Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology > Upper GI > Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are prognostic factors for cholangiocarcinoma, what is the5yr survival

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the most common metastatic sites for cholangiocarcinoma

A

Liver, lung, peritoneum, bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are prognostic factors for hepatocellular carcinoma

A

Child’s Pugh score
Performance status
Stage
Metastatic disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the three subtypes of IPMN

A

Gastric
Intestinal
Pancreatobiliary
Based on the appearance of the cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

Pancreatic intraepithelial neoplasia (PanIN)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the most common pancreatic tumour

A

Pancreatic ductal adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Where in the pancreas is pancreatic ductal adenocarcinoma most commonly located

A

The head of pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What does squamous differentiation mean for prognosis of pancreatic ductal adenocarcinoma

A

Worse prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the definition of a pancreatic neuroendocrine microadenoma

A

Well differentiated NET
<5mm
Non-functional
No mitoses

Benign and often incidental

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What two inherited genetic syndromes are most associated with pancreatic NETs

A

MEN1
VHL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the prognosis of an unresectable pancreatic ductal adenocarcinoma

A

<1 year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the names of the exocrine cells and endocrine cells of the pancreas

A

Exocrine: serous actinic cells
Endocrine: islets of langerhans. Alpha cells: glucagon, beta cells: insulin, delta cells: somatostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the epidemiological patterns of pancreatic cancer

A

Male 1.3:1
Peak incidence 60-70

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are risk factors for pancreatic cancer

A

Chronic pancreatitis
Alcohol
Smoking
Red meat
Chronic diabetes
High BMI

Familial:
-hereditary pancreatitis
-PJS
-FAMMM
-BRCA 2
-Lynch
-ataxia telangiectasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

If screening for individuals with hereditary conditions increasing risk of pancreatic cancer, what are the best investigations?

A

EUS: highest sensitivity
MRI/MRCP

No consensus on management pathway once a lesion is detected, age to initiate/ terminate screening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the usual IHC profile of pancreatic cancer

A

CK7+/CK20-
P53+
Maspin +
S100+

32
Q

What are the most common types of non-NET malignancies of the pancreas

A

Ductal adenocarcinoma
Acinar carcinoma
Pancreatoblastoma

33
Q

What must be present on IHC for the diagnosis of a pancreatic acinar carcinoma

A

Pancreatic enzymes. Ie, lipase, amylase or elastase
Trypsin and chemo trips in usually positive

34
Q

What is the epidemiology of pancreatic NETs

A

1-2% of all pancreatic tumours
M=F
Median age 40-60
No known environmental risk factors

35
Q

What IHC marker for pancreatic NETs is also commonly measurable in serum

A

Chromogranin

36
Q

What is the 5yr OS for resectable vs unresectable pancreatic ductal adenocarcinoma

A

Unresectable: 5%
Resectable: 25%. 35% local recurrence, 34% metastatic

37
Q

What proportion of patients presenting with pancreatic cancer are resectable at baseline

A

20%. But only 70% of these will actually be respected when they proceed to theatre

38
Q

What cells does GIST arise from

A

ICC: interstitial cells of Cajal
Pacemaker cells of the gut: regulate smooth muscle

39
Q

Where does GIST most frequently arise

A

Stomach, then small bowel.

40
Q

What is the epidemiological pattern of GIST

A

Usually sporadic.
M=F.
Median age 50-70

41
Q

What is the macroscopic appearance of GIST

A

Well demarcated tumour
Fleshy tan pink
Centred in muscularis propria
average size 6cm at diagnosis
May have haemorrhaged or cystic degenration

42
Q

What are the microscopic features of GIST

A

Most commonly spindle cell, but can be epithelioid or mixed

43
Q

What are the common mutations associated with GIST

A

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
Q

What are the key prognostic factors for GIST

A

Main two:
-tumour size
-mitotic rate 5+ per HPF

Others:
-lack of ckit mutation worse prognosis
-R1 resection or tumour spill
-age

45
Q

What is the IHC profile for GIST

A

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
Q

What TKI can be used to target cKIT in GIST

A

Imatinib (non specific TKI)

47
Q

How are GISTs graded

A

Based on mitotic rate only
Low: </=5
High: >5

48
Q

What are the two types of gastric dysplasia

A

Gastric type: resembles gastric foveolar cells, tubovillous folds. Apical mucin
Intestinal type: looks like colonic adenoma; tall columnar cells, hyperchromasia nuclei

49
Q

How is gastric dysplasia graded

A

Low grade: preserved polarisation (basal nuclei) and preserved architecture
High grade: prominent cytological atypia, high N:C ratio. Loss of polarity

50
Q

What is the pathway for H pylori causing gastric adenocarcinoma

A

Chronic infection -> chronic inflammation -> intestinal metaplasia-> dysplasia -> carcinoma

51
Q

What are the key risk factors for gastric adenocarcinoma

A

H pylori
EBV
Smoking
Dietary

52
Q

What are the most common/relevant morphological subtypes of gastric adenocarcinoma (WHO classification)

A

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
Q

How is it determined if a GOJ tumour is staged as oesophageal or gastric

A

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
Q

What are the two types of lymphoma that most commonly affect the stomach

A

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
Q

What cancers of the stomach is H pylori associated with

A

gastric MALToma
Gastric adenocarcinoma

56
Q

What translocation commonly renders gastric MALToma resistant to triple therapy

A

t(11:18)

57
Q

Invasion of what layer of the stomach wall distinguishes between early and advanced gastric cancer

A

The muscularis propria

58
Q

What is the IHC pattern of gastric MALToma and gastric DLBCL

A

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
Q

What were the subtypes of gastric adenocarcinoma under the old Lauren classification

A

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
Q

What are the Siewart classification of GOJ tumours (adenocarcinoma)

A

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
Q

What is the cellular process occurring in Barrett’s oesophagus

A

Metaplasia from squamous epithelium to gastric type intestinal epithelium. Columnar cells with presence of goblet cells.

62
Q

What are risk factors for Barrett’s oesophagus

A

GORD
Smoking
Obesity
Male gender
H pylori

63
Q

What is the pathogenesis to Barrett’s leading to oesophageal adenocarcinoma

A

Acid/bile reflux ->
Intestinal metaplasia ->
Mutations ->
Low grade dysplasia ->
TP53 mutations ->
High grade dysplasia ->
DNA/chromosomal instability ->
Cancer

64
Q

What is the microscopic appearance of Barrett’s oesophagus without dysplasia

A

Columnar cells with apical mucin, moderate cytoplasm, basal nuclei. Wild type p53 IHC staining

65
Q

Invasion of what layer of the oesophagus wall defines invasive carcinoma

A

Invasion through basement membrane

66
Q

What are patterns of growth of oesophageal adenocarcinoma

A

Tubular
Papillary
Signet ring
Mucinous
(Often mixed, note that these are mostly the same as gastric except for papillary)

67
Q

What are the IHC patterns of oesophageal adenocarcinoma vs SqCC

A

Adenocarcinoma: CK7+, mucin +. P63, p40, CK5/6-
SqCC: opposite to above

68
Q

What are the cytological and architectural features of oesophageal squamous dysplasia

A

Cytological: nuclear enlargement, pleomorphism, hyperchromasia, loss of polarity, overlapping nuclei
Architecture: loss of maturation

69
Q

How are low and high grade oesophageal squamous dysplasia distinguished

A

Low grade: only lower half of epithelial layer involved AND mild atypia only

70
Q

What are risk factors for oesophageal SqCC

A

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
Q

What are subtypes of oesophageal SqCC

A

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
Q

What is the annual risk of oesophageal malignancy associated with each of; Barrett’s oesophagus, LG dysplasia, HG dysplasia

A

Barrett’s: 0.2-0.5% per year
LG: 0.7% per year
HG: 7% per year

73
Q

What is the pathogenesis of hepatitis b vs hep c in HCC

A

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
Q

What percentage of pancreatic cancer over expresses HER-2

A

50%

75
Q

What is the prognosis of pancreatic adenocarcinoma

A

90% die within 1 year
5yr OS 5%

Pathology (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions