PATHOLOGY OF

GALLBLADDER &
PANCREAS

2024-2025
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 CHOLECYSTITIS
Inflammation of the gall blabber wall with or with out stone formation

CLASSIFICATION OF CHOLECYSTITIS

Acute
Onset Acute Chronic superimposed
on chronic

Calculous Acalculous
Cause 90% 10%

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 ACUTE CALCULUS CHOLECYSTITIS
Acute diffuse inflammation of the gallbladder wall 90% with stone formation
▪Incidence > middle aged F
▪ Gallbladder neck (MC) (Hartmann’s pouch )
Sites
▪ Cystic duct.
1-Chemical inflammation :
Pathogenesis

▪ Obstruction of cystic duct by stones or spasm → Abnormal concentrated bile →

toxic bile → chemical irritation & inflammation of the wall.
2. Mechanical inflammation
▪ Obstruction of cystic duct by stones → intraluminal pressure & distention of gall
bladder → disturbance of motility → obstruction of venous flow& ischemia

3- Bacterial infection: ▪ E. coli, Klebsiella , Streptococcus faecalis & Clostridium

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 ACUTE A CALCULUS CHOLECYSTITIS
Acute diffuse inflammation of the gallbladder wall 10% with out stone formation

▪Dehydration
▪Major trauma & burns
Risk factors

▪Torsion of the gallbladder

▪Sever Sepsis.
▪Recent childbirth
▪Diabetes Mellitus
▪Immunosuppression
▪Non-biliary Major Surgical Operations
▪Systemic infections (T.B, syphilis, salmonella actinomycosis).

Pathogenesis 1- Ischemic injury 2- Reflux pancreatic enzymes.

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 MORPHOLOGY OF ACUTE CHOLECYSTITIS
▪G.B: enlarged & edematous ,tense ,hyperemic,
Gross

▪Serosa: covered by fibrinous or suppurative exudate.

▪Wall: thick & edematous
▪Lumen: filled with turbid bile & pus &blood, may contain
one or more stones.

▪Diffuse PNL infiltrate all layers of gall bladder

L\M

▪Mucosal erosions \ ulceration

▪Congestion & edema

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 COMPLICATIONS OF ACUTE CHOLECYSTITIS
▪ Hydrops or Mucocele : If stones impacted in cystic duct → Distention of the gall
bladder → Bile pigment will be absorbed → contents become clear or mucus
▪ Empyema: if bladder neck is obstructed superimposed infection .
▪ Gangrenous cholecystitis: green-black necrotic gallbladder → perforations.
▪ Gallbladder perforation → Pericholecystic abscess
▪ Gallbladder rupture → diffuse peritonitis
▪ Spread of infections : Ascending cholangitis., Portal pyemia , pyemic abscess .
▪ Emphysematous cholecystitis: infection by gas-forming organisms, e.g. clostridia
▪ Chronicity→ stone formation.
▪ Gallstone ileus(Bouveret’s syndrome): Through fistula, large gallstone → bowel→
gallstone ileus or intestinal obstruction
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 CHRONIC CHOLECYSTITIS
▪Chronic inflammation of the gallbladder wall 90% with stone formation,
▪May following recurrent attacks of acute cholecystitis or start de novo

Incidence Forty or Fifty , Female , Fertile , Fatty (4F)

▪ Adhesions due to extensive fibrosis.

Complication
▪Recurrent attacks of
▪ Porcelain gallbladder: diffuse dystrophic
colicky epigastric or RT
C\P

calcification with fibrosis; high risk of cancer

upper quadrant pain,
▪ Squamous metaplasia.
▪Nausea , vomiting
▪ Malignant Transformations
▪Intolerance to fatty food
▪ Biliary enteric (Cholecystoenteric) fistula,
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 MORPHOLOGY OF CHRONIC CHOLECYSTITIS
▪ G.B: normal , or enlarged with absent mucosal folds
Gross

or contracted with exaggerated mucosal folds

▪ Serosa: fibrous adhesions .
▪ Lumen: filled with clear bile ,mucus with one or more stones
▪ Wall: thickened, opaque & gray-white fibrotic +/- calcification
▪ Mucosa: thickened, or ulcerated or flattened & atrophied , folds may be intact
L\M

▪ Mucosa: Normal - Ulceration – Atrophy –Hyperplasia – Squamous Metaplasia

▪ Wall : Chronic inflammatory infiltrate , fibrosis
invagination of epithelial mucosa deep into wall (Rokitansky-Aschoff sinuses)

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 CHOLELITHIASIS (GALLSTONES)
▪ Insoluble material found within the biliary tract & formed of bile constituents (bile
pigments, cholesterol, calcium salts) & other organic material.

Sites ▪ Gallbladder ▪ Extra hepatic biliary tract. ▪ Intrahepatic biliary tract(rare)

Pure Cholesterol Bile pigment

Calcium
10% carbonate
Types

Mixed Combined
Gallstones 80% Gallstones 10%

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 PATHOGENESIS OF CHOLELITHIASIS
Inflammation of gall bladder

▪ ↓ ↓ Bile Salts Formation → loss its emulsifying (solubilizing ) action

▪ ↑ ↑ Bile Salts Absorption → Supersaturation -→precipitation of cholesterol
▪ ↓ ↓ Motility of Gall Bladder (Stasis) → cholesterol precipitation → cholesterol
stone formation.
▪ Shredded Epithelial Cells, Pus Cells, Mucus , Fibrin act as Nuclei for stone
formation
▪ Dead bacteria (E. coli)→ Bacterial enzymes (ᵦ-glucuronidase, phospholipases)→
Unconjugated Insoluble Bilirubin, Free Fatty Acids , Unconjugated Bile Acids →
precipitation of calcium bilirubinate→ brown pigment stone formation .
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Abnormal bile composition
A. ↑↑ cholesterol concentration in blood or bile (pregnancy , ↑↑ diet or familial)
→ Bile salts Unable to keep cholesterol in solution → Supersaturates → Precipitates
B.↑↑ (unconjugated bilirubin ) in blood & bile in cases of Hemolytic Anemias.

Hpercalcemia Formation of Calcium Carbonate stone

Gall Bladder Hypomotility/ Stasis

▪ Total parental nutrition(TPN), Prolonged fasting, Pregnancy, Massive burns, OCP,
Octreotide → Gallbladder Stasis → Promote The Aggregation Of Cholesterol
crystals → formation of biliary sludge (microlithiasis)..
▪ Stasis → Infection→ Stone formation (vicious circle).
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 CHOLESTEROL STONES 7%
▪ Metabolic occurs in absence of infections Risk factors
▪ Site : gall bladder only ▪ Forty or Fifty .
Types of Gallstone

▪ Gross : Solitary, oval, large (1-5cm), soft, ▪ Female, Fertile ,OCP

mulberry (Mammillated) surface , pale yellow, ▪ Fatty ,
glistening radiating crystalline .
▪ Rapid weight reduction
▪ X-rays : radiolucent ▪ Familial
▪ Reduced gallbladder motility
▪ D.M.
▪ Hyperlipidemia.

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 PIGMENT GALLSTONES 10%
▪ Two types: black or brown Risk factors
▪ ↑↑ Unconjugated bilirubin ▪ Chronic Hemolysis.
Types of Gallstone

▪ Formed of bile pigment, calcium bilirubinate, < ▪ Parasitic Infection (Malaria)

20% cholesterol ▪ Chronic Biliary Tract Infections
▪ Site : gall bladder only ▪ Crohn Disease,
▪ Gross : multiple, irregular, soft, ▪ Cystic Fibrosis
friable ,black, brown . ▪ Alcoholic Cirrhosis
▪ X-rays : ▪ Pernicious Anemia
✓Radiolucent in brown type (> cholesterol) ▪ Advancing Age
✓Radiopaque black type( calcium)
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 COMPLICATIONS OF GALLSTONE
▪ Acute or chronic cholecystitis.
▪ Fistula with duodenum → stone to pass into lumen →Acute intestinal obstruction.
▪ Squamous metaplasia → Malignant change.
▪ Cystic duct obstruction → A. Mucocele. B. Empyema.
▪ Common bile duct obstruction causes:
A- Obstructive jaundice . B- Cholangitis. C- Secondary Biliary cirrhosis.
▪ Obstruction of ampulla of Vater → Acute Hemorrhagic Pancreatitis.
▪ Biliary colic :- radiating to the right shoulder (phrenic nerve).

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 TUMORS OF THE GALL BALDDER
Epithelial Epithelial
▪ Adenoma ▪ Adenocarcinoma 90%

Malignant
▪ Papilloma ▪ Squamous cell carcinoma
Benign

▪ Adenomyoma 5%
Mesenchymal Mesenchymal
▪ Lipoma
▪ Angioma
▪ Fibroma
▪ Leiomyoma

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 ACUTE PANCREATITIS
Acute inflammation of exocrine pancreas due to reversible injury to parenchyma
Metabolic Mechanical Drugs and toxins
▪ Alcoholism ▪ Furosemid, azathioprine
▪ Gallstones( pancreatic duct)
▪ Hyperlipoproteinemia ▪ blunt abdominal trauma ▪ Thiazides , sulfonamides,

▪ Hyperparathyroidism ▪ Iatrogenic injury. ▪ Oral contraceptives

▪ Insecticides, methanol,
Causes

▪ Hypercalcemia. ▪ Parasites (Ascaris lumbricoides)

▪ organophosphates.
Genetic Vascular Infectious
▪ Mutation in trypsinogen (PRSS1) ▪ Shock ▪ Hypothermia. ▪ Mumps,
▪ trypsin inhibitor (SPINK1) gene. ▪ Thrombosis & embolism ▪ Coxsackievirus
Idiopathic (~10–20%) ▪ Vasculitis.
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 MORPHOLOGY OF ACUTE PANCREATITIS
▪ Mild & reversible self-limiting

Gross
▪ Pancreas edematous
▪ Mild infiltration by PMN
L\M

▪ Interstitial edema
▪ Life -threatening .
Types

▪ Enlarged swollen, shows red-black ▪ Extra pancreatic fat necrosis :

Gross

hemorrhagic areas with foci of yellow- omentum , mesentery

white chalky fat necrosis subcutaneous fat
▪ Life -threatening .
▪ Extensive necrosis, hemorrhage & fat necrosis within parenchyma.
Gross

▪ In severe cases, marked hemorrhage may convert the pancreas

into a large retroperitoneal hematoma.
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 COMPLICATIONS OF ACUTE PANCREATITIS
▪ Sterile pancreatic abscess
C\P
Local

▪ Pancreatic pseudocyst.
▪ Sudden onset of severe pain in
▪ Duodenal obstruction
LT upper quadrant may radiate
▪ Infection by gram-ve. bacteria from GIT
→ back.
▪ Endotoxic shock with ATN during first week ▪ Nausea , Vomiting,
▪ DIC
Systemic

▪ Acute renal failure ▪ Fever,, Sweating,

▪ Acute respiratory distress syndrome ▪ Tachypnea , Tachycardia
▪ Hemolysis ▪ Followed By Peripheral
▪ Chemical and bacterial peritonitis. Vascular Collapse

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 CHRONIC (RELAPSING) PANCREATITIS
▪ chronic inflammation with fibrosis of pancreas [Link] by permanent &
progressive & irreversible morphologic or functional damage of exocrine
parenchyma of pancreas with destruction of endocrine parenchyma in late
stages due to repeated mild and subclinical attacks of acute pancreatitis

▪ Autoimmune pancreatitis.
▪ Chronic alcohol
▪ Familial chronic pancreatitis
Causes

▪ Cystic fibrosis of pancreas

▪ Tropical chronic pancreatitis’
▪ Long-standing obstruction of pancreatic
▪ Protein-rich diet
duct by calculi or tumor , pseudocyst , trauma
▪ Idiopathic

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MORPHOLOGY OF CHRONIC PANCREATITIS
Types ▪ Non-obstructive (95%) ▪ Obstructive.

▪ Pancreas may be enlarged or Contracted (fibrotic).

Gross

▪ Nodular , firm to hard ▪ Pseudocysts may be seen

▪ C\S: dilated ducts and calcified concretions, stones

▪ Atrophy of acini
▪ Later loss of β islets
▪ Parenchymal fibrosis
L\M

▪ Cystic dilatation of pancreatic ducts with protein plugs in its lumen.

▪ Atrophy/hyperplasia/ squamous metaplasia of duct epithelium
▪ Chronic inflammation.

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 COMPLICATIONS OF CHRONIC PANCREATITIS
▪ Severe functional damage of pancreas: ▪ Endocrine insufficiency→
▪ Exocrine insufficiency→ Malabsorption secondary D.M.
✓Weight loss . ▪ Duodenal obstruction.
✓Steatorrhoea. ▪ Biliary obstruction
✓Vitamins A, D, E , K deficiency.
✓Hypoalbuminemia edema
▪ Calcifications ▪ Splenic vein thrombosis
▪ Recurrent mild jaundice
▪ Pancreatic pseudocysts ▪ Repeated attacks of abdominal pain or
C\P
▪ Pseudoaneurysm ▪ Persistent abdominal and back pain.
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 TUMORS OF THE PANCREAS
1. Ductal tumors : 90% low-grade Malignant
2. Islet cell tumour :5% Endocrine (Islet cell)
3. Acinar (Exocrine) tumors: 2% ▪ Adenoma of G-cells (Gastrinoma)
4. Others ▪ ᾳ cell tumors (Glucagonoma )

Endocrine (Islet cell) ▪ Delta cell tumors (Somatostatinomas)

▪ Adenoma of β cells (Insulinoma) Epithelial

Benign

Malignant
Exocrine Tumors 2% ▪ Infiltrating ductal adenocarcinoma
▪ Adenoma of exocrine pancreas 90%
▪ Mucinous \ serous cystadenoma

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 PANCREATIC CARCINOMA
▪Most aggressive of solid cancers
▪2nd most common cancer of GIT after colorectal cancer
▪6% of all cancer deaths.
▪Early diagnosis very difficulty,
▪Poor prognosis .
▪Incidence 60-80yrs F=M
Sites
▪ Head 60% ▪ Body 15%
▪ Entire gland 20% . ▪ Tail 5%

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 PANCREATIC CARCINOMA
Risk Factors Inherited Predisposing conditions
▪ Cigarette smoking (strongest)
▪ Peutz-Jeghers syndrome (highest
▪ Chronic alcoholism
likelihood)
▪ Chemical carcinogens:
▪ Hereditary pancreatitis
naphthylamine, benzidine nitrosamines
▪ Strong family history 10% cases
▪ Chronic pancreatitis. ▪ High fat diets
▪ Hereditary breast & ovarian cancer
▪ Long-standing D.M. ▪ Obesity
▪ Hereditary Non-Polyposis Colorectal
▪ Familial (K-RAS. P53 mutation).
Cancer (HNPCC).
▪ H. pylori infection
▪ Lynch syndrome & FPC syndrome ,
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 MORPHOLOGY OF PANCREATIC CARCINOMA

Gross ▪ Grey-white, stellate hard gritty poorly defined mass

▪ Tumor Grades
✓Well differentiated,
✓Moderately differentiated,
L\M
✓Poorly differentiated
▪ Malignant glands \+or clusters of malignant cell
▪ Infiltrating into stroma .
▪ Prominent desmoplastic stroma.

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 SPREAD OF PANCREATIC CARCINOMA
Local spread:
▪ Perineural invasion → retroperitoneal structures as kidney, adrenals, vertebral
column, diaphragm .
▪ Directly spread → peripancreatic soft tissues, spleen, transverse colon, stomach
▪ Involvement of biliary system late.
85% at time

→ peripancreatic, gastric, mesenteric ,omental, porta-

Lymphatic spread:
of Dx

hepatic lymph nodes (mostly Cancer body and tail)

Blood spread: → liver, lungs, adrenal, and bones (mostly Cancer body and tail)

▪ Brief & progressive course (6 months). ▪ 5 years survival rare is 2%

Prognosis
▪ Usually unresectable or metastatic at the time of diagnosis.

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 PANCREATIC CARCINOMA
▪Pain (persistent & progressive) Cancer head:
▪ Obstructing common bile duct or
▪Anorexia and weight loss
Migratory Superficial ▪ Ampulla of Vater 50%→ progressive
obstructive jaundice (Early Diagnosis)
Thrombophlebitis (Trousseau Sign)
▪ Marked dilatation of gall bladder,
Cancer or its necrotic products→
▪ Obstruct duodenum.
platelet-activating factors (PAF) &
Cancer body and tail:
procoagulants → thrombosis appear
▪ Remains silent for sometimes ,
& disappear spontaneously (migratory).
▪ It may reach large size at time of discovery.
(mostly Cancer body & tail)

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