Bronchial carcinoma
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Bronchial carcinoma



this is according to the pathology dsl questions back when i was in my 2nd year of med school

this is according to the pathology dsl questions back when i was in my 2nd year of med school



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  • Angiogenesis factor=VEGF(vascular endothelial growth factor)
  • Sequence of events in cough. - There is an initial deep inspiration - Then the glottis and vocal cord closes - The diaphragm relaxes - The abdominal muscles and intercostal muscles contract - The pressure within the lungs builds up – up to 100mm of Hg - The glottis and vocal cords open resulting in a rapid release of air under pressure – speeds of upto 100 miles/hour - The sound produced is due to the turbulent flow - It helps to remove any irritant substances from the respiratory system
  • Other paraneoplastic syndrome: gynaecomastia: in adenocarcinoma Neuro: cerebellar syndrome/poly or dermatomyositis/Lambert-Eaton Myasthenic syndrome (LEMS):Ab directed to Calcium channel in presynaptic membrane  NMJ disorder Others: HPOA/clubbing

Bronchial carcinoma Bronchial carcinoma Presentation Transcript

    • 55 y/o man, a smoker of 30 pack years presented to GP d/t cough with haemoptysis, chest pain, dyspnoea, and a 6 kg LOW for the past 3 months.
    • O/E:
      • Clubbing of the finger
      • Consolidation of the Rt lower lobe
    • CXR showed a 3 cm mass lateral to Rt main bronchus.
    • After further invx, a biopsy of the mass was performed. It was subsequently diagnosed to be a carcinoma on histological evaluation.
    • State the risk factor for lung CA in this pt.
    • - smoking
    • What are the other risk factors for lung CA?
    • - industrial hazards: uranium / asbestos
    • - scarring: old infarcts/metallic FB/wounds/old healed granuloma
    • -genetic: oncogenes/tumour suppressor genes deletion (c-myc, k-ras, p53)
    • What are the precursor lesion for lung CA?
    • - goblet cell hyperplasia
    • - squamous dysplasia @ CA in situ
    • - atypical adenomatous hyperplasia
    • Explain the pathophysiology of each symptoms and signs that he presented with:
    • a) Cough
    • b) Haemoptysis
    • c) Chest pain
    • d) Dyspnoea
    • e) LOW 6 kg
    • f) finger clubbing
    • Cough:
    • - neoplasm infiltrate the AW wall  stimulate cough reflex
    • - respi infection
    • - hypersecretion of mucus
    • Haemoptysis:
    • - alveolar is highly vascular  when tumour erode blood vessels of the lung  leakage of blood into bronchial tree  blood being coughed up
    • - as tumour cell grow  it needs its own blood supply  secrete angiogenesis factor  sometimes the growth is too fast  lead to necrosis of the tumour’s center  rupture of necrotic area  bleeding
  • Cough reflex
    • Cough receptor: diffusely in respi tract / diaphragm / GIT
    • Afferent (sensory): internal laryngeal nerve (branch of CN X) to cough centre
    • Cough centre: in medulla
    • Efferent (motor): to abdominal ms, intercostal ms, diaphragm, glottis, vocal cords.
    • Mechanism:
    • Chest pain:
    • - tumour spread to the pleura  parietal pleura has somatic type of pain fibre  pleuritic pain
    • - DY/DX somatic, visceral, neuropathic pain?
    • Dyspnoea:
    • - bronchial obstruction  reduced air entry
    • LOW 6 kg:
    • - LOA
    • - tumour produce TNF  secreted into blood  hypothalamus  inhibit hunger centre
    • - increase amount of energy expenditure  BMR ↑ despite the intake of food ↓
    • Finger clubbing:
    • - ↑ growth hormone in dss state d/t ↑↑ in GF production  excessive cellular tissue in the nail bed
    • - ↑ blood flow in clubbed finger d/t vasodilatation (not hyperplasia of blood vessel in nail bed)  vasodilator eg: PG, bradykinin  vasodilatator probably inactivated in the lung of normal person but when there is dss process @ left-right shunt, defective inactivation occur
    • - clubbing occur when organs supplied by vagus nerve are affected  coz in bronchogenic CA, vagotomy causes reversal of clubbing.
    Reference: The aetiology of clubbing and hypertrophic osteoarthropathy. Dickinson CJ. Eur J Clin Invest.   1993 Jun;23(6):330-8
    • Reasons for consolidation:
    • - atelectasis
    • - secondary infection (dr effat: any obstruction that occur in liquid of the body  owez followed by infection)
    • Complications of bronchogenic CA:
    • - obstruction: partial  focal emphysema. Total  atelectasis.
    • - local invasion: pleura/pericardium/nerve/SVC/ chest wall/oesophagus/Pancoast’t tumour
    • - mets
  • Case continued..
    • Interpret the blood invx result. Explain each abnormality.
    • - Hyponatremia: release of ADH
    • - Hypercalcemia: release of PTH-related protein by tumour cell
    TEST RESULT Na 120 K 3.8 Ca 3.2
    • What is paraneoplastic syndrome?
    • - collection of symptoms/signs
    • - d/t damage to organs that are remote from the site of primary tumour or its mets
    • - mech: substances produce by tumour cells
    • What are the hormones/hormone-like factors elaborated in bronchial CA?
    • - small cell CA: ADH (SIADH) and ACTH (Cushing’s)
    • - squamous cell CA: PTH (hypercalcemia)
      • Poorly differentiated tumour cell
      • Increased mitotic xtvt
      • hyperchromatism
      • Increased N:C ratio
      • Pleomorphism (marked variation in shape & size )
    Squamous cell with keratin pearl Bronchoscopy was done and the sample taken.
  • Despite treatment, he died. Post-mortem was done.
    • Left lung
    • Tumour cell at the inferior part of lower lobe demonstrates area of central cavitation surrounded by fibrosis. (cavitation: probably because tumour outgrew its blood supply).
    • Compression of main bronchi
    • At the bottom most: consolidation.
    • Describe the basis of classification of lung CA:
    • - small cell CA
    • - non small cell CA: squamous / adenoCA / large cell
    • Features of small cell CA
    • 12. DY/DX squamous cell & adenoCA:
    • a) gender
    • b) smoking association
    • c) location
    • d) size
    • e) growth rate
    • f) microscopy
  • Quick guide to mx..