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Cathy Gibbs BSN, RNCathy Gibbs BSN, RN

Gastrointestinal Laboratory Testing and Accessory System Disorders

Gastrointestinal Laboratory Testing and Accessory System Disorders

Laboratory and Diagnostic Laboratory and Diagnostic ExaminationsExaminations• 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

Laboratory and Diagnostic Laboratory and Diagnostic ExaminationsExaminations• 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 Laboratory and Diagnostic ExaminationsExaminations

• 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 Laboratory and Diagnostic ExaminationsExaminations

• 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

Laboratory and Diagnostic Laboratory and Diagnostic ExaminationsExaminations

• 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 LiverDisorders of the Liver

•Cirrhosis• Jaundice•Hepatitis•Liver abscess•Cholecystitis•Cholelithiasis•Pancreatitis

CirrhosisCirrhosis

•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

CirrhosisCirrhosis

• Complications– Clotting dysfunction

• 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

CirrhosisCirrhosis• 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. • Treatment

– Lactulose– Neomycin

CirrhosisCirrhosis

• 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

CirrhosisCirrhosis

• Clinical manifestations/Assessment

•Early stages–Abdominal pain–Liver is firm and easy to palpate–hepatomegaly

CirrhosisCirrhosis

• Clinical manifestations/Assessment• 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

CirrhosisCirrhosis

Systemic clinical manifestations of liver cirrhosis.

Hepatomegaly and AscitesHepatomegaly and Ascites

JaundiceJaundice

JaundiceJaundice

Urine bilirubinUrine bilirubin

CirrhosisCirrhosis

• 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

CirrhosisCirrhosis

• 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

CirrhosisCirrhosis

• 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

CirrhosisCirrhosis

•Medical management/Nursing interventions– Hepatic encephalopathy

•Decrease protein in diet

•Avoid drugs which are detoxified by the liver

•Lactulose

•Neomycin

CirrhosisCirrhosis

• 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

CirrhosisCirrhosis

• 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 LaVeen Continuous Peritoneal ShuntPeritoneal Shunt

HepatitisHepatitis

• 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

HepatitisHepatitis

• 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

HepatitisHepatitis

• 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

HepatitisHepatitis

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

HepatitisHepatitis

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

HepatitisHepatitis

•Medical management/Nursing interventions– Treat symptoms– Small, frequent meals

•Low fat, high carbohydrate

– IV fluids for dehydration– Avoid unnecessary medications,

especially sedatives and alcohol

HepatitisHepatitis

•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, Disorders of the Liver, Biliary Tract, Gallbladder, and PancreasGallbladder, 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

HepatitisHepatitis

•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 AbcessLiver 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 AbcessLiver Abcess

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

Cholecystitis & CholelithiasisCholecystitis & 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 FlowPath of Bile Flow

Gall stonesGall stones

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.)

Cholelithiasis-GallstonesCholelithiasis-Gallstones

•Most common gallbladder disease

•May remain in gallbladder or lodge in bile ducts

•Gall bladder can become necrotic

Cholecystitis and Cholecystitis and CholelithiasisCholelithiasis

• 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 Cholecystitis and CholelithiasisCholelithiasis

• 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 gallbladderPalpable gallbladder

Cholecystitis and CholelithiasisCholecystitis 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

PancreatitisPancreatitis• 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

PancreatitisPancreatitis

•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

PancreatitisPancreatitis

• 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

PancreatitisPancreatitis

• 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

PancreatitisPancreatitis

• 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

PancreatitisPancreatitis

• 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

PancreatitisPancreatitis

• 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