FOM 4.

2 Hepatobiliary Obstruction and Jaundice

1. Describe the anatomy of the hepatobiliary tract:

 Biliary Tree
o biliary drainage of the liver
o right and left hepatic ducts fuse => Common Hepatic
Duct
o common hepatic duct combine w/ cystic duct =>
common bile duct
o common bile duct combine w/ pancreatic duct =>
hepatopancreatic ampulla (of vater)

2. Discuss the physiologic changes when obstruction in the

hepatobiliary tract occurs

3. Identify possible levels of obstruction in the hepatobiliary tree

4. Differentiate the following

trans FOM 4.2
a. pre-hepatic jaundice
 result of overproduction of bilirubin.
 can be either attributed to increase RBC hemolysis or
ineffective erythropoiesis.
o Hemolytic anemias cause lysis of RBCS, consequently
causing an increase in serum bilirubin. This often
overwhelms the capacity of hepatocytes, thus causing
jaundice.
o In the same manner, ineffective erythropoiesis causes
premature lysis of RBCs causing increase in serum
bilirubin.
 The ability of the liver to conjugate remains. Thus, the serum
unconjugated bilirubin is high.

b. hepatic jaundice
 Hepatic jaundice is a result of impaired hepatic function
o Can be a result of impaired uptake, impaired excretion,
 or impaired metabolism of bilirubin (e.g. Dubin-Johnson,
Criggler-Najar)
 Case no. 2 is a hepatic form of jaundice resulting from acute
viral hepatitis
o The pathophysiological process of jaundice is not as a
result of destruction of hepatocytes such as in the case
of chronic viral hepatitis, but rather an inflammation
(i.e., swelling) of the hepatocytes causing obstruction of
the bile canaliculi
o The inflammation of the hepatocytes clinically manifests
as hepatomegaly
 Chronic cases of viral hepatitis (e.g. hepatitis B, C, D) cause
apoptosis of hepatocytes, decreasing the conjugative capacity
of the liver and allowing conjugated bilirubin to spill into
circulation
o Thus, both conjugated and unconjugated bilirubin is
increased

c. post-hepatic jaundice
 Post-hepatic jaundice is a result of an obstruction along the
biliary treeCase no.1, a case of gallstone obstruction, results
to post- hepatic jaundice
 Obstruction causes bile to accumulate along the bile canaliculi
which creates an increase in pressure
o Disables the hepatocytes to excrete bile along with
bilirubin into the canaliculi
 Hepatocytes are still able to conjugate bilirubin but are unable
to excrete it
o Conjugated bilirubin spills over in circulation, thus
causing conjugated bilirubinemia
 The only treatment for this type is surgical removal of the
obstruction hence why it is also called surgical jaundice
 manifest as dark colored urine

Hepatitis

 Hepatitis is a general term used to describe inflammation of

the liver. The causes can be classified into:
o Infectious (e.g. viral, bacterial, parasitic)
o Metabolic (alcoholic, toxic, and drug-induced)
o Autoimmune
o Genetic (Alpha-1-Antitrypsin deficiency, Wilson’s
Disease)
o Others (Ischemic hepatitis, congenital/perinatal
infections)
 The most common cause worldwide is viruses, aptly name
hepatitis A to E

Gallstone/s
  Cholesterol may precipitate in the gallbladder
o Cholesterol level is determined by quantity of fat intake
 Since liver cells synthesize cholesterol from fat
metabolism
 Inflammation of the gallbladder epithelium changes
absorptive characteristic of the gallbladder mucosa
o Excessive water & bile salt absorption
 Cholesterol levels remain high
o Precipitation into small crystals of cholesterol on the
mucosal surface progressing into large gallstones

GALLSTONE OBSTRUCTION:

Cholelithiasis – general term for formation and presence of gallstones

anywhere along the biliary tree

Choledocholithiasis – presence of gallstones in the common bile duct

causing the obstruction in the passage of bile from the liver to the gall
bladder and/or small intestines

Possible Physiologic Derrangements:

 First and foremost, this will result in malnutritionBile cannot enter the
small intestines, therefore, the lipids
 found in her intestines will not be properly dissolved and
 absorbed by her bodyAbdominal pain will ensue due to production of
CCK because of the presence of lipids in her intestines and will result
in:
o Further stimulation of the gall bladder to release bileDue
to its passage being obstructed, no bile will reach the
 intestines and this will prompt the body to produce more CCK which
will result in further stimulation (constant stimulation = one the causes
of the abdominal pain)
o Due to constant stimulation, the pressure found in the
common bile ducts increases and this will cause the back flow of
bile from the gall bladder or common bile duct back into the liver
 Bile is trapped within the common bile duct which will result in the
erosion or damage of its epitheliumDepending on the location of the
obstruction, the pancreas might also be damaged
o This is due to the back flow of pancreatic enzymes which
could digest the pancreas itself
 Increase in blood serum conjugated bilirubin because the liver will
continue to process unconjugated bilirubin and convert it to its
conjugated bilirubin

o owever, since it cannot make its way into the gall bladder or
intestine, it is released back into the blood where it can be
filtered out by the kidneys (resulting in dark-colored urine)
 o This can also result in further uptake of bilirubin and
presentation of severe jaundice which is fatal

Signs and Symptoms:

 Abdominal PainThis could be due to
o Increased gall bladder stimulation due to increasing levels of
CCK in the system
 Over stimulation causes constant contraction of the
smooth muscles of the gall bladder
o Increased pressure within the common bile ducts
o Bile slowly digesting the common bile duct because its flow has
been obstructed
 Jaundice
o Because of the extra hepatic biliary duct obstruction, bilirubin is
no longer properly disposed through the GI tract
 Results in the collection of conjugated bilirubin in the
blood plasma which is deposited in the sclera, skin, and
mucosa
 Note: Serum bilirubin levels must exceed 2.0 mg to
consider for jaundice
 Acholic Stool
o Since bile flow is obstructed, no bilirubin makes its way into
the intestines. Hence the pale or "putty" colored stool.
 Dark Colored Urine
o This is the body's compensatory mechanism:
 Increase in plasma conjugated bilirubin can be filtered by
the kidneys and excreted through the urine hence the
dark color
 Since no bile is entering the intestines, bilirubin is no
longer converted into urobilinogen which gives the urine
its yellow color

Laboratory Examinations of gallstone obstruction:

 AST and ALT will both be normal, because there is still normal liver
function
 Alkaline Phosphatase will be increased because it is the liver's
response to an obstruction in the biliary tree
o Produced by the hepatocytes located adjacent to the biliary
canaliculi
 Total Bilirubin, indirect and direct bilirubin
o Total Bilirubin: increased
o Direct Bilirubin: increased
o Indirect Bilirubin: initially normal but with severe cases of
obstruction, it can also be elevated

Jaundice in Hepatitis:
 In hepatitis, hepatocytes are abnormally enlarged due to inflammation
 Hepatocytes obstruct the sinusoids in the liver causing the pressure
in the canaliculi to increase and therefore force bilirubin back into
 the blood
 Bilirubin is not excreted from the liver into the intestines via the bile
 Jaundice manifests as the serum bilirubin increases
Laboratory Examinations of Acute Viral Hepatitis
 Elevated ALT, AST, Alkaline Phosphatase Due to liver and bile duct
damage
 Decreased AlbuminLiver function is compromised
 Elevated Total, Direct & Indirect Bilirubin
o Conjugated bilirubin is released from the hepatocytes
o Liver is unable to conjugate Bilirubin
 Bilirubin is able to pass through the cells due to the
inflammation of the hepatocytes
 Increased/longer PT & PTT
o Liver function to synthesize clotting factors are compromised
o Vitamin K-dependent clotting factors II, VII, IX and X production
is also compromised due to the malabsorption of fat-soluble
vitamin K

Pathologic Changes in the Liver:

 enlarged hepatocytes
 presence of hepatits necrosis
 cell membrane ruptures
o collagen reticulum framework is left

Case: A patient was admitted due to having jaundice and a physical

examination determined a 2-cm gallstone located in the Hartmann’s pouch.
ERCP determined that the bile duct was constricted.

1. Explain how this kind of gallstone lead to jaundice.

Jaundice occurred in the patient since the gallstone is found in the

Hartmann’s pouch which is at the proximal end of the gallbladder,
near the bile duct itself. The stone was also large enough to traverse
the gap and impinge the duct so that bile flow is obstructed. As bile
is accumulated, pressure is built up and bilirubin from the bile is
shuttled back into the blood circulation. This would therefore
increase the bilirubin concentration and cause the skin and sclera to
change into a yellow color.

2. What are the expected levels of Bilirubin (Total, Direct & Indirect),
ALT & alkaline phosphatase?

Total bilirubin would be increased as the gallstone prevents its

excretion from the body. Direct bilirubin would be elevated as the
conjugated bilirubin produced in the liver are pushed back into the
blood as well since the obstruction is post-hepatic. Indirect bilirubin
is normal as the liver’s function to conjugate bilirubin is still present.
ALT levels are expected to be normal as the biliary obstructed does
not affect hepatocytes. Alkaline phosphatase is expected to increase
as bile duct cells are damaged by the gallstone.