HEPATOBILIARY

Diseases (3)

Siti balkis budin

 Liver failure
• Acute liver failure
– Caused by
• overdose certain prescription medicines such as
sulfonamides, isoniazid, halothane
• some herbal supplements
• Severe viral infections, hepatitis A, hepatitis B, and
hepatitis C
• toxins
• certain autoimmune diseases
• Chronic liver failure
– Develops more slowly. It can take months or even
years
– Often the result of cirrhosis
 ACUTE Liver Injury
• Most cases are self-limiting episodes of hepatocyte
inflammation or damage
• Resolve without causing further complications.
• Mild injury
– modest elevation of enzymes
– asymptomatic
• Severe injury
– Acute hepatic failure
– hepatic coma
– Death
• Associated with increase in
– liver injury marker (liver enzyme)
– Unconjugated bilirubin
– always not associated with low coagulation protein and
albumin levels
Cirrhosis and Chronic Liver Failure
• Cirrhosis is a late stage of liver disease
where the liver is severely scarred but may
still be able to perform its function to
support life.
• When the liver is no longer able to
perform its work adequately, its goes into
chronic liver failure.
• Most patients who develop chronic liver
failure have underlying cirrhosis.
 Clinical manifestation of Chronic Liver
Failure
• Related to the failure of the liver to carry out its normal functions.
• Fatigue, loss of appetite and weight loss
• Jaundice
– Failure of conjugation and excretion of bilirubin
• Pale stools
– In biliary obstruction bile secretion via feces is reduced, resulting in
pale stools.
• Dark urine/tea colored urine
– In biliary obstruction bilirubin are unable to be excreted via the feces,
the body compensates by increasing renal elimination of bilirubin.
• Bruising and bleeding
– Reduced in clotting factors
• Hepatic Encephalopathy
– failure of the liver to remove gut-derived toxins especially ammonia
– and cross into the central nervous system.
 Clinical manifestation of Chronic Liver
Diseases/Cirrhosis
• Portal hypertension
– increased pressure within the portal venous system as a result of
increased resistance in portal system due to obstruction of blood due
to fibrosis/cirrhosis architecture of liver;
• Varices
– Oesophageal and gastric varices as a result of portal hypertension
can burst due to high pressure leading to massive hemorrhage.
Patient may present with hematemesis (vomit out blood)
• Splenomegaly
– caused by increased pressure in the portal venous system
• Gynecomastia
– inability of the cirrhotic liver to metabolize estrogen and high estrogen
level in patient
• Ascites: Due to hypoalbuminemia and portal hypertension
– Portal hypertension also activate renin angiotensin system and lead
to sodium and water retention
 Hematemesis
Hemorrhoid

• Hepatic Failure
jaundice
 Jaundice
• Jaundice is a condition in which the skin, whites of the
eyes and mucous membranes turn yellow because of a
high level of bilirubin, a yellow-orange bile pigment.
• Types of bilirubin
– Unconjugated
– Conjugated
• Jaundice can be caused by a problem in any of the three
phases in bilirubin production
– Prehepatic
• cause high unconjugated bilirubin
– Hepatic
• cause high in unconjugated and conjugated bilirubin
– Posthepatic
• Cause high in conjugated
 Jaundice
• High in unconjugated can be due to
– prehepatic jaundice (hemolysis crisis)
– Hepatic jaundice (failure of hepatocyte to conjugate
bilirubin: acute or chronic liver failure)
• High in conjugated can be due to obstruction in
bilirubin flow
– Hepatic jaundice: due to obstruction of bilirubin flow in
canaliculi (intrahepatic cholestasis)
– Extra hepatic jaundice: extrahepatic obstruction of the
biliary tract
 Jaundice:
Bilirubin > 2mg/dl
• portal hypertension
•
Hepatocellular
Usually related to HBV & HCV
Carcinoma
• Hematogenous metastases are common
• High levels of alpha fetoprotein
• Prognosis is grim
 Liver Profile
• Liver enzyme (marker for liver cell injury)
– ALT: alanine aminotransferase (SGPT)
– AST: aspartate aminotransferase (SGOT)
– Alkaline Phosphatase
– Gamma Glutamyl Transferase (GGT)
– Lactate dehydrogenase (LDH)
• Tests of liver function
– Bilirubin
– Total Protein and serum albumin
– Bleeding profile: Prothrombin Time (PT / INR) / APTT
 ALT:

• Found primarily in hepatocytes

• Released when cells are hurt or destroyed
• Normal levels depend on the reference
range which actually differs lab to lab
• Considered normal between 5-40 U/L
• Probably should be half of this (5-20?)
 AST

• Found in many sources, including liver,

heart, muscle, intestine, pancreas
• Not very specific for liver disease
• Often follows ALT to a degree
• Elevated 2 or 3:1 (vs. ALT) in alcoholics
• Normal range: 8-20 U/L
 Alkaline Phosphatase
• Found in liver (especially biliary tract),
bones, intestines, & placenta
• “Fractionated” or “isoenzymes” to source
• Liver AP rises with obstruction or
infiltrative diseases (i.e., stones or tumors)
• Normal range: 20-70 U/L
 GGT
• GGT functions in the body as a transport molecule,
helping to move other molecules around the body.
• It plays a significant role in helping the liver metabolize
drugs and other toxins.
• GGT is concentrated in the liver, but it’s also present in
the gallbladder, spleen, pancreas, and kidney.
• GGT blood levels are usually high when the liver is
damaged.
• The GGT test is currently the most sensitive enzymatic
indicator of liver damage and disease.
• It is highest in cases of intra- or posthepatic biliary
obstruction, reaching levels some 5 to 30 times normal.
• GGT is more sensitive than alkaline phosphatase (ALP),
aspartate transaminase, and alanine aminotransferase in
detecting obstructive jaundice, cholangitis, and
cholecystitis;
• GGT rise occurs earlier than with these other enzymes
and persists longer.
 Patterns of Abnormal
• Elevations in ALT & AST only: suggests
cellular injury

• Elevations in Alk Phos & Bilirubin:

suggests cholestasis or obstruction

• Mixed pattern: ALT, AST, AP & Bili:

probably the most common scenario
 Summary
• Liver tests are numerous and somewhat
confusing
• Not all liver disease is associated with
abnormal test results
• Some of the worst liver disease has
relatively normal appearing liver enzymes
and can only be noticed with a look at
synthetic functions eg; low in albumin or
clotting protein
 Cholelithiasis
• Gallstones in the gallbladder or biliary tree
• Form in gallbladder
• Usually have multiple stones
– 50% require surgery
• Pigment gallstones
• Cholesterol gallstones
• Usually no symptoms until they begin to
move; mid-size stones are the worst
• Painful cramps in RUQ
• Nausea/vomiting
• Complications include
– cholecystitis
– pancreatitis
– perforation
– empyema of gallbladder
 Acute Cholecystitis
• Most common major
complication of
gallstones
– 90% associated
with obstruction
of the neck
• Gallbladder is
enlarged, tense, &
inflamed
• Persistent rather mild
RUQ pain to very
severe pain
 Chronic Cholecystitis
• Do not have to have a
history of acute attacks
• Almost always associated
with gallstones although
obstruction not necessary
• Mild to moderate RUQ pain
• Nausea/vomiting
• Intolerance of fatty foods