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BRONCHOGENIC CARCINOMA
DR. MD RAIHAN
MD (PATHOLOGY)
INTRODUCTION
• Malignant proliferation of cells arising from the bronchial
epithelium or mucous glands.
• Although largely preventable, carcinoma of the lung kills about 8.8 million
people each year globally.
• It is the most common cause of cancer death in men and the second most
common cause in women, after breast cancer.
ETIOLOGY
1.Cigarette smoking – both
active and passive smoking
• White area shows lung
cancer.
• Blackish area shows
discolouration due to
tobacco smoke
2. Radon gas – Colourless and odourless gas generated by
breakdown of radium which is a radioactive substance.
3.Asbestos – Has a synergistic effect with cigarette smoking in
causing lung cancer. Also causes mesothelioma(different
from lung cancer)
4.Air pollution – Fine particulates and sulphate aerosols.
5.Genetics - ~ 8%. Polymorphism on chromosomes 5, 6 and 15
6.Others – Ionisation radiation, arsenic and inorganic arsenic
compounds, hemalite, vincristine-prednisone-nitrogen
mustard-procarbazine mixture
ETIOLOGY
CLASSIFICATION
1. Squamous (35%)
2. Adenosquamous (30%)
3. Small Cell (20%)
4. Large Cell (15%)
THE MOST SIMPLE CLASSIFICATION OF LUNGS CANCER
Based on the characteristics of the disease and its response to
treatment -
- Small cell lung cancer (SCLC)
- Non-small cell lung cancer (NSCLC)
Squamous or epidermoid carcinoma
• The commonest type,
• Accounting for approximately 40% of all carcinomas.
• Most present as obstructive lesions of the bronchus leading to
infection.
• Occasionally cavitates (10%) at presentation.
• The cells are usually well differentiated
• Occasionally anaplastic.
• Local spread is common
• Widespread metastases occur relatively late.
Squamous carcinoma (keratinising)
Adenocarcinoma
• Arises from mucous cells in the bronchial epithelium.
•Invasion of the pleura and the mediastinal lymph nodes is common, as are
metastases to the brain and bones.
• Accounts for approximately 10% of all bronchial carcinomas.
•The most common bronchial carcinoma associ ated with asbestos
• Proportionally more common in
•Non-smokers
•Women
•Elderly
•Far East.
Adenocarcinoma (gland forming)
Large cell carcinomas
- Less-differentiated forms of squamous cell and
adenocarcinomas.
- Account for about 25% of all lung cancers
- Metastasize early.
Large cell carcinoma
Small-cell carcinoma
-Oftencalled oat-cell carcinoma,
-Accounts for 20-30% of all lung cancers.
-Arises from endocrinecells(Kulchitsky cells).
-Small-cell carcinoma spreads earlyand is almost always
inoperable at presentation.
-Rapidlygrowing and highly malignant.
-Responds to chemotherapy
-Prognosis remains poor
Small cell carcinoma
PANCOAST TUMOR
Pancoast syndrome
SPREAD
1. Direct
2. Lymphatics
3. Hematogenous
SPREAD
1. Direct
 Invades pleura
 Invades Chest wall
 Invades Intercostal nerves
 Invades Brachial plexus
SPREAD
2. Lymphatics
Mediastinal lymph nodes Compressing:
• Pericardium
• Esophagus
• Superior vena cava
• Trachea
• Phrenic/ left recurrent laryngeal nerve
SPREAD
3. Hematogenous
 Liver
 Bone
 Brain
 Adrenal
 Skin
TNM CLASSIFICATION
TNM CLASSIFICATION
• Tumour (T)
T1: <3 cm and not involving main bronchus or pleura
T2: >3 cm, or involving main bronchus and visceral pleura
T3: any size, invading chest wall, or within 2 cm of carina
T4: invading mediastinum, great vessels, trachea
• Node (N)
N0: no regional node metastases N1:
ipsilateral hilar node metastases
N2: ipsilateral mediastinal or subcarinal node metastases
N3: contralateral mediastinal or hilar nodes
• Metastases (M)
M0: no distant metastasis
M1: distant metastasis
CLINICAL FEATURES
• These may be due to:
1. Local tumour effects
2. Metastatic tumour effects
3. Paraneoplastic manifestations.
• Many patients have no specific signs.
• In some, the lung cancer may be an incidental finding on CXR
or CT performed for another reason.
CLINICAL FEATURES
• Local Tumour effects
Persistent cough or change in usual cough
Haemoptysis
Chest pain (suggests chest wall or pleural involvement)
Unresolving pneumonia or lobar collapse
Unexplained dyspnoea (due to bronchial narrowing or obstruction)
Wheeze or stridor
Shoulder pain (due to diaphragm involvement)
Pleural effusion (due to direct tumour extension or pleural
metastases)
CLINICAL FEATURES
• Local Tumour effects
Hoarse voice (tumour invasion of the left recurrent laryngeal nerve)
Dysphagia
Raised hemidiaphragm (phrenic nerve paralysis)
SVCO
Horner’s syndrome (miosis, ptosis, enophthalmos, anhydrosis) due to
apical or pancoast’s tumour damaging sympathetic chain
Pancoast’s tumours can also directly invade the rib and brachial
plexus, causing C8–T1 dermatome numbness, shoulder pain, and
weakness of small muscles of the hand.
CLINICAL FEATURES
• Metastatic Tumour effects
Cervical/supraclavicular lymphadenopathy (common, present in
30%, and may be an easy site for diagnostic biopsy)
 Palpable liver edge
 Bone pain/pathological fracture due to bone metastases
 Neurological sequelae 2° to cerebral metastases
Hypercalcaemic effects (due to bony metastases or direct tumour
production of parathyroid hormone (PTH)-related peptide or PTH)
 Dysphagia (compression from large mediastinal nodes).
CLINICAL FEATURES
• Paraneoplastic syndromes
• Endocrine syndromes are due to the ectopic production of hormones or
hormonally active peptides.
• Neurological syndromes are due to antibody-mediated CNS damage.
 Cachexia and wasting
 Clubbing (up to 29% of patients; any cell type, more common in squamous and
adenocarcinoma)
 Hypertrophic pulmonary osteoarthropathy
CLINICAL FEATURES
 Gynaecomastia
 Ectopic ACTH (Cushing’s syndrome)
 Cerebellar syndrome (usually SCLC)
Limbic encephalitis (SCLC, also breast, testicular, other
cancers).
 Dermatomyositis/polymyositis
 Glomerulonephritis.
CLINICAL FEATURES
INVESTIGATIONS
• In outpatients
1. History and examination, including smoking and occupational histories
2. Spirometry pre-biopsy or surgery
3. CXR (PA and possibly lateral)—location of lesion, pleural involvement, pleural
effusion, rib destruction, intrathoracic metastases, mediastinal
lymphadenopathy. CXR can be normal
4. Blood tests, including sodium, calcium, and LFTs. Check clotting if biopsy
planned
5. Sputum cytology only indicated in patients who are unfit for bronchoscopy
or biopsy
6. Diagnostic pleural tap, if effusion present
7. FNA of enlarged supraclavicular or cervical lymph nodes.
INVESTIGATIONS
• Radiology
1. CT neck, chest, liver, adrenals (contrast-enhanced) to assess tumour site and
size
2. USG of neck or liver may provide information about enlarged lymph nodes or
metastases suitable for biopsy
3. MRI Used to answer specific questions relating to tumour invasion/ borders.
4. Bone scan Indicated if any suggestion of metastatic disease such as bony pain,
pathological fracture, hypercalcaemia, raised ALP,highly suggestive of bony
metastases if multiple areas of increased uptake.
5. CT head Indicated if any neurological evidence of metastatic
6. Positron Emission Tomography (PET) scanning Imaging technique
MANAGEMENT
1. Surgical resection in patients with ipsilateral
peribronchial or hilar node involvement
2. Radiotherapy
3. Chemotherapy
4. Laser therapy
5. General managment
MANAGEMENT
General Management
 Pain relief
 Good diet
 Specific therapy to treat anxiety & depression
 Treat Hypercalcemia
 Manage malignant pleural effusions.
Prognosis
Clinical features
bronchogenic.pptx

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bronchogenic.pptx

  • 1. BRONCHOGENIC CARCINOMA DR. MD RAIHAN MD (PATHOLOGY)
  • 2. INTRODUCTION • Malignant proliferation of cells arising from the bronchial epithelium or mucous glands. • Although largely preventable, carcinoma of the lung kills about 8.8 million people each year globally. • It is the most common cause of cancer death in men and the second most common cause in women, after breast cancer.
  • 3. ETIOLOGY 1.Cigarette smoking – both active and passive smoking • White area shows lung cancer. • Blackish area shows discolouration due to tobacco smoke
  • 4. 2. Radon gas – Colourless and odourless gas generated by breakdown of radium which is a radioactive substance. 3.Asbestos – Has a synergistic effect with cigarette smoking in causing lung cancer. Also causes mesothelioma(different from lung cancer) 4.Air pollution – Fine particulates and sulphate aerosols. 5.Genetics - ~ 8%. Polymorphism on chromosomes 5, 6 and 15 6.Others – Ionisation radiation, arsenic and inorganic arsenic compounds, hemalite, vincristine-prednisone-nitrogen mustard-procarbazine mixture ETIOLOGY
  • 5. CLASSIFICATION 1. Squamous (35%) 2. Adenosquamous (30%) 3. Small Cell (20%) 4. Large Cell (15%)
  • 6. THE MOST SIMPLE CLASSIFICATION OF LUNGS CANCER Based on the characteristics of the disease and its response to treatment - - Small cell lung cancer (SCLC) - Non-small cell lung cancer (NSCLC)
  • 7. Squamous or epidermoid carcinoma • The commonest type, • Accounting for approximately 40% of all carcinomas. • Most present as obstructive lesions of the bronchus leading to infection. • Occasionally cavitates (10%) at presentation. • The cells are usually well differentiated • Occasionally anaplastic. • Local spread is common • Widespread metastases occur relatively late.
  • 9. Adenocarcinoma • Arises from mucous cells in the bronchial epithelium. •Invasion of the pleura and the mediastinal lymph nodes is common, as are metastases to the brain and bones. • Accounts for approximately 10% of all bronchial carcinomas. •The most common bronchial carcinoma associ ated with asbestos • Proportionally more common in •Non-smokers •Women •Elderly •Far East.
  • 11. Large cell carcinomas - Less-differentiated forms of squamous cell and adenocarcinomas. - Account for about 25% of all lung cancers - Metastasize early.
  • 13. Small-cell carcinoma -Oftencalled oat-cell carcinoma, -Accounts for 20-30% of all lung cancers. -Arises from endocrinecells(Kulchitsky cells). -Small-cell carcinoma spreads earlyand is almost always inoperable at presentation. -Rapidlygrowing and highly malignant. -Responds to chemotherapy -Prognosis remains poor
  • 18. SPREAD 1. Direct  Invades pleura  Invades Chest wall  Invades Intercostal nerves  Invades Brachial plexus
  • 19. SPREAD 2. Lymphatics Mediastinal lymph nodes Compressing: • Pericardium • Esophagus • Superior vena cava • Trachea • Phrenic/ left recurrent laryngeal nerve
  • 20. SPREAD 3. Hematogenous  Liver  Bone  Brain  Adrenal  Skin
  • 22. TNM CLASSIFICATION • Tumour (T) T1: <3 cm and not involving main bronchus or pleura T2: >3 cm, or involving main bronchus and visceral pleura T3: any size, invading chest wall, or within 2 cm of carina T4: invading mediastinum, great vessels, trachea • Node (N) N0: no regional node metastases N1: ipsilateral hilar node metastases N2: ipsilateral mediastinal or subcarinal node metastases N3: contralateral mediastinal or hilar nodes • Metastases (M) M0: no distant metastasis M1: distant metastasis
  • 23. CLINICAL FEATURES • These may be due to: 1. Local tumour effects 2. Metastatic tumour effects 3. Paraneoplastic manifestations. • Many patients have no specific signs. • In some, the lung cancer may be an incidental finding on CXR or CT performed for another reason.
  • 24. CLINICAL FEATURES • Local Tumour effects Persistent cough or change in usual cough Haemoptysis Chest pain (suggests chest wall or pleural involvement) Unresolving pneumonia or lobar collapse Unexplained dyspnoea (due to bronchial narrowing or obstruction) Wheeze or stridor Shoulder pain (due to diaphragm involvement) Pleural effusion (due to direct tumour extension or pleural metastases)
  • 25. CLINICAL FEATURES • Local Tumour effects Hoarse voice (tumour invasion of the left recurrent laryngeal nerve) Dysphagia Raised hemidiaphragm (phrenic nerve paralysis) SVCO Horner’s syndrome (miosis, ptosis, enophthalmos, anhydrosis) due to apical or pancoast’s tumour damaging sympathetic chain Pancoast’s tumours can also directly invade the rib and brachial plexus, causing C8–T1 dermatome numbness, shoulder pain, and weakness of small muscles of the hand.
  • 26. CLINICAL FEATURES • Metastatic Tumour effects Cervical/supraclavicular lymphadenopathy (common, present in 30%, and may be an easy site for diagnostic biopsy)  Palpable liver edge  Bone pain/pathological fracture due to bone metastases  Neurological sequelae 2° to cerebral metastases Hypercalcaemic effects (due to bony metastases or direct tumour production of parathyroid hormone (PTH)-related peptide or PTH)  Dysphagia (compression from large mediastinal nodes).
  • 27. CLINICAL FEATURES • Paraneoplastic syndromes • Endocrine syndromes are due to the ectopic production of hormones or hormonally active peptides. • Neurological syndromes are due to antibody-mediated CNS damage.  Cachexia and wasting  Clubbing (up to 29% of patients; any cell type, more common in squamous and adenocarcinoma)  Hypertrophic pulmonary osteoarthropathy
  • 28. CLINICAL FEATURES  Gynaecomastia  Ectopic ACTH (Cushing’s syndrome)  Cerebellar syndrome (usually SCLC) Limbic encephalitis (SCLC, also breast, testicular, other cancers).  Dermatomyositis/polymyositis  Glomerulonephritis.
  • 30. INVESTIGATIONS • In outpatients 1. History and examination, including smoking and occupational histories 2. Spirometry pre-biopsy or surgery 3. CXR (PA and possibly lateral)—location of lesion, pleural involvement, pleural effusion, rib destruction, intrathoracic metastases, mediastinal lymphadenopathy. CXR can be normal 4. Blood tests, including sodium, calcium, and LFTs. Check clotting if biopsy planned 5. Sputum cytology only indicated in patients who are unfit for bronchoscopy or biopsy 6. Diagnostic pleural tap, if effusion present 7. FNA of enlarged supraclavicular or cervical lymph nodes.
  • 31. INVESTIGATIONS • Radiology 1. CT neck, chest, liver, adrenals (contrast-enhanced) to assess tumour site and size 2. USG of neck or liver may provide information about enlarged lymph nodes or metastases suitable for biopsy 3. MRI Used to answer specific questions relating to tumour invasion/ borders. 4. Bone scan Indicated if any suggestion of metastatic disease such as bony pain, pathological fracture, hypercalcaemia, raised ALP,highly suggestive of bony metastases if multiple areas of increased uptake. 5. CT head Indicated if any neurological evidence of metastatic 6. Positron Emission Tomography (PET) scanning Imaging technique
  • 32. MANAGEMENT 1. Surgical resection in patients with ipsilateral peribronchial or hilar node involvement 2. Radiotherapy 3. Chemotherapy 4. Laser therapy 5. General managment
  • 33. MANAGEMENT General Management  Pain relief  Good diet  Specific therapy to treat anxiety & depression  Treat Hypercalcemia  Manage malignant pleural effusions.