GALL BLADDER

CHOLELITHIASIS
• Bile formation  elimination of excess cholesterol from the
body.
• TYPE :
CHOLESTEROL STONE, PIGMENT STONE & MIXED
• COMPLICATION :
CHOLECYSTITIS, OBSTRUCTIVE JAUNDICE, LIVER ABSCESSES,
PANCREATITIS, AND CRCINOMA
• PATHOLOGY:
NORMAL, MUSCULAR HYPERTROPHY, LOSS OF THE MUCOSAL
PAPILLARY FOLD, INFLAMMATION, CYSTIC
• Cholesterol  water-soluble by aggregation with bile salts and lecithins. When
cholesterolconcentrations exceed the solubilizing capacity of bile (supersaturation) no longer
remain dispersed  crystallizes. Cholesterol gallstone formation is enhanced by hypomobility of the
gallbladder (stasis), which promotes nucleation, and by mucus hypersecretion, with consequent
trapping of the crystals, thereby enhancing their aggregation into stones.
• Formation of pigment stones  presence of unconjugated bilirubin in the biliary tree, as occurs in
hemolytic anemias and infections of the biliary tract. The precipitates are primarily insoluble calcium
bilirubinate salts.
• The major risk factors :
• Age and gender. The prevalence of gallstones increases throughout life. ♀:♂= 2:1
• Ethnic and geographic. Cholesterol gallstone prevalence approaches 50% to 75% in certain Native
American populations—the Pima, Hopi, and Navajos—whereas pigment stones are rare; the prevalence
seems to be related to biliary cholesterol hypersecretion.
• Heredity. In addition to ethnicity, a positive family history imparts increased risk, as do a variety of
inborn errors of metabolism such as those associated with impaired bile salt synthesis and secretion.
• Environment. Estrogenic influences, including oral contraceptives and pregnancy, increase hepatic
cholesterol uptake and synthesis, leading to excess biliary secretion of cholesterol. Obesity, rapid weight
loss, and treatment with the hypocholesterolemic agent clofibrate also are strongly associated with
increased biliary cholesterol secretion.
• Acquired disorders. Any condition in which gallbladder motility is reduced predisposes to gallstones,
such as pregnancy, rapid weight loss, and spinal cord injury. In most cases, however, gallbladder
hypomotility is present without obvious cause.
• 70% to 80% of individuals with gallstones remain
asymptomatic throughout life, with the risk of
symptoms diminishing over time.
• However, some minority have the symptoms. There
is usually pain, often excruciating, which typically
localizes to the right upper quadrant or epigastric
region and can be constant or, less commonly,
spasmodic. Such “biliary” pain is caused by
gallbladder or biliary tree obstruction, or by
inflammation of the gallbladder itself.
 CHOLECYSTITIS
• Inflammation of the gallbladder may be acute, chronic, or acute
superimposed on chronic, and almost always occurs in association with
gallstones
• It is a common cause of abdominal pain in the right hypochondrium.

ACUTE CHOLECYSTITIS
• EMPYEMA: INFECTION : E. COLI, KLEBSIELLA
• GANGRENOUS: ISCHAEMIC AETIOLOGY

CHRONIC CHOLECYSTITIS
• ACALCULOUS CHOLECYSTITIS
• EMPHYSEMATOUS CHOLECYSTITIS; GAS IN THE WLL & LUMEN
• XANTHOGRANULOMATOUS
• PORCELAIN GALL BLADDER: DYSTROPHIC CALCIFICATION IN BROAD BAND OF
MUCOSA
• Acute cholecystitis
 Usually associated with gallstones
 Initially sterile, then infected
 Complications include empyema and/or rupture
 The diagnosis is based on the detection of gallstones by ultrasonography, typically
accompanied by evidence of a thickened gallbladder wall

• Chronic cholecystitis
 Invariably associated with gallstones
 Fibrosis and Rokitansky–Aschoff sinuses  a pathologic diagnosis based on the
examination of the resected gallbladder.
 Attention to this disorder is important because of the potential for the following serious
complications:
• Bacterial superinfection with cholangitis or sepsis
• Gallbladder perforation and local abscess formation
• Gallbladder rupture with diffuse peritonitis
• Biliary enteric (cholecystenteric) fistula, with drainage of bile into adjacent
organs, entry of air and bacteria into the biliary tree, and potentially gallstone-
induced intestinal obstruction (ileus)
• Aggravation of preexisting medical illness, with cardiac, pulmonary, renal, or liver
decompensation
CHOLECYSTITIS
Rokitansky–Aschoff sinuses
 NEOPLASM
BENIGN
MUCOSAL POLYPS
• CHOLESTEROLE POLYPS
• INFLAMMATORY POLYPS
• ADENOMATOUS POLYPS
MESENCHYMAL NEOPLASM
• RARE
CARCINOMA
PREDISPOSING FACTORS
• GALLSTONE
• PORCELAIN GALLBLADDER
SARCOMA AND CARCINOSARCOMA
1,5% OF MALIGNANT
GALLBLADDER TUMOR
LYMPHOMA MALIGNUM: VERY
RARE
Adeno carcinoma
PANCREAS
 PANCREATITIS
• Pancreatitis (inflammation of the pancreas) can be
acute or chronic. Overlap occurs as patients with
chronic pancreatitis can have acute exacerbations.
• In acute pancreatitis, function can return to normal if
the underlying cause of inflammation is removed.
• By contrast, chronic pancreatitis is defined by
irreversible destruction of exocrine pancreatic
parenchyma.
 ACUTE PANCREATITIS

AETIOLOGY
• OBSTRUCTION OF BILE DUCT gallstones >>
• BILE REFLUX
• ACUTE INTOXICATION OF ALCOHOL >>
• ACUTE VASCULAR INSUFFISCIENCY
• MUMPS VIRUS INFECTION
• TRAUMA

CLINICL FEATURE
• SUDDEN ONSET OF SEVERE ABDOMINAL PAIN
• NAUSEA, VOMTING
• RAPID CLINICAL DETERIORATION
• SHOCK

• Amylase released into blood serves as diagnostic test

 Morphology of acute pancreatitis

• Haemorrhage
• Inflammasi akut
• Fat necrosis
• Pseudo cyst
 CHRONIC PANCREATITIS

AETIOLOGY
• CHRONIC EXCESSIVE ALCOHOL CONSUMPTION >>
• FAMILIAL PANCREATITIS
• PROLONGED OBSTRUCTION OF PANCREATIC DUCT
• SCARRING TISSUE FOLLOWING ACUTE PANCREATITIS
• FAT CONSUMPTION

CLINICAL FEATURE
• INTERMETTEN UPPER ABDOMINAL & BACK PAIN
• WEIGHT LOSS  Intestinal malabsorption and diabetes

MORPHOLOGY
• Continuing inflammatory process with exocrine atrophy and fibrosis
Chronic Pancreatitis
 CARCINOMA OF THE PANCREAS

• Carcinoma of exocrine pancreas is usually ductal adenocarcinoma

• Very poor prognosis

AETIOLOGY
• CIGGERETTES SMOKING >>
• DIABETES MELITUS
• FAMILIAL PANCREATITIS

PATHOLOGY
• ADENOCARCINOMA
• DESMOPLASTIC STROMA

LOCATION
• MOSTLY IN HEAD OF PANCREAS

METASTASIS
• HEMATHOGEN LIVER
• LIMPHOGEN LYMPHNODE
 PANCREAS NEOPLASM
• Pancreatic cancer probably arises from noninvasive precursor
lesions (most commonly, PanINs), developing by progressive
accumulation of characteristic mutations of oncogenes (e.g.,
KRAS) and tumor suppressor genes (e.g., CDKN2A/p16, TP53,
and SMAD4).
• Typically, these neoplasms are ductal adenocarcinomas that
produce an intense desmoplastic response.
• Most pancreatic cancers are diagnosed at an advanced stage,
accounting for the high mortality rate.
• Obstructive jaundice is a feature of carcinoma of the head of
the pancreas; many patients also experience debilitating pain.
• Morphology :
 Cell differentiation : DUKTAL, ASINAR, ENDOKRIN
 Configuration : SOLID, CYSTIC, INTRADUCTAL
 Adenocarcinoma

Carcinoma of the pancreas. A, A cross-section through the head of the pancreas and adjacent common bile duct
showing both an ill-defined mass in the pancreatic substance (arrowheads) and the green discoloration of the duct
resulting from total obstruction of bile flow. B, Poorly formed glands are present in a densely fibrotic (desmoplastic)
stroma within the pancreatic substance.
Adenokarsinoma duktal
Karsinoma asinar
Undifferentiated carcinoma