GI

Question 1

Subepithelial neural appearing nodule

Answer 1

DDX:

• mucosal schwann cell hamartoma (S100+)
• perineurioma (Glut1+)

Question 2

HCV vs late acute cellular rejection

Answer 2

• HCV should NOT have plasma cells or pericentral vein inflammation
• late ACR (or de novo AIH) can have plasma cells or pericentral vein inflammation

Question 3

Portal triad: size of ducts vs arteries

Answer 3

• arteries should be smaller than ducts

- when arteries are larger it tell you there is a vascular problem

Question 4

Portal vein thrombosis

Answer 4

-can see splitting of the veins in the liver

Question 5

Prominent oxyntic rugal folds

Answer 5

-consider ZE

Question 6

Collagenous colitis and lymphocytic colitis

Answer 6

-should be diffuse processes (meaning affecting more than one site of colon)

Question 7

Subtype of hepatic adenomas

Answer 7

1. HNF-1alpha mutations:
   - fat and no cytologic atypia
2. Beta catenin activating mutations:
   - cytologic atypia, acini, more likely to transform to HCC
3. Inflammatory/telangiectatic, IL6ST mutations:
   - chronic inflammation
   - sinusoidal dilatation
   - increased IL6 signaling

Question 8

Reactive changes in small intestine

Answer 8

• foveolar metaplasia

- goblet cell depletion

Question 9

“Atypical HCC” by imaging

Answer 9

-do a CK7 to rule out cholangiocellular component

Question 10

IPMN gross

Answer 10

• multilocular, papillary
• usually NOT unilocular
• should see messed up background pancreas due to obstruction

Question 11

MCN gross

Answer 11

-usually multilocular

Question 12

DDX cystic pancreatic tumor

Answer 12

• cystic NET (can be unilocular, looks like an eyeball)
• MCN
• IPMN

Question 13

Crystals

Answer 13

• kayexylate (fish scales)
• sevelamer (fish scales)
• cholestyramine (dont cause mucosal injury)

Question 14

Signet ring type adenoca in rectum

Answer 14

consider a NET too

Question 15

LAMN

Answer 15

low grade appendiceal mucinous neoplasm

Question 16

Major Patterns of Liver Injury

Answer 16

• predominantly portal inflammation
• prominent lobular injury
• ductular reactions
• steatosis
• fibrosis

Question 17

Prominent ductular reaction

Answer 17

biliary disease

Question 18

Mild ductular reaction

Answer 18

can indicate chronic viral hepatitis

Question 19

Pathognomonic feature of PBC

Answer 19

florid duct lesion: non-necrotizing granuloma surrounding damaged bile duct (granulomatous duct destruction)

Question 20

Pathognomonic feature of sinusoidal obstruction syndrome

Answer 20

AKA “veno-occlusive disease”

occluded central veins

Question 21

Predominantly portal inflammation

Answer 21

• chronic viral hepatitis
• autoimmune hepatitis
• drug/toxin induced hepatitis
• chronic biliary diseases (PBC, PSC, strictures)
• metabolic disease (Wilson’s and alpha1antitrypsin)
• neoplastic (leukemia/lymphoma)

Question 22

Chronic Hep C

Answer 22

• 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

Question 23

collagen in cecum and rectum

Answer 23

can normally have increased collagen band; increase your threshold for collagenous colitis

Question 24

cirrhotic background bile duct adenoma

Answer 24

have very high threshold, can see normally in cirrhosis

Question 25

superficial mucosal inflammation of gallbladder

Answer 25

can see in downstream obstruction

Question 26

Chronic Hep B

Answer 26

• 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

Question 27

Autoimmune Hepatitis

Answer 27

• 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

Question 28

Acute Hepatitis

Answer 28

• 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

Question 29

Chronic Biliary Disease

Answer 29

• 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

Question 30

Pathognomonic feature of PSC

Answer 30

-concentric periductal inflammation, fibrosis, and bile duct scars

Question 31

Predominantly Lymphocytic Inflammation in Portal Tracts

Answer 31

• HCV
• HBV
• Autoimmune
• Acute Hepatitis
• Chronic Biliary Disease

Question 32

Predominantly Plasmacytic Inflammation in Portal Tracts

Answer 32

• 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

Question 33

Predominantly Mixed Inflammation in Portal Tracts

Answer 33

• 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

Question 34

Predominantly Eosinophilic Inflammation in Portal Tracts

Answer 34

• 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

Question 35

Predominantly Granulomatous Inflammation in Portal Tracts

Answer 35

• 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

Question 36

Features of “granulomatous hepatitis”

Answer 36

-portal, lobular, parenchymal hepatitis around the granuloma as well as away from it; eos may or may not be prominent

Question 37

Hyalinizing cholecystitis

Answer 37

• 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