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Tumours of the Respiratory Tract
Bronchial carcinoma is the most common, accounting for 95% of primary tumours of the lung. Alveolar cell carcinoma
accounts for 2% and other less malignant or benign tumours account for the remaining 3%.
TYPES
(MALIGNANT) BRONCHIAL CARCINOMA
Bronchial carcinomas are broken into small cell lung carcinoma (SCLC) and non-small cell lung carcinoma (NSCLC).
Small cell lung carcinoma
Type Freq. Macroscopic Microscopic Metastases/Spread Features
SMALL CELL 20- Seldom in periphery Homogenous population Metastasise widely Only 1% occur in non-
CARCINOMA 25% (hilar or central) of (small) oat-like cells and early (most smokers
(oat-cell - Little cytoplasm aggressive)
carcinoma) Usually don’t cavitate - Round/oval shapes Poor prognosis
Metastasis is via
Dense-core lymphatics/blood and is Ectopic hormone
neurosecretory usually present at production is common
granules as they arise diagnosis
from neuroendocrine Therapy: CT &/or RT
cells. Virtually incurable
with surgery
Non-small cell carcinomas
Three main types:
Squamous cell carcinoma (SCC)
Adenocarcinoma (AdenoCa)
(Undifferentiated) Large cell carcinoma
Type Freq. Macroscopic Microscopic Metastases/Spread Features
Squamous cell 25- Come from larger, Intercellular bridges Tends to spread Most present as
carcinoma – 40% more central visible locally & metastasise obstructive lesions of the
most common bronchi Keratin present later in its course, but bronchus leading to
type Cells form does tend to grow more infection
Cavitation sometimes whorl/nest pattern rapidly in their original
and necrosis location bronchial Common in men
May be squamous obstruction & sequelae Hx of smoking
metaplasia/dysplasia &
foci of carcinoma in-situ Lymphatic spread is May secrete PTH-like
in the epithelium next to more common than peptide Ca
the mass haematogenous
Often an initial response to
RT (not CT)
About 60% are surgically
resectable but recurrence
is common
Type Freq. Macroscopic Microscopic Metastases/Spread Features
Adenocarcinoma 10% Typically peripherally From mucous cells in Grows more slowly
the bronchial Invasion of the than SCC
Bronchial-derived epithelium pleural and
Adenocarcinoma mediastinal lymph M=F
(common) Small and vary from nodes is common.
well-differentiated with Not as closely
SUBTYPE: glandular elements to Metastases to the associated with
Bronchioloalveolar papillary lesions to solid brain and bones are smoking
carcinoma (1-2% of lung masses common.
Ca) (better 20-50% 5 year 80% contain mucin Incidence increasing
survival)
Single nodule or more In pulmonary Most common
commonly, multiple diffuse parenchyma in terminal bronchial carcinoma
nodules that may coalesce regions. associated with
into consolidation (like asbestos
pneumonia)
Type Freq. Macroscopic Microscopic Metastases/Spread Features
Large cell 10- Tend to be in Anaplastic carcinoma with Metastasise early Very poor prognosis
(undifferentiated) 25% periphery large, more polygonal cells
tumour & vesicular nuclei.
More likely to be SCC &
adenoCa so undiff. that it
can’t be recognised.
(Cells same size as SCC,
but no characteristic whorls)
Some have:
Intracellular mucin
Mutlinucleate cells
(giant cell Ca.)
Cleared cells (clear cell
Ca.)
Spindly appearance
(spindle cell Ca)
PRE-CURSOR LESIONS (may not actually progress to lung cancer)
Squamous dysplasia/carcinoma in-situ
Atypical adenomatous hyperplasia
Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia
BENIGN EPITHELIAL TUMOURS
Pulmonary hamartoma (most common benign lesion)
Usually seen on the X-ray as a well-defined round lesion 1-2cm in diameter in the periphery of the lung
Growth is very slow (but the tumour can reach several cm in diameter)
Bronchial carcinoid (not actually benign, but it is a low grade tumour)
Rare tumour ressembling intestinal carcinoid tumour
It is locally invasive, eventually spreading to mediastinal lymph nodes and distant organs
Highly vascular tumour that projects into the lumen of a major bronchus recurrent haemoptysis
Grows slowly, but eventually blocks the bronchus lobar collapse
May produce ACTH (are foregut derivatives)
Cylindroma, Chrondroma, Lipoma
Extremely rare. They tend to grow and cause obstruction
Tracheal tumours – squamous papilloma, leiomyoma, haemangioma
MESOTHELIAL TUMOURS
Malignant Mesothelioma
Due to asbestos exposure (latent period of 20-50 years)
Presents with chest pain, dyspnoea, pleural effusion
Histology: Often biphasic (epithelioid/sarcomatous)
Treatment: Nil effective (only palliative)
Prognosis: Poor – death within 10 months on average
Secondary mesothelioma (lung, breast)
SECONDARY TUMOURS TO THE LUNG
Metastases to the lung are common and usually present as round shadows (1.5-3cm diameter).
Typical sites for the primary tumour are: kidney, prostate, breast, bone, GIT, cervix, ovary
Metastases nearly always develop in the parenchyma and are often fairly asymptomatic even when the CXR shows
extensive pulmonary metastases. (Rarely, they can develop in the bronchi and the patient can present with haemoptysis).
Carcinoma, especially of the stomach, pancreas and breast can involve mediastinal glands and spread along the
lymphatics of both lungs (lymphangitis carcinomatosa) progressive and severe breathlessness. See streaky basal
shadowing fanning out over both lung fields on the CXR as well as bilateral lymphadenopathy.
Occasionally, metastases may be only a solitary, round shadow on an X-ray of an asymptomatic patient. This is most
commonly due to renal cell carcinoma, but DDx. Includes:
Primary bronchial carcinoma, tuberculoma, benign tumour of the lung, hydatid cyst
PRESENTATION
Part of the reason that lung cancers have such poor survival is that they are generally diagnosed at a late stage.
Those arising centrally (bronchial tree) typically present with chest symptoms (e.g. haemoptysis)
Peripheral tumours may grow silently without causing local symptoms until quite advanced
Thus, many tumours are found coincidentally on a CXR or present with non-specific general symptoms (e.g. weight loss),
with effects of metastases (e.g. to brain, bone (pain)) or with non-metastatic “paraneoplastic” syndromes (as a result of
hormones, peptides, antibodies, prostaglandins or cytokines produced by the tumour)
Symptoms Signs
Cough (46%) Clubbing (14%)
Dyspnoea (40%) Atelectasis (10%)
Haemoptysis (32%) Effusion (9%)
Chest pain (30%) Hepatomegaly (8%)
Anorexia (25%) SVC obstruction (5%)
Fatigue (24%) Hypertrophic pulmonary osteoarthropathy (2%)
Weight loss >10% (17%) Paralysed diaphragm (2%)
Wheeze (12%) Supraclavicular nodes (2%)
Bone pain (10%) Pancoast’s syndrome (2%)
Hoarseness (9%) Horner’s syndrome (1%)
Dysphagia (4%) NO clinical signs (53%)
Asymptomatic (13%)
Metastases may cause bone tenderness, hepatomegaly, confusion, fits, local CNS deficit, cerebellar syndrome, proximal myopathy or
peripheral neuropathy.
Paraneoplastic syndromes:
Endocrine changes:
o Hypercalcaemia due to PTH-like substance secretion from SCC
o Hyponatremia due to ADH secretion by small cell carcinomas
o Cushing’s (ACTH) – ectopic secretion by small cell carcinoma
o Gynaecomastia – due to excessive gonadotrophin secretion
o Hypoglycaemia – release of insulin-like peptide from SCC
Neurological signs:
o Eaton-Lambert syndrome (progressive muscle weakness) and retinal blindness due to small cell carcinoma
o Peripheral neuropathy
o Subacute cerebellar degeneration
o Polymyositis
o Cortical degeneration
o Horner’s syndrome (partial ptosis of the eyelid, miosis of pupils, lack of sweating) – due to interruption of the sympathetic
innervation of the eye by apical tumours (usually associated with pain in an ulnar nerve pattern)
Haematological features:
o Migrating venous thrombophlebitis
o Disseminated intravascular coagulation
o Anaemia
Skin changes:
o Acanthosis nigricans (brown to black velvety elevations of the epidermis due to confluent papillomas, usually in the axillae
& nape of the neck)
o Dermatomyositis (papules over the knuckles)
PATHOGENESIS
There is overwhelming evidence that cigarette smoking is a major cause of lung cancer (including passive smoking)
The specific causative agents in cigarette smoke are uncertain but potential carcinogenic substances such as poly-
aromatic hydrocarbons, phenols & radioisotopes are implicated
Many smoke particles are so small that they penetrate far into the lung (although most bronchogenic carcinomas
originate in the large bronchi this may be because the large bronchi are exposed to a higher [ ] of tobacco smoke
products as the material is transported from the peripheral regions by the mucociliary system)
Other factors include: radiation, asbestos, air pollution, nickel, chromates, arsenic
These exposures are thought to act by causing genetic alterations in the lung cells, which accumulate and
eventually neoplasia (multi-hit theory of cancer)
In lung cancers, it is estimated that 10-20 mutations have occurred by the time the cancer is clinically apparent. As in
most cancers, there is a role for dominant oncogenes and the frequent loss & inactivation of recessive tumour
suppressor genes.
o Oncogenes: c-myc (growth responsive gene) in small cell carcinomas & K-ras (cellular transduction of
GPCR) in adenocarcinomas
o TSG: p53, Rb – both important in stopping the progression of the cell cycle
There is a familial clustering of lung cancer – suggesting a genetic basis for susceptibility that may involve
these genes or the cytochrome P450-A1 gene
NOTE – these genetic changes are not currently used for diagnosis or prognosis.
