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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
squamnous cell carcinoma
25-40% pul carcinoma smoking local spread met late
26
adenocarcinoma development
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
in situ
round can remove not in interstitium
28
mutations in adenoCa
mutually exclusive precursor type 2 pneumocyte/club cell smoker - K ras mutation, DNA methylation, p53 non-smoker - EGFR mutation/amplification, ALK, ROS
29
histology of adenocarcinoma
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
large cell carcinoma
poorly diff tumour large cell no histological evidence of glandular/squamous differentiation electron microscopy = glandular/squamous/neuroendocrine diff poor prognosis
31
histology of small cell carcinoma
``` 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
treatment of small cell lung cancer
chemoradiotherapy | surgery rare - already met
33
mon-small lung cancer prognosis and treatment
``` 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
treatment of squamous cell carcinoma
fatal haemorrhage from anti-angiogenic therapy Bevacizumab | give chemotherapeutic agent
35
treatment of adenoCa
some chemo works better in adenoCa- pemetrexed | molecular abnormalities provide targets only in adenoCa - ALK, ROS, EGFR, ret mutations
36
evolution of targeted therapy
non-small lung cancer - 1 disease histology based subtyping: squamous and adenoCa subdivided by mutations adenoCa - main use of molecular therapy
37
EGFR
``` membrane receptor tyrosine kinase regulates: angiogenesis prolif apoptosis cellular migration ```
38
EGFR in NSCLC
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
ALK +ve adenoCa
``` gene rearrange protein test FISH show translocation male young non-smoker large response to treatment in 6months ```
40
basis behind immunomodulatory therapy
tumour express new antigens PD-L1 from tumour interact with PD1 evade the immune system inhibit cytotoxic T cell attacking tumour
41
immunomodulatory therapy
inhibit PDL1 dramatic response immune system attack tumour
42
role of histopathologist
confirm diagnosis determine histopathological type determine stage - pleural involvement, lymph node involvement molecular pathology
43
confirming the diagnosis
look at sputum bronchial wash and blush pleural fluid endoscopic fine needle aspiration of tumour/nodes
44
next steps if adenoCa
molecular testing
45
next steps if adenoCa/squamoCa
PDL1 testing for immunotherapy
46
Bronchoscopy
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
CT
when have cough for >4/6wks | screen people >55 who are heavy smoking - reduce their death by 25%
48
when there is spread to lymph nodes
look at the nodes | give staging and diagnosis at the same time
49
PET
``` 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
ultrasound
see gland in real time needle in area - take sample send sample to pathologist
51
stain with Ab
gives molecular fingerprint
52
Transthoracic CT biopsy
``` 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
diagnostic strategy
``` 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
biopsy
central tumour - bronchoscopy | peripheral -CT guided, through chest wall
55
surgical biopsy
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
staging
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
how does staging affect treatment
how does staging affect treatment
58
staging - T
``` tumour T1-4 size invasion pleura invasion other structures ```
59
staging - N
lymph node met N0-3 N0 - not invaded N1-3 node involved by tumour
60
staging - M
``` distant met M0 or 1 in liver bone brain separate tumour nodule in different lobe of lung ```
61
what does staging do
give info on prognosis and operability | can be clinical, radiological or pathological
62
what is paraneoplastic syndrome
systemic effect of tumour | expression of hormones and other factors not normally expressed in tissue where tumour occurs
63
example of paraneoplastic syndrome
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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