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Cancer > Lung cancer > Flashcards

Lung cancer Flashcards

1
Q

Risk factors lung cancers

A

Smpking - 10 fold
Asbestos - x 5
synergistic - together = 50 x risk
exposure to arsenic, Radon, Nicke, Chromate , Aromatic hydrocarbon, Cryptogenic fibrosing alveolitis
Radiotheraoy to breast or chest, exposure in workpleace, medical imaging tests ef CT, atomic bomb radiation
Air pollution
FH
HIV
beta carotene supplements

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2
Q

What is more common type of lung cancer

A

Non samll cell - 80%

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3
Q

What types of cancer is included in non small cell lung cancer

A

SCC - 25%
Adenocarcinoma - 40% - most common in smokers
Large cell carcinoma - 10%

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4
Q

What are small lung cell cancers

A

Neuro endocrine differntiation
Large AWs strong smoking ass

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5
Q

Primary lung cancer tumour symptoms

A

Cough - progresisive
Haemoptysis
Dysponiea
Chest pain - dull and persistent, shar if pleuritic involvement
Wheezing or stridor
Recurrent chest infections
Anorexia and weight loss

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6
Q

Symptoms of regional lung cancer spread

A

Hoarseness
Dysphagia
SVC obstruction
Pancoast tumour

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7
Q

What causes hoarseness in lung cancer

A

recurrent laryngeal nerve involvement.

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8
Q

Distance metastatsis related symptoms

A

Bone pain esp spine, pelvis, long bones
Neurological symptoms - brain mets
Abdo pain or jaundice - liver mets
Adrenal insufficiency - adrenal mets

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9
Q

Paraneoplastic symptoms

A

Hypercalcemia
Cushigns syndrome - ACTH production
SIADH -> hyponatremia
Lambert Eaton myasthenic syndrome - LEMS - neuromuscular disorder antibodies against voltage gated calcium channels in presynaptic
Clubbing

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10
Q

when refer for 2 week wait lung cacner

A

CXR suggestive
>40 unexplained haemoptysis

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11
Q

When offer an urgent CXR lung cancer

A

> 40 + 2 or more following or if ever smoked and 1 or more of -
Cough
Fatigue
SOB
Chest pain
Weight loss
Appetite loss

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12
Q

When do you consider an urgent CXR for lung cancer

A

Persistent or recurrent chest infection
Finger clubbing
supraclavicular lymphadenopathy or persistent cervical lymphadenopathy
Chest signs consistent with lung cnacer
Thrombocytosis

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13
Q

Investigation of choice for suspected lung cancer

A

CT chest

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14
Q

Investigations for lung cancer

A

CXR first line
CT chest
Bronchoscopy - biopsy, endo US
PET scan - non small lung cacner - curative or palleative

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15
Q

How does PET scan work

A

18-fluorodeoxygenase taken up preferentially by neoplastic tissue seen on scan

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16
Q

Epidemiology of sage of lung cancer at presentation

A

75% stage III/IV

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17
Q

First line treatment for stage I or II lung cancer

A

Surgical resection - lobectomy with hilar and mediastinal lymph node resection and sampling
Curative intent

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18
Q

First line for lung cancer stage I-III if unfit for surgery

A

Radiotherapy
Curative intent

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19
Q

What is offered for lung cancer stage III or IV

A

Chemotherapy - improve survival and QOL
3rd gem chemo eg docetael, paclitacel, gemcitabine
Platinum agent - carboplatin or cisplatin
Alos consider for chemoradiotherapy

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20
Q

Which lung cancer paitents are offered adjuvant chemotherapy

A

Complete resection

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21
Q

Which lung cancer paitents are offered adjuvant Radidotherapy

A

Incoplete resection of tumour

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22
Q

What is limited stage small cell lung cancer

A

SCLC without distant mets

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23
Q

First line for SCLC limited disease

A

4-6 cycles of cispltin based combination therapy
Radiotherapy adjunct or concurrent only considered if good response

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24
Q

What is extensive stage SCLC

A

Distant mets

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25
Q

First line treatment for extensive SCLC

A

Platinum based combo therapy - reassess for response after each cycle - up to a maximum of 6 cycles
Concurrent or adjunct radio if good response to chemo at primary and metastatic sites

26
Q

Relapsed lung cancer treat

A

6 cycles max of chemo
Palliatuive radiotherapy symptom control

27
Q

Complications of local spread of lung cancer

A

Nerve plasy
SVC
Pericarditis

28
Q

Metastatic spread of lung cancer

A

Brain, spina cord, bone, liver, adrenal glands

29
Q

Palliative therapy in lung cnacer

A

Radiotherpay - symptom control
Endobrachial stenting or debulking for bronchial obstruction
Pleural drainage or aspiration for pleural effusion
Dexamethasone therapy for symptomatic brain mets
Opioid therapy relieve cough and SOB

30
Q

Survival rate small cell LC

A

5 year surival of 30-40% very early stage - v rare
10-15% IIIA
5-10% IIIB
IV - 1-3%

31
Q

NSCLC surivval 5 years

A

IB - 45-55%
IIA - 40-50%
IIB - 30-40%
IIIA - 20-30%
IIIB - 10-15%
IV -<5%

32
Q

Factors affecting lung prognosis

A

Age - older = poorer
Overall health - cormorbidites
Tumour size and location - near vital strucutres etc
Molecular markers - EGFR mutations, ALK rerrangements - impact treatment options

33
Q

What is pancoasts syndrome

A

Chest wall pain
Horners syndrome
Pain in T1 dermatome - apical tumour invading chest wall

34
Q

Horners syndrome symptoms

A

Miosis
Anhydrosis
Partial ptosis and enophtalmos

35
Q

Gender epidemiology lung cancer

A

3:1

36
Q

How does lung cancer spread

A

Spread is circumferential and longitudinal along the bronchus of origin
Tumours frequently involve regional lymphatics
Spread is to ipsilateral peribronchial and hilar nodes, followed by mediastinal, contralateral hilar and supraclavicular nodes
There is a propensity to disseminate widely via the bloodstream and virtually any site may be involved

37
Q

Where are SCLCs more common

A

Central tumour
Larger AWs

38
Q

Mutations in SCLC

A

RB1 and TP53
Abnormal DNA methylation of cyclin D2 gene

39
Q

Types of lung cancer with higher metatastic spread vs less

A

Adrenocarcinoma - peripherally occuring from bronchial muscosal glands - high risk metatastic spread often to mediastinal lymph and pleura -> effusion
Large cell - can be paraneoplastic features - high risk mets poor differentiate
SCC spead locally, less likely mets

40
Q

Investigations for radical treatment in SCLC

A

pulmonary function tests
contrast CT scan of the thorax and upper abdomen
V/Q scan
MRI scan
ultrasound scan
mediastinoscopy, laryngoscopy, PET-CT
additional investigation if clinical, biochemical or radiological suspicion of metastatic disease.

41
Q

Investigations for lung cncare

A

Bronchoscopy
Fine needle aspirate from lympg node or CT guided transthoracic biopsy
Fluid cytology from pleural effusion
MRI OR PET/CT to determine operability

42
Q

Adverse prognostic factors lung cancer

A

Pulmonary symptoms
Large tumour size >3cm
Nonsquamous histology
Mets to multiple lymph nodes
Vascular invasion

43
Q

Low risk adverse prognostic factors

A

Poor performance status

Any site metastasis

Increased serum LDH

44
Q

Medium adverse prognostic factors

A

Bone metastasis

Liver metastasis

Male gender

> 5% weight loss

45
Q

High risk adverse prohnostic factors

A

Brain mets
>65 years
Non squamous tyoe
Prev RT

46
Q

Where does squamous cell carcinoma originate

A

Near a bronchus

47
Q

Mutations of subsets of adrenocarcinoma of lung

A

MAPK
EGFR
P13K

48
Q

Core biopsy vs FNA

A

Core biopsy provides more tissue to pathologise - larger and more resprecsenative smaple

49
Q

Best approach biopsy specimen lung cancer

A

Biopsy from R supraclavicular fossa mass

50
Q

Most likley cause of confusion in lung cancer

A

Calcium

51
Q

What can be offered as treatment if EGFR mutations present

A

EGFR tyrosine kinase inhibitors - gefitinib, erlotinib

52
Q

Curative radiotherapy for lung cacner

A

f continuous hyperfractionated accelerated radiotherapy (CHART), delivered in 3 fractions per day for 12 days

53
Q

Genetics in NSCLC

A

EGFR mutations strongly predict the improved response rate and progression-free survival of inhibitors of EGFR. Fusions of ALK with EML4 and other genes form translocation products that occur in ranges from 3% to 7% in unselected NSCLC and are responsive to pharmacological inhibition of ALK by agents such as crizotinib. The MET oncogene encodes hepatocyte growth factor receptor. Amplification of this gene has been associated with secondary resistance to EGFR tyrosine kinase inhibitors. Recurrent fusions involving the ROS1 gene are observed in up to 2% of NSCLCs and are responsive to treatment with crizotinib and entrectinib. NTRK gene fusions can occur in up to 1% of NSCLCs and can be treated with the TRK inhibitors, larotrectinib and entrectinib.”1

54
Q

Disease related complications in NSCLC

A

Local invasion
SVC obstruction
Pleural effusion
Distant metastasis
Brain, liver, bone
Non-metastatic
Hypercalcaemia
Cushing syndrome
SIAD
Neurological syndromes

55
Q

What is caused by SVC obstruction

A

Compression, invasion, thrombosis in superior mediastinum

56
Q

symptoms of SVC obstruction

A

Dyspnoea
Facial swelling
Head fullness
Cough
Arm swelling
Chest pain
Venous distention of neck or chest wall
Facial oedema
Cyanosis
Plethora of face
Oedema of arms

57
Q

Causes of SVC obstruction

A

Lung cancer
Lymphoma
Other malignancies - primary or secondary
nonneoplastic
Undiagnosed

58
Q

CXR findings on SVC obstruction

A

15% normal
Supreior mediastinal widening
Pleural effusion
R hilar mass
Bilateral diffuse infiltrates, cardiomegaly, calcified paratrahceal nodes, ant mediastinal mass

59
Q

Brain mets presentation

A

Headache (70-80%)
Cognitive dysfunction (40%)
Neurological deficit (40%)
Seizures (15-20%)

60
Q

How do steroids treat brain mets

A

Decrease peritumoral oedema
Minimal mineralcorticoid actiit
Can double surival
10 mg stat iv, followed by 16 mg per 24 hours

61
Q

Treatment for brain mets

A

Dexamethasone
Anticonvulsants eg phenyotin if seizures
Surgery - limited ecisend
Radiotherapy
Chemoterhapy - often doesnt cross BBB

Cancer (22 decks)

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