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Upper GI Flashcards

1
Q

What is the IHC profile of HCC vs cholangiocarcinoma

A

HCC:
Positive: Cam 5.2, HepPar-1, Albumin ISH, AFP (50%), CEA (pattern of positivity specific)
Negative: AE1/AE3neg (an exception to normal rule of carcinomas being positive), CK20/CK7

Cholangio:
Positive: AE1/AE3, cam5.2, CK20/CK7, CEA ( pattern of positivity specific)
Negative: HepPar1, albumin ISH (but positive in intrahepatic cholangio), AFP

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2
Q

What is the epidemiology and risk factors for HCC

A

Males >. Females
Leading cause of cancer mortality worldwide
Higher incidence in areas with high rates of hep b/c
Risk factors:
Hep b/c infection (80% of cases)
Injected drug use
Liver Cirrhosis
Obesity
Diabetes
Smoking
Alcohol use
Haemochromatosis

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3
Q

What is the typical presentation of HCC

A

Painless liver mass, without symptoms directly related to cancer
More likely to have signs and symptoms of underlying liver disease
-Cancer related: pain, weight loss, early satiety, diarrhoea, fever, fatigue
-decompensated cirhosis: ascites, encephalopathy, jaundice, variceal bleeding

Associated paraneoplastic syndromes including cutaneous; worse prognosis

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4
Q

What are the typical epidemiological features and risk factors for cholangiocarcinoma

A

No definite age predisposition
Present age 50-70
Higher rates south east Asia eg Thailand.

Risk factors:
-Primary sclerosing cholangitis (younger age of presentation). Lifetime risk 5-20%
-hepatobiliary lithiasis
-Liver flukes
-cystic fibrosis
-Le Fraumeni
-smoking
-hep b/c
-cirrhosis
-inflammatory bowel disease
-obesity, diabetes (also risk factors for HCC)

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5
Q

What are the microscopic features of cholangiocarcinoma

A

Usually adenocarcinoma
Significant peritumoural desmoplasia (lower yield of biopsy)
Typically multi focal
High rates of perineural invasion
Polysomy on FISH

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6
Q

What are prognostic factors for cholangiocarcinoma, what is the5yr survival

A

Age, stage, grade, margin status.
2-30% 5yr OS

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7
Q

What are the most common metastatic sites for cholangiocarcinoma

A

Liver, lung, peritoneum, bone

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8
Q

What blood tests should be done for a suspected liver cancer

A

Hep b/c (both, more HCC)
CEA (both)
CA19-9 (CCA)
AFP (HCC)
CBC
Coagulation screen (PT/INR)
Albumin
Liver enzymes, bilirubin

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9
Q

What scoring system is used for liver cirrhosis and what are it’s components?

A

Child’s Pugh
-total score groups into class A, B, C. C is worst class

-total bilirubin
-serum albumin
-PT or INR
-ascites (absent, moderate, severe)
-encephalopathy

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10
Q

What are the American screening recommendations for HCC

A

Anyone with chronic hep b infection and/or cirrhosis. Unless Child’s Pugh C and NOT on transplant list (ie prognosis too poor to warrant screening)

6 monthly USSand AFP

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11
Q

What is the microscopic appearance of hepatocellular carcinoma

A

May be one or several discrete lesions, or diffusely infiltrating the liver
Macroscopically pale or yellow (fatty) or green due to bile. May invade veins
Well/moderately differentiated: cells resembling hepatocytes, marked cellular atypia in poorly differentiated
Thick plates or trabeculae, pseudoglandular structures.

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12
Q

What is a typical presentation of cholangiocarcinoma

A

Presents early with small tumours due to signs and symptoms of biliary tract obstruction
Intrahepatic can present later, usually in individuals without liver cirrhosis. RUQ pain, weight loss.
1/3 have nodal Mets at diagnosis

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13
Q

What are the typical microscopic features of cholangiocarcinoma

A

Typically well to moderately differentiated
Adenocarcinoma features
Glandular/tubular structures lined by malignant epithelial cells
Abundant fibrous stroma
LVSI, PNI common

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14
Q

What imaging is used in the work up of hepatocellular carcinoma

A

MRI or
4 phase CT: pre contrast, hepatic arterial phase, portal venous phase, delayed phase

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15
Q

What are prognostic factors for hepatocellular carcinoma

A

Child’s Pugh score
Performance status
Stage
Metastatic disease

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16
Q

What does IPMN stand for, and where in the pancreas are they most commonly located. What is its radiological appearance

A

Intraductal papillary mucinous neoplasm
Head of pancreas, either in the main pancreatic duct or it’s branches
Cystic appearance on imaging (solid more concerning for invasive malignancy)

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17
Q

What are the three subtypes of IPMN

A

Gastric
Intestinal
Pancreatobiliary
Based on the appearance of the cells

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18
Q

What is the pre invasive lesion that is most commonly a precursor to pancreatic ductal adenocarcinoma

A

Pancreatic intraepithelial neoplasia (PanIN)

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19
Q

What is the most common pancreatic tumour

A

Pancreatic ductal adenocarcinoma

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20
Q

Where in the pancreas is pancreatic ductal adenocarcinoma most commonly located

A

The head of pancreas

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21
Q

What is the typical microscopic appearance of a pancreatic ductal adenocarcinoma

A

Well to moderately differentiated
Duct-like glandular structures that haphazardly infiltrate
Desmoplasia
PNI in 90%
LVSI in 50%

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22
Q

What does squamous differentiation mean for prognosis of pancreatic ductal adenocarcinoma

A

Worse prognosis

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23
Q

What four key driver gene mutations are commonly associated with pancreatic ductal adenocarcinoma, which is highly specific

A

KRAS (>90%)
p53 (50-80%)
p16 (CDKN2A) (95%)
SMAD4 (50%) highly specific
Ie these are molecular tests that can be done

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24
Q

What is the definition of a pancreatic neuroendocrine microadenoma

A

Well differentiated NET
<5mm
Non-functional
No mitoses

Benign and often incidental

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25
What two inherited genetic syndromes are most associated with pancreatic NETs
MEN1 VHL
26
What is the prognosis of an unresectable pancreatic ductal adenocarcinoma
<1 year
27
What are the names of the exocrine cells and endocrine cells of the pancreas
Exocrine: serous actinic cells Endocrine: islets of langerhans. Alpha cells: glucagon, beta cells: insulin, delta cells: somatostatin
28
What are the epidemiological patterns of pancreatic cancer
Male 1.3:1 Peak incidence 60-70
29
What are risk factors for pancreatic cancer
Chronic pancreatitis Alcohol Smoking Red meat Chronic diabetes High BMI Familial: -hereditary pancreatitis -PJS -FAMMM -BRCA 2 -Lynch -ataxia telangiectasia
30
If screening for individuals with hereditary conditions increasing risk of pancreatic cancer, what are the best investigations?
EUS: highest sensitivity MRI/MRCP No consensus on management pathway once a lesion is detected, age to initiate/ terminate screening
31
What is the usual IHC profile of pancreatic cancer
CK7+/CK20- P53+ Maspin + S100+
32
What are the most common types of non-NET malignancies of the pancreas
Ductal adenocarcinoma Acinar carcinoma Pancreatoblastoma
33
What must be present on IHC for the diagnosis of a pancreatic acinar carcinoma
Pancreatic enzymes. Ie, lipase, amylase or elastase Trypsin and chemo trips in usually positive
34
What is the epidemiology of pancreatic NETs
1-2% of all pancreatic tumours M=F Median age 40-60 No known environmental risk factors
35
What IHC marker for pancreatic NETs is also commonly measurable in serum
Chromogranin
36
What is the 5yr OS for resectable vs unresectable pancreatic ductal adenocarcinoma
Unresectable: 5% Resectable: 25%. 35% local recurrence, 34% metastatic
37
What proportion of patients presenting with pancreatic cancer are resectable at baseline
20%. But only 70% of these will actually be respected when they proceed to theatre
38
What cells does GIST arise from
ICC: interstitial cells of Cajal Pacemaker cells of the gut: regulate smooth muscle
39
Where does GIST most frequently arise
Stomach, then small bowel.
40
What is the epidemiological pattern of GIST
Usually sporadic. M=F. Median age 50-70
41
What is the macroscopic appearance of GIST
Well demarcated tumour Fleshy tan pink Centred in muscularis propria average size 6cm at diagnosis May have haemorrhaged or cystic degenration
42
What are the microscopic features of GIST
Most commonly spindle cell, but can be epithelioid or mixed
43
What are the common mutations associated with GIST
Mostly mutually exclusive, C-kit: activating tyrosine kinase mutation. 75% of tumours PDGFRa: activating mutation (platelet derived growth factor receptor alpha SDH mutation: succinct dehydrogenase (syndrome also associated with paraganglioma/phaeochromocytoma and SDH associated RCC)
44
What are the key prognostic factors for GIST
Main two: -tumour size -mitotic rate 5+ per HPF Others: -lack of ckit mutation worse prognosis -R1 resection or tumour spill -age
45
What is the IHC profile for GIST
Positive: DOG1 CD117 (ckit) CD34 (non specific) Negative: -S100 (Schwannoma positive and CD117 neg, multiple others S100 positive) -Desmin (positive in smooth muscle tumours)
46
What TKI can be used to target cKIT in GIST
Imatinib (non specific TKI)
47
How are GISTs graded
Based on mitotic rate only Low: 5
48
What are the two types of gastric dysplasia
Gastric type: resembles gastric foveolar cells, tubovillous folds. Apical mucin Intestinal type: looks like colonic adenoma; tall columnar cells, hyperchromasia nuclei
49
How is gastric dysplasia graded
Low grade: preserved polarisation (basal nuclei) and preserved architecture High grade: prominent cytological atypia, high N:C ratio. Loss of polarity
50
What is the pathway for H pylori causing gastric adenocarcinoma
Chronic infection -> chronic inflammation -> intestinal metaplasia-> dysplasia -> carcinoma
51
What are the key risk factors for gastric adenocarcinoma
H pylori EBV Smoking Dietary
52
What are the most common/relevant morphological subtypes of gastric adenocarcinoma (WHO classification)
Tubular: most common Poorly cohesive: includes signet ring (intracellular mucin) No well formed glands. Second most common Mucinous: >50% of tumour has malignant cells in extra cellular mucin pools Gastric adenocarcinoma with lymphoid stroma: often EBV associated.
53
How is it determined if a GOJ tumour is staged as oesophageal or gastric
Sievert Oesophageal: tumour crosses the GOJ and epicentre is within 2cm of GOJ Gastric: tumour doesn’t cross the GOJ or if it does the epicentre of tumour is >2cm into stomach from GOJ
54
What are the two types of lymphoma that most commonly affect the stomach
Extranodal DLBCL: similar molecular/IHC profile to nodal DLBCL. Still determine if germinal centre type or activated. Less aggressive than nodal DLBCL MALToma: h pylori associated, may be cured with H pylori triple therapy. Extranodal Marginal zone lymphoma
55
What cancers of the stomach is H pylori associated with
gastric MALToma Gastric adenocarcinoma
56
What translocation commonly renders gastric MALToma resistant to triple therapy
t(11:18)
57
Invasion of what layer of the stomach wall distinguishes between early and advanced gastric cancer
The muscularis propria
58
What is the IHC pattern of gastric MALToma and gastric DLBCL
MALT: CD20, Pax5 positive (b cell markers), CD34. H pylori positive DLBCL: EBV negative, CD20, CD19, Pax5, CD79a positive. Check for MYC and BCL2 alterations
59
What were the subtypes of gastric adenocarcinoma under the old Lauren classification
Intestinal type: well differentiated Diffuse type: poorly differentiated. Basically signet ring/ e cadherin loss. Associated with worse prognosis, early lymphatic dissemination, peritoneal carcinomatosis, highly metastatic.
60
What are the Siewart classification of GOJ tumours (adenocarcinoma)
Class 1: arise from metaplasia 1-5cm above GOJ, but still involves GOJ. Class 2: arise 1cm above GOJ to 2cm below Class 3: arise 2-5cm below GOJ, but still involves GOJ Class 1 and 2 treated as oesophageal cancer. Class 3 treated as Gastric
61
What is the cellular process occurring in Barrett’s oesophagus
Metaplasia from squamous epithelium to gastric type intestinal epithelium. Columnar cells with presence of goblet cells.
62
What are risk factors for Barrett’s oesophagus
GORD Smoking Obesity Male gender H pylori
63
What is the pathogenesis to Barrett’s leading to oesophageal adenocarcinoma
Acid/bile reflux -> Intestinal metaplasia -> Mutations -> Low grade dysplasia -> TP53 mutations -> High grade dysplasia -> DNA/chromosomal instability -> Cancer
64
What is the microscopic appearance of Barrett’s oesophagus without dysplasia
Columnar cells with apical mucin, moderate cytoplasm, basal nuclei. Wild type p53 IHC staining
65
Invasion of what layer of the oesophagus wall defines invasive carcinoma
Invasion through basement membrane
66
What are patterns of growth of oesophageal adenocarcinoma
Tubular Papillary Signet ring Mucinous (Often mixed, note that these are mostly the same as gastric except for papillary)
67
What are the IHC patterns of oesophageal adenocarcinoma vs SqCC
Adenocarcinoma: CK7+, mucin +. P63, p40, CK5/6- SqCC: opposite to above
68
What are the cytological and architectural features of oesophageal squamous dysplasia
Cytological: nuclear enlargement, pleomorphism, hyperchromasia, loss of polarity, overlapping nuclei Architecture: loss of maturation
69
How are low and high grade oesophageal squamous dysplasia distinguished
Low grade: only lower half of epithelial layer involved AND mild atypia only
70
What are risk factors for oesophageal SqCC
Smoking Alcohol Very hot beverages Achalasia Caustic ingestion Most prevalent SE Asia HPV infection often present, but not thought to be contributing to malignancy.
71
What are subtypes of oesophageal SqCC
Verrucous- exceedingly well differentiated Spindle cell- high grade spindle cell component Basaloid. Solid or nested growth of Basaloid cells. (No HPV associated unlike the oropharynx equivalent
72
What is the annual risk of oesophageal malignancy associated with each of; Barrett’s oesophagus, LG dysplasia, HG dysplasia
Barrett’s: 0.2-0.5% per year LG: 0.7% per year HG: 7% per year
73
What is the pathogenesis of hepatitis b vs hep c in HCC
Both: -acute infection -> chronic infection -> chronic liver disease/inflammation -> cirrhosis -> increased hepatocyte division -> HCC Hep C - RNA virus that does not integrate in host DNA, so no direct carcinogenic effect Hep B -DNA virus that integrates into host DNA, causing genomic instability which causes activation of oncogenes and loss of tumour suppressors -> HCC
74
What percentage of pancreatic cancer over expresses HER-2
50%
75
What is the prognosis of pancreatic adenocarcinoma
90% die within 1 year 5yr OS 5%

Pathology (16 decks)

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