Lung cancer Flashcards

1
Q

Learning outcomes

A
  • Classify lung tumours as benign/malignant; primary/secondary
  • Explain how primary lung carcinomas are classified and outline their histogenesis
  • List complications of lung tumours resulting from invasion of local structures, integrating with current anatomy teaching
  • List common anatomical sites that lung cancers metastasise to and outline the TNM staging system
  • Explain what is meant by paraneoplastic syndrome. Give examples of paraneoplastic syndromes specific to lung cancer
  • Define malignant mesothelioma and recognise the significance of its association with asbestos exposure
  • Explain why a molecular pathology classification of lung cancer may yet replace existing histopathological classification systems
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2
Q

Classification of lung tumours

A

Primary (benign) lung tumours:
•pulmonary hamartoma/chondroma

Primary ( malignant ) lung tumours:
•(pulmonary carcinoid) ( indolent low grade malignant)
•Bronchogenic carcinoma
•Malignant mesothelioma
•Malignant Lymphoma
•Certain types of soft tissue (mesenchymal) sarcoma

Metastases to lungs
•As common or indeed more common than primary malignant lung tumours
•Multiple bilateral tumours
•Haematogenous spread can give large impressive cannonball tumours from sarcomas, melanomas, malignant testicular germ cell tumours and carcinomas like renal cell carcinoma
•Lymphatic spread can result in a more diffuse pattern of involvement: Lymphangitis carcinomatosaegspread from breast carcinoma
•Malignantpleural effusions
METASTASES

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3
Q

Metastases- pathway of spread

A
  • Direct seeding of body cavities or surfaces (Transcoelomic)
  • Lymphaticspread
  • Haematogenousspread – i.e. by blood vessels
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4
Q

Pulmonary chondroma/hamartoma

A
Chondroma•Benign tumour of cartilage
•May be ossified
•Females > males
•Peripheral > central
•May be associated with Carney’s triad and multiple•Example of benign tumour
Hamartoma•Disordered proliferation of mature cartilage, fat, smooth muscle with entrapped respiratory epithelial lined clefts
•Males > Females
•Central > peripheral
•Solitary
•Example of hamartoma
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5
Q

Classification of primary lung carcinoma

A

Classified on the basis of histology (currently!)•Squamous Carcinoma (20–30 %)
•Adenocarcinoma (30–40 %)
•Large cell (undifferentiated carcinoma) (10–15%)

Sometimes the above 3 are classified together as “Non-small cell carcinoma”
•Small cell carcinoma (15–20%)

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6
Q

Pathogenesis

A
  • Cigarette smoking and other causes of repeated injury to bronchial epithelium (e.g. bronchiectasis) are associated with metaplasia: a permanent change from a respiratory ciliated bronchial epithelial lining to an abnormal squamous epithelium
  • Dysplastic change may supervene with progression to carcinoma in situ and eventually invasive squamous carcinoma, often centrally situated, close to hilum of the lung
  • Adenocarcinomas often develop more peripherally, associated with areas of fibrous scarring and the precursor lesion is thought to be atypical adenomatous hyperplasia
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7
Q

Local effects

A
  • Mass Effect
  • Ulceration
  • Invasion of local anatomical structures

•Collapse of Lung distal to tumour: atelectasis, infection
•Ulceration of pulmonary artery or veins/branches: haemoptysis
•Superior vena cava: fixed elevated JVP
•Recurrent laryngeal nerve: hoarseness
•Phrenic nerve: elevation of hemidiaphragm
•Pericardium: malignant pericardial effusion; atrial fibrillation and other arrythmias
•Pleura: Malignant pleural effusion
•Invasion of carina, oesophagus and vertebra
Lecture 58 for diagrams- underwood’s pathology a clinical approach

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8
Q

Pancoast tumour

A
  • The growing tumour can cause compression of the superior vena cava resulting in a fixed raised jugular venous pressure
  • Compression/infiltration of the sympathetic/stellate ganglion can result in Horner’s syndrome: miosis, ptosis and anhidrosis
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9
Q

Lung cancer staging

A

•TNM System adopted for most malignant tumours
•Staging is informed by clinical examination and radiological investigations: clinical Stage
•Staging is also informed by pathological examination of specimens: p prefix used
Metastatic Lung Carcinoma :Sometimes described as Stage IV disease
Not curable by conventional treatments

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10
Q

Paraneoplastic syndrome

A

•Syndromes not explained by local effect or metastases or by production of hormones indigenous to the tissue from which the tumour arose
•Occur in about 10% of patients with malignancy
•Arise from tumour secretion of hormones, peptides, or cytokines or from immune cross-reactivity between malignant and normal tissues
Most commonly associated malignancies include•Small cell lung cancer •Breast cancer •Gynaecological tumours•Haematological malignancies
Recognition of these syndromes may permit diagnosis of cancer in patients with confusing mixture of symptoms and signs

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11
Q

Examples of paraneoplastic syndromes

A
Neurologic Paraneoplastic syndromes
•Eaton-Lambert syndrome
Endocrine Paraneoplastic syndromes
•Cushing's syndrome
Musculoskeletal
•Hypertrophic osteoarthropathy
Other Paraneoplastic Syndrome
•Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH),
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12
Q

Eaton- Lambert syndrome

A
  • An immune-mediated, myasthenia-like syndrome –weakness usually affecting the limbs and sparing ocular and bulbar muscles
  • The syndrome can precede, occur with, or develop after the diagnosis of cancer
  • It occurs most commonly in menwith intrathoracictumours (70% have small cell lung carcinoma)
  • Symptoms and signs includefatigability, weakness, pain in proximal limb muscles, peripheral paraesthesias, dry mouth, erectile dysfunction and ptosis (droopy eyelid)
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13
Q

SIADH

A
  • The Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH),
  • Hypo-osmotic, euvolemic hyponatremia (Decreased sodium levels),
  • Affects 1–2% of all patients with cancer
  • Small cell lung cancer – approximately 10% to 45% of all patients with small cell lung cancer develop SIADH
  • Arises from tumour cell production of antidiuretic hormone (ADH) and atrial natriuretic peptide
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14
Q

Cushing’s syndrome

A
  • Approximately 5–10% of cases of Cushing syndrome are paraneoplastic
  • Approximately 50–60% of these paraneoplastic cases are lung tumours (Small cell lung cancer and bronchial carcinoids)
  • Patients often present with symptoms of paraneoplastic Cushing syndrome beforea cancer diagnosis is made
  • Approximately 5–10% of cases of Cushing syndrome are paraneoplastic
  • Approximately 50–60% of these paraneoplastic cases are lung tumours (Small cell lung cancer and bronchial carcin
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15
Q

Hypertrophic osteoarthropathy

A

•Prominent with certain lung cancers
•Manifests as
1.Painful swelling of the joints (knees, ankles, wrists, elbows, metacarpophalangeal joints)
2.Finger-clubbing

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16
Q

Malignant mesothelioma

A
  • Malignant tumour arising from mesothelial lining cells of pleura
  • Strongly associated with exposure to asbestos; may see calcified pleural plaques on Cxror CT
  • Most commonly shipyard workers, electricians , plumbers
  • Notifiable to coroner: Coroners autopsy required in all cases to confirm cause of death/diagnosis
  • Civil litigation very common
17
Q

Lung cancer- oncological causes

A
  1. Mutation- EGFR, BRAF, HER2
  2. Fusions- ALK, ROS1, RET, NTRK1, NRG1 > Targeted therapy with specific inhibitors
  3. Exon skipping- MET >amplification, over expression
  4. Drivers not found yet, high mutation load, PD-L1 high expression > immunotherapy