HEPATOBILIARY

SYSTEM
BY
PRANJAL KULKARNI
NEHA MANE
Introduction
Hepatobiliary system refers to Liver, Gall
bladder, and Bile ducts and how they
work together to make bile.
Bile consists of water ,electrolytes, bile
acids, cholesterol, phospholipids and
conjugated bilirubin.
THE LIVER

• Also called ‘ hepar ’

• Largest/heaviest solid organ in body.
• Weighs about 1600gm in males and
1300gm in females.
• Occupies right hypogastrium ,
epigastrium , & left hypochondrium.
• Most part of liver is covered by ribs
and costal cartilage
• It is covered by network of connective
tissues (Gilsson’s capsule).
 Functions of liver
 Glucose metabolism – Glucose is converted into
glycogen and stored in hepatocytes.
 Ammonia conversion – the liver converts ammonia into
urea.
 Protein metabolism – the liver synthesizes almost all
plasma protein by amino acids.
 Fat metabolism – fatty acids can be broken down for
production of energy and production of ketone bodies.
 Vitamin and iron storage – vitamin A,B & D and several
of B complex vitamins are stored in large amounts in
liver.
 Bile formation – formed by hepatocytes .

 Bilirubin excretion .

 Drug metabolisation.
 GALLBLADDER
 Pear shaped sac , about 7 to 10 cm long .
 Lying on visceral surface of right lobe of the liver in a
fossa between right & quadrate lobes .
 It stores 30 to 50 ml of bile.
 It is divided into -
1. Fundus
2. Body
3. Infundibulum
4. Neck
 Jaundice
Definition –
 Yellowish pigmentation of skin, sclera and mucous
– membrane by elevated level of bilirubin in blood
i.e. more than 2.5 mg/dl (normal – 0.3-1.3mg/dl)
 Jaundice is not a disease but rather a sign that
occur in many different diseases. Jaundice is the
yellowish staining of the skin and sclera.
 There are 3 main types of jaundice

1) Hemolytic jaundice – Massive lysis of RBC’s in

hemolytic anemia e.g. sickle cell anemia and G6PD
deficiency anemia and hemolytic transfusion
reaction.
2) Obstructive jaundice – Conjugated bilirubin is
prevented from passing to the intestine. As in
Gallstone.
3) Hepatocellular jaundice – liver damage (by
hepatitis or cirrhosis) causes low conjugation
efficiency leading to increase unconjugated (indirect)
bilirubin in blood.
 Symptoms of jaundice
 Yellow coloration of the eyes, skin tongue and urine.
 Loss of appetite.
 Dull pain in the liver region.
 Nausea.
 Severe constipation.
 Extreme weakness.
 Fever.
 Headache and undue fatigue.
 Treatment
• Treatment depend on underlying cause.
1) Anemia – induced jaundice may be treated by
iron supplementation.
2) Hepatitis induced jaundice by antiviral or steroid
medication.
 Portal
Hypertension
• Definition – It is characterized by increase in portal
venous pressure.
- Normal portal pressure : 5-10mmHg.
- Raised portal venous pressure Is termed portal
hypertension.
- Normal portal blood flow : 1-1.5L/minute.
 Causes
1) Common – Extra hepatic – Sepsis (umbilical)
- Unknown (50-75 %)
• Intrahepatic presinusoidal – schistasomiasis
• Intrahepatic parenchymal – cirrhosis
2) Other causes –
• Thrombosis
• Pregnancy
• Abdominal trauma.
• Congenital
• Budd – Chiari Syndrome
• Cystic liver disease
• Secondary malignant disease
 Pathogenesis
• Portal hypertension can result from :
1) Increase in resistance to portal flow and/or
2) Increase in portal vines flow

• Clinical features :
1) Splenomegaly
2) Hematemesis and melena
3) Ascites
4) Rectal varies
 Complication
1) Varies : Esophageal; gastric, anorectal
2) Congestive gastropathy
3) Caput medusa
4) Ascites
5) Hepatic encephalopathy

• Investigation :
1) USG – show feature of PHT and splenomegaly.
2) Portal venography – cause of venous obstruction.
3) LFT – for any liver disease

• Management :
1) Treat the underlying disease
2) Nitrates reduce venous return
3) Vasodilators
4) Sx – Endoscopic variceal band ligation
Ascites
• Accumulation of excess fluid within the peritoneal
cavity
 Clinical features of ascites
Symptoms:- 1.abdominal distention
2.bloated feeling in abdomen
3.dyspnoea and orthopnea
4. indigestion and heartburn

Signs :- 1.abdominal distention and fullness of flanks

2.umbilicus may be flat or everted
3. skin of abdomen is stretched and shiny
with straie albicans
4. caput medusae
5. shifting dullness
6. fluid thrill in tense ascites
• Investigations in ascites:-
1. USG
2. Diagnostic paracentesis
3. Laparoscopy and peritoneal biopsy if needed
4. Ascites fluid examination i.e. transudatetive or
exudative

• D/D: -
1. Cirrhosis of liver
2. Chylous ascites
3. Budd- chiari syndrome
4. Malignant ascites
5. Tubercular peritonitis
 Management of ascites

• Sodium and water retention

• Diuretics
• Paracentesis
Viral Hepatitis
Liver Abscess
There are 2 types:

1. Pyogenic liver abscess.

2. Amoebic liver abscess.
• FEATURES:-
1. May be solitary, multilocular and multiple. Single
and multiple abscesses occur in equal frequency.
2. Increased incidence is seen in-
a) Old age.
b) Diabetics .
c) Immunosuppressed patients .

• Causative organism:-
• E.coli , streptococci, staphylococci, mixed infection.
• E.coli is responsible for 1/3rd cases.
• Causes :-
1. Via portal vein in appendicitis or diverticulitis.
2. Via hepatic artery as in sepsis and general
septicemia.
3. Direct spread of infection from neighborhood as in
subhepatic abscess.
4. After hepatic trauma like cholangitis secondary to
biliary calculi.

• Clinical features:- Fever

-Anorexia, Nausea and Vomiting
- Upper Rt. Abd discomfort & Pain
- Mild jaundice
- Tender hepatomegaly
• Investigation:
1. Blood examination - leucocytosis and raised ESR.
2. USG - confirms the diagnosis
3. Culture – Aspiration of pus, for culture sensitivity.
4. CT scan – show source of abscess ( usually from
colon ).

• Treatment :
1. Combination of ampicillin , gentamicin and
metronidazole ( duration 4-8 wks ).
2. USG guided aspiration – s/o large abscess with
impending rupture. Abscess size > 6 cm.
3. Surgical drainage if needed.
 Amoebic liver abscess
• It is a complication of amoebic dysentery .
• Lower socio-economic status is usually affected.
• Common in immunocompromised patients.
• Common site – upper & post. Of Rt. lobe of liver
• It is usually superficial.

• Etiology :

- Entamoeba histolytica.
- E. multilocus (rare).
• Pathology:
food contaminated with cysts ,especially water and vegetables

Feco-oral route

Cyst (Infective form)

Trophpozoites in small intestine

Adult trophozoites in cecum

Sigmoid colon Rt./ Lt. Asymptomatic

iliac fossa

Liver , lung , Diarrhea Perforation

stomach
• Portal of entry :
- via liver lymphatic's.
- can spread directly through peritoneum.

• Clinical features :
1. Dull aching chronic pain in Rt . Hypochondrium.
2. Fever.
3. Diarrhea.
4. Anorexia , nausea, vomiting , wt. loss ,anemia.
5. Hepatomegaly with tenderness.
• Investigations :

1. Blood examination –
a) TLC increases.
b) Hb decreases.
c) S.bilirubin and Alkaline phosphate increases.
d) SGOT and SGPT increases.
e) USG and CT scan.
f) Aspiration and Culture of pus – s/o RBC’s ,
odorless and Pus looks like green (contaminated
with bile) or chocolate sauce (yellow).
• Treatment :
1. Appropriate medicinal treatment.
2. Aspiration and drainage of abscess – done in case
of impending rupture.

• Complications:
1. Rupture in various organs . Pleural and peritoneal
rupture is commonest.
2. Hemorrhage .
3. Superinfection and secondary infection.
Hydatid cysts
• It is a zoonotic disease.
• Causative agent is Echinococcus granulosus.

Life cycle:
• Definitive host is dog or other canine.
• Intermediate host is sheep , cattle , camel.
• Human is accidental host.
• Infective stage is egg
• MAN IS A DEAD END HOST.
Life cycle
• Clinical features :

1. Mostly asymptomatic.
2. Cysts larger than 5 cm in diameter – pressure
symptom.
3. Most common symptom is abdominal pain ,
vomiting , dyspepsia.
4. Jaundice in 10% of patients – biliary tract
obstruction.
5. Bacterial infection of cysts present as pyogenic
liver abscess.
6. Most frequent sign is hepatomegaly / palpable
mass.
• Investigations :-
1. Routine blood test- 25% esinophilia and raised
bilirunbin.
2. ELISA are the most widely used methods for
detection
3. Casoni’s intradermal test.
4. USG for primary diagnosis of cysts.
5. CT scan and MRI.

• Treatment:
1. Medical Rx – Mebendazole (3-6 months orally)
albendazole( 3-6 months orally)
2. Surgical Rx- for large liver cysts with multiple
daughter cysts. Or Infected cysts
Cirrhosis of liver
• It is a diffused disease having following features:
1. It involves entire liver , normal architecture of liver is
disorganized .
2. There is a formation of nodules separated from one
another by irregular bands of fibrosis.
3. It occurs following hepatocellur necrosis ,it is a
totally irreversible phenomenon.
 Alcoholic liver cirrhosis
• All those who drink alcohol donot develop liver
damage following reasons are necessary to
develop cirrhosis -:
1. Drinking pattern – more than 80 gm of any type of
alcoholic beverage for atleast 10 years is likely to
develop alcoholic cirrhosis.
2. Malnutrition – absolute or relative malnutrition of
proteins and vitamins is regarded as contributary
factor in evolution of cirrhosis . Than recurrent
infection with hepatitis (HAV , HBV, HCV, HDV)
leads to cirrhosis.
3. Genetic factor - is also responsible for
development of cirrhosis.
 Pathogenesis of cirrhosis
• Cirrhosis in general is initiated by hepatocellular
necrosis there is continuous destruction of
hepatocytes causes collapse of normal lobular
hepatic parenchyma followed by fibrosis.
• This mechanism is continuous untill whole liver cells
are destoryed.
• There are 2 morphologies of liver in cirrhosis:-
1. Micronodular cirrhosis – there is diffused involment
of hepatic lobule and forms small nodules which
are separated by bands of fibrosis.
2. Macronodular cirrhosis – in this type nodules are
larger separated from fibrosis band.
 Pathologic changes
• Alcoholic fatty liver : - In this liver becomes enlarged
yellow and greasy . There is a deposition of droplet
of fats inside the hepatocytes which causes
enlargement of liver.
• Alcoholic hepatitis :- It occurs following heavy
drinking there is inflammation of hepatocytes with
infiltration of inflammatory cells inside the
hepatocytes . This both stages are curable.
• Alcoholic cirrhosis :- It is progressive alcoholic liver
disease in which there is abnormal lobular
architecture with irreversible cell injury .i.e. necrosis
of hepatocytes occurs.
 Clinical features of cirrhosis

1. Weakness
2. Weight loss
3. Muscle wasting
4. Anorexia , nausea , vomiting
5. Jaundice
6. Recurrent infection
7. Low grade fever
8. Symptoms of hepatic insufficiency
9. Ascites
 Complications

1. Portal hypertension
2. Ascites
3. Portal vein thrombosis
4. Peritonitis
5. Hepatocellular carcinoma
6. Hepatic encephalopathy
 Investigation in cirrhosis
• CBC – Anemia , leucopenia , thrombocytopenia
Acanthocytosis (spur like projections on RBC).
• LFT – Hyperbilirubinaemia
- A : G ratio is reversed (A and G )
- AST : ALT ratio more than 2 in alcoholic
cirrhosis.
• USG – ascites , size of portal vein , size of liver.
• Liver biopsy – confirms the diagnosis.
 Treatment of cirrhosis

• Remove the cause (drugs , alcohol)

• Multivitamin supplement.
• Specific treatment for complication.
Wilson’s Disease
• Autosomal recessive inheritance.
• In wilson disease total body copper is increased
due to abnormal copper metabolism.
• Wilson’s disease is characterized by following
abnormalities:-
1. Excessive accumulation of copper in body
2. Failure to synthesize ceruloplasmin.

Pathology :-
The excess copper is deposited in various tissues
resulting in damage – liver , kidneys , brain ,eyes and
skeleton.
 Clinical features of Wilson disease
1. Presents between 5 and 30 years .
2. LIVER INVOLMENT :-
a) Asymptomatic hepatosplenomegaly.
b) Acute hepatitis.
c) Chronic hepatitis.
d) Cirrhosis of liver.
e) Hepatic failure.
3. BRAIN INVOLMENT :-
a) Neurological manifestations – muscle disorders,
especially resting and intention tremors.
b) Psychological manifestation – bizarre behavioural
disturbances similar to schizophrenia.
4. EYE MANIFESTATION :-
a) Greenish brown or golden brown ring around the
periphery of cornea , appearing first at the upper
periphery. It is best detected by slit lamp
examination.
b) Disappears with treatment.
c) KAYSER-FLEISEHER RINGS.
 Investigations
1. Slit examination of eyes for kayser-fleischer ring.
2. Low total serum copper concentration.
3. High urinary copper excretion.
4. High hepatic copper content.

Management
1. Chelating drugs penicillamine 1g/day life long.
2. Zinc acetate for asymptomatic patients or after
maximal improvement with penicillamine.
3. Patients with neurological involvement , not
improved by penicillamine may be treated
intramuscular dimercaprol.
4. Liver transplant in hepatic failure.
5. All siblings of patients should be screened for wilsons
disease and treated even if they are asymptomatic.
Cholelithiasis
 Gallstones
• Incidence :
Gallstones are not common in general population .
Incidence increases after 21 years and reaches the
peak in 5th and 6th decade .
Females are more commonly affected than male.
 Etiology
• Depends upon 4 factors :-
1. METABOLIC FACTOR:
- Cholesterol excess due to obesity , increased
calorie diet ,medication usually cholesterol is
emulsified by bile but the ratio drops cholesterol
precipitates and stone is formed.
2. BILE STASIS : pregnancy and prolong total parental
nutrition leads to gallstone formation.
3. HEMOLYTIC ANEMIA : like sickle cell anemia ,
thalassemia causes calcium bilirubinate stones
4. PARASITIC INFECTION : like ascaris and ankylostoma.
5. SAINT’S TRAID : gallstones , mackle's diverticulum ,
hiatus hernia.
6. INFECTION : with bacteria are from tonsil ,tooth ,
and bowel which reaches gall bladder through blood
stream.

Types
1. Cholesterol stones: -it is a single solitary stone.
2. Brown pigmented stone: -it is mixture of calcium
bilirubinate and cholesterol .
3. Mixed stone: - some are cholesterol stone and
some are bilirubin stone.
 Clinical features
• In Gall bladder :
1. Asymptomatic gallstones.
2. Hydrops of gall stones.
3. Flatulent dyspepsia.
4. Gallstone colic.
5. Mucocele .
6. Empyema .
7. Chronic cholecystitis.
8. CA gall bladder.
• In common bile duct:
1. Obstructive jaundice.
2. Liver failure.
3. Acute or recurrent pancreatitis.

• In Pancreas:
1. Acute pancreatitis
2. Acute Relapsing pancreatitis
3. Chronic pancreatitis
• In intestine :
It Leads to acute intestinal obstruction

Investigation
1. Straight x-ray – to demonstrate radiopaque stone
2. Blood examination – Reveal leukocytosis
3. Cholecystography
4. USG
 Treatment

• Treatment of gall stone is cholecystectomy.

• In acute conditions – antibiotic, analgesics to
control inflammatory process and pain.
• IV fluids should be administered if needed.
Cholecycstitis
• Acute bacterial inflammation of gall bladder is
called cholecystitis.

Types –
1. Calculus cholecystitis (inflammation of gall
bladder with stone)
2. Acalculus cholecystitis (inflammation of gall
bladder without stone)

Causative bacteria: E. coli, Streptococci, salmonella.

 Pathogenesis
STONE

OUTLET OBSTRUCTION MUCOSAL EROSION

STASIS DESTRUCTION OF
CELLS BY TOXIC
BILE SALTS.

BACTERIAL PROLIFERATION
BACTERIAL PROLIFERATION

NECROSIS
PERFORATION
 Clinical features
• Fatty fertile female typical victim of cholecystitis
(3f’s)
• Patients present with severe upper abdominal pain
with nausea and vomiting.
• Patients also has low grade fever with loss of
appetite.

Signs – Murphy’s signs is positive keep the finger in right

hyperchondrium and ask patients to take a deep
inspiration at the height of inspiration (last part of
inspiration) there is pain.
Boa’s sign – Area of hyperesthesia between 9th to 11th
ribs on right side.
 Investigation
• Total WBC Count – Is always raised
• Blood and Urine Sugar – To rule out DM
• Plain X-ray Abdomen – To confirm diagnosis
• USG
 Liver
Function
Tests (LFTs)
 Objectives
•Understand the major metabolic functions of the
liver and causes of liver dysfunction.
•Discuss markers of liver function tests such as liver
enzymes, bilirubin, albumin and prothrombin time
that can diagnose hepatic injury and assess hepatic
function.
 Liver Function Tests
(LFTs)
Broadly classified as:

1. Tests to detect hepatic injury:

• Mild or severe; acute or chronic
• Nature of liver injury (hepatocellular or
cholestasis)

2. Tests to assess hepatic function

 Classification of LFTs
Group I: Markers of liver dysfunction

▫ Serum bilirubin: total and conjugated

▫ Urine: bile salts and urobilinogen
▫ Total protein, serum albumin and
albumin/globulin ratio
▫ Prothrombin Time
 Classification of LFTs
Group II: Markers of hepatocellular injury

▫ Alanine aminotransferase (ALT)

▫ Aspartate aminotransferase (AST)
 Classification of LFTs
Group III: Markers of cholestasis

▫ Alkaline phosphatase (ALP)

▫ g-glutamyltransferase (GGT)
 Limitations of LFTs
• Normal LFT values do not always indicate
absence of liver disease
o Liver a has very large reserve capacity

• Asymptomatic people may have abnormal

LFT results
o Diagnosis should be based on clinical
examination
 Serum Albumin
• The most abundant protein synthesized by the liver

• Normal serum levels: 3.5 – 5 g/dL

• Synthesis depends on the extent of functioning liver

cell mass

• Longer half-life: 20 days

• Its levels decrease in all chronic liver diseases

 Serum Globulin
• Normal serum levels: 2.5 – 3.5g/dL

• a and b-globulins mainly synthesized by the liver

• They constitute immunoglobulins (antibodies)

• High serum g-globulins are observed in chronic

hepatitis and cirrhosis:
o IgG in autoimmune hepatitis
o IgA in alcoholic liver disease
 Albumin to globulin
(A/G) ratio
• Normal A/G ratio: 1.2/1 – 1.5/1

• Globulin levels increase in hypoalbuminemia

as a compensation
 Aspartate
aminotransferase (AST)
• Normal range: 8 – 20 U/L

• A marker of hepatocellular damage

• High serum levels are observed in:

o Chronic hepatitis, cirrhosis and liver cancer
Alanine aminotransferase
(ALT)
• More liver-specific than AST
• Normal range (U/L):
▫ Male: 13-35
▫ Female: 10-30
• High serum levels in acute hepatitis (300-1000U/L)
• Moderate elevation in alcoholic hepatitis (100-
300U/L)
• Minor elevation in cirrhosis, hepatitis C and non-
alcoholic steatohepatitis (NASH) (50-100U/L)
Alanine aminotransferase
(ALT)
• Appears in plasma many days before clinical signs
appear

• A normal value does not always indicate absence

of liver damage

• Obese but otherwise normal individuals may have

elevated ALT levels
 Alkaline phosphatase
(ALP)
• A non-specific marker of liver disease

• Produced by bone osteoblasts (for bone

calcification)
• Present on hepatocyte membrane

• Normal range: 40 – 125 U/L

• Modearte elevation observed in:

o Infective hepatitis, alcoholic hepatitis and hepatocellular
carcinoma
 Alkaline phosphatase
(ALP)
• High levels are observed in:
o Extrahepatic obstruction (obstructive
jaundice) and intrahepatic cholestasis

• Very high levels are observed in:

o Bone diseases
 g-glutamyltransferase
(GGT)
• Used for glutathione synthesis

• Normal range: 10 – 30U/L

• Moderate elevation observed in:

o Infective hepatitis and prostate cancers

• GGT is increased in alcoholics despite normal liver

function tests
o Highly sensitive to detecting alcohol abuse