Biliary Tract and Pancreas

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Biliary Tract • 70% associatedBiliary General

andPathology
with inflammatory
Tract bowel disease,
Pancreas
Bile particularly1ulcerative
December 07
colitis
• Two major functions • M:F = 2:1, third through fifth decades
o Elimination of bilirubin, excess cholesterol, and • Progressive fatigue, pruritus, jaundice
xenobiotics that are insufficiently water soluble to be • Chronic course
excreted in urine • Increased risk for cholangiocarcinoma
o Emulsification of dietary fat in the gut by bile acids
(cholic acid, chenodeoxycholic acid)
• Unconjugated → Conjugated
• Reabsorbed in terminal ileum (enterohepatic circulation)

Cholestasis
• Systemic retention of not only bilirubin but also other solutes
eliminated in bile, particularly bile salts and cholesterol
• Due to hepatocellular dysfunction or biliary obstruction
• Accumulation of bile pigment within the hepatic parenchyma
– Kupffer cells
Cholelithiasis
• Bile ductular proliferation
• Very common
• Bile lakes
• Cholesterol stones
• Portal tract fibrosis
o Bile is supersaturated with cholesterol
o Gallbladder stasis
Secondary Biliary Cirrhosis
o F>M
• Most common cause is extrahepatic cholelithiasis
• Biliary atresia, malignancies of the biliary tree and head of o Obesity
the pancreas, and strictures o Advancing age
• Cholestasis • Pigment stones – calcium bilirubinate salts
• Bile duct proliferation with surrounding neutrophils o Asian more than Western
• Periportal fibrosis o Chronic hemolytic syndromes
• Clinical Features
Primary Biliary Cirrhosis o Asymptomatic
• Middle-aged women o Biliary colic
• M:F = 1:10 o Cholecystitis
• Possibly autoimmune
o Gallstone ileus
o Autoantibodies to mitochondrial pyruvate
dehydrogenase 90%
• Insidious onset, usually presenting with pruritus
• Hyperbilirubinemia, jaundice, cirrhosis late
• ↑ alkaline phosphatase, cholesterol

Figure 1-Nonsuppurative, granulomatous destruction of medium-sized


intrahepatic bile ducts = florid duct lesion

Primary Sclerosing Cholangitis


• Inflammation, obliterative onion-skin fibrosis, and segmental
dilatation of the obstructed intrahepatic and extrahepatic bile
ducts
• String of beads on ERCP
General Pathology – Biliary Tract and Pancreas by VGY Page 2 of 10

Cholecystitis • Complete obstruction of bile flow caused by destruction or


• Acute calculous absence of all or part of the extrahepatic bile ducts
o Obstruction of GB neck or cystic duct • Acquired inflammatory disorder
o RUQ pain radiating to right shoulder • Normal stools to acholic stools
o Fever, nausea, leukocytosis • Bile ductular proliferation on liver bx
o Potential surgical emergency • Cirrhosis by 3 to 6 months of age.
• Acute acalculous – seriously ill pts • Require liver transplantation
• Chronic
o Recurrent attacks of pain
o Nausea and vomiting
o Associated with fatty meals

Gallbladder Carcinoma
• Seventh decade
• F>M
• Discovered at late stage, usually incidental
• Exophytic and infiltrating types
• Adenocarcinoma
• Local extension into liver, cystic duct, portahepatic LNs
• Mean 5 yr survival 1%

Choledocholithiasis
• Stones within the biliary tree
• West – from gallbladder
• Asia – primary ductal and intrahepatic stone formation
• Symptoms due to:
o Biliary obstruction
o Pancreatitis Cholangiocarcinoma
o Cholangitis • Older pts
• M>F
o Hepatic abscess
• Painless jaundice, N/V, weight loss
• Opisthorchis sinensis (liver fluke),inflammatory bowel
Cholangitis
disease
• Acute inflammation of bile ducts
• Tumors usually small at dx yet not resectable
• Due to biliary obstruction, usually choledocholithiasis
• Klatskin tumor – arises at bifurcation
• Bacterial infection from gut, i.e., gram negative aerobes
• Adenocarcinoma
o Fever, chills, abdominal pain, jaundice
• Mean survival 6 to 18 months
• Latin America and Near East: Fasciola hepatica,
schistosomiasis
• Far East: Clonorchis sinensis, Opisthorchis viverrini
• AIDS: cryptosporidiosis

Biliary Atresia
• 1/3 of cases of neonatal cholestasis
• 1 in 10,000 live births
General Pathology – Biliary Tract and Pancreas by VGY Page 3 of 10

Head of Pancreas
• Includes uncinate process
• Flattened structure, 2 – 3 cm thick
Pancreas
Brief History • Attached to the 2nd and 3rd portions of duodenum on the
• Herophilus, Greek surgeon first described pancreas. right
• Wirsung discovered the pancreatic duct in 1642. • Emerges into neck on the left
• Pancreas as a secretory gland was investigated by Graaf in • Border b/w head & neck is determined by GDA insertion
1671. • SPDA and IPDA anastamose b/w the duodenum and the rt.
• R. Fitz established pancreatitis as a disease in 1889. lateral border
• Whipple performed the first pancreatico-duodenectomy in
1935 and refined it in 1940. Neck of Pancreas
• 2.5 cm in length
Pancreas
• Straddles SMV and PV
• Gland with both exocrine and endocrine functions
• Antero-superior surface supports the pylorus
• 6-10 inch in length
• 60-100 gram in weight • Superior mesenteric vessels emerge from the inferior border
• Location: retro-peritoneum*, 2nd lumbar vertebral level • Posteriorly, SMV and splenic vein confluence to form portal
• Extends in an oblique, transverse position vein
• Parts of pancreas: head, neck, body and tail • Posteriorly, mostly no branches to pancreas

Embryology
• Endodermal origin
• Develops from ventral and dorsal pancreatic buds
• Ventral bud becomes the uncinate process and inferior head
of pancreas
• Dorsal bud becomes superior head, neck, body and tail
• Ventral bud duct fuses with dorsal bud duct to become mail
pancreatic duct (Wirsung)

Body of Pancreas
• Elongated, long structure
• Anterior surface, separated from stomach by lesser sac
• Posterior surface, related to aorta, lt. adrenal gland, lt. renal
vessels and upper 1/3rd of lt. kidney
• Splenic vein runs embedded in the post. Surface
• Inferior surface is covered by tran. mesocolon

Tail of Pancreas
• Narrow, short segment
• Lies at the level of the 12th thoracic vertebra
• Ends within the splenic hilum
• Lies in the splenophrenic ligament
General Pathology – Biliary Tract and Pancreas by VGY Page 4 of 10

• Anteriorly, related to splenic flexure of colon


• May be injured during splenectomy (fistula)

Pancreatic Duct
• Main duct (Wirsung) runs the entire length of pancreas
• Joins CBD at the ampulla of Vater
• 2 – 4 mm in diameter, 20 secondary branches
• Ductal pressure is 15 – 30 mm Hg (vs. 7 – 17 in CBD) thus
preventing damage to panc. duct
• Lesser duct (Santorini) drains superior portion of head and
empties separately into 2nd portion of duodenum Lymphatic Drainage
• Rich periacinar network that drain into 5 nodal groups
Arterial Supply of the Pancreas o Superior nodes
• Variety of major arterial sources (celiac, SMA and splenic) o Anterior nodes
• Celiac à Common Hepatic Artery à Gastroduodenal Artery o Inferior nodes
à Superior pancreaticoduodenal artery which divides into o Posterior PD nodes
anterior and posterior branches o Splenic nodes
• SMA à Inferior pancreaticoduodenal artery which divides
into anterior and posterior branches Innervation of Pancreas
• Anterior collateral arcade b/w anterosuperior and • Peptidergic neurons that secrete amines and peptides
anteroinferior PDA (somatostatin, vasoactive intestinal peptide, calcitonin gene-
• Posterior collateral arcade b/w posterosuperior and related peptide, and galanin
posteroinferior PDA • Rich afferent sensory fiber network
• Body and tail supplied by splenic artery by about 10 • Ganglionectomy or celiac ganglion blockade interrupt these
branches somatic fibers (pancreatic pain*)
• Three biggest branches are • Peptidergic neurons that secrete amines and peptides
o Dorsal pancreatic artery (somatostatin, vasoactive intestinal peptide, calcitonin gene-
related peptide, and galanin
o Pancreatica Magna (midportion of body)
• Rich afferent sensory fiber network
o Caudal pancreatic artery (tail)
• Ganglionectomy or celiac ganglion blockade interrupt these
somatic fibers (pancreatic pain*)

Histology-Exocrine Pancreas
• 2 major components – acinar cells and ducts
• Constitute 80% to 90% of the pancreatic mass
• Acinar cells secrete the digestive enzymes
• 20 to 40 acinar cells coalesce into a unit called the acinus
• Centroacinar cell (2nd cell type in the acinus) is responsible
for fluid and electrolyte secretion by the pancreas
• Ductular system - network of conduits that carry the
exocrine secretions into the duodenum
Venous Drainage of Pancreas
• Follows arterial supply • Acinus à small intercalated ducts à interlobular duct à
• Anterior and posterior arcades drain head and the body pancreatic duct
• Interlobular ducts contribute to fluid and electrolyte secretion
• Splenic vein drains the body and tail
along with the centroacinar cells
• Major drainage areas are
o Suprapancreatic PV
Histology-Endocrine Pancreas
o Retropancreatic PV
• Accounts for only 2% of the
o Splenic vein
pancreatic mass
o Infrapancreatic SMV • Nests of cells - islets of
• Ultimately, into portal vein Langerhans
• Four major cell types
General Pathology – Biliary Tract and Pancreas by VGY Page 5 of 10

o Alpha (A) cells secrete glucagon o secreted as proenzymes and require activation for
o Beta (B) cells secrete insulin proteolytic activity
o Delta (D) cells secrete somatostatin o duodenal enzyme, enterokinase, converts trypsinogen
o F cells secrete pancreatic polypeptide to trypsin
• B cells are centrally located within the islet and constitute o Trypsin, in turn, activates chymotrypsin, elastase,
70% of the islet mass carboxypeptidase, and phospholipase
• PP, A, and D cells are located at the periphery of the islet • Within the pancreas, enzyme activation is prevented by an
antiproteolytic enzyme secreted by the acinar cells
Physiology – Exocrine Pancreas
• Secretion of water and electrolytes originates in the Insulin
centroacinar and intercalated duct cells • Synthesized in the B cells of the islets of Langerhans
• Pancreatic enzymes originate in the acinar cells • 80% of the islet cell mass must be surgically removed
before diabetes becomes clinically apparent
• Final product is a colorless, odorless, and isosmotic alkaline
• Proinsulin, is transported from the endoplasmic reticulum to
fluid that contains digestive enzymes (amylase, lipase, and
the Golgi complex where it is packaged into granules and
trypsinogen)
cleaved into insulin and a residual connecting peptide, or C
• 500 to 800 ml pancreatic fluid secreted per day
peptide
• Alkaline pH results from secreted bicarbonate which serves
• Major stimulants
to neutralize gastric acid and regulate the pH of the intestine
o Glucose, amino acids, glucagon, GIP, CCK,
• Enzymes digest carbohydrates, proteins, and fats
sulfonylurea compounds, β-Sympathetic fibers
• Major inhibitors
Bicarbonate Secretion
• Bicarbonate is formed from carbonic acid by the enzyme
o somatostatin, amylin, pancreastatin, α-sympathetic
carbonic anhydrase fibers
• Major stimulants
Glucagon
Secretin, Cholecystokinin, Gastrin, Acetylcholine
• Secreted by the A cells of the islet
• Major inhibitors
• Glucagon elevates blood glucose levels through the
Atropine, Somatostatin, Pancreatic polypeptide and
Glucagon stimulation of glycogenolysis and gluconeogenesis
• Secretin - released from the duodenal mucosa in response • Major stimulants
to a duodenal luminal pH < 3 o Aminoacids, Cholinergic fibers, β-Sympathetic fibers
• Major inhibitors
Enzyme Secretion o Glucose, insulin, somatostatin, α-sympathetic fibers
• Acinar cells secrete isozymes
o amylases, lipases, and proteases Somatostatin
• Secreted by the D cells of the islet
• Major stimulants • Inhibits the release of growth hormone
o Cholecystokinin, Acetylcholine, Secretin, VIP
• Inhibits the release of almost all peptide hormones
• Synthesized in the endoplasmic reticulum of the acinar cells
• Inhibits gastric, pancreatic, and biliary secretion
and are packaged in the zymogen granules
• Released from the acinar cells into the lumen of the acinus • Used to treat both endocrine and exocrine disorders
and then transported into the duodenal lumen, where the
enzymes are activated. Exocrine Pancreas
• The final product of the exocrine pancreas is a clear isotonic
Enzymes of the Pancreas solution with a pH in the range of 8. The 2 distinct
• Amylase components of exocrine secretion are enzyme secretion and
o only digestive enzyme secreted by the water+electrolyte secretion.
pancreas in an active form • Cholecystokinin is the most potent endogenous hormone
o functions optimally at a pH of 7 known to stimulate enzyme secretion.
o hydrolyzes starch and glycogen to glucose, • Secretin is the most potent endogenous stimulant of
maltose, maltotriose, and dextrins pancreatic electrolyte secretion.
• Lipase
Endocrine Pancreas
o function optimally at a pH of 7 to 9
o emulsify and hydrolyze fat in the presence of bile salts • The release of insulin into the portal blood is controlled by
• Proteases the concentration of blood glucose, vagal interactions, and
o essential for protein digestion local concentrations of somatostatin.
General Pathology – Biliary Tract and Pancreas by VGY Page 6 of 10

• The major stimulus for glucagon release is a fall in serum pseudocyst, phlegmon, abscess or ongoing acute
glucose. pancreatic inflammation.
o Elevated amylase levels may occur in other acute
• Pancreatic polypeptide appears to function for regulation of
abdominal conditions, though levels rarely exceed 500
pancreatic exocrine secretion and biliary tract motility.
IU/dL
• Somatostatin has a broad inhibitory spectrum of o Urinary amylase excretion is increased and this may be
gastrointestinal activity very helpful in cases where the serum amylase level
has returned to normal.
Congenital anomalies o Other lab. Findings
• Agenesis  Moderate leukocytosis
• Pancreas divisum  Mild bilirubin elevation (<2mg/dL)
• Annular pancreas  Raised Haematocrit
• Ectopic pancreas  Hypocalcaemia (Calcium being complexed with
fatty acids)
Acute Pancreatitis
• Nonbacterial inflammatory disease caused by activation, • Radiographic Findings
interstitial liberation, and autodigestion of the pancreas by o CXR and PFA non-specific findings
its own enzymes.  Sentinel loop
• Inconclusive evidence regarding pathogenesis  Pleural effusion (Left)
o Partial or intermittent ductal obstruction and increased o Abdominal Ultrasonography
ductal pressure  Lithiasis of biliary tract
o Biliary reflux  Pancreatic swelling
o Duodenal juice reflux o Computed Tomography with iv contrast

• Etiology • Clinical Course


o Gallstones and Alcohol account for 90% o Early identification of patients at greater risk of
o Hyperlipidemia complications allows them to be managed more
o Hypercalcemia aggressively, which appears to decrease the mortality
o Familial rate.
o Pancreatic duct obstruction o The severity and prognosis of an attack of acute
 Tumour pancreatitis can be predicted by use of routinely
 Pancreas divisum available laboratory determinations.
o Viral infection o Just the single finding of fluid sequestration exceeding
o Scorpion venom 2 L/d for more than 2 days is reasonably accurate
o Drugs dividing line between severe and mild to moderate
disease.
o Idiopathic

• Ranson’s criteria for severity


• Signs and Symptoms
o On admission
o Midepigastric abdominal pain
 Age >55 years
o Radiating to the back
 WBC >16000
o Nausea and vomiting
 Blood Glucose >200 mg/dL
o Fever and tachycardia
 LDH >350 iu/L
o Epigastric tenderness
 AST (SGOT) > 250 iu/dL
o Abdominal distention
o Bluish discoloration in the flank (Grey Turner’s sign) o After 24 hours
o Bluish discoloration periumbilically (Cullen’s sign)
 Hematocrit fall >10%
 BUN rise >8mg/dL
• Diagnosis  Serum Ca <8mg/dL
o It is supported by appropriate laboratory determinations  Arterial PO <60 mmHg
and radiographic findings  Base deficit > 4mEq/L
o Serum amylase is the most widely used lab test
 Fluid sequestration >600 mL
o Hyperamylasemia is commonly observed within 24 hrs. o Predicted Mortality Rates
of the onset and gradually returns to normal 0-2 criteria = 2%
o Persistent hyperamylasemia beyond the initial week 3 or 4 criteria = 15%
may indicate the development of pancreatic 5 or 6 criteria = 40%
General Pathology – Biliary Tract and Pancreas by VGY Page 7 of 10

7 or 8 criteria = 100% o Infection à Abscess


o Rupture à Severe chemical peritonitis
• Glasgow prognostic system o Haemorrhage

Chronic Pancreatitis
• Is an entity encompassing recurrent or persistent abdominal
pain of pancreatic origin combined with evidence of exocrine
and endocrine insufficiency and marked pathologically by
irreversible parenchymal destruction.
• It is associated with alcohol abuse, Hyperparathyroidism,
congenital anomalies of the pancreatic duct and pancreatic
trauma. It may also be idiopathic.

Neoplasms of the Pancreas


Exocrine Tumours
• Treatment
A. Periampullary Carcinoma
Goals of medical treatment
• Cancer of the head of pancreas 85%
o Reduction of pancreatic secretory stimuli
• Ampullary carcinoma 10%
o Correction of fluid and electrolyte derangements
• Duodenal carcinomas <5%
• Complications • Distal Common Bile Duct Ca <5%
o Abscess • Signs and Symptoms
o Jaundice
o Pseudocyst formation o Weight loss
o Anorexia
o Pancreatic ascites o Vague abdominal pain
o Elevated bilirubin, Alk. Phosphatase, AST, ALT
o Chronic pleural effusion
o Tumour markers CA 19-9 not sufficiently accurate
o Gastrointestinal bleeding o CT scan to determine the size and to detect
metastatic spread
o Acute splenic vein thrombosis o Selective celiac and mesenteric angiogram
combined with portal venography to assess
o Chronic Pancreatitis resectability.
• Treatment
o Palliation with Drainage of biliary tree with stents
o Duodenal obstruction poorly palliated non-
Pancreatic Pseudocyst
operatively
• The term pseudocyst denotes absence of an epithelial lining o Surgical treatment is feasible
in contrast to true cysts o Only 40% of pre-operatively resectable tumours
• Encapsulated collections of fluid with high enzyme are resectable, and this rate is even lower for
concentrations that arise from the pancreas. adeno-Ca of head of pancreas.
• They are usually located either within or adjacent to the o Whipple’s pancreaticoduodenectomy
pancreas in the lesser sac. • Prognosis
• The walls of a pseudocyst are formed by inflammatory o Overall 5 year survival 25%
fibrosis of the peritoneal, mesenteric and serosal o Head of pancreas Ca 5-year survival <20%
membranes which limits spread of the pancreatic juice as o Other periampullary Ca 5 year survival ~60%
the lesion develops. o Chemotherapy alone not significant benefit
• Early or late presentation
o Combined Radio-chemotherapy and local radiation
• Pain is the most common finding therapy have shown some benefit at least in local
• Fever, weight loss, tenderness, palpable mass tumour control.
• Jaundice rarely
• Elevated amylase and WBC in ~ 50% B. Carcinoma of Body and Tail
• CT scan is the investigation of choice • 30% of all cases of pancreatic Cancer
• D/D Abscess, phlegmon, neoplastic cysts • Weight loss and abdominal pain
• Complications • CT scan and ERCP
General Pathology – Biliary Tract and Pancreas by VGY Page 8 of 10

• Resectability rate <7% o Sonography


• Poor prognosis (mean survival 5 to 6 months) o ERCP
o Selenomethionine Scan
Neoplasms of the Pancreas o Duodenal Aspiration
Endocrine Tumours o Serum Test:
• Pancreatic islet cell endocrine tumour are rare and are  Span-1
presumed to originate from neural crest cells.  CA 19-9
• Functional endocrine tumours are conventionally named  CEA
according to the major hormone produced by the hormone. • 2/3-head, 1/3-body & tail
• Malignancy is determined by the presence of local invasion, • Poorly delineated, yellowish gray CS
the spread to regional lymph nodes, or the existence of • Duodenal wall à direct extension
hepatic or distant metastases.
• Up to 25% of pancreatic endocrine tumours are classified as
• Non-neoplastic area à extensive atrophy, chronic
non-functional based on the absence of a clinical syndrome inflammation, fibrosis
and the lack of elevated serum hormone levels.
• Non-functioning tumours frequently have clinical
manifestations similar to the more common exocrine
malignancies
• Non-functioning tumours are associated with a higher
malignancy rate than are their functioning counterparts.
• Principles of Management
o Recognition of the abnormal physiologic mechanism or • Microscopic features:
characteristic syndrome o Well differentiated à dx is extremely difficult
o Detection of hormone elevations in serum by
o LPO – glands are well formed, 1-2 layers
radioimmunoassay
o HPO – marked nuclear pleomorphism, loss of polarity,
o Localization and staging of the tumour in preparation for
prominent nucleoli
operative therapy.
o Perinueral invasion – 90%
o Goals of treatment:
o Pan IN / CIS
 control of symptoms due to hormone excess
• IHC
 Excision of maximal neoplastic tissue
o Mucin (gastric & SI types)
 Prevention of tumour recurrence.
o Keratin, EMA
• Endocrine Pancreatic Tumours
o CEA, CA19-9 B72.3
a. Insulinoma
o Pancreatic CA Associated antigens
o Most common endocrine tumour
o DU PAN-2
o 90% benign solitary pancreatic adenomas
o Y Pan-1
b. Gastrinoma
o Second most common o Tn
o Peptic ulcer disease. o Sialosyl-Tn-Antigens
o Elevated serum gastrin o DF3 Antigen
c. VIP-oma o M1
o Watery diarrhea, hypokalemia, achlorydria o Cathepsin E
d. Somatostatinoma o Pepsinogen II
o Villin
Ductal Adenocarcinoma o Laminin
• 85 % of pancreatic malignancies Silver stain
Chromogranin
• 4th most common CA in the US
Islet cell hormones
• Risk factors:
• Cytogenetics:
o Cigarette smoking
o Structural rearrangements
o Chronic pancreatitis
o Mutations/ accumulation of p53
o Pancreaticobiliary ductal anomaly
o K-ras oncogene mutation
o Elderly
o HER2neu overexpression
• Diagnosis
o Aneuploid
o CT Scan
• Variants
o MRI
o Adenosquamous CA
o Celiac angiography
General Pathology – Biliary Tract and Pancreas by VGY Page 9 of 10

o Oncocytic CA Mucinous Cystic Neoplasm


o Clear cell CA • Younger age group
o Signet ring • Women
o Mucinous CA • Large multiloculated or unilocular lined by tall mucin
• Most common Sites of Metz producing cells
o peritoneum • High levels of CEA
o Lung • Mucinous Cyst Adenoma vs. Mucinous CystadenoCA –
o Adrenal distinction not always clear cut
o Bone
o Distal lymph nodes
o skin
o CNS
• Cytology
o Duodenal secretion
o Pancreatic Juice
o Percutaneous FNA
o Intraop FNA
• Treatment: Surgical
o Body & tail – distal pancreatectomy Intraductal Neoplasm
o Head – Whipple operation + retroperitoneal resection • Intraductal Papillary Carcinoma
o Paliative bypass operation o Involve major ducts, multicentric
• Mucus secreting or Mucin Producing Duct-Ectatic Tumor
Giant Cell Tumor o Dilated ducts filled with mucus
• large & hemorrhagic o Columnar, mucin producing, well diff
• Dual population: o Overexpression or c-erb-2
o Spindle cells
o Multinucleated giant cells Acinar Cell Tumor & Tumor-like Conditions
• Some cases, clear cut glandular appearance • Acinar Cell Hyperplasia
• Acinar Cell Adenoma
• Acinar Cell Carcinoma

Microcystic Cystadenoma
• A.k.a.glycogen-rick cystadenoma
• Large multinucleated mass, small cysts filled with clear Acinic Cell Carcinoma
serous fluid • IHC
• Microscopic: small flat to cuboidal lining o Trypsin
Layer of myoepithelium o Lipase
• IHC: EMA, LMW keratin o Chymotrypsin
• Elderly o amylase
• Abundant ER on EM
• Metastasis present in the time of diagnosis

Papillary & Solid Epithelial Neoplasm


• Young women
• Large with areas of necrosis and hemorrhage, some with
well developed capsule
• Microscopic: very cellular, simulates islet cell tumor
Microcystic Adenocarcinoma
o Pseudopapillae covered by layers of epithelial cells
• Similar to microcystic adenoma but with nuclear atypia,
pleomorphism, metastasis o Nuclei are ovoid and folded
o Distict nucleoli, few mitoses
General Pathology – Biliary Tract and Pancreas by VGY Page 10 of 10

o Hyaline globules
o Thick fibrovascular core with mucinous change
• Ultrastructure
o Acinar, ductal, & endocrine differentiation
• IHC
o Keratin, desmoplakin, trypsin, chymotrypsin, amylase &
vimentin
o Focal reactivity: NSE, islet cell hormones

Haay, ang haba…

Feeling ko tlga ndi na kmi trans nito e.

Oist, new year na! Magbagong buhay na kau! :-p

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