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Respiratory System > 8. Lung Cancer Pathology > Flashcards

8. Lung Cancer Pathology Flashcards

1
Q

What are the symptoms of lung cancer?

A 
• Most patients are asymptomatic
• Symptomatic
- cough
- haemoptysis
- recurrent infections
- chest wall pain
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2
Q

What can pathologists look at when determining lung cancer, in terms of cytology?

A 
(study of individual cells)
• sputum
• bronchial washings and brushings
• pleural fluid
• endoscopic fine needle aspiration
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3
Q

What can pathologists look at when determining lung cancer, in terms of histology?

A

(study of tissues)
• Biopsy at bronchoscopy - central tymours
• Percutaneous CT guided biopsy - peripheral tumours
• Mediastinoscopy and lymph node biopsy - staging
• Open biopsy at time of surgery
• Resection specimen

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4
Q

What are the characteristics of a benign lung tumour?

A
  • Don’t metastasise

* Local complications e.g. obstruction of airways

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5
Q

What are the characteristics of a malignant lung tumour?

A
  • Potential to metastasise
  • Invade adjacent tissues
  • Most common: epithelial tumours (carcinomas)
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6
Q

What are the 3 types of Non-Small Cell Carcinoma

A
  • Squamous Cell Carcinoma
  • Adenocarcinoma (most common lung cancer among non-smokers)
  • Large Cell Carcinoma
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7
Q

How is Small Cell Carcinoma different to Non-small Cell Carcinoma?

A

• Worst form of lung cancer
(• Worse prognosis than non-small cell)
• Unusual to find early stage - rapid and more aggressive

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8
Q

What are the trends in the incidence of Non-Small Cell Carcinoma?

A
  • Incidence of Squamous Cell Carcinoma is decreasing (association with smoking)
  • Incidence of adenocarcinoma is increasing (as incidence of smoking is decreasing, or less tar in cigarettes)
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9
Q

Where do squamous cell carcinomas and adenocarcinomas tend to arise?

A
  • Squamous - near the mediastinum, in airways (there has been an increase in peripheral)
  • Adenocarcinoma - periphery
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10
Q

What are the main causes of lung cancer?

A

• Smoking
- 75% of smokers and 25% of non smokers (passive smoking)
- Tumour initiators: polycyclic aromatic hydrocarbons
- Tumour promoters: N Nitrosamines, Nicotine, Phenols
- Complete carcinogens: Nickel, Arsenic
• Asbestos Exposure
• Radiation
• Rare metals

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11
Q

How do genes affect lung cancer?

A

• Familial lung cancers are very rare
• Susceptibility genes:
- Nicotine addiction
- Chemical modification of carcinogens (Cytochrome P450 enzymes and Glutathione S transferases)
• Susceptibility to chromosome breaks and DNA damage

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12
Q

How does a carcinoma generally develop?

A
  • Disordered growth
  • Loss of cell adhesion
  • Invasion of tissue
  • Stimulation of new vessel formation
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13
Q

How does a Squamous Cell Carcinoma develop?

A
  • Airway epithelium toughens after irritation by cigarette smoke (hyperplasia)
  • Repeated exposure - squamous metaplasia
  • No cilia => mucus stays => carcinogens accumulate
  • Squamous cells acquire mutations - dyplasia
  • More disordered => carcinoma in sity
  • Further mutations => invasive
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14
Q

Is Squamous Cell Carcinoma reversible?

A
  • Remove exposure to the irritant up to the metaplastic squamous cell stage
  • Can revert back to ciliated epithelial cells
  • Further along the pathway, mutations are irreversible
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15
Q

Describe the cytology of Squamous Cancer Cells

A
  • Large nuclei

* Keratin in the cytoplasm

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16
Q

Describe the histology of Squamous Cancer tissues

A
  • Keratinisation

* Intracellular ‘prickles’ represent desmosomes

17
Q

Describe the development of adenocarcinomas

A

• Forms from glandular epithelium
• Increasing in incidence because of deeper inhalation
• Precursor lesion - atypical adenomatous hyperplasia
- proliferation of atypical cells lining the alveolar walls
• Walls thicken
• Cells grow larger
• Cells form enzymes that break down the stroma (connective tissue)
• Inflammation
• Invasion

18
Q

Describe the cytology of an adenocarcinoma

A
  • Produces mucin
  • Big atypical nuclei
  • Rest of cytoplasm filled with mucin globule
19
Q

Describe the histology of adenocarcinoma

A
  • Multi-focal in the lungs
  • Tends to spread early
  • Glandular differentiation
20
Q

What are the molecular pathways in adenocarcinoma?

A

• Smoker - K ras mutation (DNA methylation + P53)
- can’t respond to targeted therapy
• Non-Smoker - EGFR mutation/amplification
- responder mutation: almost complete regression to targeted therapy
- resistance mutation

21
Q

Describe the histology of large cell carcinoma

A

• Poorly differentiated tumours
• No evidence of glandular, squamous or neuroendocrine differentiation
- apart from on electron microscopy
• Probably poorly differentiated adenocarcinoma or squamous cell carcinoma
• Poorer prognosis

22
Q

Describe the cytology of small cell carcinoma

A
  • Small cells
  • Nuclei with a small amount of cytoplasm
  • Look like lymphocytes
23
Q

Describe the histology of small cell carcinoma

A
  • Central near the bronchi
  • 80% of cases present with advanced disease
  • Lot of paraneoplastic syndromes (involves altered immune response)
  • Lots of mitoses
  • Often outgrows its blood supply and becomes necrotic
24
Q

What is the prognosis like for small cell carcinoma?

A
  • Chemosensitive due to high growth rate

* However, awful prognosis - can relapse after treatment

25
Q

Compare the survival rate of small cell carcinoma with non-small cell carcinoma

A

Small cell carcinoma
• General survival of 2-4 months untreated
• General survival of 10-20 months with current treatment
(• Chemoradiotherapy)

Non-small cell carcinoma
• Early Stage 1: 60% 5 year survival 
• Late Stage 4: 5% 5 year survival
• 20-30% have early stage tumours suitable for surgical resection
(• Less chemosensitive)
26
Q

Why is it important to subtype Non-small cell carcinoma in terms of treatment?

A
  • If treated with Bevacizumab and actually have squamous cell carcinoma - may develop fatal haemorrhage
  • Some chemo e.g. Pemetrexed, works better in adenocarcinoma instead due to specific characteristics e.g. EGFR, ALK, ros, ret mutations
27
Q

Give an example of a way you can predict the response to conventional chemotherapy

A

• Excision Repair Cross-Complimentation Group 1 Protein (ERCC1)
• This marker determines response to cisplatin
• Advanced stage non-small cell lung cancer:
- ERCC1 positive tumours have a poor response to cisplatin based chemotherpy
- ERCC1 protein removes drug-DNA adducts

28
Q

How can EGFR (Epidermal Growth Factor Receptor) be used as a target for treatment?

A
  • Membrane receptor Tyrosine Kinase
  • Regulates angiogenesis, proliferation, apoptosis and migration
  • Mutation/amplification of EGFR => adenocarcinoma (mainly non-smokers)
  • Target of a Tyrosine Kinase Inhibitor
29
Q

What is the ALK gene and what does a mutation in it lead to + treatment?

A
  • Gene with instructions for production of ALK receptor tyrosine kinase (regulating cell growth)
  • Mutation in the gene occurs in a small number of adenocarcinomas
  • Stain to look for mutations
  • Treated with anti-ALK mediation
30
Q

What is PDL-1?

A
  • Protein expressed by tumour cells
  • Hides the tumour from cytotoxic T-cells
  • Immunotherapy - medication can be used to block PDL-1 so the T-cell can recognise the tumour cells
31
Q

Which of the following tumour staging is the gold standard:
• clinical
• radiological
• pathological

A

Pathological

32
Q

What are the local effects of a bronchogenic carcinoma?

A

• Proximal tumour - squamous cell or small cell carcinoma
• Bronchial obstruction
- collapse of distal lung => shortness of breath
- impaired drainage of the bronchus => chest infection
• Invasion of local airways and vessels => haemoptysis
• Invasion around large vessels - Superior Vena Cava syndrome => venous congestion of the head and arm, oedema and ultimately circulatory collapse
• Dysphagia - difficulty swalling
• Horner’s syndrome - tumour on sympathetic nervous system => miosis (constricted pupil) and ptosis (weak, droopy eyelid)

33
Q

What are the effects when bronchogenic carcinoma extends through the pleura/pericardium?

A
  • Pleuritis or pericarditis with effusions => breathlessness
  • Cardiac compromise => effusion can affect cardiac function
  • Diffuse lymphatic spread within lung => shortness of breath, poor prognostic features
34
Q

What are the systemic effects of bronchogenic carcinoma?

A
  • Brain => fits
  • Skin => lumps
  • Liver => pain, deranged function tests
  • Bone => pain, fracture
  • Paraneoplastic Syndrome => abnormal expression of factors by tumour cells, not normally expressed by the tissue it came from
35
Q

Give examples of endocrine paraneoplastic syndromes

A
  • Anti-diuretic hormone (ADH) => SIADH (high ADH) - hyponatremia
  • Low adrenocorticotropic hormone (ACTH) => Cushing’s Syndrome (especially small cell carcinoma)
  • Parathyroid hormone-related peptides => hypercalcaemia (especially squamous cell carcinoma)
  • Calcitonin => Hypocalcaemia
  • Gonadotrophins => Gynaecomastia
  • Seratonin => Carcinoid Syndrome
36
Q

What do non-endocrine paraneoplastic syndromes affect?

A
  • Haematologic/coagulation defects
  • Skin
  • Muscular
  • Miscellaneous
37
Q

What is the cause of mesothelioma (a malignant pleural tumour) and how does it present?

A
  • Asbestos
  • Currently a peak in incidence
  • Fatal
  • Long lag time (develops decades after exposure)
  • More common in males
  • Shortness of breath, chest pain
  • Awful prognosis

Respiratory System (18 decks)

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