Brainscape's Knowledge GenomeTM

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


See full index

Pathology > neoplasia > Flashcards

neoplasia Flashcards

1
Q

What are some other terms for “pre-malignant”

A

dysplasia (intraepithelial neoplasia)

carcinoma in situ - high end dysplasia, but not yet invasive

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

difference between benign neoplasm + dysplasia

A

benign = ordered

dysplasia = disordered, premalignant lesion, mutation

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

definition of progression from in-situ dysplasia to carcinoma

A

invasion - malignant cells breach BM to invade underlying stroma

no have access to lymphatic/vascular invasion -> metastatic spread to lymph nodes, distant organs

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

which are the low-risk types of HPV? and which are high risk

A

low risk - 6+11

  • mild cause of genital warts
  • CIN1

high risk - 16+18

  • CIN2-3
  • squamous cell carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

pathogenesis of Barrett’s oesophagus

risk

A

chronic reflux oesophagitis -> repetitive mucosal injury by gastric acid + duodenal content (bile, pancreatic enzymes)

=> cellular proliferation

=> likely exposure to carcinogens

=> re-epithelialisation by columnar epithelium

risk: malignant transformation

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

histo changes in barrett’s oesophagus

A
  • inflammation of epithelium -> proliferative response
    => hyperplasia + expansion of basal cell response
  • oedematous response in epithelium
  • eosinophils + lymphocutes

see transition of squamous epithelium -> glandular epithelium (not gastric but its own epithelium)

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

describe barrett’s epithelium

A

glands wtih large number of goblet cells (intestinal-type)

also expresses intestinal type proteins

=> intestinal metaplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Barrett’s oesophagus -> neoplasia

what do you see in

  • low grade dysplasia
  • high grade dysplasia
  • intramucosal carcinoma
  • deep invasive adenocarcinoma
A

low grade = enlarged, atypical nuclei, bit more disorganised + hyperchromatic

high grade dysplasia = severe nuclear atypia (not yet invasive)

intramucosal = fusion of glands (has got to lamina propria - bad bc there are lymphatics there)

deep invasive - deeply invade muscle layers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what needs to be breached for progression to invasive carcinoma

cervix
oesophagus
colon
breast
prostate
A

all = access to lymphatics + blood = metastatic potential

cervix = BM
oesophagus = BM
colon = muscularis mucosae (no lymph in lamina propria)
breast = myoepithelial cell layer loss
prostate = basal cell layer loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is familial adenomatous polyposis?

A

autosomal dom syndrome

have APC mutation

> 100 adenomatous polyps in large bowel

=> high incidence of early onset colorectal carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

histology of an adenomatous polyp

A

abnormal crypt architecture (tubular or viliform)

dysplasia

  • crowded cells
  • enlarged, hyperchromatic, pseudostrat nuclei
  • goblet cell depletion
  • more mitoses

no invasion beyond musc mucosae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

colon - where are the lymphatics?

A

beyond the musc mucosae - none in lamina propria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Genetic pathways of colorectal cancer

- which are most common in sporadic CRC

A

chromosomal instability
(change number, copies, translocation)
= FAP
- 75-85% of sporadic`

microsatellite instability
= HNPCC/Lynch
- 15% of sporadic

CpG island methylator phenotype
~15% of sporadic
- common in prox bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are common genetic changes in dysplasia-carcinoma sequence

A

loss of APC function

  • ↓cell adhesion, ↑cell proliferation
  • is early event in adenoma formation

chromosomal instability
- increased nuclear DNA content

accumulated mutations

  • proto-oncogenes: K-RAS, B-RAF
  • tumour suppressor - SMAD4/2, p53
  • activation of telomerase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is lynch syndrome (hereditary non-polyposis colorectal cancer)

A

most common familial colorectal cancer syndrome

autosomal dom

inherit mutation in DNA mismatch repair gene

early onset colorectal cancer (45yo)

also get extracolonic cancers - endometrium, renal pelvis/ureter, stomach, small bowel, ovary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the microsatellite instability pathway? (neoplasia)

example in colorectal

A

defective DNA mistmatch repair

=> get widespread mutations in DNA microsatellites

microsatellites - mono or di-nucleotide repeats

inc mutations in proto-oncogenes, tumour suppressor genes, DNA repair genes

example: loss of MLH1 protein (tumour suppressor DNA repair gene)

17
Q

Sessile serrated adenoma/polyp

  • where does it typically arise
  • features (histo/morph)
  • what mutations are comonly seen
  • why might they be missed at colonoscopy
  • what might they mean
A

proximal colon

features: mixed hyperplastic + dysplastic
- saw-tooth architecture
- more complex branching than hyperplastic polyp of crypts (prolfieration of cells)
- elongated, vesicular nuclei, prominent nuceloli
- increased atypia with dysplasia
- non invasive

freq: BRAF V600E mutation - precursor for CRC

is sessile -> hard to see on colonoscopy

risk of interval tumours

18
Q

macroscopic features of colorectal cancer:

  • growth patterns
  • cut surface
  • what do you assess for invasion
A

prox colon - bulky, polypod, exophytic (bulge in lumen, but doesn’t cause obstruction)

distal colon, rectum - annular, stenosing (apple core), ulcerated
=> bleeding, alternating constipation + diarrhoea

cut surface - firm, white (desmoplasia), necrotic
mucoid in mucinous tumours

invasion: muscularis mucosae, muscularis propria, lymph nodes, adj organs, perforation into peritoneal cavity

19
Q

Staging of colon cancer - Modified Duke’s (ABCD)

A

A - invades beyond musc mucosa

B - invades beyond musc propria

C - lymph node metastases

D - distant metastase

20
Q

staging of colon cancer - TNM

A 
T = depth of tumour invasion
Tis - insitu
T1 - musc mucosa
T2 - musc propria
T3 - beyond 
T4 - other organs/perforates

N = nodes
N0 - none
N1 - in 1-3 LN
N2 - 4+ LN

M - metastases
Mx - can’t be assessed
M0 - none
M1 - distant

21
Q

common site of colon cancer metastasis

A

liver -> portal blood

22
Q

what are some high risk features of colorectal cancer?

A

If high grade
- tumour predominately solid, rather than gland formin

If T3 with localised perforation, or T4

if has close, indeterminate, positive margins

if lymphovascular invasion (inc likelihood of mets)

if <12 nodes examined (may have understaged)

23
Q

features of nuclear atypia

A 
irrecular contours
variable size, shape
mitoses
abnormal chromatin
increased nuclear:cytoplasmic ratio
24
Q

what are some targeted therapies for coloncancer, what are they targeting

what mutations render it ineffective

A

target EGFR - block its signalling - inhibit growth
= cetuximab, panitumumab

K-RAS and B-RAF are activating mutations -> inneffective

MSI can improve outcomes

25
Q

what clinicopathological features raise suspicion of a familial syndrome

A

early onset CRC ( prob inactivating mutation in one TSG

Pathology (3 decks)

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