to third spacing of fluids Measure amylase levels, preferably the Amylase P, which is more specific to pancreatic pathology. Levels more than 3 times higher than normal strongly suggest the diagnosis of acute pancreatitis Lipase levels also are elevated and remain high for 12 days. In patients with chronic pancreatitis (usually caused by alcohol abuse), lipase may be elevated in the presence of a normal serum amylase level Perform liver function tests (eg, alkaline phosphatase, serum glutamic-pyruvic transaminase [SGPT], serum glutamic-oxaloacetic transaminase [SGOT], G-GT) and bilirubin, particularly with biliary origin pancreatitis

Pancreatitis Medical management/Nursing interventions NPO/NG tube-to avoid stimulating pancreatic activity IV fluids Antiemetics Pain management Demerol 75-100 mg every 3-4 hours Do not give morphine-causes spasms at the sphincter of oddi which surrounds the lower end of the pancreatic duct/common bile duct Anticholinergics- to decrease pancreatic activity Antacids or Tagamet-prevent ulcers from high gastric pH Hyperalimentation- TPN, lipids