Pancreas

Question 1

Acute pancreatitis

Answer 1

Reversible if stimulus is withdrawn associated with inflammation
- associated with biliary tract disease (gallstones) or alcoholism
- also hereditary pancreatitis
Morph: mild interstitial edema and inflammation to extensive necrosis and hemorrhage
- vascular leakage with edema
- acute inflammation
- necrosis of regional fat by lipolytic enzymes
- proteolytic destruction of pancreatic substance
- vascular injury with interstitial hemorrhage
Path: parenchymal autodigestion by activated pancreatic enzymes and inappropriate activation for trypsinogen
- pancreatic inflammation and thrombosis with tissue proteolysis, lipolysis, hemorrhage
Mech: pancreatic duct obstruction, primary acinar cell injury, defective intracellular transport of proenzymes, alcohol
Sx: abdominal pain, nausea, anorexia, elevated amylase and lipase
- hypocalcemia possible

Question 2

Pancreas divisum

Answer 2

Most common pancreatic congenital anomalies

• failure of ventral and dorsal fetal duct systems to fuse
• causes pancreatic secretions to drain through smaller minor papilla
• causes stenosis predisposes to chronic pancreatitis

Question 3

Annular pancrease

Answer 3

Bandlike ring of normal pancreatic tissue around second portion of duodenum
- causes duodenal obstruction

Question 4

Ectopic pancreas

Answer 4

Parenchyma in abnormal location is common

• stomach, duodenum, jejunum, meckel diverticulum, ileum
• submucosal single or multiple

Question 5

Hereditary pancreatitis

Answer 5

Recurrent bouts of pancreatitis beginning in childhood
Inheritance: auto dom mutations in cationic trypsinogen gene (PRSS1)
- auto recessive mutations in serine protease inhibitor Kazal type 1 gene (SPINK1)

Question 6

Acute necrotizing pancreatitis

Answer 6

Gray white parenchymal necrosis and chalky white fat necrosis

Question 7

Chronic pancreatitis

Answer 7

Inflammation with irreversible parenchymal destruction and fibrosis
- starts exocrine and then endocrine destroyed
Cause: alcoholism, ductal obstruction from pseudocysts, tumors, calculi, pancreas divisum, hereditary pancreatitis, CFTR gene mutations
Path: ductal obstruction by concretion, toxic effects, oxidative stress,
Morph: replacement of pancreatic acinar tissue by dense fibrous CT sparing islet of langerhans
Sx: silent or recurrent attacks of pain and/or jaundice
- precipitated by alcohol, overeating, opiates
- late complications: malabsorption, DM, pseudocyts

Question 8

Lymphoplasmacytic sclerosing pancreatitis

Answer 8

autoimmune pancreatitis is characterized by mixed inflammatory cell infiltrates, venulitits, and IgG4 producing plasma cells

Question 9

Congenital cysts

Answer 9

anomalous development of pancreatic ducts in congenital polycystic disease
- in von Hippel Lindau disease
Morph: unilocular and thin-walled

Question 10

Pseudocysts

Answer 10

Collections of necrotic-hemorrhagic material rich in pancreatic enzymes
- walled off areas of fat necrosis

Question 11

Cystic neoplasms

Answer 11

Painless slow-growing masses

• serous cystadenoma: solitary, well circumscribed nodules with central stellate scar, benign and resection is curative
• mucinous cystic neoplasm: multiloculated cystic neoplasms filled with thick mucinous material and mucin producing columnar cells within a dense stroma
• -> women and slow growing painless masses in body or tail of gland
• -> 1/3 have invasive adenocarcinoma
• intraductal papillary mucinous neoplasm: men more than women at head of gland
• -> 1/3 malignant
• solid pseudopapillary tumor: round and well circumscribed neoplasms have solid and cystic regions
• -> young women with abdominal discomfort
• -> aggressive activating beta-catenin

Question 12

Pancreatic carcinoma - precursor

Answer 12

Infiltrating ductal adenocarcinoma, fourth leading cause of CA deaths

• progression from non-neoplastic epithelium to small ductal non-invasive lesions to invasive carcinoma
• pancreatic intraepithelial neoplasms

Question 13

Pancreatic carcinoma

Answer 13

Path: KRAS most frequently altered oncogene in pancreatic cancer
- CDKN2A inactivated in majority
- SMAD4 tumor suppressor gene inactivated in more than half
- p53 inactivation loss of checkpoint
Cause: smoking increases risk 2 fold
- high fat diet, family history, DM increases risk
Morph: 60% in head of gland, 15% in body, 5% in tail, 20% whole organ
- highly invasive and elicit intense host scarring response
- head of pancreas causes obstruction leading to jaundice
- micro: differentiated glandular patterns resembling ductal epithelium
–> adenosquamous carcinoma and undifferentiated carcinoma
Sx: weight loss, pain, obstructive jaundice
- metastasis common: liver, migratory thrombophlebitis

Question 14

Acinar cell carcinoma

Answer 14

acinar cell differentiation with zymogen granules and production of exocrine enzymes (trypsin); lipase release causes metastatic fat necrosis

Question 15

Pancreatoblastoma

Answer 15

Rare malignant tumors, in childhood; micro there are squamous islands admixed with acinar cells