Brainscape's Knowledge GenomeTM

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


See full index

Path > Neoplasia - lung, CRC, cervical > Flashcards

Neoplasia - lung, CRC, cervical Flashcards

1
Q

define neoplasm

A

formation of new tissue

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

benign nomenclature

A

finish in oma
eg: adenoma

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

malignant nomenclature

A

finshes in sarcoma
eg: fibrosarcoma, osteo sarcoma

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

emsenchymal tissue (fibrous) benign and malignant name

A

fibroma
fibrosarcoma

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

smooth muscle benign and malignant names

A

leiomyoma
leiomyosarcoma

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

bone benign and malignant names

A

osteoma
osteosarcoma

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

epithelial (glandular) benign and malignant names

A

adenoma
carcinoma (adenocarcinoma)
90% of cancers

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

benign neoplasms - characteristics

A

well differentiated
encapsulated
low mitotic rate (slow division)

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

define mitotic rate

A

number of cells dividing (spindles)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

=malignant neoplasms - characteristics

A

abnormal proliferation (high mitotic rate)
no differentiation (diff to adjacent tissues)
abnormal nuclei (high N:C ratio)
for tumours
undergo metastasis AND angiogenesis

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

metasitasis overview - 2steps

A
  1. in situ - cancer cells are still above the basement membrane
  2. invasive - move through BM and degrade ECM to move to adjacent vessels to migrate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

pathways of metastasis

A
  1. haematogenous - blood flow usually to liver and lungs
  2. lymphatic system
  3. direct (organ to organ)
  4. perineurally - via neural sheath (head and neck cancer)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

metastasis definition

A

movement from primary to secondary site
secondary tumour is named after origin
eg: breast cancer metastises to lungs its called metastatic breast cancer

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

define pleomorphism

A

variability in shape and size

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

anaplasia definition

A

lack of differentiation

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

dysplasia

A

disordered growth
pleomorphic
hyperchromatic nuclei

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

metaplasia definition

A

change of cell type

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

progression of cancer sequence

A

normal -> metaplasia -> dysplasia

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

grade classification

A

T tumour size
N nodes involved
M metastasis

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

stage classification

A

more useful when there is metastasis/high grade
uses the stage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

requirements of malignant cells (8)

A

self sufficient growth signals
insensitive to growth inhibition signals
evade apoptosis
achieve limitless replication potential
sustain angiogenesis
ability to invade and metastasise
reprogram their energy metabolism
avoid detection + destruction by immune cells

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

normal cell division - cell cycle

A

by mitosis to replace damaged/dead cells
RB, P53 (tumour supressor genes) monitors cell cycle and cause repair or apoptosis.
growth factor tyrosine kinase - binds to receptor causing signal transduction, then mvmt into nucleus and proliferation occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

cell types of cell cycle that are dysregulated in cancer + its effects

A

DNA repair genes = no repair
proto oncogenes = overstimulation of proliferation
tumour supressor genes = loss of breaking proliferation

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

roles of RB and p53

A

breaks of proliferation

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

roles of proto oncognese

A

proliferation

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

accumulated development of cancer

A

start with normal epithelium
several mutations occur causing dysplasia (low then high grade) = carcinoma in situ
- more mutations cause metastasis past BM = invasive carcinoma

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

carcinogens defintion, examples

A

cause DNA mutations
chemicals (asbestos, coal, tobacco smoke, sawdust)
UV rays, x rays, cathode rays
ionisation radiation
oncogenic viruses

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

proto-oncogene -> oncogene

A

proto-oncogene to oncogene ahppens from mutations that cause hyper active gene product, increased trasncription, gene amplification.
translocation of a gene from one chromosome to another = generate a protein

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

BCR - ABL proto-oncogene example

A

normally: ABL on on echromosome and BCR on another
mutation: after translation, both genes on sam chromosome
causes: production of a functional protein that drives leukemia

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

BRCA1/2

A

usually a tumour supressor and usually repair.
mutation = increased risk of breast, ovarian, prostate, pancreatic and colon cancer

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

P53 normal function VS mutation

A

normally: tumour supressor gene, repair and apoptosis
mutation = damaged cells proliferate instead of apoptosis

32
Q

P53 normal function VS mutation

A

normally: tumour supressor gene, repair and apoptosis
mutation = damaged cells proliferate instead of apoptosis

33
Q

paraneoplastic syndromes

A

accumulation of symptoms that can occur with tumours but arent directly associated with cancer mass effect/invasion
rare disorders triggered by abnormal immune response to cancerous tumour
T cells attack normal cells in the nervous system by mistake = neuro symptoms
middle aged -> older ppl
in with lung, ovarian, lymphatic, breast cancers
eg: cushings syndrome from ACTH mutation

34
Q

normal skin - basal cells

A

some basal cells are progenitor cells that will divide into 1 progenitor and one daughter cells that ill migrate up and differentiate.
basal cell become keratinocytes to make keratin
Melanocytes are on BM and produce melanin

35
Q

squamous cell carcinoma

A

UV light exposure
cells on top - terminally differentiated
older ppl
just proliferation problem (not a big issue)

36
Q

basal cell carcinoma

A

UV light causes transformation on basal cells
more aggressive because they are progenitor cells so will replicate much faster
can cause harm/mortality

37
Q

melanocytes -> melanoma

A

melanocytes arise on BM
melanin protects from light effects
UV light causes damage to DNA
damage to melanocytes = dysplastic neavi development
some are harmless but others are associated with the development of melanoma

38
Q

melanocytic tumour genetic predisposition

A

ppl can be born with p16 gene mutation (p16 regulates cell cycle)
autosomal dominant mutation

39
Q

UV damage to proto-oncogenes + tumour supressors

A

BRAF
p53
NRAS

40
Q

define proto-oncogene

A

a mutated growth factor which drives cellular proliferation

41
Q

melanoma - radial growth phase (RGP)

A

first stages
in situ
no potential to for tumour and metastasis
horizontal growth only - contained in BM
can take it out if early recognition

42
Q

mole and melanoma ABCDE

A

asymmetry
border irregularity
colour variation
diameter (>6mm)
evolution/elevation - vertical growth

43
Q

multistage carcinogenesis of melanocytes - sequence

A

melanocyte gets mutated = increased proliferation to form a nevus
nevus gets mutated = dysplastic nevus
more mutation = RGP melanoma
more mutation = VGP melanoma (invasive)

44
Q

oncogenic viruses - method, examples, causes

A

they integrate their DNA into our genome
can reain latent there for year
HPV = cervical cancer
can live in us and not cause anything until we get some immunosuppression

45
Q

normal cervical epithelium

A

progenitor cells also sit on BM and divide into 1 cell that differentiates and migrates up

46
Q

Cervical cancer - dysplasia cause and features

A

virus gets in and down to the progenitor cells and into their nucleus to insert its genome.
high N:C ratio, increases with CIN levels
progression = cervical intraepithelial neoplasia (CIN), 1, 2, 3
all still within epithelial layer - hasn’t metastasis hence = in situ (can be in situ for many years or very fast)

47
Q

koilocytes

A

squamous epithelial cells with a different appearance from HPV infection
2-3x larger nucleus
hyperchromatic
halo around nucleus

48
Q

HPV - human papilloma virus, process

A

diff strands:
HPV-16, 18 most common
viral genes:
- E6 binds our p53 (no apoptosis)
- E7 interferes with p53 transcription + binds to RB (no limiting cell growth) + inactivates p21

49
Q

gardasil

A

vaccine targets HPV
not live virus
elicits B and T cell response : develops antibodies against HP 6, 11, 16, 18

50
Q

SIL

A

cytology version of CIN
= squamous intraepithelial lesion
low grade of high grade SIL

51
Q

colorectal cancer - risk factors

A

age
obesity
T2DM
smoking
alcohol
dietlack of PA
poyposis syndrome
Ulcerative colitis or Crohns disease
family hx

52
Q

colorectal cancer - signs and symptoms

A

intial:
- iron deficiency aneamia (Rsided)
- changes in bowel habit, bleeding, abnominal discomfort (L sided)

later
- abdomnial pain
- weight loss
- abdomnial mass

53
Q

growth patterns of cancer in hollow organ

A

exophytic, ulcerative and difusely infiltrative

54
Q

colorectal cancer - pathogenesis

A

adenoma-carcinoma sequence
start with a polyp (adenoma), accumulation of mutations = carcinoma
in hereditary cases, genetic changes are there at birth

55
Q

adenoma def

A

benign neoplasm

56
Q

polyp def

A

adenoma
can be sessile and serrated OR pedunculated (on a stork)

57
Q

colorectal cancer - aberrant crypt formation (ACF)

A

clusters of abnormal tube-like glands in colon and rectum lining
forms pre polyps - earlier changes of cancer that cna be seen
apoptosis resistant

58
Q

mismatch repair

A

can have a mutation of genes that usually repair mismatches and insertions or deletions.
when they are mutated, repair cant occur

59
Q

benign to malignant - APC beta pathway

A

mostly in L sided CRC

60
Q

benign to malignant - mismatch repair pathway

A

mostly in R sided CRC

61
Q

colorectal cancer metastasis

A

heamatogenously - portal vein to liver
lymphatic system
direct contact
called secondary metastatic colon cancer

62
Q

lung epithelia

A

changes:
bronchus - ciliated Pseudostratified columnar
bronchioles - cilliated simple cuboidal
alveolus - squamous

63
Q

lung cancer - risk factors

A

heavy smoking, recent stopped smoking
females
second hand smoke
industrial exposures
scarring from other disease
radiations

64
Q

lung cancer def + patterns of growth

A

invasive malignant neoplasm arriving from epithelia of lungs ( bronchi, bronchioles, alveoli)
exophytic, ulcerative and infiltrative

65
Q

bronchogenic carcinomas

A

make up most of 1˚lung cancers
adenocarcinoma and squamous cell carcinoma, large cell carcinoma (together = non small cell lung carcinoma)
small cell carcinoma

66
Q

adenocarcinoma

A

malignant epithelial tumour with glandular differentiation or mucin production
can be preceeded by precursor lesion: atypical adenomatous hyperplasia.

67
Q

atypical adenomatous hyperplasia

A

precursor for adenocarcinoma
proliferative lung lesion from alveolar epithelium associated with invasive adenocarcinoma

68
Q

squamous cell carcinoma

A

proceeded by changes in airways from smoking (cillia, mucous cells..)
starts at the epithelial cells lining the bronchi that has undergone squamous metaplasia from carcinogen. squamous metaplasia progresses to malignant epithelial tumour with keratinisation

69
Q

lung cancer sequence

A

normal -> (carcinogen) -> metaplasia -> dysplasia

70
Q

invasive squamous cell carcinoma (SCC) fts

A

forms keratin pearls + intercellular bridges between keratin layers
eosinophilic cytoplasm (very pink)
pleomorphic nuclei
hyper chromatic nuclei
tumour necrosis

71
Q

small cell carcinoma (oat cell) - fts, causes, effects

A

hyper-chromatic nuclei
pleomorphic nuclein
hgih N:C ratio
high mitotic rate
small undifferentiated cells
cell of origin = neuroendocrine progenitor cell of bronchial epithelium (not epithelial cell) = fast spread along bronhi
mutations: p53, RB
narrowing of airways

72
Q

molecular pathogenesis

A

common mutations in oncogenesis lung cancer: KRAS, c-MET, EGFR, c=KIT
common mutation in tumour suppressor genes: p53, RB1, p16

73
Q

lung cancer - clinical presentations

A

cough - w blood sometimes
SOB
post obstructive pneumonia
pain from pleural/chest wall invasion by tumours
weight loss
tracheal/oesophageal obstruction
Hoarseness

74
Q

secondary lung cancer

A

goes to :
liver, adrenals, bone, skin
will have lung tissue markers

75
Q

metastatic cancers to lungs

A

melanoma, prostate, carcinoma (kidney, breast, bowel), sarcoma

76
Q

malignant pleural mesothelioma (MPM)

A

exposure to asbestos where fibres cause an incurable cancer

77
Q

asbestos exposure - consequences, where from

A

contributes to lung cancer
asbestosis
mesothelioma
mining, construction, demolition, boiler makers
exposure and smoking increases risk of lung cancer more than individual risk factors together

Path (8 decks)

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