Elimination (Liver, Pancreas, & Gallbladder)
Pathophysiology Case Study & Integration Concept Map
Case 1
L.B. is a 45-year-old Caucasian woman with three children—ages 4, 6, and 10 years. She
works long hours as an instructor at a local college to support her three children and
husband who is disabled. She has had a 6-month history of severe bouts of abdominal pain
associated with indigestion, gas, and steatorrhea. Fatty foods seem to exacerbate the
symptoms. L.B. is about 40 pounds overweight. A CT scan of L.B.’s abdomen revealed
multiple stones in her gallbladder. She was scheduled for a cholecystectomy.
Discussion Questions
1. What risk factors does L.B. have that predispose her to development of gallstones?
Risk factors that predisposed L.B. to cholelithiasis are, she is female, Caucasian, & obese.
2. Why are fatty foods often associated with an exacerbation of symptoms?
Increase in fatty food intake increases GB to contract & release bile that is saturated with cholesterol
that turns into bile salts (crystals) and cause hypomotility or stasis of bile in the bile duct. The stasis of
bile crystals then fuses together to form gallstones in the GB.
3. What is the relationship between gallstones and cholecystitis?
The relation between gallstones & cholecystitis is the ongoing presence of gallstones in the
gallbladder will cause walls of the gallbladder to become inflamed with fibrosis & wall thickening.
Case Study 2
F.C. is a 54-year-old man with a history of chronic heavy alcohol use. He has frequent
bouts of gastrointestinal bleeding for which he has been hospitalized on six separate
occasions over the years. He continues to drink and exhibits most of the common
manifestations of alcoholic cirrhosis. He was recently hit by a car and was hospitalized for
a broken leg. He appeared to be under the influence of alcohol at the time of the accident
and had a blood alcohol level of 1.8. F.C.’s family reports that his mental functioning has
deteriorated significantly over the past few months.
Discussion Questions
1. What are the common manifestations of alcoholic cirrhosis? Which of these are
secondary to hepatocellular failure? Which are secondary to portal hypertension?
a) Some common manifestations of cirrhosis are hepatomegaly, fever (due to inflammation of the
liver cells), abdominal pain, weight loss (anorexia – d/t multiple failure of liver functions),
changes in bowel habits, hypoalbuminemia (causes edema in lower extremities, working its way
up), ascites & anemia,
b) Secondary to hepatocellular failure is jaundice.
c) Secondary to portal HTN is gastroesophageal varices.
2. Why is F.C. at particular risk for GI bleeding?
F.C. is at risk for GI bleeding because cirrhosis leads to portal HTN that cause gastroesophageal varices.
Once formed, patient is at risk for hemorrhage due to rupture of vessel from increased portal
pressure. Pt may also be experiencing hypokalemia which reduces clotting factors.
3. What is the probable cause of F.C.’s progressive mental deterioration?
F.C.’s mental deterioration is possible caused by an increased level of ammonia in the blood that has not
been detoxified in the liver. Hepatic encephalopathy results from severe chronic liver disease.
4. Draw a concept map of the development of portal hypertension caused by cirrhosis.
See the following page
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Alcoholic Cirrhosis
Alcohol abuse
Accumulation of fat in liver cells
ETOH converts into acetahyde in the liver
Acetahyde causes fibrosis of the liver
Scar tissue & nodules forms
Scarring & thickening of liver wall
prevent entry of blood flow into liver
Blood flow begins to back up in the portal
vein
Pressure begins to build, leaking out of
vessel & into the peritoneal space
Portal hypertension
Other types of
cirrhosis:
 Postnecrotic
 Biliary
 Cardiac
Diagnosis:
 Liver Bx
 Hepatic profile
 ERCP
Complications:
 Ascites
 Gastroesophageal
varices
 Caput medusa
 Coagulopathy
Treatment:
 Aiming to reduce Sx
 Medication (Actigall,
Colchicine,
 Liver transplantation
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Case 3
D.W. is a 47-year-old man being evaluated for complaints of fatigue, anorexia, and
abdominal distention. On examination, it skin is noted that the skin is jaundiced and the
liver enlarged. D.W. denies significant alcohol or drug use. He denies any known exposure
to hepatitis and has never been vaccinated for hepatitis. He is taking no medication.
Laboratory tests reveal the following, and a diagnosis of acute hepatitis B is made:
AST (5-40)
142 IU/L 
ALT (5-35)
120 IU/L 
GGT (10-48)
42 IU/L
Alk Phos (35-15)
84 IU/L
Total bilirubin
1.0 mg/dl
(<1.0)
Albumin (3.5-5.5) 4.3 g/dl
HBsAg (negative) positive +
Anti-HBS
negative
Anti-HCV
negative
HIV
negative
Discussion Questions
1. Review and analyze the laboratory data. Which findings support the diagnosis of acute
hepatitis B?
Finding that supports the diagnosis of Hepatitis B is the postive Hep B surface antigen.
2. What are the usual modes of hepatitis B transmission? What further risk factor
assessment is indicated to identify the source of infection?
a) Hep B usual mode of transmission are prenatally, percutaneous (IV drug use, ACCIDENTAL
NEEDLE STICK PUNCTURES), or body fluids and tissue (saliva, organ tissue transplantation,
sex-semen and vaginal secretions).
b) Further risk factors to asses is if pt has had any blood transfusion or organ transplants, drug use,
and sexually active. History of rash, joint pain, or kidney disease.
3. What precautions should D.W. take to avoid transmitting the disease to others?
To avoid transmission, D.W. should use protection during sexual intercourse, to not donate blood or do
anything that can expose another person to be in contact with his blood, and no kissing or any other ways
that body fluids may be transmitted.
Case Study 4
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BK is a 63-yr-old women who is admitted to the medical-surgical floor from ED with
nausea & vomiting and epigastric and LUQ abdominal pain that is severe, sharp, and
boring and radiates through to her mid-back. The pain started 24 hours ago and awoke her
in the middle of the night. BK is divorced, retired sales manager who smokes a ½ pack of
cigarettes daily. The ED nurse reports that BK is anxious and demanding. Her
VS: 100/70, 97, 30, 100.2o F (tympanic), SaO2 88% on room air and 92% on 2 L of O by
N/C.
The ED nurse giving you the report states that the admitting diagnosis is acute pancreatitis.
Unfortunately the CT scanner is down and won’t be fixed until morning. However, an US
of the abdomen was performed, and “no cholelithiasis, gallbladder wall thickening, or
choledocholithiasis was seen. The pancreas was not well visualized due to overlying bowel
gas.” Admitting labs reveal lipase 3000 units/L , amylase 2000 units/L , alkaline
phosphatase 350 units/L , alanine transaminase (ALT) 90 units/L , aspartate
transaminase (AST) 150 unites/L , total bilirubin 2.0 mg/dl , albumin 3.0 g/dl, BUN
26 mg/dl , creatinine 1.0 mg/dl, WBC 17.5 thou/cmm , and Hct 36%. A clean-catch
urine sample was just sent to the lab, the urine was dark.
1. What are the possible causes of pancreatitis?
Possible causes of pancreatitis are hypertrygliceremia, high estrogen levels, gallstones, post-ERCP,
drugs, alcohol, hypercalcemia, biliary sludge & microlithiasis, trauma, pancreas divisium, pregnancy,
infections & toxins, vascular disease, post-op pancreatitis, Hereditary pancreatitis, & structural
abnormalities.
2. If a CT scan is planned for the morning, what orders would you expect?
Orders to expect for a CT scan scheduled for the morning would be to check for pt’s allergies, NPO after
midnight, & if CT is w/wo contrast, CKD, pregnancy, medical Hx (asthma).
3. Which labs are the most important to monitor in acute pancreatitis? Why are they
significant?
a) Amylase & lipase levels (norm: below 200) are important to monitor.
b) Elevated levels indicates inflammation of the pancreas caused by an immune response. Activation of
enzymes in the pancreas (abnormal effect) then starts to damage pancreas.
Lipase not able to breakdown fat in the duodenum so in turns also increases cholesterol level
4. What do the BUN and creatinine tell you about her renal function and volume status?
A slight increase in the BUN suggests that BK is beginning to have diminished renal function. This is due
to the decrease in blood flow to the renal. Vasculature insufficiency is due to interstitial edema causing
hypovolemia.
Creatinine is WNL or considered borderline.
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