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Pathology > Hepatopancreatobilary > Flashcards

Hepatopancreatobilary Flashcards

1
Q

35F head of pancreas lesion
Dx?
Key features?
IHC?

A

solid pseudopapillary neoplasm.
Well-demarcated, large mass
Solid, monomorphic sheets of polygonal cells
Delicate vessels surrounded by hyalinized or myxoid stroma
Characteristic degenerative change leading to pseudopapillae
Cytoplasmic eosinophilic hyaline globules, PAS-D positive
Uniform round to oval nuclei with finely dispersed chromatin
Neoplastic cells often have nuclear grooves

IHC: Immunohistochemistry: Nuclear β-catenin, loss of membrane E-cadherin, nuclear progesterone receptor, positive TFE3 and SOX11

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2
Q

acinar cell carcinoma of pancrease

(+) IHC

A

(+) chymotrypsin, trypsin, lipase, BCL10 (antibody directed against the -COOH terminal portion of BCl10 protein is highly specific). NB: Also can be (+) for AFP, Hep-PAR-1, glypican 3, albumin mRNA.

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3
Q

pancreas

solid pseudopapillary neoplasma IHC

A

nuclear b-catenin (+); CD10, CD56 (+)
E-cadherin shows lost membraneous staining

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4
Q

pancreatic ductal adenocarcinoma

Most common mutation?

A

KRAS activation point mutations.
> 90% show this (also in PanIN)

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5
Q

solid pseudopapillary neoplasm

immunophenotype:

A

Consistently (+) for:
- PR
- Abnormal beta-catenin
- vimentin
- alpha-1-antitrypsin
Consistently (-) chromogranin

Variable expression other neuroendocrine markers: SYN, CD56, NSE; epithelial markers EMA/keratin; other hormone receptors: OR/inhibin

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6
Q

Frequently mutated genes in pancreatic ductal adenocarcinoma vs IPMN

A
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7
Q

Types of IPMN and immunophenotype

A
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8
Q

ductal adenocarcinoma vs chronic pancreatititis

ductal adenocarcinoma vs chronic pancreatitis

A
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9
Q

38F pancrease

dx?

A

Neuroendocrine tumour

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10
Q

well circumscribed lesion head of pancreas
Dx?
Key features?
IHC?

A

Acinar cell carcinoma

Key features:
Unlike conventional ductal adenocarcinoma, this tumor is highly cellular and with scant fibrous stroma
Cells show moderate amounts of granular eosinophilic cytoplasm containing PAS positive diastase resistant zymogen granules
Nuclei are uniform with a typically present, single and prominent nucleolus
Can have different architectures and growth patterns, including cystic, acinar, glandular and intraductal

IHC:
(+): CK7, CK8/18, CK19, BCL10, trypsin
(-): chromo/synapto

Image: showing monomorphic nuclei with prominent nucleoli. NB: atypical and amorphous zymogen material

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11
Q

IPMN

subtypes (3) and which is most common?
Major mutations

A

Gastric (most common, 70%); gastric foveolar type epithelium + scattered goblet cells, most are low-grade

Intestinal type (2nd most common), intestinal type epi forming villous papillae, tall columnar cells with cigar shaped nuclei. Usu reveal HGD

Pancreatobiliary (least common):

Mutations: KRAS and GNAS (although KRAS is nearly a precursor to PDAC, GNAS is rarely found in these neoplasms)

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12
Q

IPMN vs IOPN vs ITPN

IHC comparison

A
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13
Q

cystic lesions in the pancreas

ddx

A

IMPN
IOPN
ITPN
Mucinous cystic neoplasm
Retention cysts

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14
Q

IMPN

IPMC may be associated with invasive carcinoma. Describe the types of carcinoma associated with which IPMN subtypes

A

The invasive ca can be of 2 main types:
1. Colloid carcinoma: infiltrating epithelial elements separated by abundant stromal mucin arising in a/w intestinal type IPMN.
2. Tubular (ductal) adenocarcinoma which is morphologically similar to conventional PDAC, arises either in a/w pancreaticobiliary type or gastric type IPMN.

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15
Q

60F pancreatic head lesion, cystic

Dx
IHC

A

IPMN, gastric type
IHC: CK7+, CK20-, EMA-, MUC2 -, MUC5AC+, MUC6 -/+, CDX2-

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16
Q

55M head of pancreas lesion

dx
IHC

A

IPMN, intestinal type
IHC

17
Q

62M cystic lesion pancreas head

dx
IHC

A

IPMN, pancreaticobiliary

Note: the image shows cells to have little mucin production and enlarged round nuclei.

18
Q

70M cystic lesion head of pancreas

dx
IHC

A

IPMN, intestinal type with HGD
IHC

NB: image shows complex architecture and the nuclei are stratified, hyperchromatic, and pleomorphic.

19
Q

Neuroendocrine neoplasms of pancreas

types and grading

A
20
Q

mixed neuroendocrine neoplasm

Diagnosis, % of each component etc

A

For a tumour to qualify as MiNEN, each component should account for ≥ 30% of the tumour cell population. Non-neuroendocrine carcinomas with scattered neuroendocrine cells by immunohistochemistry do not fulfil this criterion; the presence of focal (< 30%) neuroendocrine differentiation can be mentioned but does not affect the diagnostic categorization. MiNEN is a conceptual category rather than a discrete entity; individual diagnoses indicating the specific cellular components should be applied (i.e. mixed acinar-neuroendocrine carcinoma, mixed ductal-neuroendocrine carcinoma, etc.)

21
Q

pancreatic neuroendocrine neoplasms

commonly mutated gene

A

The MEN1 gene is somatically inactivated in about 40% of PanNETs (TSG).
Approximately 40% of PanNETs showed mutation in either DAXX or ATRX. The function of DAXX and ATRX proteins is to maintain chromatin remodelling at telomeric and pericentromeric regions.

22
Q

head of pancreas lesion, 67F

dx
IHC

A

Pancreatic neuroendocrine carcinoma, small cell type

Essential: a poorly differentiated neoplasm of small or large cells, with vague neuroendocrine features; usually weak expression of neuroendocrine markers; mitotic count of > 20 mitoses/2 mm2 and Ki-67 proliferation index > 20%.

Desirable: Ki-67 proliferation index > 50%.

23
Q

acinar cell carcinoma

IHC

A

(+) trypsin, chymotrypsin, BCL10 (ab directed against the -COOH terminal portion of BCL10 protein) - highly specific and sensitive); CK7, CK19

NB: can be (+) for AFP, Hep-par 1, glypican 3, ablumin mRNA (FISH)

NB: can have focal + for chromo and synapta

24
Q

serous cystadenoma (pancreas)

Associated with which condition

A

von Hippel Lindau disease

25
Q

autoimmune pancreatitis

differences b/w type 1 and type 2

A
26
Q

solid pseudopapillary neoplasm

key features and IHC

A

Nuclear grooves, foamy cells, eosinophilic DPAS globules, pseudopapillae, (+) ofor CD10 and nuclear beta catenin

27
Q

PDAC vs chronic pancreatitis key features

A
28
Q

cholecystectomy

Dx?
& key features.

A

Dx: adenomyoma.
Key features: Cystically dilated benign biliary glands accompanied by smooth muscle hypertrophy of gallbladder wall, thickened / fibrotic subserosa

29
Q

IHC for HCC:

A

HSP70, glypican 3 and glutamine synthetase
Positivity for at least two of these markers strongly indicates HCC, with a near 100% specificity and 72% sensitivity. (WHO)

30
Q

In terms of premalignant lesions for HCC, what is the difference between dysplastic nodules and dysplastic foci?

A

Dysplastic foci are < 1mm in diameter and are incidental lesions discovered on histo examination of livers w/ advanced fibrosis. Further subclassified into large-cell change, small-cell change and iron-free foci.

DN are usu 5-15 mm in diameter and detected either macroscopically or by imaging in cirrhotic livers. Classified into low-grade or high-grade based on the degree of cytological and architectural atypia. The vascular remodelling of DNs leads to a progressive shift from a venous to an arterial blood supply. Portal tracts are commonly retained in DNs, but they may be reduced in number as newly formed unpaired lobular arteries gradually increase from LG DN to HG DN to HCC.

31
Q

Describe four morphological patterns of intracholecystic papillary neoplasm and associated IHC?

What % are a/w inv carcinoma.

A

Biliary: CK7/EMA (+)
Gastric morphology: (gastric foveolar). diffusely (+) MUC5AC.
Intestinal morphology: Resembles colonic adenoma. (+) CK20, CDX2, MUC2
Oncocytic: Diffusely (+) for EMA and NO labelling for MUC6

An associated invasive ca is identified in about half of all ICPNs.

32
Q

Described the histological features (7) used to distinguish pancreatic ductal adenocarcinoma from chronic pancreatitis?

A
32
Q

mutations in IPMNs and Mucinous cystic neoplasms

A

IPMN: KRAS, GNAS
MCN: KRAS

33
Q

molecular pathology for solid pseudo papillary neoplasm

A

somatic activating mutation in exon 3 of CTNNB1 is the only genetic alteration known in SPNs.

34
Q

Hepatocellular adenoma
RF
subtypes
Morphological features of subtypes

DDX + how to differentiated

A

RF: OCP, anabolic steroids, glycogenesis types 1 and 3, galactosaemia, tyrosinaemia.

Subtypes:
HNF1A-inactivated
Inflammatory HCA
beta-catenin activated HCA
beta-catenin activated inflammatory HCA

Morphology:
ALL: ill defined tumours, lacks fibrous capsule, b/g liver usu non-cirrhotic; cell plates 1-2 cells thick.
HNF1A-inactived: lobulated contours, diffuse macro/microsteatosis, ballooned and clear cells +/-pseudoglands
Inflammatory: sinusoidal dilatation, congestion, foci of inflammation, thick arteries+/- ductalr reaction. Fibrotic bands and nodular organization may be misleading for FNH.
b-acatenin-activated: cytoarchitectural atypia, pseudoglands, andpigments.

Ddx:
FNH (ddx for iHCA): map-like GS and (+) staining with inflammatory markers (serum amyloid A and C-reactive protein) in IHCA
HCC: thick cell, freq pseudoglands, small cell change, mitoses, and loss/fragmentation of the reticulin network are typical of HCC. IHC: glypican 3, HSP70, GS. Arterialised sinusoids (CD34+) are freq seen in HCCs (but can be seen in benign lesions include focal nodular hyperplasia and HCA)

Epithelioid angiomyolipoma: can show diffuse GS staining. demonstration of myomelanocytic differentiation by IHC confirms dx.

Pathology (23 decks)

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