lung cancer Flashcards

1
Q

how common in lung cancer and who is it most common in?

A

1/3 most common cancer

most common in men after 75 yrs

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2
Q

where do the majority of lung cancers arise from?

A

95% are bronchial carcinomas

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3
Q

which tumours metastasise to the lung?

A

GIT
breast, prostate, kidney
bone
cervix and ovaries

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4
Q

how can we classify lung cancers?

A
small cell 
non small cell - majority
   - adenocarcinoma - most common
   - squamous cell carcinoma
   - large cell 
   - carcinoid tumour 
   - bronchioalveolar cell tumour
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5
Q

where do non-small cell lung cancers arise from?

A

non small cell mainly arise from smaller airways.

squamous cell have a central location

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6
Q

where do small cell lung cancers arise from?

A

arise from APUD cell (high amine precursor uptake, high decarboxylase)
arise from larger airways and tend to be central tumours

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7
Q

what are the risk factors for lung cancer?

A
smoking
lung disease - TB, COPD, pulmonary fibrosis 
FHx
toxins - radon, asbestos, arsenic
HIV 
age
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8
Q

what is the 2WW CXR referral guidelines?

A

urgent CXR 2ww referral for those >40 and 2 of the following symptoms or 1 symptom + smoker:

  • cough
  • SoB
  • chest pain
  • fatigue
  • loss of appetite
  • weight loss

urgent 2ww for >40 and one of symptoms:

  • persistent recurrent chest infections
  • finger clubbing
  • supraclavicular/ cervical lymphadenopathy
  • chest signs consistent with lung cancer
  • thrombocytosis
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9
Q

what is the 2ww for cancer MDT referral criteria?

A

CXR finding suggestive of cancer

>40yrs and unexplained haemoptysis

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10
Q

how do squamous cell lung cancers mainly present?

A

obstruction of bronchus leading to infection

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11
Q

how do squamous cell lung cancers mainly spread?

A

local spread is common but wide spread metastasis is rare

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12
Q

what is the most common bronchial tumour associated with asbestos and most common in non-smokers?

A

adenocarcinoma

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13
Q

do large cell lung cancer metastasise early or late?

A

less differentiated and metastasise early

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14
Q

describe the growth pattern of small cell lung cancer? what does this mean about the prognosis?

A

rapid growth and highly malignant
small primary tumour and lots of nodes involved.
almost always inoperable at time of presentation
respond well to chemo but poor prognosis

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15
Q

what investigations would you need in someone you suspect has lung cancer?

A
bloods - FBC, LFTs (mets and baseline before drugs) , bone profile, UEs, CRP (rule out infection),  serum calcium, INR, tumour markers. 
CXR
CT - chest abdomen pelvis 
F-deoxyglucose PET scan 
CT head/ MRI brain 
radionucleotide bone scan
USS of liver 
biopsy 
sputum culture and cytology 
thoracentesis
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16
Q

what are the tumour markers?

A
CEA 
CA19-9
PSA
AFP
CA125 
B-hCG
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17
Q

what might be seen on CXR in lung cancer?

A
peripheral circular opacity / consolidation 
hilar enlargement / lymphadenopathy
pleural effusion 
collapse 
bony metastasis
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18
Q

what is the role of a PET scan?

A

F deoxyglucose is given and taken up by active tumour cells.

the scan will detect the emission from this positron emitting radionucleotide to show up active lesions

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19
Q

what are the different methods of biopsying in lung cancer?

A
bronchoscopy 
Neck USS guided FNA of nodes 
CT guided tumour biopsy 
surgical biopsy if other methods fail
thoracentesis and cytology of pleural fluid
20
Q

what is a biopsy needed for?

A

gold standard diagnosis to confirm it is a tumour
test for mutations e.g. EGFR, PD1, ALK , KRAS
helps predict prognosis and aid treatment.

21
Q

what is the WHO performance status scoring?

A

0 - normal no restrictions
1 - restricted in strenuous physical exercise
2 - incapable of carrying out work
3 - 50% bed/chair bound of waking hours, limited self care
4 - always in bed/ chair , completely disabled
5 - dead

number one predictor of prognosis in any cancer

22
Q

how do lung cancer patients present?

A

specific to the lung cancer:

  • cough (most common presentation, but not specific so often missed)
  • dyspnoea, chest pain, haemoptysis
  • slow resolving pneumonia

from obstruction:

  • Pancoast syndrome
  • dysphagia, stridor, wheeze

local spread:
- rib erosions, pericarditis, AF

systemic upset:
- fever, malaise, weight loss, weakness, lethargy, signs of dehydration and finger clubbing

paraneoplastic syndromes
metastatic presentation

23
Q

what is Pancoast syndrome?

A

apical tumours can cause obstructive problems and present as the following:

  • Horners syndrome (miosis, partial ptosis, and anhidrosis and enopthalmos) due to compression of sympathetic nerves
  • Brachial plexus compression - arm and should pain, weakness in hand muscles, paraesthesia in T1/C8 and wasting of hand muscles
  • compression of vessels - arm oedema
  • SVC obstruction
  • recurrent laryngeal nerve palsy - hoarseness of voice
  • phrenic nerve involvement
  • ipsilateral reflex sympathetic dystrophy of arm (CRPS) - with enhanced sensitivity and skin changes
24
Q

what type of lung cancer are majority of Pancoast tumours?

A

adenocarcinoma - 1/2

squamous cell carcinoma - 1/2

25
Q

what paraneoplastic syndromes are seen in lung cancer?

A
anaemia - pale conjunctiva, pallor
DIC, thrombocytosis 
small cell:
    - ADH - SiADH - hyponatraemia 
    - ACTH - cushings syndrome, bilateral adrenal hyperplasia and hyperkalaemic acidosis 
    - acanthosis nigricans 
    - dermatomyositis 
    - lambert eaton syndrome  

squamous cell carcinoma:

- PTH - high Ca 
- hyperthyroid 
- hypertrophic pulmonary osteoarthropathy (HPOA)

adenocarcinoma - gynaecomastia
others: hypoglycaemia, mononeuritis multiplex, encephalomyelitis, MND, nephrotic syndrome, glomerulonephritis, polymyopathy, subacute sensory neuropathy.

subcut: erythema multiforme, thrombophlebitis migrans, pruritic and urticaria

26
Q

how can lambert eaten syndrome and dermatomyositis present?

A

can present after lung cancer or can actually precede the cancer. thus anyone presenting with these syndromes should be screened regularly.

lambert eaton (auto Ab to VG Ca channels) - myasthenia like syndrome
dermatomyositis - muscle weakness and skin changes
27
Q

how does metastatic lung cancer present?

A

supraclavicular/ cervical/ axillary lymphadenopathy
bone - pain, pathological fractures, hypercalcaemia
spinal mets - peripheral neuropathy
liver - hepatomegaly, ascites
adrenals - Addison’s
brain - headaches, N&V, focal neurology, visual changes, personality changes, cerebellar syndrome, seizures

28
Q

describe the TNM staging for non-small cell lung cancer.

A

Tx - positive cytology but no lesion seen
T0 - no evidence of primary tumour

T1 - diameter = 3cm, surrounded by lung/ pleura. T1a <2cm, T1b 2-3cm

T2 - 3-7cm diameter, involves main bronchus, >2 cm from carina, associated with atelectasis/ obstructive pneumonitis that extends to hilar but doesn’t involve whole lung. T2a 3-5cm, T2b 5-7cm

T3 - >7cm diameter, directly invades chest wall, diaphragm, phrenic nerve, mediastinal pleura or parietal pericardium. <2cm from carina but no involvement. associated with atelectasis/ pneumonitis that involves entire lung

T4 - invasion of mediastinal organs (oesophagus, bronchus, great vessels, heart, vertebral body). malignant pleural effusion. separate ipsilateral nodes, recurrent laryngeal nerve involvement.

N0 - no nodes
N1 - ipsilateral bronchopulmonary or hilar nodes
N2 - ipsilateral mediastinal/ subcarinal nodes
N3 - contralateral mediastinal , hilar or supraclavicular nodes

M0 - no mets
M1 - distant med, includes nodules in different lobes (M1a)

29
Q

describe the clinical staging for lung cancer (non small cell)

A
IA - T1
IB - T2
IIA - T1N1
IIb - T2N1 or T3
IIIA - T1-3, N2 or T3 N1
IIIB  - any T4 or any N3
IV - M1
30
Q

based on staging, which cancers are curative and which are not for non-small cell lung cancer?

A

stage 1 to 3 are curative

stage 3b and 4 are inoperable and chemo used to improve symptoms and control disease

31
Q

what is the management for non small cell lung cancer?

A

encourage to stop smoking - improves outcome and post surgical complication

surgery:
- lobar resection. during resection also sample the hilar/ mediastinal nodes

radiotherapy: (CHART)
- offered to all patients 1- 3 which are not suitable for surgery and radical radiotherapy if WHO performance score is good.
- can also be used in palliative care

chemotherapy:
- offered to all patients with III or IV with good performance status. e.g. cisplatin or docetaxel
- adjuvant chemo for those who have had complete resection and good performance status and good post op recovery.

32
Q

what can be done Pre op for lung cancer surgery?

A

assessment and throacoscore to calculate the risk of death
lung function tests
CVS risk assessed

33
Q

what are the contraindications to lobectomy?

A

FEV1 <1.5
stage III or IV
SVCO
vocal cord paralysis

34
Q

what investigations do you need before lung radiotherapy?

A

Pulmonary function tests, must be adequate to continue.

35
Q

what is CHART?

A

continuous hyperfractionated accelerated radiotherapy
can be used for radical or palliative care

3 fractions / day for 12 days

36
Q

which type of non-small cell lung cancer is highly responsive to chemo?

A

squamous cell

37
Q

how is stage 3b/ 4 non small cell lung cancer treated?

A

chemoradiotherapy
radical RT
palliative chemo
palliative RT

immunotherapy, targeted therapies

38
Q

what determines what treatment for lung cancer is used?

A
type and stage
expression of markers
lung function
comorbidities
WHO performance
patients wishes
39
Q

describe specific mutations seen in non small cell lung cancer and how they are treated?

A

EGFR tyrosine kinase mutations - targeted therapies against tyrosine kinase (tyrosine kinase inhibitors) - these are very specific to certain tyrosine kinase molecules

PDL1 mutations - pembrolizumab - monoclonal Ab against PDL1 to allow immune system to recognise tumour cells and kill them (PDL1 is expressed to appear as self to T cells which have PDL1 receptor). this is known as immunotherapy as it enhances immunity

40
Q

how does the mutational status differ between non-smokers and smokers?

A

non smokers get very specific single mutations which drive the tumour to grow e.g. EMRF-ALK translocation

smokers - have multiple mutations (tumour mutational burden) that together drive the tumour to grow. PDL1 mutations are most commonly associated with smokers.

41
Q

how are small cell lung cancers staged?

A

limited stage disease:

  • confined to one hemithorax
  • involves ipsilateral hilar nodes
  • involves ipsilateral/ contralateral supraclavicular/ mediastinal nodes

extensive disease:

  • metastatic lesions in contralateral lung
  • distant metastasis
42
Q

how are small cell lung cancers managed?

A

stop smoking
if less than or equal to 5cm can consider surgical removal (if good performance status and no lymph node involvement). then give adjuvant chemo.

otherwise chemoradiotherapy
consider prophylactic cranial RT

relapse - best supportive care/ chemo/ immunotherapy

43
Q

how do small cell lung cancers respond to chemo?

A

very well

but relapse rates are high

44
Q

what is the prognosis for small cell lung cancer?

A

limited - 18-30 months

extensive - 7-12 months

45
Q

discuss different methods for supportive/ palliative care for lung cancer..

A

breathlessness - opioids, fan on face, breathing techniques

bronchial obstruction - external beam radiotherapy, debulking bronchoscopic proceedures, stents

pleural effusion - pleural aspiration, drainage, pleurodesis

cough / pain - codeine/ morphine, radiotherapy

SVCO - chemo/radiotherapy, stent

bone pain - analgesia
cerebral mets - steroids, radiotherapy
spinal cord compression - steroids and emergency radiotherapy/ surgery

46
Q

how is lung cancer prevented?

A

discourage smoking
smoking caessation services
prevent occupational exposure to carcinogens.