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Block 7 - GI > Pathology 3 > Flashcards

Flashcards in Pathology 3 Deck (22):
1

What causes physiological neonatal jaundice?

unconjugated hyperbilirubinemia from increased bilirubin - hemolysis going from low oxygen environment to high

2

What disorders can cause prolonged jaundice or jaundice after the first week of life?

sepsis
neonatal hepatitis
biliary atresia
choledochal cysts
syndromes or diseases that result in paucity of intrahepatic bile ducts

3

What are extra hepatic biliary tract tumors?

adenocarcinoma of gallbladder
extrahepatic cholangiocarcinoma

4

What are extrahepatic biliary tract tumors associated with?

cholelithiasis
fibrocystic diseases of bile ducts
biliary tract inf
IBD
PSC
thorotrast exposure

5

Where do cholangiocarcinomas develop?

20-25% intrahepatic
50-60% perihilar - fork of hepatic ducts
20-25% distal, extrahepatic

6

What is periampullary carcinoma?

carcinoma of distal common bile duct, proximal pancreatic carcinoma, and carcinoma of small intestine in ampulla of Vater
obstruction and jaundice at early stage

7

What are risk factors for the development of pigment stones?

non-western countries
chronic hemolytic anemias and GI dz, CF

8

What is a possible complication of cholelithiasis?

gallstone ileus - stones at ileocecal valve

9

What causes cholecystitis?

phospholipases from damaged mucosa hydrolyze other molecules which become toxic to mucosa - detergent action of bile salts further damages wall - released prostaglandins inflame
distension of gallbladder increases pressure and compromises flow since cystic A. is end artery

10

What can cause acalculous cholecystitis?

ischemic injury of GB - PAN, bile sludge, post-op, postpartum, trauma/burns, sepsis

11

What histologic findings are present in acute vs. chronic cholecystitis?

acute - neutrophils, ulcers, possible empyema
chronic - lymphocytes, plasma cells, Rokitansky-Aschoff sinuses

12

Other than secretion of enzmes in inactive form, what other protective mechanisms are in place to protect pancreas from damage?

proenzymes in zymogen granules in acinar cells - enzymes in lysosomes can degrade if normal acinar secretion blocked
acinar cells resistant to many activated enzymes
most enzymes inactive in bicarb rich pancreatic fluid
trypsinogen and trypsin inhibitors (SPINK1) present in ductal secretions
trypsin has self recognition cleavage site in situations of high local concentrations

13

What three processes cause acute pancreatitis?

ductal obstruction
direct acinar cell injury
defective intracellular transport of enzymes

14

What is the histology of acute pancreatitis?

fat necrosis w/i and outside pancreas
acute inflammation
parenchymal destruction
fibrinoid necrosis of blood vessel walls - hemorrhage if severe

15

What are causes of/risk factors for acute pancreatitis?

Alcoholism and biliary tract disease (stones)
Infection/inflammatory
Ischemia
Drugs
Metabolic
Congenital anomalies - pancreas divisum
Trauma
Hereditary - PRSS1 (trypsinogen) and SPINK1 (trypsin inhibitor) gene mutations

16

What are complications that can result from acute pancreatitis?

hypocalcemia and electrolyte imbalance
shock and multiorgan failure
DIC
pancreatic abscess
pancreatic pseudocyst formation - no epithelium, lined by fibrotic tissue
chronic pancreatitis and pancreatic insufficiency

17

What are complications that can result from chronic pancreatitis?

exocrine pancreatic insufficiency (steatorrhea, malabsorption)
diabetes
pancreatic pseudocyst
pancreatic carcinoma if hereditary causes

18

What are the different types of pancreatic neoplasias?

pancreatic ductal adenocarcinoma - most common
pancreatic serous neoplasms - benign or malignant
mucinous cystic neoplasms - benign or malignant
intraductal papillary mucinous neoplasms - adenomas or carcinomas growing into lumen
acinar cell carcinoma
neuroendocrine (or endocrine) tumors - low grade functional or non-functional, small and large cell carcinomas
solid psuedopapillary tumor - benign in young women
pancreaticoblastoma - malignant, infants/children

19

What are risk factors for pancreatic ductal adenocarcinoma development?

smoking - doubles risk
chronic pancreatitis and diabetes
hereditary disorders - Tumor syndromes (Peutz Jegher syndrome, BRCA2 mutation, HNPCC and FAP syndromes), hereditary pancreatitis mutations (PRSS1), CFTR mutation

20

Where are most pancreatic ductal adenocarcinomas located?

head of pancreas - can lead to biliary obstruction and jaundice

21

What genetic alterations lead to the dev of pancreatic ductal adenocarcinoma?

telomere shortening
K-ras mutations and activation
inactivation of p16
SMAD4 tumor suppressor activation
p53 tumor suppressor gene activation

22

What are the features of IPMN?

more common in men
arise in main ducts
lack cell stroma of mucinous neoplasms
can have dysplasia and invasion