1
Q
Subepithelial neural appearing nodule
A
DDX:
- mucosal schwann cell hamartoma (S100+)
- perineurioma (Glut1+)
2
Q
HCV vs late acute cellular rejection
A
- HCV should NOT have plasma cells or pericentral vein inflammation
- late ACR (or de novo AIH) can have plasma cells or pericentral vein inflammation
3
Q
Portal triad: size of ducts vs arteries
A
- arteries should be smaller than ducts
- when arteries are larger it tell you there is a vascular problem
4
Q
Portal vein thrombosis
A
-can see splitting of the veins in the liver
5
Q
Prominent oxyntic rugal folds
A
-consider ZE
6
Q
Collagenous colitis and lymphocytic colitis
A
-should be diffuse processes (meaning affecting more than one site of colon)
7
Q
Subtype of hepatic adenomas
A
- 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
8
Q
Reactive changes in small intestine
A
- foveolar metaplasia
- goblet cell depletion
9
Q
“Atypical HCC” by imaging
A
-do a CK7 to rule out cholangiocellular component
10
Q
IPMN gross
A
- multilocular, papillary
- usually NOT unilocular
- should see messed up background pancreas due to obstruction
11
Q
MCN gross
A
-usually multilocular
12
Q
DDX cystic pancreatic tumor
A
- cystic NET (can be unilocular, looks like an eyeball)
- MCN
- IPMN
13
Q
Crystals
A
- kayexylate (fish scales)
- sevelamer (fish scales)
- cholestyramine (dont cause mucosal injury)
14
Q
Signet ring type adenoca in rectum
A
consider a NET too
15
Q
LAMN
A
low grade appendiceal mucinous neoplasm
16
Q
Major Patterns of Liver Injury
A
- predominantly portal inflammation
- prominent lobular injury
- ductular reactions
- steatosis
- fibrosis
17
Q
Prominent ductular reaction
A
biliary disease
18
Q
Mild ductular reaction
A
can indicate chronic viral hepatitis
19
Q
Pathognomonic feature of PBC
A
florid duct lesion: non-necrotizing granuloma surrounding damaged bile duct (granulomatous duct destruction)
20
Q
Pathognomonic feature of sinusoidal obstruction syndrome
A
AKA “veno-occlusive disease”
occluded central veins
21
Q
Predominantly portal inflammation
A
- chronic viral hepatitis
- autoimmune hepatitis
- drug/toxin induced hepatitis
- chronic biliary diseases (PBC, PSC, strictures)
- metabolic disease (Wilson’s and alpha1antitrypsin)
- neoplastic (leukemia/lymphoma)
22
Q
Chronic Hep C
A
- 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
23
Q
collagen in cecum and rectum
A
can normally have increased collagen band; increase your threshold for collagenous colitis
24
Q
cirrhotic background bile duct adenoma
A
have very high threshold, can see normally in cirrhosis
25
superficial mucosal inflammation of gallbladder
can see in downstream obstruction
26
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
27
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
28
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
29
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
30
Pathognomonic feature of PSC
-concentric periductal inflammation, fibrosis, and bile duct scars
31
Predominantly Lymphocytic Inflammation in Portal Tracts
- HCV
- HBV
- Autoimmune
- Acute Hepatitis
- Chronic Biliary Disease
32
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
33
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
34
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
35
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
36
Features of "granulomatous hepatitis"
-portal, lobular, parenchymal hepatitis around the granuloma as well as away from it; eos may or may not be prominent
37
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
Surgical Pathology
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