GI Flashcards
Subepithelial neural appearing nodule
DDX:
- mucosal schwann cell hamartoma (S100+)
- perineurioma (Glut1+)
HCV vs late acute cellular rejection
- HCV should NOT have plasma cells or pericentral vein inflammation
- late ACR (or de novo AIH) can have plasma cells or pericentral vein inflammation
Portal triad: size of ducts vs arteries
- arteries should be smaller than ducts
- when arteries are larger it tell you there is a vascular problem
Portal vein thrombosis
-can see splitting of the veins in the liver
Prominent oxyntic rugal folds
-consider ZE
Collagenous colitis and lymphocytic colitis
-should be diffuse processes (meaning affecting more than one site of colon)
Subtype of hepatic adenomas
- HNF-1alpha mutations:
- fat and no cytologic atypia - Beta catenin activating mutations:
- cytologic atypia, acini, more likely to transform to HCC - Inflammatory/telangiectatic, IL6ST mutations:
- chronic inflammation
- sinusoidal dilatation
- increased IL6 signaling
Reactive changes in small intestine
- foveolar metaplasia
- goblet cell depletion
“Atypical HCC” by imaging
-do a CK7 to rule out cholangiocellular component
IPMN gross
- multilocular, papillary
- usually NOT unilocular
- should see messed up background pancreas due to obstruction
MCN gross
-usually multilocular
DDX cystic pancreatic tumor
- cystic NET (can be unilocular, looks like an eyeball)
- MCN
- IPMN
Crystals
- kayexylate (fish scales)
- sevelamer (fish scales)
- cholestyramine (dont cause mucosal injury)
Signet ring type adenoca in rectum
consider a NET too
LAMN
low grade appendiceal mucinous neoplasm
Major Patterns of Liver Injury
- predominantly portal inflammation
- prominent lobular injury
- ductular reactions
- steatosis
- fibrosis
Prominent ductular reaction
biliary disease
Mild ductular reaction
can indicate chronic viral hepatitis
Pathognomonic feature of PBC
florid duct lesion: non-necrotizing granuloma surrounding damaged bile duct (granulomatous duct destruction)
Pathognomonic feature of sinusoidal obstruction syndrome
AKA “veno-occlusive disease”
occluded central veins
Predominantly portal inflammation
- chronic viral hepatitis
- autoimmune hepatitis
- drug/toxin induced hepatitis
- chronic biliary diseases (PBC, PSC, strictures)
- metabolic disease (Wilson’s and alpha1antitrypsin)
- neoplastic (leukemia/lymphoma)
Chronic Hep C
- lymphoid follicles
- +/- mild epithelial bile duct damage due to direct infection
- lipogranulomas
- macrovesicular steatosis
- steatosis and insulin resistance associated with tx resistance and progression to fibrosis
collagen in cecum and rectum
can normally have increased collagen band; increase your threshold for collagenous colitis
cirrhotic background bile duct adenoma
have very high threshold, can see normally in cirrhosis
superficial mucosal inflammation of gallbladder
can see in downstream obstruction
Chronic Hep B
- predominantly portal mononuclear inflammation, lymphoid aggs not as frequent as HCV
- ground glass (cytoplasmic) hepatocytes is suggestive but not specific (can be seen in certain drugs and TPN)
- IHC for HepB surface Ag can be helpful
Autoimmune Hepatitis
- characterized by mixture of portal and periportal inflammation and marked lobular activity
- plasma cells are characteristic but not always prominent
- eos are usually present, albeit in very small numbers
- lymphoid aggs/follicles may be present and if surrounding a bile duct and causing epithelial damage, should exclude an overlap syndrome with PBC
- prior to tx show marked interface and lobular activity with hepatocyte necrosis, loss, and in particular, confluent necrosis
- confluent necrosis often around central veins, or may bridge central portal or portal-portal areas (“bridging necrosis”) or involve entire lobules (“parenchymal collaspse”)
- when confluent necrosis extends to portal tract, a ductular reaction often become prominent
Acute Hepatitis
- prominent lobular inflammation and hepatocyte necrosis
- usually also accompanied by variable amount of portal inflammation
- most commonly from hepatotropic viruses (HAV, HBC (+/-HDV), HCV, HEV), drugs/toxins, and non-hepatotropic viruses (CMV, HSV, adenovirus- these usually do not show prominent portal inflammation)
- EBV, however, is associated with a portal mononuclear infiltration to a degree that it may mimic HCV or HBV
Chronic Biliary Disease
- demostrate prominent portal lymphocytic inflammation
- PBC stage 1 shows portal lymphocytic inflammation, lymphoid aggregates, and follicles and associated with bile duct damage
- nonspecific findings such as ductular reaction or copper accumulation in periportal hepatocytes
Pathognomonic feature of PSC
-concentric periductal inflammation, fibrosis, and bile duct scars
Predominantly Lymphocytic Inflammation in Portal Tracts
- HCV
- HBV
- Autoimmune
- Acute Hepatitis
- Chronic Biliary Disease
Predominantly Plasmacytic Inflammation in Portal Tracts
- autoimmune hepatitis (more likely to show extensive interface hepatitis and/or confluent necrosis)
- PBC (more likely to show biliary features: ductular rxn, chronic cholestasis)
- IgG4 disease associated sclerosing cholangitis
- in allografts can indicate recurrent autoimmune hepatitis, recurrent PBC, or late cellular rejection
Predominantly Mixed Inflammation in Portal Tracts
- acute cellular rejection is the prototype and includes lymphocytes, neutrophils, macrophages, eosinophils
- be careful if allograft also has hx of HCV b/c it may be difficult to appreciate a portal mononuclear infiltrate with a mixed inflammatory background
- other things include Hodgkin and extramedullary hematopoiesis
Predominantly Eosinophilic Inflammation in Portal Tracts
- parasitic infection (schistosoma targets the portal venous system)
- inflammatory myofibroblastic tumor
- inflammatory pseudotumor
- LCH
- Hodgkin
- may be plentiful (although not predominant) in autoimmune hepatitism, PBC, PSC, and drug induced liver injury
Predominantly Granulomatous Inflammation in Portal Tracts
- caseous necrosis suspect infection
- fibrin ring granulomas susggest Q fever, allopurinol or griseofulvin toxicity
- granulomas of different ages, cellularity, and sclerosis often with asteroid bodies suggest sarcoidosis
Features of “granulomatous hepatitis”
-portal, lobular, parenchymal hepatitis around the granuloma as well as away from it; eos may or may not be prominent
Hyalinizing cholecystitis
- Be VERY careful- they probably have cancer
- look super carefully at every cell to look for atypia
- submit the whole thing or submit a lot
- example: a gallbladder that you have to peel off a stone- probably has cancer (submit whole thing)
- now thought that these hyalinizing ones more likely to have cancer than porcelain ones
