Repiratory Pathology

Question 1

Which gene does smoking damage?

Answer 1

p53 gene

Question 2

Clinical features of lung cancer

What do to after this?

Answer 2

Haemoptysis (coughing up blood)
Persistent (>3 weeks) of cough, chest pain, finger clubbing
Chest Xray then CT scan, exercise+ pulmonary function tests

Question 3

TNM classfication

Answer 3

T= tumour (size, infiltrating major organ)
N= nodes (location)
M= metastasis

Question 4

Types of lung cancer

Answer 4

Small cell lung cancer: highly malignant form, with shorter doubling time and earlier metastases

Non small cell lung cancer: subdivided to adenocarcinomas, squamous cell cancer or large cell cancer

Question 5

FDG-PET-CT

Answer 5

Radioactively labelled glucose injected
Cells that use glucose a lot (cancer) detected
Additional specimen collection required

Question 6

Trans-thoracic CT biopsy
Advantages?
Disadvantages?

Answer 6

Real-time
High sensitivity
Quick
Easy

Risk of pneumothorax
No immediate intrabronchial treatment possible if bleeding occurs

Question 7

Reason for MRI on brain instead of PET scan on body

Answer 7

PET scan looks at glucose metabolism but brain always shows high levels

Question 8

Reason why lung cancer= difficult to have a high survival rate

Answer 8

Adenocarcinoma diagnosis done very late+ tumours can spread before you see them

Question 9

Lung cancer causes

Answer 9

Smoking

In non-smokers:
Asbestos exposure
Radiation
Genetic predispostion

Question 10

Development of Carcinoma
Leads to?
Features?

Answer 10

Multistep accumulation of mutations
Disordered growth
Loss of cell adhesion
Invasion of tissue by tumour
Metastasis

REVERSIBLE= stimulation of new vessel formation around tumours

Question 11

Benign vs Malignant

Most common malignant?

Answer 11

Benign= don’t metastasise, local complications (e.g. airway obstruction)
Malignant most common= carcinomas (epithelium)

Question 12

Types of malignant epithelial tumours

Treatment?

Answer 12

Small cell carcinoma
Undifferentiated, aggressive, central near bronchi, often outgrow blood supply
Chemoradiotherapy= fast response but fast relapse

Non-small cell carcinoma (subtypes)
Less chemosensitive because detected too late

Question 13

Non-small cell carcinoma types

Answer 13

Squamous cell carcinoma- cilitated epithelium= irritated by triggers= changes under metaplasia to squamous which is more resistant to smoke chemicals but no cilia= inhaled carcinogens sit in airway= dysplasia= potential to metastasise

Adenocarcinoma- tumour of glandular epithelium, develops around lung periphery.
Precursor stage= small lesions with atypical cells growing along alveolar wall, sometimes stop growing+ turn into fibrous scar, sometimes expand+ progress to cancer.
Smokers usually have K ras mutation, non-smoker= EGFr mutation, mutations= MUTUALLY EXCLUSIVE (won’t have both)

Large cell carcinoma- poorly differentiated tumours composed of large cells

Question 14

Targets of treatment

Membrane receptor?

Answer 14

1. EGFR gene
   Tyrosine kinase- regulates angiogenesis, proliferation apoptosis, migration, continually switched on= unregulated growth
   Tyrosine kinase inhibitors
2. Immunemodulatory Therapy
   Tumour cells express PDL1: inhibits Cytotoxic T cells from targetting tumour cells so PDL1 inhibitor= used

Question 15

Types of biopsy

Answer 15

Normal done through bronchoscopy

Surgical= tumour exposed+ biopsy done, if benign then excised+ patient closed up. If tumour= malignant, surgery proceeds

Question 16

Local effects of lung cancer

Answer 16

Bronchial obstruction
Collapse of distal lung= shortness of breath
Impaired drainage of bronchus= chest infection
Invasion of local vessels= haemoptysis
Invasion of large vessels= venous congestion= head+ arm oedema
Oesophagus= dysphagia (swallowing problems)
Chest wall= pain
Inflammation of pleura/ pericardium= breathlessness+ cardiac compromise