HEPATITIS
Hepatitis means inflammation of liver,
It is most commonly caused by viruses but also be caused by drugs,
chemicals, autoimmune disease and metabolic abnormalities.
ETIOLOGY
Viral hepatitis
Alcohol hepatitis
Autoimmune hepatitis
Non alcoholic steatohepatitis (NASH)
VIRAL HEPATITIS
Five types of hepatitis have been identified : Hepatitis A, B, C , D , E
Hepatitis A and E viruses typically cause only acute or short term infections
while B, C and D are most likely to become ongoing and chronic.
Except HBV all are RNA virus .
Other less common viruses can also cause liver disease. These include CMV,
Herpes virus , rubella virus , Epstein –barr virus (EBV).
Hepatitis A and E are infectious, transmitted by fecal-oral route, whereas B, C
and D cause serum hepatitis and transmitted mainly by parenteral route.
Clinical manifestation
PRODROMAL STAGE
Easy fatigue and generalized malaise due to systemic effects of liver
inflammation.
Anorexia, mild weight loss
Fever, nausea and vomiting
Right upper quadrant tenderness
Dark coloured urine and clay coloured stool
CLINICAL STAGE
Worsening of all symptoms of prodromal stage
Itching from increased bilirubin in blood
Abdominal pain and tenderness
Jaundice from increased bilirubin in blood.
RECOVERY STAGE
The patient’s symptoms subside and appetite returns.
OTHER TYPES OF HEPATITIS
CHRONIC HEPATITIS
It is defined as asymptomatic , biochemical or serological evidence of
continuing or relapsing hepatic disease for more than 6 months.
Seen with HCV and HBV.
c/f are variable fatigue, anorexia and mild jaundice.
FULMINANT HEPATITIS
It is defined as hepatic insufficiency that progresses from onset of symptoms to
hepatic encephalopathy within 2-3 weeks in individuals who do not have chronic
liver disease.
CARRIER STATE
The individual harbors and can transmit the organism but is asymptomatic.
HCV ≫ HBV
PATHOLOGICAL CHANGES
ACUTE HEPATITIS
Swelling of the hepatocytes called “ballooning”
Presence of apoptotic hepatocytes giving rise to councilman bodies. Apoptosis of
a single hepatocyte is called spotty necrosis.
Disruption of lobular architecture of the liver.
Necrosis connecting portal to portal, portal to central , central to central regions
of adjacent lobules is called bridging necrosis.
Infiltration of portal tract with inflammatory cells .
Spilling of inflammatory cells in the adjacent parenchyma causing necrosis of
adjacent cells (Interface hepatitis or piecemeal necrosis)
CHRONIC HEPATITIS
Elementary lesion in chronic hepatitis are:
Spotty necrosis
Confluent lytic necrosis
Portal inflammation
Interface hepatitis/ piecemeal necrosis
Fibrosis – hallmark of chronic liver damage. It can be intralobular, septal to
periportal , portal to portal, portal to central
Cirrhosis – ongoing necroinflammation and fibrosis along with regeneration will
eventually lead to cirrhosis (post – necrotic)
Diagnostic tests
Hepatitis profile studies
SGOT , SGPT increased
Serum bilirubin level
Prothrombin time is prolonged
Liver biopsy
AMEBIC LIVER ABSCESS
Most of the liver abscesses are of bacterial origin and less often they are
amebic or hydrated.
It is a complication of amebic dysentery which is caused by Entamoeba
Histolytica.
Pathology
The protozoa passes from the colonic lesion via the portal vein into the liver,
usually into the upper and posterior portions of right lobe.
Liver infection begins with intrahepatic portal thrombosis and infarction , the
cytolytic activity starts and leads to liquefaction of the surrounding stromal
and parenchymal structures , resulting in formation of large single abscess.
30% have more than one abscess.
CLINICAL MANIFESTATION
Fever
Chills, nausea and vomiting
Anorexia , weight loss and weakness
Right upper quadrant abdominal pain and tenderness
Hepatomegaly
Anemia and sometimes jaundice
Investigation
Blood examination- leukocytosis in early cases, anemia in chronic cases
Radiography
Sigmoidoscopy reveals characterstic amebic ulcers.
Diagnosis is 100 % confirmed by aspiration of liver abscess , anchovy sauce is
quiet diagnostic.
Treatment
Management of amoebic abscess is mainly drug therapy with amoebicidal
drugs, few abscess particularly the large ones may require needle aspiration.
CIRRHOSIS OF LIVER
DEFINITION
Cirrhosis of liver is a chronic, progressive disease characterized by widespread
fibrosis (scarring) and nodule formation. Cirrhosis occurs when the normal
flow of blood , bile and hepatic metabolites is altered by fibrosis.
Types
ALCOHOLIC CIRRHOSIS-Most common due to chronic alcoholism. Scar tissue
characteristically surrounds the portal area.
POST NECROTIC CIRRHOSIS- There are broad bands of scar tissue due to late
results of acute viral hepatitis , post intoxication with industrial chemicals.
BILIARY CIRRHOSIS- Scaring occurs around bile duct in liver, results from
chronic biliary obstruction and infection.
CARDIAC CIRRHOSIS- Associated with severe right sided long term heart
failure.
Risk factors
Drinking too much alcohol.
Being overweight- non alcoholic fatty liver disease and Non alcoholic
steatohepatitis.
Having viral hepatitis-not everyone with chronic hepatitis will develop
cirrhosis , but its one of the world’s leading cause of liver disease.
CAUSES
Alcoholic liver disease- injure the liver by blocking the normal metabolism of
proteins , fats and carbohydrates.
Chronic hepatitis C
Chronic hepatitis B- probably the most common cause of cirrhosis worldwide.
Non alcoholic steatohepatitis (NASH)- In this fat builds up in the liver and
eventually causes scar tissue. This type of hepatitis appears to be associated
with diabetes , malnutrition, obesity , coronary artery disease and treatment
with corticosteroid medication.
Primary biliary cirrhosis
Autoimmune hepatitis
PATHOPHYSIOLOGY
SYMPTOMS
Fatigue
Loss of appatite
Nausea
Swelling in leg, feet and ankle (edema)
Jaundice
Ascites
Spider like blood vessels on skin
Redness in palm of hand
Males- gynecomastia
Confusion , drowsy and slurred speech (hepatic encephalopathy)
DIAGNOSIS
Complete blood count
Liver function test including alkaline phosphatase, SGPT
Serum albumin
Liver biopsy
Liver scan
Upper GI barium swallow
CT of the abdomen
MRI of the abdomen
Ultrasound of the abdomen.
DEFINITION
Acute or chronic inflammation causing
painful distention of the gall bladder. It is
usually associated with gallstones impacted
in cystic duct.
ACUTE CHOLECYSTITIS
Acute inflammation of gall bladder with or without
gall stones.
TYPES
1) CALCULOUS CHOLECYSTITIS-It is the obstructive cholecystitis
due to gall stones having the most common variety in which
around 90 percent of people having gall stones suffer.
2) ACALCULOUS CHOLECYSTITIS-It is the non obstructive type
which is common in person suffering from major illness such
as severe sepsis, diabetes mellitus, burns, dehydration,
multiple injury etc.
3) ACUTE EMPHYSEMATOUS CHOLECYSTITIS- begins
with acute cholecystitis followed by ischemia or
gangrene of GB wall and infection by gas producing
organisms.
CHRONIC CHOLECYSTITIS
It is always associated with gallstones and results
from repeated bouts of subacute or acute
cholecystitis or mechanical irritation of gall bladder
wall. It may appear as asymptomatic then may
progress to symptomatic gall bladder disease with
complications.
PATHOLOGICAL CHANGES
Grossly the gall bladder is distended and tense
There are frank abscess in the wall of gall bladder.
The gall bladder shows inflammatory edema , congestion
and neutrophilic exudates
ACUTE PANCREATITIS
It is an acute inflammatory process of the
pancreas.
The degree of inflammation varies from mild
edema to severe hemorrhagic necrosis.
It is most common in middle aged men and
women. It affects male and female equally.
Causes of pancreatitis
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps / malignancy
Autoimmune
Scorpion sting
Hypertriglycerides or hypercalcemia
ERCP
Drugs (HCTZ, Pentamidine, azathioprine)
PATHOPHYSIOLOGY
ETIOLOGICAL FACTORS (gall stones, ethanol, trauma)
ACTIVATION OF PANCREATIC ENZYMES
TRYPSINOGEN TRYPSIN
ACTIVATES PROTEASES WHICH CAUSES AUTODIGESTION OF PANCREAS AND
ACTIVATION OF OTHER PROTEOLYTIC ENZYMES
ELASTASE HEMMORHAGE
PHOSPHOLIPASE FAT NECROSIS
CLINICAL FEATURES
Severe abdominal pain is predominant symptoms
Pain located in upper quadrant and midepigastrium
Severe deep piercing and continuous or steady in nature
Nausea vomiting
hypotension
Pathological findings
GROSS-
Pancreas is swollen and edematous.Later grey white pancreatic
necrosis, chalky white fat necrosis and blue black hemmorhages
are seen.
MICROSCOPIC-
Necrosis of pancreatic lobules and ducts
Necrosis of the arteries and arterioles with areas of hemmorhage.
Fat necrosis
Inflammatory reaction chiefly with polymorphs.
Mortality in acute pancreatitis is high (20-30%).
Patients succumb to hypotensive shock infection,
acute renal failure and DIC.
SYSTEMIC COMPLICATIONS
Chemical and bacterial peritonitis.
Endotoxic shock
Acute renal failure
Diagnostic findings
Primary tests
Serum amylase – increased (≥200 U/L)
Serum lipase – elevated
Secondary tests
Blood glucose- hyperglycemia
Serum calcium- hypocalcemia
Serum triglyceride- hyperlipidemia
COMPLICATIONS
SYSTEMIC COMPLICATIONS
Chemical and bacterial peritonitis
Endotoxic shock
Acute renal failure
LOCAL SEQUELAE
Pancreatic abscess
Pancreatic pseudocyst
Duodenal obstruction
CLASSIFICATION
BENIGN TUMORS
Hepatic hemangioma (most common benign tumor of liver)
Focal nodular hyperplasia
Hepatic adenoma
MALIGNANT HEPATIC TUMOR
Hepatocellular carcinoma
Hepatoblastoma
Cholangiosarcoma
Cystadenocarcinoma
Embryonal sarcoma
ETIOPATHOGENESIS
A number of etiologic factors are implicated for
growth of malignant tumors in liver.
1) Hepatitis B infection
2)Hepatitis C infection
3)Cirrhosis of liver
4) Alcoholism
5)Mycotoxins as Aspergillus flavus, aflatoxins B1
PATHOPHYSIOLOGY
CHEMICAL CARCINOGENS, PARASITIC INFECTIONS,
TOBACCO SMOKING
GENETIC MUTATIONS
MUTATED GENE INACTIVATES THE TUMOR SUPRESSOR
ONCOGENES
DISRUPTION OF NORMAL GROWTH CONTROL
LIVER CELL DYSPLASIA
LIVER CARCINOMA
CLINICAL FEATURES
Undetected and asymptomatic in the initial stage
Hepatomegaly
Palpable mass in liver
Right upper quadrant pain and tenderness
Jaundice , fever and hemmorhage from esophageal varices
Weight loss, weakness, anorexia related to increased tumor growth
Dependent edema secondary to tumor invasion and obstruction of
portal vein.
DIAGNOSTIC METHODS
Needle biopsy of the liver cells confirms cell type.
Serum enzymes and bilirubin are elevated indicating
abnormal LFT.
Alpha fetoprotein levels are elevated
Chest Xray reveal possible metastasis.
Serum electrolyte studies reveal hypernatremia and
hypercalcemia.
CARCINOMA OF GALL BLADDER
It is malignant tumor of the biliary tract.
It is more frequent in the women with peak incidence in
seventh decade of life.
Gall bladder carcinoma is commonly adenocarcinoma.
ETIOPATHOGENESIS
Cholelithiasis
Cholecystitis
Chemical carcinogens
Genetic factors
Pathological changes
Irregular area of diffuse thickening and induration
of gall bladder wall
Deep ulceration in the wall of gallbladder
Friable, papillary or cauliflower like growth.
Invasion of gall bladder wall and liver bed.
Clinical manifestation
Pain
Jaundice
Noticeable mass
Anorexia and weight loss
Intense itching/ pruritus
Metastasized growth to adjacent organs.
Diagnostic methods
Biopsy
Liver function test
TUMORS OF PANCREAS
Pancreatic cancer is one of the visceral cancers occurring
between the age of 60 and 80 years.
Pancreatic duct adenocarcinoma being the most common.
RISK FACTORS
Cigarette smoking
Consumption of a diet rich in fat
Chronic pancreatitis
Diabetes mellitus
Alcohol consumption
SITE- the majority of the pancreatic carcinoma arise in the
head , followed by body and tail of pancreas.
GROSS- they are usually hard, stellate, gray white color and
appear as poorly defined masses
MICROSCOPY- They are adenocarcinoma in which tumor cells
are arranged in glandular pattern.
Clinical features
Abdominal pain
Obstructive jaundice
Dark colored urine
Clay colored stool
Weight loss
Anorexia
Generalised malaise and weakness
Trousseau syndrome- migratory thrombophlebitis
Courvoisier sign- carcinoma in head of pancreas causes distended palpable
gallbladder.
VERY POOR PROGNOSIS
