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Category Archives: Pancreas
Serous microcystic adenoma
Serous microcystic adenoma
Gross Features
- Most frequently occur in tail
- Single, well-circumscribed slightly bosselated, round lesions with diameters ranging from 1-25 cm in greatest dimension (average, 6-10 cm)
- Sponge-like and made up of numerous tiny cysts filled with serous fluid
- Cysts range from 0.01-0.5 cm but can be up to 2 cm in diameter
- Cysts are arranged around a centrally located, dense fibronodular core from which thin fibrous septae radiate to the periphery (central stellate scar)
Microscopic Features
- Cyst pattern resembles that of a sponge on low power
- Cysts contain proteinaceous fluid are lined by a single layer of cuboidal/flattened epithelial cells
- Cellular cytoplasm is clear and only rarely eosinophilic and granular
- Centrally located nuclei, round to oval in shape, uniform, with an inconspicuous nucleolus
- PAS positive, PASD and Alcian blue negative
- No mitoses or cytologic atypia
- Central fibrous stellate core formed of hyalinised tissue with a few clusters of tiny cysts
• Serous oligocystic adenoma
• Serous cystadenocarcinoma
Posted in Pancreas
Tagged , Pancreas serous cyst, Pancreatic serous cysts, Pancreatic serous neoplasms, Serous cystadenocarcinoma, Serous microcystic adenoma, Serous oligocystic adenoma
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Mucinous cystic neoplasms
Mucinous cystic neoplasms
Gross Features
- Arise in the body/tail of the pancreas; present as painless, slow growing masses
- Cysts are filled with thick, tenacious mucin
- Neoplasms show no attachment to main pancreatic ducts
Microscopic Features
- Cysts are lined by columnar mucinous epithelium with a dense stroma resembling ovarian stroma
- Benign mucinous cystadenomas lack cytologic or architectural atypia
- Borderline mucinous cystadenomas possess cytologic atypia and demonstrate cellular pseudostratification and pseudopapillary formation (architectural atypia) but do not invade the stroma
- Mucinous cystadenocarcinomas demonstrate cytologic and architectural atypia with definite stromal invasion
Posted in Pancreas
Tagged , Mucinous cystic neoplasms, Pancreas cyst, Pancreas mucinous cancer, Pancreatic mucinous neoplasms
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Intraductal Papillary Mucinous Neoplasms
Intraductal Papillary Mucinous Neoplasms
Gross Features
- Arise in the head of the pancreas (males>females)
- Cysts are filled with mucin
- Neoplasm is connected to main pancreatic duct
Microscopic Features
- Cysts are lined by columnar mucinous epithelium lacking a dense ovarian-type stroma
- Benign mucinous cystadenomas lack cytologic or architectural atypia
- Borderline mucinous cystadenomas possess cytologic atypia and demonstrate cellular pseudostratification and pseudopapillary formation (architectural atypia) but do not invade the stroma
- Mucinous cystadenocarcinomas demonstrate cytologic and architectural atypia with definite stromal invasion
Posted in Pancreas
Tagged , Intraductal papillary mucinous neoplasms, Mucinous cystadenocarcinomas, Mucinous neoplasm, Pancreas mucinous neoplasm
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Serous Pseudopapillary Tumor
Serous Pseudopapillary Tumor
Gross Features
- Large, well-circumscribed masses with cystic and solid zones
- Cystic spaces contain hemorrhagic debris
Histology and Microscopic Features
- Cells grow as sheets or as papillary projections
Posted in Pancreas
Tagged , Pancreas neoplasm, Pancreas tumor, Serous pseudopapillary tumor
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Pancreatic Cystic Lesions
Pancreatic Cystic Lesions
Cystic lesions of the pancreas
Classification
• Non-neoplastic cysts
- Pseudocysts
- Congenital cysts
• Neoplastic cysts
o Serous cystic neoplasms
- Serous microcystic adenoma
- Serous oligocystic adenoma
- Serous cystadenocarcinoma
o Mucinous cystic neoplasms
- Benign
- Borderline
- Malignant
o Intraductal papillary mucinous neoplasms
- Benign
- Borderline
- Malignant
o Solid-pseudopapillary tumor
Posted in Pancreas
Tagged , Congenital cysts, Cyst pancreas, Intraductal papillary mucinous neoplasms, Mucinous neoplasm, Pancreatic cysts, Pseudocysts, Serous cystic neoplasms, Solid-pseudopapillary tumor
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Acute Pancreatitis
Acute pancreatitis
Causes of Acute Pancreatitis
• Metabolic
o Alcoholism
o Hyperlipoproteinemia
o Hypercalcemia
o Drugs (eg. thiazide diuretics)
• Mechanical
o Trauma
o Gallstones
o Iatrogenic injury (perioperative injury, endoscopic procedures with dye injection)
• Vascular
o Shock
o Atheroembolism
o Polyarteritis nodosa
• Infectious
o Mumps
o Coxsackie virus
o Mycoplasma pneumoniae
• Idiopathic/genetic
o Hereditary pancreatitis (mutations in cationic trypsinogen gene)
o Mutations in SPINK1 (serine protease inhibitor Kazal type 1)
Gross features
• Chalky-white fat necrosis
• Areas of hemorrhage within pancreatic parenchyma
Pathogenesis
• Due to autodigestion of pancreatic substance due to inappropriately activated pancreatic enzymes
• Activated enzymes (trypsin, lipase, phospholipase, elastase) cause disintegration of fat cells, and damage blood vessel walls.
• Trypsin converts prekallikrein to its activated form and also activates Hagemann factor. This activates the kinin cascade and the clotting and complement cascades which in turn leads to increased inflammation and thrombosis of small vessels (causing congestion and rupture of already weakened vessels).
• Three proposed mechanisms by which pancreatic enzymes are inappropriately activated:
o Pancreatic duct obstruction
- Increase in intrapancreatic ductal pressure, causes production of enzyme-rich interstitial fluid. Lipase secreted in active form injures fat cells causing local fat necrosis. Injured tissues, myofibroblasts, and leukocytes secrete cytokines causing local inflammation and promoting interstitial edema (which in turn compromises blood flow, causing ischemic injury to acinar cells).
o Primary acinar cell injury
o Defective intracellular transport of proenzymes within acinar cells
- May occur with pancreatic duct obstruction or exposure to alcohol
Complications
• ARDS
• DIC
• Shock
• ATN
• Pancreatic abscess
• Pancreatic pseudocyst
• Gram negative infection of necrotic debris in acute necrotizing pancreatitis
References: Robbins & Cotran Pathologic Basis of Disease, Seventh Edition
by: Vinay Kumar, Nelso Fausto, Abul Abbas
Posted in Pancreas
Tagged Acute Pancreatitis, Acute Pancreatitis Complications, Acute Pancreatitis Pathogenesis, Pancreatitis
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Pancreatitis
Pancreatitis
Complications of acute pancreatitis
- systemic organ failure – shock, ARDS, ARF
-DIC
- pancreatic abscess
- pancreatic pseudocyst
-duodenal obstruction
Five causes
- alcohol
- gallstones
- post-ERCP
- infections
- trauma
Pathogenesis
- inappropriate activation of trypsin which in turn leads to activation of other proenzymes and activation of the kinin system leading to inflammation and thrombosis.
Mechanisms of pancreatic enzyme activation
- pancreatic duct obstruction – ie. gallstones
- primary acinar cell injury – ie, viral damage ( mumps), drugs, trauma or ischemia
- defective intracellular transport of proenzymes- ie. alcohol, hereditary pancreatitis
Gross findings
- enlarged and soft pancreas
- chalky white foci of fat necrosis
- hemorrhage in more severe cases
Microscopy
- edema
- acute inflammation
- fat necrosis
Clinical and laboratory manifestations
- epigastric pain that often radiates to back
- elevated serum amylase
- diffuse pancreatic enlargement on imaging
Pancreas Hereditary Syndromes
Pancreas Hereditary Syndromes
Preneoplastic lesion
PanIN – pancreatic intraepithelial neoplasia
2 herditry familial syndromes associated with pancreatic cancers:
HNPCC –MSH2 and MLH1
BRCA2
FAMM ( familial atypical multiple melanoma syndrome) – p16
Hereditary pancreatitis ( loss of site on trypsin for it’s own autodestruction) – PRSS1
Peutz –Jeger =STK11/LKB
Posted in Pancreas
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Pancreas Cancer Mutations
Pancreas Cancer Mutations
- most common mutation found in cancers of the pancreas include:
KRAS – in >90% of pancreatic cancers
Posted in Pancreas
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Pseudocyst
Pancreatic Pseudocyst
What is it?
- localized collection necrotic material rich in pancreatic enzymes, usually following acute pancreatitis which becomes walled off by granulation tissue or fibrous tissue
Management
Supportive care
Some may require surgical drainage