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

2. 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

3. 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

4. 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

5. 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

6. 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

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

8. 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

9. 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

10. 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

11. 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

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

13. 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

14. Systemic clinical manifestations of liver cirrhosis.

15. Hepatomegaly and Ascites

16. Jaundice

17. Jaundice

18. Urine bilirubin

19. 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

20. 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

21. 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

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

23. 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

24. 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)

25. LaVeen Continuous Peritoneal Shunt

26. 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

27. 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

28. 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

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

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

31. 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

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

33. 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

34. 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

35. 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

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

37. 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

38. Path of Bile Flow

39. 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

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

41. 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

42. 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

43. Palpable gallbladder

44. 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

46. 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

47. 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

48. 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

49. 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

50. 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

51. 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

52. Pancreatitis Medical management/Nursing interventions
NPO/NG tube-to avoid stimulating pancreatic activity
IV fluids
Antiemetics
Pain management
Demerol 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