Bronchial carcinoma

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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

    1. 1. BRONCHIAL CA
    2. 2. SCENARIO <ul><li>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. </li></ul><ul><li>O/E: </li></ul><ul><ul><li>Clubbing of the finger </li></ul></ul><ul><ul><li>Consolidation of the Rt lower lobe </li></ul></ul><ul><li>CXR showed a 3 cm mass lateral to Rt main bronchus. </li></ul><ul><li>After further invx, a biopsy of the mass was performed. It was subsequently diagnosed to be a carcinoma on histological evaluation. </li></ul>
    3. 3. <ul><li>State the risk factor for lung CA in this pt. </li></ul><ul><li>- smoking </li></ul><ul><li>What are the other risk factors for lung CA? </li></ul><ul><li>- industrial hazards: uranium / asbestos </li></ul><ul><li>- scarring: old infarcts/metallic FB/wounds/old healed granuloma </li></ul><ul><li>-genetic: oncogenes/tumour suppressor genes deletion (c-myc, k-ras, p53) </li></ul><ul><li>What are the precursor lesion for lung CA? </li></ul><ul><li>- goblet cell hyperplasia </li></ul><ul><li>- squamous dysplasia @ CA in situ </li></ul><ul><li>- atypical adenomatous hyperplasia </li></ul>
    4. 4. <ul><li>Explain the pathophysiology of each symptoms and signs that he presented with: </li></ul><ul><li>a) Cough </li></ul><ul><li>b) Haemoptysis </li></ul><ul><li>c) Chest pain </li></ul><ul><li>d) Dyspnoea </li></ul><ul><li>e) LOW 6 kg </li></ul><ul><li>f) finger clubbing </li></ul>
    5. 5. <ul><li>Cough: </li></ul><ul><li>- neoplasm infiltrate the AW wall  stimulate cough reflex </li></ul><ul><li>- respi infection </li></ul><ul><li>- hypersecretion of mucus </li></ul><ul><li>Haemoptysis: </li></ul><ul><li>- alveolar is highly vascular  when tumour erode blood vessels of the lung  leakage of blood into bronchial tree  blood being coughed up </li></ul><ul><li>- 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 </li></ul>
    6. 6. Cough reflex <ul><li>Cough receptor: diffusely in respi tract / diaphragm / GIT </li></ul><ul><li>Afferent (sensory): internal laryngeal nerve (branch of CN X) to cough centre </li></ul><ul><li>Cough centre: in medulla </li></ul><ul><li>Efferent (motor): to abdominal ms, intercostal ms, diaphragm, glottis, vocal cords. </li></ul><ul><li>Mechanism: </li></ul>
    7. 7. <ul><li>Chest pain: </li></ul><ul><li>- tumour spread to the pleura  parietal pleura has somatic type of pain fibre  pleuritic pain </li></ul><ul><li>- DY/DX somatic, visceral, neuropathic pain? </li></ul><ul><li>Dyspnoea: </li></ul><ul><li>- bronchial obstruction  reduced air entry </li></ul><ul><li>LOW 6 kg: </li></ul><ul><li>- LOA </li></ul><ul><li>- tumour produce TNF  secreted into blood  hypothalamus  inhibit hunger centre </li></ul><ul><li>- increase amount of energy expenditure  BMR ↑ despite the intake of food ↓ </li></ul>
    8. 9. <ul><li>Finger clubbing: </li></ul><ul><li>- ↑ growth hormone in dss state d/t ↑↑ in GF production  excessive cellular tissue in the nail bed </li></ul><ul><li>- ↑ 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 </li></ul><ul><li>- clubbing occur when organs supplied by vagus nerve are affected  coz in bronchogenic CA, vagotomy causes reversal of clubbing. </li></ul>Reference: The aetiology of clubbing and hypertrophic osteoarthropathy. Dickinson CJ. Eur J Clin Invest.   1993 Jun;23(6):330-8
    9. 10. <ul><li>Reasons for consolidation: </li></ul><ul><li>- atelectasis </li></ul><ul><li>- secondary infection (dr effat: any obstruction that occur in liquid of the body  owez followed by infection) </li></ul><ul><li>Complications of bronchogenic CA: </li></ul><ul><li>- obstruction: partial  focal emphysema. Total  atelectasis. </li></ul><ul><li>- local invasion: pleura/pericardium/nerve/SVC/ chest wall/oesophagus/Pancoast’t tumour </li></ul><ul><li>- mets </li></ul>
    10. 11. Case continued.. <ul><li>Interpret the blood invx result. Explain each abnormality. </li></ul><ul><li>- Hyponatremia: release of ADH </li></ul><ul><li>- Hypercalcemia: release of PTH-related protein by tumour cell </li></ul>TEST RESULT Na 120 K 3.8 Ca 3.2
    11. 12. <ul><li>What is paraneoplastic syndrome? </li></ul><ul><li>- collection of symptoms/signs </li></ul><ul><li>- d/t damage to organs that are remote from the site of primary tumour or its mets </li></ul><ul><li>- mech: substances produce by tumour cells </li></ul><ul><li>What are the hormones/hormone-like factors elaborated in bronchial CA? </li></ul><ul><li>- small cell CA: ADH (SIADH) and ACTH (Cushing’s) </li></ul><ul><li>- squamous cell CA: PTH (hypercalcemia) </li></ul>
    12. 13. <ul><li>RIGHT SIDE: </li></ul><ul><ul><li>Poorly differentiated tumour cell </li></ul></ul><ul><ul><li>Increased mitotic xtvt </li></ul></ul><ul><ul><li>hyperchromatism </li></ul></ul><ul><ul><li>Increased N:C ratio </li></ul></ul><ul><ul><li>Pleomorphism (marked variation in shape & size ) </li></ul></ul>Squamous cell with keratin pearl Bronchoscopy was done and the sample taken.
    13. 14. Despite treatment, he died. Post-mortem was done. <ul><li>Left lung </li></ul><ul><li>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). </li></ul><ul><li>Compression of main bronchi </li></ul><ul><li>At the bottom most: consolidation. </li></ul>
    14. 15. <ul><li>Describe the basis of classification of lung CA: </li></ul><ul><li>- small cell CA </li></ul><ul><li>- non small cell CA: squamous / adenoCA / large cell </li></ul><ul><li>Features of small cell CA </li></ul><ul><li>12. DY/DX squamous cell & adenoCA: </li></ul><ul><li>a) gender </li></ul><ul><li>b) smoking association </li></ul><ul><li>c) location </li></ul><ul><li>d) size </li></ul><ul><li>e) growth rate </li></ul><ul><li>f) microscopy </li></ul>
    15. 17. Quick guide to mx..
    16. 18. PREVIOUS LEARNING ISSUE <ul><li>KIESSELBACH’S PLEXUS </li></ul>ICA ↓ OPHTALMIC ARTERY ECA

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