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Respiratory system > Lung cancer > Flashcards

Lung cancer Flashcards

1
Q

Risk factors

A

main smoking - many carcinogens, if smoke cells will be exposed
radon
asbestos

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2
Q

mutational compensation

A

all cells have a tendency to become immortal
p53 gene prevents this by apoptosis
smoking stops this - process is unchecked in smoker
have genetic tendency too - oncogenes too.

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3
Q

smoking and prevalence of lung cancer

A

the curves of prevalence of cancer and smoking are out of phase by 10 years but match up
there is a significant risk of cancer in passive smokers, dose dependant effect of the number of cigarettes smoked
there is a commulative risk of smoking - still risk increases if continue smoking at age 60 - always worth stopping

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4
Q

Symptoms

A 
haemoptysis - cough up blood 
symptoms that are unexplained that last >3 wks: 
cough 
shoulder/chest pain
dyspnoea 
hoarseness
finger clubbing - angle between nail and nail bed more obtuse, nail bed more boggy 
weight loss 
lethargy 
declining appetite
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5
Q

features seen on examination with lung cancer

A

clubbing of fingers
nicotine staining
cachexia - loss of appetite and weight
diminished air entry into R base

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6
Q

survival according to stage

A

related to suitability for surgery
considered in stage 1, 2 and 3a
need to detect early
5% overall risk and 10% major complications

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7
Q

prognosis

A

80% die in a year

5yr survical/cure rate <6%

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8
Q

where does lung cancer arise

A

large airway
terminal airway
alveoli

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9
Q

causes of lung cancer

A

smoking - 75% attributable - 25% attributed to passive smoking; tumour initiators, promoters and complete carninogens - polycyclic aromatic hydrocarbons, phenols, Nickle and arsenic
asbestos
radiation - radon exposure and therapeutics
genetic predisposition - rare
heavy metals - chromates, arsenic nickle
molecular abnormality
risks multiplicative

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10
Q

Development of carcinoma

A

multistep accumulation of mutations cause:
metastasis
disordered growth
loss of cell adhesion
invasion of tissue by tumour
stimulation of new vessel formation around tumours
mutations in epi cells and stem cells
pathways diff for diff tumour types - molecular therapies
early stages can be reversible
reflected in histology of tumours

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11
Q

benign lung tumours

A

don’t metastasise
local complications
chondroma - airway obstruction

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12
Q

malignant lung tumours

A 
potential to met
variable clinical behaviour 
commonest epithelial - carcinoma
non-epi - sarcoma and lymphoma 
non-small cell 80% 
small cell 20% `
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13
Q

non-small cell carcinoma

A

squamous - 20-40%
adenocarcinoma 20-40%
large cell carcinoma - uncommon

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14
Q

small cell carcinoma

A

advance
aggressive
small survival
poor prognosis

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15
Q

presentation with lung cancer

A 
asymptomatic 
symptoms vague: 
cough 
haemoptysis 
recurrent infection 
weight loss/malaise
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16
Q

local effects

A

bronchial obstruction - collapse of distal lung = shortness of breath or impaired drainage of bronchus - chest infection = pneumonia/abscess
invasion local structures - airways and vessels = haemoptysis and cough, large vessel = SVC syndrome - venous congestion of head arm oedema and upper circ collapse, oesophagus = dusphagia, chest wall = pain, nerves = horners syndrome
inflame/irritation/invasion of pleura/pericardium - pleuritus or pericarditis with effusion = breathlessness, cardiac compromise, fluid needs to be drained

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17
Q

systemic effects of bronchogenic carcinoma

A 
don't present with primary cancer 
fits - brain met 
lumps on skin - stained to show primary lung 
liver pain/deranged LFTs - liver met 
bone pain/fracture - bones 
paraneoplastic syndromes
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18
Q

change in classification of tumour

A

used to be small lung cancer/non-lung small cancer
now more sub groups
immunotype the tumour
see if squamous cell carcinoma
adenocarcinoma
adenosquamos carcinoma
molecular phenotype - have different phenotypes

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19
Q

molecular phenotype of cancers

A

look at molecular fingertype
PDL-1 - death ligand - if >50% then the patients are suitable for immunotherapy
adenocarcinoma - tumour of EGFR gene for tyrosine kinase, ALK gene, ROS -1, kRAS - can give targeted treatment if mutations in these are present (crizotinib for AlK gene mutation)

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20
Q

Treatment

A

small cell cancer - rapidly dividing - chemo
non-small cell lung cancer - slow - cut out and can use chemo/radio after surgery
non-metastatic manifestations of lung cancer - eg wrist pain from tumour or increased Ca causing swelling - chemo/immunotherapy

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21
Q

death from malignant change of different types of cancer

A

squamous - 9.6
adenocarcinoma - 17.6
undifferentiated - 9.4
small cell - 3.2

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22
Q

squamous cell carcinoma development

A

squamous epithelium
not normally in lung
cilia irritated by carcinogens - metaplasia to squamous
more resistant to smoke
cant remove debris
chronic cough
dysplasia - disordered growth and differentiation
carcinoma in situ
mutation produce enzymes and MMP so invade stroma
metastasise

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23
Q

molecular and genetic changes in development of squamous cell carcinoma

A 
3pLOH microsatellite alterations 
Myc overexpression and telomerase dysregulation 
neoangiogenesis 
gene methylation P16ink4 
K-ras mutation
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24
Q

location of squamous cell carcinoma

A

previously in central airway
now smoke breathed more deeply
in lower airways SqCC - peripheral

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25
Q

squamnous cell carcinoma

A

25-40% pul carcinoma
smoking
local spread
met late

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26
Q

adenocarcinoma development

A

glamndular epi
periphery - around terminal airways and interstitium
precurser is atypical adenomatous hyperplasia - prolif in atypical cells lining alveolar walls - <5mm in size
become invasive or become fibrous scar
from adenocarcinoma in situ to mixe2d pattern adenoCa - need invasive phenotype

27
Q

in situ

A

round
can remove
not in interstitium

28
Q

mutations in adenoCa

A

mutually exclusive
precursor type 2 pneumocyte/club cell
smoker - K ras mutation, DNA methylation, p53
non-smoker - EGFR mutation/amplification, ALK, ROS

29
Q

histology of adenocarcinoma

A

increasing incidence - 25-40% pul carcinomas
common in far east, females, non-smokers
peripheral
multicentriuc
extrathoracic met - common and early
glandular diff- capillaries produce mucin
multipke legions at different stages
large nuclei and mucin vacuoles in cytologyu

30
Q

large cell carcinoma

A

poorly diff tumour
large cell
no histological evidence of glandular/squamous differentiation
electron microscopy = glandular/squamous/neuroendocrine diff
poor prognosis

31
Q

histology of small cell carcinoma

A 
20-25% 
central - near bronchi 
smoking 
80% present with advanced disease 
chemosensitive 
abysmal prognosis - high and quick recurrence 
18months with treatment
2months without 
paraneoplastic syndromes
outgrow blood supply - necrotic
32
Q

treatment of small cell lung cancer

A

chemoradiotherapy

surgery rare - already met

33
Q

mon-small lung cancer prognosis and treatment

A 
early stage 1 - 60% 5yr survival 
late stage 4- 5% year survival
20-30% have early stage tumours for surgical resection 
less chemoreceptive
diagnosis - late in disease
34
Q

treatment of squamous cell carcinoma

A

fatal haemorrhage from anti-angiogenic therapy Bevacizumab

give chemotherapeutic agent

35
Q

treatment of adenoCa

A

some chemo works better in adenoCa- pemetrexed

molecular abnormalities provide targets only in adenoCa - ALK, ROS, EGFR, ret mutations

36
Q

evolution of targeted therapy

A

non-small lung cancer - 1 disease
histology based subtyping: squamous and adenoCa
subdivided by mutations
adenoCa - main use of molecular therapy

37
Q

EGFR

A 
membrane receptor tyrosine kinase 
regulates: 
angiogenesis
prolif
apoptosis 
cellular migration
38
Q

EGFR in NSCLC

A

always on from mutation = unregulated growth
non-smoker
female
asian
an inhibitor can act anywhere along the pathway
inhibitor = prolongued survival compared to chemo

39
Q

ALK +ve adenoCa

A 
gene rearrange 
protein test 
FISH show translocation 
male 
young 
non-smoker 
large response to treatment in 6months
40
Q

basis behind immunomodulatory therapy

A

tumour express new antigens
PD-L1 from tumour interact with PD1
evade the immune system
inhibit cytotoxic T cell attacking tumour

41
Q

immunomodulatory therapy

A

inhibit PDL1
dramatic response
immune system attack tumour

42
Q

role of histopathologist

A

confirm diagnosis
determine histopathological type
determine stage - pleural involvement, lymph node involvement
molecular pathology

43
Q

confirming the diagnosis

A

look at sputum
bronchial wash and blush
pleural fluid
endoscopic fine needle aspiration of tumour/nodes

44
Q

next steps if adenoCa

A

molecular testing

45
Q

next steps if adenoCa/squamoCa

A

PDL1 testing for immunotherapy

46
Q

Bronchoscopy

A

camera down the airways
lung cancer = a lot of mucous secretion so can see mucous artefacts
use forceps to take biopsy of tumour so can see what pathology is

47
Q

CT

A

when have cough for >4/6wks

screen people >55 who are heavy smoking - reduce their death by 25%

48
Q

when there is spread to lymph nodes

A

look at the nodes

give staging and diagnosis at the same time

49
Q

PET

A 
only imaging 
give radiolabelled glucose 
taken up by highly active cells 
shouldn't be in lung 
additional specimen collection is required to confirm diagnosis
50
Q

ultrasound

A

see gland in real time
needle in area - take sample
send sample to pathologist

51
Q

stain with Ab

A

gives molecular fingerprint

52
Q

Transthoracic CT biopsy

A 
use scanner 
needle into lung tissue 
real time - quick 
sensitivity 70-100% 
25-30% pneumothorax
small sample size
if bleed - no intrabronchial treatment possible
53
Q

diagnostic strategy

A 
non-specific symptoms 
chest xray - abnormal 
refer to respiratory 
pul func tests, CT scan of the thorax, exercise tests
diagnosis and staging 
PET-CT, PFTS, MRI brain (cant use PET because always active) 
lung function see how fit 
discussed in MDT
54
Q

biopsy

A

central tumour - bronchoscopy

peripheral -CT guided, through chest wall

55
Q

surgical biopsy

A

mediastinal lymph node biopsy - staging
open biopsy during op - frozen section
resection specimen - confirm excision and staging
background of lung - predisposistion of cancer eg asbestos
look at size, if invaded pleura, subtype
how far from resection margin - ensure all removed

56
Q

staging

A

TNM
tumour - size and where
node - lymph
metastasis
certain number for T but gets upstaged if touch chest wall, major vessels, heart, diaphragm
nodes - consider the contralateral lymph nodes - if nodes on the other side of the body, then the tumour has spread more
M - increased staging if spread to brain

57
Q

how does staging affect treatment

A

how does staging affect treatment

58
Q

staging - T

A 
tumour 
T1-4
size
invasion pleura 
invasion other structures
59
Q

staging - N

A

lymph node met
N0-3
N0 - not invaded
N1-3 node involved by tumour

60
Q

staging - M

A 
distant met 
M0 or 1 
in liver
bone 
brain
separate tumour nodule in different lobe of lung
61
Q

what does staging do

A

give info on prognosis and operability

can be clinical, radiological or pathological

62
Q

what is paraneoplastic syndrome

A

systemic effect of tumour

expression of hormones and other factors not normally expressed in tissue where tumour occurs

63
Q

example of paraneoplastic syndrome

A

syndrome of inappropriate ADH = hyponatraemia in small cell cancer
expression of PTH in liver - high Ca
hematologic/coagulation defects

Respiratory system (23 decks)

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