Repiratory Pathology Flashcards
Which gene does smoking damage?
p53 gene
Clinical features of lung cancer
What do to after this?
Haemoptysis (coughing up blood)
Persistent (>3 weeks) of cough, chest pain, finger clubbing
Chest Xray then CT scan, exercise+ pulmonary function tests
TNM classfication
T= tumour (size, infiltrating major organ) N= nodes (location) M= metastasis
Types of lung cancer
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
FDG-PET-CT
Radioactively labelled glucose injected
Cells that use glucose a lot (cancer) detected
Additional specimen collection required
Trans-thoracic CT biopsy
Advantages?
Disadvantages?
Real-time
High sensitivity
Quick
Easy
Risk of pneumothorax
No immediate intrabronchial treatment possible if bleeding occurs
Reason for MRI on brain instead of PET scan on body
PET scan looks at glucose metabolism but brain always shows high levels
Reason why lung cancer= difficult to have a high survival rate
Adenocarcinoma diagnosis done very late+ tumours can spread before you see them
Lung cancer causes
Smoking
In non-smokers:
Asbestos exposure
Radiation
Genetic predispostion
Development of Carcinoma
Leads to?
Features?
Multistep accumulation of mutations Disordered growth Loss of cell adhesion Invasion of tissue by tumour Metastasis
REVERSIBLE= stimulation of new vessel formation around tumours
Benign vs Malignant
Most common malignant?
Benign= don’t metastasise, local complications (e.g. airway obstruction)
Malignant most common= carcinomas (epithelium)
Types of malignant epithelial tumours
Treatment?
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
Non-small cell carcinoma types
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
Targets of treatment
Membrane receptor?
- EGFR gene
Tyrosine kinase- regulates angiogenesis, proliferation apoptosis, migration, continually switched on= unregulated growth
Tyrosine kinase inhibitors - Immunemodulatory Therapy
Tumour cells express PDL1: inhibits Cytotoxic T cells from targetting tumour cells so PDL1 inhibitor= used
Types of biopsy
Normal done through bronchoscopy
Surgical= tumour exposed+ biopsy done, if benign then excised+ patient closed up. If tumour= malignant, surgery proceeds