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CPRS > L74: Lung Carcinoma > Flashcards

L74: Lung Carcinoma Flashcards

1
Q

Lung cancer epidemiology in HK

A

Male:

  • 1st in incidence
  • 1st in mortality

Female:
- 3rd in incidence
- 1st in mortality
- high prevelance in Asian female:
—> Passive smoking: more sensitive to cigarette smoke
—> Genetics: susceptibility loci found in GWAS
—> Hormonal: higher estrogen receptor level —> induce cell proliferation
—> other factors

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2
Q

Causes of lung cancer

A
  1. Tobacco
    —> ROS —> Cancer
    —> DNA adducts —> Cancer
  2. Chronic inflammation —> ROS
  3. Occupation carcinogen: heavy metals (chromium) —> oxidative stress
  4. Environmental carcinogens: radon, benzopyrene
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3
Q

Genetic factors for lung cancer

A

SNP genes:

  1. P450 enzymes (carcinogen activation) —> fast activator
  2. Glutathione enzymes (detoxification) —> slow detoxifier
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4
Q

Chronic inflammation and lung cancer

A 
Chronic inflammation
—> inflammatory cells and macrophage
1. inflammatory mediator
—> damage lung epithelium, activate growth factor
—> induce cell proliferation for repair
—> persistent cell proliferation
—> mistakes in DNA replication
  1. ROS, free radicals
    —> damage lung epithelium and DNA
    —> mistakes in DNA replication

Overall: accumulation of enough DNA mutation: Malignancy

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5
Q

Carcinogenesis in lung CA

A
  1. Cumulative damage to DNA (genetic progression)
  2. Dysplasia (morphological progression)

Squamous Cell Carinoma model

  1. Normal
  2. Hyperplasia / Metaplasia (glandular —> squamous)
  3. Dysplasia (prominent nuclei, N/C ratio increase, hyperchromatic)
  4. Carcinoma-in-situ (whole thickness of epithelium abnormal)
  5. SCC (invade/metastasise)

Adenocarcinoma model (glandular cell cancer)

  1. Dysplasia
  2. Carcinoma-in-situ
  3. Adenocarcinoma
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6
Q

Classification of Primary Lung Carcinoma (4 histological type)

A

Non-SCLC

  1. Adenocarcinoma (smoker 20% + non-smokers 70%): 50%
  2. Squamous cell carcinoma (smokers): 30%
  3. Large cell carcinoma: 10%

SCLC
4. Small cell lung carcinoma (smokers): 10%

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7
Q

Adenocarcinoma

A
  • Peripheral part of lung: Type II pneumocyte
  • More common nowadays due to filter in cigarette: small particles —> distal lung

Gland-forming

  • Acinar predominant (gland)
  • Papillary predominant (finger-like)
  • Lepidic predominant
  • Solid AD

Mucinous:

  • cough with sputum
  • pneumonia-like (no response to antibiotic)
  • poor prognosis
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8
Q

Squamous cell carcinoma

A
  • Central part of lung: glandular epithelium —> squamous epithelium (metaplasia)
  • Keratin formation
  • Intercellular bridges (shrinkage of cytoplasm: prominent cell junction)
  • Smoking highly associated
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9
Q

Small cell carcinoma

A
  • Arise from neuroendocrine cells —> may produce hormone-like peptides
    1. small tumour cells (2-4x lymphocyte size)
    2. hyperchromatic nuclei
    3. indistinct nucleoli
    4. scanty cytoplasm
  • Smoking strongly associated
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10
Q

Large cell carcinoma

A

Large (4x lymphocyte), poorly differentiated tumour cell

  • not well understood
  • no features of SCC, AD or SCLC in microscopy (lack squamous/glandular differentiation)
  • high grade
  • aggressive
  • poor prognosis
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11
Q

Features of lung cancer spread

A
  1. Irregular edges
  2. Necrosis, haemorrhage (outgrowing blood capillaries —> dead tumour cells)
  3. Solid, obstructed lumen —> bronchiectasis
  4. Infiltrated lung/pleura
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12
Q

Methods of lung cancer spread

A
  1. Direct spread
    - brachial plexus —> pain in arm
    - esophagus —> dysphagia
    - pleura, pericardium —> effusion
    - chest wall —> mass
  2. Lymphatic spread
    - hilar (1st place)
    - mediastinal (carina, aorta, trachea)
    - supraclavicular (lower neck)
    - pleural lymphatics —> pleural effusion
  3. Haematogenous spread
    - liver, adrenals, bond, brain
    - SCLC, AD
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13
Q

TNM staging

A

Tumour (T0-T4):

  • size
  • extent

Node (N0-N3):

  • site (hilar, mediastinal, supraclavicular)
  • same side (ipsilateral, contralateral)

Metastasis (M0-M1)
- spread/no spread to distant organ

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14
Q

Clinical presentation of lung cancer

A
  1. Local:
    - cough
    - haemoptysis
    - obstruction, collapse
  2. Metastatic:
    - pleural effusion
    - brain tumour —> stroke
  3. Paraneoplastic syndrome
    - circulating tumour-derived factors (may present even earlier than tumour)
    - removal of tumour —> symptoms relief
    - General symptoms: fever, fatigue, weight loss (TNF-alpha, IL6)
    - Ectopic hormone: ACTH, ADH, PTH (common in SCLC)
    - Autoimmune effects: autoantibodies cross react with body tissue —> neuromuscular symptoms (sensory impairment, muscle pain)
  4. Often no pain due to lack of nerve endings within lung (only in pleural surface)
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15
Q

Diagnosis of lung cancer

A
  • Metastatic tumours in lung are much more common
  • always exclude metastatic tumour first

Secondary/Metastatic lung tumour:
Blood borne from all organs (esp. GI, breast, ovary)

Secondary/Metastatic pleural tumour:
Lymphatic/blood spread

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16
Q

Comparison of SCLC vs Non-SCLC

A

SCLC:

  • aggressive
  • early blood spread
  • poor prognosis (3 month survival)
  • Chemotherapy and radiotherapy: good response
  • Surgery not appropriate (due to blood spread)

Non-SCLC

  • less aggressive
  • local spread
  • outcome depends on stages
  • Early: Surgical resection
  • Late: Chemotherapy
17
Q

Target therapy of lung cancer

A
  1. Epidermal growth factor receptor (EGFR): AD associated
    - Gene mutation
    - mutated receptor —> ligand-independent firing —> autonomous cell proliferation, increased survival of tumour
    - Gefitinib: anti-EGFR targeted therapy
    - 50% survival 4 months longer in EGFR mutation type
    - worse prognosis when used in EGFR wild type
  2. ALK fusion gene (5%, esp in AD)
    - Chromosomal translocation
    - ligand-independent firing
    - respond to ALK-targeted therapy
18
Q

Flow diagram to prescribe treatment for lung cancer

A

Morphological diagnosis:
—> Early Non-SCLC: surgery

—> Late Non-SCLC: chemotherapy

—> SCLC (early/late): chemotherapy

—> AD —> EGFR, ALK status (molecular diagnosis) —> wild type: chemotherapy, mutant: targeted therapy

CPRS (75 decks)

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