PATHOLOGY

GALLBLADDER AND PANCEAS

Dr. Janet L. Dy

November 29, 2011

Pathogenesis:
A. Formation of cholesterol stones
- Supersaturation of bile with cholesterol
Congenital dilations of the common bile duct
- When cholesterol concentrations exceed the solubilizing
Predispose to stone formation, cholangitis, stenosis and
capacity of bile (supersaturation), cholesterol can no
stricture, pancreatitis, obstructive biliary complications
longer remain dispersed and nucleates into solid
Increased risk of bile duct carcinoma in older patients
cholesterol monohydrate crystals
most often in children before 10 years with non-specific
- Cholesterol gallstone formation involves 4 simultaneous
symptoms of jaundice and/or recurrent abdominal pain
conditions:
a. Bile must be supersaturated with cholesterol
Cholelithiasis/ Gallstones
b. Hypomotility (stasis) of gallbladder promotes
More than 80% are silent
nucleation
90% are cholesterol stones (crystalline cholesterol monohydrate)
c.
Cholesterol nucleation in bile is accelerated
10% are pigment stones (bilirubin calcium salts)
d. Hypersecretion of mucus ion gallbladder traps
2 Types of Stone:
nucleated crystals
1. Cholesterol stone (cholesterol monohydrate)
Biliary
hypersecretion of cholesterol Bile
- Usually solitary, oval and 2-3 cm in length
supersaturation Formation of solid cholesterol stone
- Has a radiating, glistening cut surface & a tiny dark
(yellowish and solitary)
central deposit
B. Formation of pigment stones
- Most common
- Complex mixture of abnormal insoluble calcium salts of
- Almost always pure cholesterol monohydrate
unconjugated bilirubin along with inorganic calcium salts
2. Pigment stones (bile Ca salts)
- Elevated levels of unconjugated bilirubin increases the
- Multiple
risk of developing pigment stones
- Faceted due to tendency of cholesterol salts to
1. Hemolytic syndromes
aggregate together.
2. Severe ileal dysfunctions
- Greenish-black in color
3. Bacterial contamination (E. coli infection, biliary
- Associated with hemolytic conditions
Ascariasis, liver fluke)
Morphology:
- Mucin glycoproteins constitute the scaffolding and
interparticle cement of all stones
- Cholesterol stones:
Pale yellow, round to ovoid
Appears radiolucent if largely composed of cholesterol
Appears radiopaque if sufficient calcium carbonate is
found
- Pigment stones:
Fig. 1. Left: Numerous yellow-green cholesterol in an inflamed gallbladder. Right:
1. Black pigment stones
Brown and black pigment (bilirubin) stones
Found in sterile gallbladder
Risk Factors:
Contain oxidized polymers of calcium salts of
1. Sex: Female
unconjugated bilirubin
2. Age: > 40 years old (prevalence of cholesterol gallstones
Small yet present in large quantities and crumble
increases throughout life)
easily
3. Obesity: Increased biliary cholesterol secretion
2. Brown pigment
4. Estrogen
Found in infected intra and extrahepatic ducts
- Oral contraceptives, pregnancy
Contain pure calcium salts of unconjugated bilirubin
- Stimulates hepatic HMG-CoA reductase activity
Few, tend to be soft with a greasy soaplike
Increase cholesterol uptake and biosynthesis
consistency
Note:
Clinical
features:
Four Fs Female, forty, fat, fertile
- Majority of patients with gallstones are without
5. Clofibrate: Excess biliary secretion of cholesterol
symptoms
6. Rapid Weight Loss
- Biliary pain (prominent symptoms)
7. Ethnic & Geographic
Excruciating and constant or colicky (spasmodic)
8. Hemolytic syndrome: Elevated levels of unconjugated
Result of obstructive nature of gallstones
bilirubin
- Other symptoms: Bloating, intolerance to fatty foods, nausea
9. Bacterial contamination of biliary tree parasitic infection
Complications:
- Setting in which pigment gallstones arise
- Acute cholecystitis (gallbladder inflammation)
10. Parasitic Infection
- Cholangitis (biliary tree inflammation)
11. GIT disease
- Empyema (gall bladder with pus)

GALLBLADDER
Choledocal Cyst

Note:
The 1st 5 factors mentioned above are associated more
with cholesterol gall stone formation

SECTION B

- Pancreatitis (reflux of pancreatic secretion due to obstruction of

hepatopancreatic duct)
- Gallstone ileus / Bouverets syndrome (intestinal obstruction,
occassionaly, due to a large stone eroding directly into an
adjacent loop of small bowel)
- Gallbladder carcinoma

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Choledocholithiasis
Presence of stones within the bile ducts of the biliary tree
Stones are usually pigmented and associated w/ biliary tract
infection
May be asymptomatic
Clinical Features:
- Symptoms include obstructions, pancreatitis, cholangitis,
hepatic abscess, secondary biliary cirrhosis, acute calculous
cholecystitis
Note:
Cholangitis: acute inflammation of the wall of bile ducts

Fig. 2.Common bile duct is opened to reveal several small calculi within the lumen,
indicative of choledocholithiasis. Note that the gallbladder to the right is dilated.
Stones from the gallbladder, if small enough can pass through (or impact within) the
neck of the gallbladder and gain access to the common bile duct, a condition known
as choledocholithiasis.

Cholecystitis
Acute inflammation of the gallbladder
90% associated with gallstone obstruction of neck or cystic
duct
Causes: Obstruction by gallstones, chemical irritation,
secondary to bacterial infection

Acute Cholecystitis
Types:
A. Acute Calculous Cholecystitis (with gallstones)
- Precipitated 90% of the time by obstruction of neck or
cystic duct
- Primary complication of gallstones
- Most common reason for emergency cholecystectomy
Pathogenesis:
- Inflammation of obstructed gallbladder Bile stasis
Release of chemical mediators, phospholipases
Phospholipase hydrolyzes lecithins to toxic
lysolecithins Disruption of mucosal layer
Mucosal epithelium exposed to bile salts Acute
inflammation
- Chemical irritation (direct detergent action of bile
salts) Gallbladder dysmotility Distension and
increase intraluminal pressure Compromise blood
flow to mucosa Ischemia
- Occur in the absence of bacterial infection
- Frequently develops in diabetic patients who have
- Symptomatic gallstones

B. Acute Acalculous Cholecystitis (without gallstones)

- 5-12% of cases
- Result from ischemia (cystic artery is an end artery with
no collateral circulation)
- Occur in the absence of gallstones
Risk Factors:
1. Postoperative nonbiliary major surgery
2. Major trauma and burns
3. Sepsis with hypotension and multisystem organ failure
4. Prolonged intravenous hyperalimentation
5. Postpartum
6. Immunosuppression
7. Diabetes mellitus
8. Infections
Morphology:
- No specific morphologic difference bet acalculous and
calculous except for absence/presence of stones
- Enlarged and tense gallbladder
- Bright red or blotchy, violaceous to green-black
discoloration, imparted by subserosal hemorrhages
- In mild cases, the wall is thicked, edematous and hyperemic
- In severe cases, serosal covering layered by fibrin and
suppurative coagulated exudates (fibrinopurulent exudates)
- Empyema of gallbladder
Gallbladder contains an exudates that is virtually pure
pus
- Gangrenous cholecystitis
Green-black necrotic organ in more severe cases
- Histologic picture:
Extensive necrosis
Numerous neutrophils in the mucosa and lumen (gall
bladder does not have a submucosa; neutrophils are
found in the muscle layer)
Mucosal erosion
Clinical Features:
- Attack begins with progressive right upper quadrant or
epigastic pain
Often radiate to right shoulder
Pain maybe colicky when stone is present in the ducts
or neck
- Tenderness
- Presence of conjugated hyperbilirubinemia suggests
obstruction of common bile duct
- Mild fever, anorexia, tachycardia, sweating, nausea,
vomiting
- Mild to moderate luekocytosis
Complications:
- Gangrene (incidence higher in acalculous)
- Perforation (incidence higher in acalculous)
- Secondary bacterial infection w/ subsequent cholangitis
sepsis

Chronic Cholecystitis

Fig. 3. Acute Cholecystitis. Enlarged and hyperemic GB. Note the exudate.

Associated with cholelithiasis in more than 90% of cases

E. coli and enterococci are most common pathogen
Obstruction of gallbladder outflow is not a requisite (unlike
acute calculous cholecystis)
Symptoms from biliary colic to RUQ pain and epigastric
distress (just like in acute cases)
Etiology:
- May be a sequel to repeated bouts of acute cholecystitis but
may arise de novo
- In many instances, it develops in apparent absence of
antecedent attacks
- Affects similar px population as acute cholecystitis

Fig. 4. Microscopic features. Black arrow: Mucosa. White arrow: PMNs

SECTION B

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Morphology:
- Fibrosis (due to thickening of the wall Very important
sign!)
- Chronic inflammation
- Velvety appearance of mucosa
- 95% of cases gall stones are present
- Thickening of gall bladder wall is due to fibrosis

Cholesterolosis (strawberry gallbladdder)

- Microscopically, the mucosa in cholesterolosis of the
gallbladder
contains many foamy macrophages which
produce the grossly visible strawberry-like appearance
(green-red-yellow streaks)

Fig. 9: Left: Gross. Right: Histology The mucosa in cholesterolosis of the GB

contains many foamy macrophages which produce the grossly visible strawberrylike appearance

Fig. 5. Chronic Cholecystitis

- Histology
Perimuscular fibrosis
Chronic inflammation cells
Hypertrophy of muscle layer
Mucosa begins to crack which will progress to sinuses
(Aschoff-Rokitansky sinuses)
- Aschoff-Rokitansky sinuses
Outpouchings of the mucosal epithelium through wall
Entrapped mucosa that outpouches due to weak ms
layer
Note:
Remember, weakness due to absent submucosa
Protruding inward Forming sinuses

Fig. 6. Chronic Cholecystitis with cholesterol stones

Hydrops of the gallbladder

- Atrophic, chronically obstructed gallbladder containing only
clear secretions
- Due to obstruction of cystic duct, maybe due to a solitary
stone

Fig.10. Hyrdops Gallbladder

Clinical Features:
- Recurrent attacks of either steady or colicky epigastric or
RUQ pain
- Nausea, vomiting, and intolerance for fatty foods are
frequent accompaniments.
Complications:
- Bacterial superinfection (cholangitis or sepsis)
- GB perforation and lical abscess formation
- GB rupture with diffuse peritonitis
- Biliary enteric (cholecystenteric) fistula
- Gallstone-induced intestinal obstruction (ileus)
- Aggravation of pre-existing medical illness
- Predisposition to gallbladder malignancy

Gallbladder Carcinoma

Fig. 7. Histology: Chronic Cholecystitis Thick muscularis layer with fibrosis,

presence of AR sinuses and chronic inflammatory cells

Xanthogranulomatous cholecystitis
- Gallbladder has massively thinkened wall, is shrunken,
nodular, and chronically inflamed with foci of necrosis and
hemorrhage
Porcelain Gallbladder
- Produced by extensive dystrophic calcification within
gallbladder
- Increased incidence of associated cancer
- Wall and surfaces of the gallbladder are enlarged, hard and
tan-white like a porcelain vase

Fig. 8. Porcelain Gallbladder: Wall and surface of the gallbladder are hard and
tan-white like a porcelain vase. This is one end result of chronic cholecystitis,
increase risk of cancer development.

SECTION B

Associated with gallstones

Most common malignancy of the extrahepatic biliary tract
Mean 5-year SR 5-12% despite surgical intervention
Cholelithiasis is present in 95% of cases however, only 0.5%
of patients with gallstones develop gallbladder cancer after 20
or more years
Gallbladders containing stones or infectious agents develop
cancer as a result of irritative trauma and chronic
inflammation
Presence of abnormal choledochopancreatic duct junction is
considered to be risk factor
Morphology:
- Most GB carcinomas are adenocarcinoma that arises from
mucosa and cholecystitis
- Maybe papillary, poorly differentiated or undifferentiated
infiltrating tumors
- By the time gallbladder cancers are discovered, most have
invaded the liver directly and many have extended to the
cystic duct and adjacent bile ducts and portal hepatic lymph
nodes.
- 2 patterns of GB carcinoma growth:
1. Infiltrating pattern
- More common
- Poorly defined area of diffuse thickening and
induration of the GB wall
- Scirrhous and firm
2. Exophytic pattern
- Grows into lumen as an irregular, cauliflower mass
while invading the underlying wall

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Clinical Features:
- Symptoms are typically indistinguishable from those
associated with cholelithiasis (abdominal pain, jaundice,
anorexia, nausea, vomiting)
- Prognosis is poor because of late presentation
Due to anatomy, gall bladder is a deep tissue
Hence, manifestations appear in advanced disease

Fig. 11. Gallbladder Carcinoma: Fungating mass in the middle (arrow) with white
pebbles are gallstones. In the lower right shows chronic cholecystitis as evidence by
the flattened mucosa with thickening of the wall

- Other causes:
Bile reflux (other reasons for obstruction such as
periampullary neoplasms, choledocheles and parasites)
Medications e.g. furosemide, azathioprine
Ischemic injury Vascular insufficiency (shock),
vascular thrombosis, embolism and vasculitis
Infections Mumps, coxsackie and M. pneumoniae
Metabolic disorder Hyperparathyroidism,
hypertriglycerdiemia
Hypothermia
Trauma Blunt abdominal trauma and iatrogenic
injury during surgery
Inherited gene alteration Cationic trypsinogen
(PRSS1) and trypsin inhibitor (SPINK1) [if this is
mutated, the pancreatic enzyme will be resistant to
inactivation thus prolonging the activation and
destroying even the acinar cells]

Fig. 12. Tumor is formed with glands lined with neoplastic cells and arises from the
lining mucosa. Presence of desmoplastic reaction, lymphocytes. Cells are
pleomorphic hyperchromic and disorganized. Slide shows glandular appearance
infiltratingthe muscularis layer and abnormal mucosal lining. Take note that the
muscularis layer are thick which is another evidence of chronic cholecystitis.

PANCREAS
Three clinically significant disorders of the exocrine pancreas:
1. Congenital abnormalities: Cystic Fibrosis
2. Inflammation and its sequelae: Acute Pancreatitis and
Chronic Pancreatitis
3. Neoplasm

Congenital Anomalies
1. Agenesis
- Totally absent pancreas
- Due to PDX1 (critical for development of pancreas)
mutation
2. Pancreas Divisum
- Most common congenital anomaly of pancreas
- Failure of fusion of the fetal duct systems of the dorsal and
ventral pancreatic primordial
- Bulk of pancreas drains through the dorsal pancreatic duct
and small caliber minor papilla
3. Annular Pancreas
- Band like ring of normal pancreatic tissue that completely
encircles the second portion of the duodenum
4. Ectopic Pancreas
- Aberrantly situated pancreatic tissue
- Favored sites: Duodenum and stomach
- Histologic exam: Normal appearing pancreatic acini,
glands and sometimes islets of langerhans

Acute Pancreatitis
Reversible pancreatic parenchymal injury associated with
inflammation
Acute inflammatory process of the pancreas with abdominal
pain and increased levels of serum amylase and lipase
Manifested as acute abdominal pain
Etiology:
- Biliary tract disease and alcoholism- account for 80% of
cases in Western countries
Gall stones Obstruction of pancreatic duct system
Alcohol Damages acinar cells leading to release of
proenzymes

SECTION B

Fig. 13 Pathogenesis of acute pancreatitis

Pathogenesis:
- Autodigestion of the pancreatic substance by inappropriately
activated pancreatic enzymes
- Inappropriate activation of trypsinogen Important triggering
event in acute pancreatitis
Inappropriately activated trypsin Activate other
proenzymes such as prophospholipase and proelastase
Degrade fat cells and damage elastic fibers of blood
vessels
Trypsin Converts prekallikrein to active form
Activation of Hageman factor Activate clotting and
complement systems
Note:
Remember that these enzymes can cleave any
macromolecules. Hindi basta basta i-activate because it may
digest even the normal tissue like what happened to Pancreatitis.
- Three possible events by which activation of pancreatic
enzymes are initiated (refer to figure above)
1. Pancreatic duct obstruction
Gallstones or biliary sludge impaction Raise
intrapancreatic ductal pressure Accumulation of
enzyme rich fluid Lipase can cause local fat
necrosis Injury
Injured tissues Proinflammatory cytokines
Inflammation Interstitial edema
Edema Compromise blood flow Ischemic
injury to acinar cells
2. Primary acinar cell injury
Caused by certain viruses (e.g. mumps), drugs and
trauma; also ischemia and shock

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3. Defective intracellular transport of proenzymes

within acinar cells
Proenzymes Inappropriately delivered to
intracellular compartment containing lysosomal
hydrolases Activation of proenzymes
Disruption of hydrolases Activated enzymes
released
Note:
To make the story short, enzymes in pancreas are activated
due to these 3 possible events, then destroy the tissue itself with
some complication like ischemia etc. thus pancreatitis is formed.
- Alcohol consumption
Chronic alcohol ingestion Secretion of protein-rich
pancreatic fluid Deposition of inspissated protein
protein plugs Obstruction
Also increases pancreatic exocrine secretion,
contraction of sphincter of Oddi and has direct toxic
effects on acinar cells.
- Acinar cell injury + excessive intake of alcohol Release of
inactivated from of enzymes which are eventually activated
Activated enzymes are toxic to pancreatic cells Acinar
cell injury
- Example:
Activated elastase: Hemorrhage due to blood vessel
damage
Protease: Necrosis
Morphology:
- Basic alterations
Swelling Edema due to microvascular leakage
Fat necrosis due lipolytic enzymes
Acute inflammation
Proteolytic destruction of pancreatic parenchyma
Destruction of blood vessels and interstitial
hemorrhage
Ca2+ binding leading to hypocalcemia
- Acute Interstitial Pancreatitis
Milder form
Alterations: Mild inflammation, interstitial edema and
focal areas of fat necrosis
- Acute Necrotizing Pancreatitis
More severe form
Acinar and ductal tissues are necrotic
Macroscopically: areas of red-black hemorrhage
interspersed with foci of yellow-white chalky fat necrosis
Fat necrosis appears grossly as tan-yellow flecks of soft
material within and on the surface of pancreas as well
as on mesentery
- Acute Hemorrhagic Pancreatitis
Most severe form
Extensive parenchymal necrosis accompanied by
dramatic hemorrhage within the substance of the gland
With numerous neutrophils
Only small area left viable
Clinical Features:
- Abdominal pain Cardinal manifestation
Pain Constant, intense and referred upper back or to
left shoulder
Frequently accompanied by anorexia, nausea and
vomiting
- Full blown acute pancreatitis Medical emergency due to
release of toxic enzymes and mediators resulting in
leukocytosis, hemolysis, ARDS and diffuse fat necrosis
- Lab diagnosis
Increase serum amylase and lipase
Diagnostic: Elevation of amylase during first 24 hrs,
followed by increase in serum lipase within 72-96 hr
Hypocalcemia (due to precipitation of calcium
soaps in necrotic fat) Poor prognosis

SECTION B

Management: Resting the pancreas by total restriction of oral

intake and supportive therapy with IV fluids and analgesia
Complications: (in severe Acute pancreatitis)
- DIC Disseminated Intravascular Coagulopathy
- ARDS Adult Respiratory Distress Syndrome
- Shock
- ATN Acute Tubular Necrosis
Note:
Sequelae of surviving patient: sterile pancreatic abscess
and pancreatic pseudocyst

Fig. 14. Acute Pancreatitis: These figures reveal hemorrhage with some focal area
of pale fat necrosis in the peripancreatic fat.

Fig. 15. Acute Pancreatitis with fat necrosis. Microscopically, acute pancreatitis
has necrosis of pancreatic parenchyma (lower left) with acute inflammation and fat
necrosis (right and upper part of photograph). Fat necrosis appears grossly as tanyellow flecks of soft material within and on the surface of pancreas as well as on
mesentery.

Fig. 16. Acute Hemorrhagic Pancreatitis showing numerous neutrophils with

extensive hemorrhage throughout the slide.

Chronic Pancreatitis
Defined as inflammation of the pancreas with irreversible
parenchymal damage and scar formation. (This distinction will
differ from the acute pancreatitis.)
Long term alcohol abuse Most common cause
Lesson common causes:
o Long standing obstruction of pancreatic duct
o Recurrent bouts of clinically silent acute pancreatitis
o Tropical pancreatitis
o Hereditary pancreatitis (PRSS1 and SPINK1 mutation)
o CFTR gene mutations (cystic fibrosis- cause obstruction
but sweat chloride level is normal in chronic pancreatitis)
Pathogenesis:
- Acute pancreatitis initiates sequence of: Perilobular fibrosis,
duct distortion and altered pancreatic secretions Lead to
loss of parenchyma and fibrosis
- Proposed events for development of chronic pancreatitis
1. Ductal obstruction by concretions
Increase protein concentration in pancreatic juice
Ductal plugs May calcify and form calculi
Further obstruction
2. Toxic effects Direct toxic effect of alcohol on acinar
cells
3. Oxidative stress Alcohol induced generation of free
radicals

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Morphology:
- Characterized by:
Parenchymal fibrosis
Reduced number and size of acini, relative sparing of
Islets of Langerhans
Dilation of pancreatic ducts
- Ducts: Dilated and contain protein plugs
- Ductal epithelium Hyperplastic or atrophied
- Acinar loss Constant feature
- Chronic inflammatory infiltrate around remaining lobules and
ducts
- Glandular atrophy
- Grossly:
Hard with visible calcified concretions
Not enlarged
Sometimes with extremely dilated ducts
- Lymphoplasmacytic sclerosing pancreatitis
Autoimmune, characterized by duct-centric mixed
inflammatory cell infiltrate, venulitis and inc. numbers of
IgG4-producing plasma cells.
Clinical Features:
- Associated with repeated attacks of moderately severe
abdominal pain, recurrent or persistent abdominal and back
pain
- May be silent until pancreatic insufficiency and DM develop
- May be precipitated by alcohol abuse, overeating or use of
drugs
- Diagnosis requires high degree of suspicion
- Gallstone-induced obstruction Jaundice and elevated
alkaline phosphatase
- Weight loss and hypoalbuminemic edema from
malabsorption caused by pancreatic exocrine insufficiency
- Not an immediately life-threatening condition
- 20-25 year mortality rate of 50%

Morphology:
- Distribution
Head = 60%
Body = 10 %
Tail = 10%
Diffuse involvement = 20%
- Hard (due to increased fibrosis), stellate, gray white, poorly
defined masses/ irregular infiltrative borders (malignant)
- Two features characteristic of pancreatic CA
Highly invasive
Elicits an intense non-neoplastic host reaction Desmoplastic response
- Carcinoma in head of pancreas Obstruct distal common
bile duct Distention of biliary tree Jaundice
- Carcinoma In body and tail Do not impinge biliary tract
Remain silent, quite large and widely disseminated
- Directly invade spleen, adrenals, vertebral column,
transverse colon and stomach; distant metastases in liver,
lungs and bones
- Microscopically:
Moderately to poorly differentiated adenocarcinoma
Forms abortive tubular structures or cell clusters
Aggressive, deeply infiltrative growth pattern
Malignant glands: Lined by pleomorphic cuboidal to
columnar epith cells. ductal adenocarcinomas (welldifferentiated)

Fig. 17. Pancreatic Carcinoma

Complications:
- Chronic malabsorption (lack of lipases)
- Chronic malabsorption (pancreatic exocrine insufficiency)
- Secondary diabetes mellitus if islets are destroyed
Fig. 18: Malignant glands in a dense fibrous stroma

Pancreatic Carcinoma

Infiltrating ductal adenocarcinoma of pancreas ;deadly CA

4th most common CA death in male & 5th in female
Increasing incidence rate
5th decade of life, male predilection
Predisposing Factors:
o Smoking (strong association)- doubles risk
o 7,12-dimethylbenzanthracene
o Diet- high in meat & fat
o DM
o Chronic pancreatitis (Some confusion whether it is a
preceding factor or it is one of the complication of
pancreatic CA. why? Because a small tumor can cause
obstruction in pancreatic duct thus pancreatitis.
o Genetic (mutational activation of k-ras & over expression
of erb B2. Inactivated p16, p53, SMAD4. BRCA2)
o Arise from precursor lesions such as dysplasia and
carcinoma in situ.
KRAS Most frequently altered oncogene in pancreatic
Ca that can cause impairment of intrinsic guanosine
triphosphate activity of Kras protein
CDKN2A (p16) Most frequent inactivated tumor
suppressor gene in pancreatic carcinoma that has a role
in control of cell cycle
SMAD4 Role in signal transduction from TGF-B
receptors but is inactivated in 55% which its function is to
suppress growth and promote apoptosis
p53 In 50-70% of pancreatic CA and has a role in cell
cycle checkpoint, apoptosis and cellular senescence
Majority of Pancreatic carcinoma arise from the ductal
epithelial cells

SECTION B

Clinical Features:
- Pain is first symptom
- Weight loss, anorexia, weakness, malaise- advanced
disease
- Courvosiers sign Acute painless dilatation of GB +
jaundice Lesion in the head
- Migratory thrombophlebitis Trousseau syndromehypercoagulable state (tumor secretes platelet aggregating
factors)
1. Serine proteaseactivates plasma factor X
2. Release of intracellular tissue thromboplastin
3. Plasma membrane vesicles
- Other symptoms (relatively non-specific)
Abdominal pain due to neural tissue affectation
Body malaise
Weight loss (apparent within 3- 4 months)
Poor prognosis (given 3-6 months after being diagnosed)
Note:
Jaundice is an early manifestation of pancreatic head
carcinoma. This type is detected earlier compared to the
carcinoma located in the tail.
Course: Brief and progressive and fewer than 20% are
resectable at time of diagnosis
Note:
Since walang lecture dito and sabi ni Dr. Dy na yung topic lang sa ppt
yung kasama, di niya namin sinama yung ibang diseases. We tried to
explain, hopefully magets niyo yung mga pathogenesis =D. Basta puro
obstruction tapos injury na then inflammation. Hahaha!! Gallstone =
Cholecystitis; Enzyme digestion = Pancreatitis. =)

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