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Hepatobiliary Disorders: A Comprehensive Study Guide, Exams of Nursing

Chamberlain College of NursingNursing

This study guide provides a detailed overview of hepatobiliary disorders, focusing on cholelithiasis, cholecystitis, and hepatitis. It covers the causes, symptoms, diagnosis, and treatment of these conditions, including detailed explanations of the different types of hepatitis and their clinical courses. The guide also includes numerous exercises and questions to test understanding and reinforce learning.

Typology: Exams

2024/2025

Available from 03/30/2025

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PATH 1017 – HEPATOBILIARY EXAM
STUDY SET
disorders of the gallbladder
- cholelithiasis (gallstones)
- acute and chronic cholecystitis
- choledocholithiasis (not tested)
- cholangitis (not tested)
cholelithiasis (gallstones)
cholesterol, calcium salts or mixed
acute and chronic cholecystitis
inflammation caused by irritation due to concentrated bile
what is cholelithiasis caused by
precipitation of cholesterol (80%) and 20 % bilirubin - black, brown pigment
composed of myucin, glycoprotein, and calcium salt.
Gallbladder sludge
-thickened gallbladder mucoprotein with tiny trapped cholesterol crystals
-precursor to formation of stones
why is cholelithiasis associated with obesity?
liver makes more cholesterol, therefore more gallstones are produced
why is cholelithiasis associated with women?
estrogen causes fewer bile acids to be produced, which break down
cholesterol (there is a higher risk for pregnant women and those on birth control
due to estrogen decreasing bile synthesis causing more cholesterol to be
excreted by liver to the bile)
symptoms of cholelithiasis
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PATH 1017 – HEPATOBILIARY EXAM

STUDY SET

disorders of the gallbladder

  • cholelithiasis (gallstones)
  • acute and chronic cholecystitis
  • choledocholithiasis (not tested)
  • cholangitis (not tested) cholelithiasis (gallstones) cholesterol, calcium salts or mixed acute and chronic cholecystitis inflammation caused by irritation due to concentrated bile what is cholelithiasis caused by precipitation of cholesterol (80%) and 20 % bilirubin - black, brown pigment composed of myucin, glycoprotein, and calcium salt. Gallbladder sludge
  • thickened gallbladder mucoprotein with tiny trapped cholesterol crystals
  • precursor to formation of stones why is cholelithiasis associated with obesity? liver makes more cholesterol, therefore more gallstones are produced why is cholelithiasis associated with women? estrogen causes fewer bile acids to be produced, which break down cholesterol (there is a higher risk for pregnant women and those on birth control due to estrogen decreasing bile synthesis causing more cholesterol to be excreted by liver to the bile) symptoms of cholelithiasis
  • no symptoms until obstruction of blood flow (transient)
  • symptoms include jaundice, severe right upper quadrant pain, and indigestion what is obstructed bile flow? when the gallstones block the bile duct or cystic duct factors contributing to the formation of gall stones
  • abnormal composition of bile
  • stasis of bile (anything that slows ongoing forward movement, allowing crystals and substances to sit there and form stones)
  • increased level of cholesterol
  • gallbladder sludge (contracts the crystals and allows them to form)
  • inflammation of gallbladder(alters abosorptive characteristics of mucosal layer allowing increase in absorption of water and bile salts.) what will happen to the gallstones in cholelithiasis? either pass or go back to the gallbladder acute cholecystitis
  • inflammation caused by irritation caused by bile due to complete or partial obstruction of the cystic duct by stone(s)
  • more concentrated bile because of blockage
  • associated with presence of gallstones (85-90%) what happens to the mucosa in acute cholecystitis?
  • mucosal phospholipase is released and disrupts the mucosa, exposing mucosa to bile salts (goes through mucosal lining)
  • results in inflammation, edema, and bile stasis what may occur/develop in acute cholecystitis?
  • secondary bacterial infections (acalculous cholecystitis)
  • gangrenous changes and perforation (bc of transmural infarction rather than inflammation changes with stone) manifestations in acute cholecystitis? VARY IN SEVERITY
  • pain (right upper quadrant pain)
  • more vague than acute and may have exacerbations
  • intolerance to fatty foods, belching
  • episodes of colicky pain when bile outflow is obstructed
  • gallbladder size may be normal or increased/decreased (enlarged, shrunken, or normal size, fibrous and thick)
  • may develop pancreatitis, Bladder Ca diagnosis of cholecystitis
  • ultrasound (detect size (1cm or more) and shows thickening of gallbladder wall indicating inflammation)
  • cholescintigraphy a.k.a "gallbladder scan: (nuclear scan) (repeats scans to show passageway of the bile duct and show obstruction) treatment of cholecystitis
  • diet (avoid fatty foods)
  • surgery (cholecystectomy - removal of gallbladder, no problems)
  • non-surgical (shock wave treatment - to break up stones to pass) hepatitis
  • inflammation of the liver
  • can be acute or chronic causes of hepatitis
  • autoimmune disorders
  • infectious disorders outside liver causing secondary hepatitis
  • viruses that attack liver
  • chronic alcoholism, drug toxicity what are the two mechanisms of liver injury in viral hepatitis infections?
  • direct cell injury
  • induced immune responses against infected cells types of viral hepatitis
  • Hepatitis A (HAV)
  • Hepatitis B (HBV)
  • Hepatitis B-Associated Delta Virus (HDV)
  • Hepatitis C (HCV)
  • Hepatitis E (HEV) diagnosis of hepatitis
  • viral antigen and antigen antibody tests (bloodwork)
  • liver function tests
  • liver biopsy (chronic cases or if patient's is severely ill) what are the results of liver function tests in viral hepatitis?
  • increased aminotransferase (AST) (indicates damage)
  • increased bilirubin (shows jaundice) clinical course of hepatitis
  • varies with different viruses
  1. acute asymptomatic infection
  2. acute symptomatic infection
  3. chronic hepatitis
  4. carrier state
  5. fulminant acute asymptomatic infection of hepatitis
  • infected with no symptoms
  • can spread virus
  • resolved in 6 months acute symptomatic infection of hepatitis
  • infected with symptoms
  • can spread virus
  • resolved in 6 months chronic hepatitis
  • virus present in blood for 6 or more months OR have symptoms (liver inflammation) for 6 months or more
  • can spread virus
  • sometimes acute leads to this what is chronic hepatitis caused by?

manifestations of fulminant hepatitis

  • jaundice (and GI symptoms at the beginning)
  • hepatic encephalopathy (bc liver is failing)
  • other signs of liver failure (ex: hemorrhage) (bc liver is failing)
  • increased LFTs, increased ammonia (causing swelling in brain) treatment options for fulminant hepatitis
  • supportive care
  • liver transplant (death without = 85%, death with = 35%) stages of the acute symptomatic course of hepatitis
  1. prodromal (preicteric)
  2. icterus
  3. convalescence
  • depending on the type of hepatitis, can go through all 3 stages prodromal (preicteric) stage of acute symptomatic course
  • abrupt onset of manifestations
  • increased AST and ALT (blood work - see signs of liver damage)
  • severe flu-like manifestations (muscle aches, fatigue, GI symptoms, fever, chills)
  • occurs with HAV and HBV icterus stage of acute symptomatic course
  • occurs 5-10 days after prodromal stage
  • worsening of prodromal symptoms (start to have more symptoms specific to hepatitis)
  • jaundice, severe pruritus, liver tenderness, dark urine
  • increased bilirubin (causing jaundice) and increased liver enzymes convalescence stage of acute symptomatic course
  • improvement in symptoms and appetite
  • jaundice disappears
  • people with chronic do not go through this stage how long does it take to go through the stages of acute symptomatic infection?
  • hepatitis A takes 2 months
  • acute hepatitis B takes 4 months (most progress to chronic or stuck in icterus phase) hepatitis A
  • replicates in the liver, excreted in bile and shed in feces
  • able to resist digestion of acid in stomach
  • person sheds virus before any signs of infection transmission of hepatitis A
  • fecal-oral route
  • may be contracted through consumption of contaminated water, milk, shellfish, international travel and institutional settings incubation period of hepatitis A average 25-30 days manifestations of hepatitis A
  • sudden onset (flu-like illness)
  • jaundice is common (75%) clinical course of hepatitis A
  • usually self-limiting acute course of 2 months
  • RARE fulminant hepatitis (1-3%)
  • less likely in children hepatitis B
  • DNA based virus
  • linked to hepatitis D
  • most common worldwide
  • high rate of carriers and infected in Asia
  • decreased rate in North America due to vaccines transmission of hepatitis B
  • found in most bodily fluids (blood, sexual contact, infants born to HBV+ mother)
  • common in sexual contact (mostly infected by teens or adults and drug users)
  • defective RNA virus
  • must have HBV to get
  • outcome if have HBV is worse who does hepatitis D occur in?
  • only in those infected with HBV as a co-infection OR superimposed infection
  • common in injection drug users
  • common in sexual contact (mostly infected by teens or adults and drug users) transmission of hepatitis D
  • similar to HBV
  • found in most bodily fluids (blood, sexual contact, infants born to HBV+ mother) incubation period of hepatitis D
  • similar to HBV
  • 40 - 180 days (average 75 days) clinical course of hepatitis D acute or chronic hepatitis treatment of hepatitis D
  • no treatment
  • prevented by preventing hepatitis B infection with vaccines hepatitis E
  • unenveloped, single-stranded RNA virus transmission of hepatitis E
  • fecal-oral transmission
  • especially in contaminated water (international travel - Asia, India, Africa, Mexico, rarely seen in North America) incubation period of hepatitis E 14 - 60 days manifestations of hepatitis E
  • similar to HAV
  • sudden onset (flu-like illness)
  • jaundice is common (75%) clinical course of hepatitis E
  • typically acute pattern similar to HAV (resolves after)
  • may lead to fulminating hepatitis in pregnant women (20% die) treatment of hepatitis
  • education on preventing spread
  • supportive care
  • avoid alcohol, caution with drugs (hepatotoxic)
  • antivirals tend to be ineffective
  • peginterferons in chronic hepatitis (need to meet certain criteria - expensive)
  • liver transplant if end stage liver disease vaccinations are available for which hepatitis infections?
  • HAV
  • HBV (indirectly protects from HAD) vaccinations are NOT available for which hepatitis infections?
  • HCV
  • HDV
  • HEV cirrhosis
  • end stage liver disease where functional liver tissue has been replaced by fibrous tissue
  • scaterm-83r tissue wraps around hepatic ducts and restricts so hepatocytes can't do their job
  • liver has nodules and bumps due to scar tissue
  • 25% will end up with cirrhosis what is cirrhosis usually associated with?
  • alcoholism
  • can develop from viral hepatitis