•
PATHOLOGY OF THE RESPIRATORY SYSTEM
Congenital abnormalities
Upper portion of resp. system.
-cyclopia
-choanal
atresia
-cleft
lip and palate
-Pierre
Robin sequence
(hypomandibulosis,
glossoptosis and cleft lip and palate)
Larynx
-stenosis
-atresia
•
Cong.
Abnorms continua.
Trachea
-agenesis,
bronchi originating from oesophagus, stenosis, etc
Tracheal and bronchial cartilage
-Tracheomalasia,
bronchomalasiaà lung collapse
Bronchociliary
-Kartagener’s
syndrome (sinusitis, brochiectasis & situs inversus) (dynein arm problem)
•
Congenital
abnormalities of lung
•
Agenesis
(unilateral or bilateral)
•
Sequestrstration
(intralobar & extralobar)
•
Adenomatoid
malformation
•
Pulmonary
hypoplasia
•
PULMONARY ATELECTASIS
•
Is incomplete expansion of the lungs or collapse of
previously inflated lung tissue
•
Atelectasis neonatorum occurs due to failure of lung
to expand in the new born
•
Acquired atelectasis can be obstructive
(absorptive), compressive (pleural effusion) or contraction type (scarring)
•
Patchy atelectasis occurs in the new born due to
lack of lung surfactant
•
ACUTE (ADULT) RESPIRATORY DISTRESS SYNDROME (SHOCK
LUNG)
•
Is also called diffuse alveolar damage (DAD),
traumatic wet lung, or acute alveolar injury.
•
This actually refers to a diffuse alveolo-capillary
injury xrised by rapid onset of life threatening respiratory insufficiency,
tachycardia, cyanosis and severe arterial hypoxia that is refractory to oxygen
therapy and may progress to extra-pulmonary multisystem organ failure.
•
Most pts have severe pulmonary oedema.
•
Lung compliance is decreased
•
Causes include: shock (hypovol, septic, etc),
diffuse pulm. infections especially viral, oxygen toxicity, inhalation of
toxins, narcotic overdose, hypersensitivity to organic solvents, aspiration
pneumonitis, cardiac surgery
•
Pathogenesis of ARDS
•
The initial injury in ARDS is either to the
capillary endothelium or sometimes alveolar epithelium but eventually both are
affected.
•
The injury leads to increased vascular permeability
and alveolar flooding, loss of diffusion capacity, and widespread surfactant
abnormalities (damage to type II pneumocytes).
•
The injury is mediated by polymorphs attraction and
activation by macrophage secretory products (IL-8, IL-1, & TNF). The
polymorphs release oxidants, proteases, PAF, and leukotrienes that cause active
tissue damage.
•
The exudate and tissue damage do not resolve
resulting into organisation with scarring leading to chronic pulmonary disease
•
Morphology of ARDS
•
A) Early stage.
The
lungs are heavy, firm, red and boggy.
They exhibit congestion, oedema and
inflammation, fibrin deposition, necrosis of epithelial
cells with formation of hyaline membranes.
Intra-alveolar haemorrhage and patchy
atelectasis also occur.
•
B) Late stage. Proliferative or
organising stage.
The
alveoli become lined by cuboidal or columnar type II pneumocytes.
Variable
intra-alveolar and interstitial fibrosis also occur.
•
Clinical course
•
Usually a hospitalised pt for the predisposing cause
and initially without pulmonary symptoms suddenly develops profound dyspnoea
and tachypnoea with initially normal CXR but subsequently develops cyanosis,
hypoxia and respiratory failure. Later CXR will reveal diffuse bilateral
infiltrates.
•
Hypoxia then becomes unresponsive to oxygen therapy
and respiratory acidosis develops.
•
Mortality is very high and even in the USA with
their modern facilities, it is as high as 50%.
•
PULMONARY INFECTIONS
•
Pneumonia refers to inflammation of the lung tissue.
•
For pulmonary infections to set in, the normal
pulmonary defense mechanisms have to be defeated.
The
pulmonary defense mechanisms are:
a)
Cough reflex
b)
Nose, pharynx (trapping of organisms).
c)
Mucociliary action of lower respiratory tract.
d)
Phagocytosis and elimination of organisms by alveolar macrophages.
•
Factors affecting the defense mechanisms
•
Loss or suppression of cough reflex as in coma,
anaesthesia, drugs, chest pain, etc.
•
Injury to mucociliary apparatus as in smoking,
inhalation of hot or corrosive gases
•
Viral diseases
•
Genetic disturbances such as immobile cilia syndrome
•
Phagocytic or bactericidal function of alveolar
macrophages as in alcoholism, tobacco smoking, oxygen toxicity, etc.
•
Pulmonary congestion and oedema
•
Accumulation of secretions as in cystic fibrosis,
bronchial, obstruction.
•
PNEUMONIA
•
BRONCHPNEUMONIA
•
LOBAR PNEUMONIA
•
BRONCHOPNEUMONIA
•
It is xrised by patchy consolidation of the lungs
•
Usually represents a pre-existing bronchitis or
bronchiolitis
•
Occurs in the two extremes of life (elderly and
infants)
•
Also occurs in debilitated patients, progressive
heart failure & pts with disseminated cancer.
Etiology:
Common
agents include staph, strept, pneumococci, H influenzae, P. aerugenosa and
coliforms
Morphology:
*patchy
consolidation that can affect one lobe, both lobes,
bilateral or basal parts of the lung(s).
*The
areas of consolidation are foci of suppurative inflammation
*Well
developed lesions are about 3-4 cm slightly elevated, dry,
granular, gray-red to yellow in colour and poorly delineated
*Confluence
of these foci gives rise to confluent broncopneumonia
•
Morph.
Continua.
•
Histologically:
Suppurative exudate that fills bronchi,
bronchioles and adjacent alveolar spaces.
Neutrophils are dominant
Aggressive organisms may lead to lung
abscess due to necrosis of lung tissue
Residual fibrin may be present
Exudate may completely resolve
Clinical course: Depends on virulence of
the organism and extent of involvement.
Temp
380-39.50c, cough with expectoration and rales in one or
more lobes
Mild
to moderate respiratory difficulty
CXRay
will show focal opacities.
•
Complications of bronchopneumonia
•
Lung abscess
•
Emphysema
•
Suppurative pericarditis
•
Metastatic abscesses
•
LOBAR PNEUMONIA
•
This is an acute bacterial infection of a large
portion of a lobe or the entire lobe which tends to occur at any age but
relatively uncommon in infancy and late life (elderly).
•
Is now uncommon in the western world because of
effective antibiotics.
•
Aetiology and Pathogenesis
•
The host defense mechanisms must be overcome before
infection can set in as discussed earlier.
•
90% are caused by pneumococci (Strept. Pneumoniae)-
types 1, 3, 7 and 2
•
Occasionally can be caused by Klebsialla pneumoniae,
staph, H Influenzae, pseudomonas and proteus
•
The most common portal of entry is the air passages
•
Extensive exudation leads to spread through the pores
of Kohn
•
Mucoid encapsulation of pneumococci protects the
organisms from immediate phagocytosis and thus favours spread
•
Morphology of lobar pneumonia
•
Sequence
of changes that occur in the morphology of L pneumonia
•
Stage
of congestion
•
Stage
of red hepatisation
•
Stage
of gray hepatisation
•
Stage
of resolution
Because of present day effective
antibiotics, the disease does not go through all the stages without been
aborted
•
Stage
of congestion
•
This is the stage of development of bacterial
infection and lasts for about 24 hours
•
Is xrised by vascular engorgement
•
There is fluid exudation into the alveoli, few
polymorphs and numerous bacteria
•
Grossly the lungs are boggy, red, and sub-crepitant
•
Stage of red hepatisation
•
There is increased number PMN, pptation of fibrin to
fill alveolar spaces
•
Massive confluent exudation obscures the normal
architecture
•
Extravasation of RBCs makes the lung red hence the
term red hepatisation
•
WBCs contain engulfed bacteria
•
Fibrinous or fibrinopurulent pleuritis is invariably
present
•
Grossly: the lobe affected is red, firm, airless
with liver-like consistency hence the term red hepatisation
•
Stage of gray hepatisation
•
There is continuing accumulation of fibrin
associated with progressive disintegration of WBCs & RBCs
•
This exudate contracts to yield a clear zone
adjacent to the alveolar walls
•
The progressive breakdown of WBCs & RBCs along
with persistence of fibrino-suppurative exudate gives the grayish-brown dry
surface and hence it is again likened to a gray liver-like tissue (gray
hepatisation)
•
Extension into the pleura leads to empyema
•
Stage of resolution
•
This occurs in cases with favourable outcome
•
Progressive digestion of the consolidated exudate
within the alveolar spaces produces granular semi-fluid debris that are either
resorbed, ingested by macrophages or coughed out
•
With these going on, normal lung parenchyma is
restored
•
Pleural reaction may slightly resolve but more often
organises leaving fibrous thickening or adhesions
•
Complications
of lobar pneumonia
•
Excessive mucoid secretions as in type 3 pneumococci
and Klebsiella
•
Abscess formation
•
Solidification of the lung
•
Bacterial dissemination
•
Clinical course
•
In classic cases there is sudden on set of dx with chills,
fever, cough with expectoration of sputum in stages (purulent, sometime
haemorrhagic)
•
Temperature may go up to 400C or 410C
•
Auscultation reveals crepitations, bronchial breath
sounds, etc
•
There is dull percussion note over the area
•
CXRay findings are classical
•
TUBERCULOSIS
•
This is a disease caused by mycobacteria
•
Human tuberculosis is mainly caused by Myco. Tb
hominis and Myco. Bovis
•
Myco. Tb hominis is the major cause of pulmonary
infections
•
Tb is estimated to affect 1.7 billion individuals
worldwide
•
After HIV, Tb is the leading infectious cause of
death in the world
•
Recent increase in Tb in the industrialised nations
is because of the increased number of cases among HIV infected patients
•
Infection by myco. Tb typically leads to the
development of delayed hypersensitivity to myco. Tb Ags and this can be
detected by Mantoux test
•
A positive Mantoux test signifies cell-mediated
hypersensitivity to tubercular Ags.
•
Tb continua.
•
Tuberculosis is
becoming a world-wide problem. War, famine, homelessness, and a lack of medical
care all contribute to the increasing incidence of tuberculosis among
disadvantaged persons.
Patterns of Infection
•
There are two
major patterns of disease with TB:
•
Primary
tuberculosis: seen as an initial infection, usually in children. The initial
focus of infection is a small subpleural granuloma (Ghon focus).
When accompanied by granulomatous hilar lymph node ininvolment, these two make-up the Ghon complex. In nearly all cases, these
granulomas resolve and there is no further spread of the infection. However, in
exceptional cases such as infants and children and the immunodef. progressive
spread may occur leading to primary progressive tuberculosis.
•
Secondary
tuberculosis: seen mostly in adults as a reactivation of previous infection (or
reinfection), particularly when health status declines. The granulomatous
inflammation is much more florid and widespread. Typically, the upper lobes of lung are most affected, and cavitation can occur.
•
Tb continua.
•
When resistance
to infection is particularly poor, a "miliary" pattern of spread can
occur in which there are a myriad of small millet seed-sized (1-3 mm) granulomas, either in lung or in other
organs.
•
Pathogenesis of Tbc
•
The pathogenesis is simply the development of
delayed type of hypersensitivity reaction.
•
Tb
AgàLNCD4 of
TH1 are sensitised and re-circulated to site of infectionrelease of
cytokinesrecruitment of monocytes
•
Morphology of 20 tuberculosis
•
Most cases represent reactivation of an old
sub-clinical infection
•
20 tuberculosis tends to produce more
damage to the lungs than 10 tbc
•
20 tbc is located in the apex of one or
both lungs usually
•
It begins as a small focus of consolidation, <3cm
in diameter
•
In most instances regional LNs develop foci of tbc
activity
•
In favourable cases, there will be an area of
necrosis without cavitation with progressive fibrous encapsulation and scarring
followed by spontaneous healing
•
In progressive lesions, coalescent granulomas and
caseation necrosis occur over a period of months to years with further
pulmonary and distant organ involvement resulting into:à cavitary
fibrocaseous, miliary or Tb bronchopneumonia
•
Cavitary fibrocaseous
•
Erosion into a bronchiole drains caseous focus
transforming it into a cavity which may remain apical
•
Formation of cavity favours multiplication of
bacteria b/c of increased O2 tension
•
The cavity is usually linned by yellow-gray caseous
material
•
Contents of the cavity may be coughed out and on its
way out lead to endobronchial or endotracheal tbc
•
Spread may also occur through lymphatics leading to Tb
adenitis
•
Pleural involvement may lead to effusion, Tb empyema
&/or obliterative fibrous pleuritis
•
Miliary tuberculosis
•
Lymphohaematogenous spread may lead to seeding of
other tissues or organs with formation of small granulomas of millet seed size
called miliary Tbc.
•
Tuberculous bronchopneumonia
•
This is seen in highly susceptible individuals
•
Spreads rapidly throughout large areas of the lungs
in the form of diffuse bronchpneumonia
•
CHRONIC OBSTRUCTIVE AIRWAY DISEASES
•
This is a group of conditions accompanied by chronic
or recurrent obstruction to air flow within the lungs
They include:
•
EMPHYSEMA
•
CHRONIC BRONCHITIS
•
BRONCHIAL ASTHMA
•
BRONCHIECTASIS
•
EMPHYSEMA
•
This
is an abnormal permanent dilatation of the air spaces distal to the terminal
bronchiole accompanied by destruction of their walls
•
There
are 4 different types:
•
Centriacinar.
-central
or proximal portions of acini formed by resp. bronchioles are affected while distal
alveoli are spared
-both
emphysematous and normal air spaces exist within the same acinus and lobule
-this
form is more common and usually more severe in the upper lobes particularly
apical segments
-inflammation
around bronchi, bronchioles and septae is common
-moderate
to severe degrees of emphysema occur predominantly in male smokers often
associated with chronic bronchitis
-causes
include smoking and coal dust
•
Enphysema
continua.
b) Pancinar
emphysema
-the
acini are uniformly affected from the level of respiratory bronchiole to the
terminal blind alveoli
-it
tends to occur more commonly in the lower zones and in the anterior margins of
the lungs
-it
is usually most severe at the bases
-this
is the type associated with α1AT deficiency
c) Paraseptal
emphysema
-the
proximal part of acinus is normal but the distal part is dominantly affected
-the
emphysema is more striking adjacent to the pleura along the lobular connective
tissue septa
-occurs
adjacent to areas of fibrosis, scarring or atelectasis
-usually
more severe in the upper ½ of the lung
-probably
underlies many cases of spontaneous
pneumothorax in young adults
•
Emphysema
contin.
•
Irregular emphysema
-so
called because the acinus is irregularly affected
-is
almost invariably associated with scarring
-it
may be the most common form of emphysema but may remain undiagnosed until at
post mortem
-usually
there is irregular enlargement of acini adjacent to scars, accompanied by
destructive changes
-it
is most often asymptomatic, mostly discovered at post mortem
•
Pathogenesis of emphysema
•
For
centriacinar and panacinar emphysema, the pathogenesis is unresolved but
several factors may be involved.
•
Other
forms of emphysema are thought to be due to an imbalance between protease and
anti-protease (elastase) activity leading to destruction of the alveolar walls
•
Morphology
of emphysema
•
The
important criteria for the diagnosis and classification of emphysema are
derived from naked eye (hand lens) examination of the lungs fixed in a
state of inflation.
•
CHRONIC BRONCHITIS
•
This is a clinical condition xrised by chronic cough
with expectoration of sputum for at least consecutive 3/12 in at least 2
consecutive years
•
Is common among smokers and inhabitants of
smog-laden cities
•
It is divided into simple chronic bronchitis and obstructive
chronic bronchitis with physiologic evidence of airway obstruction
•
Is more frequent in middle-aged men
•
Pathogenesis of chronic bronchitis
•
Chronic irritation by inhaled substances such as
cigarette smoking
•
Microbiologic infections
The hallmark and earliest feature of
chronic bronchitis is hyper-secretion of mucus which starts in large airways
and is associated with hypertrohy of the submucous glands in trachea and
bronchi
As CB persists there is hypertrophy and
hyperplasia of goblet cells of the small airways, this may lead to obstruction
When CB is accompanied by moderate to
severe airflow obstruction, co-existent emphysema is the predominant feature
The role of infection appears to be
secondary
•
Morphology of Chronic Bronchitis
•
Hyperrhaemia
, swelling and puffiness of the mucosa with mucopurulent secretions
•
Mucus
casts or plugs may be present in bronchial lumina
•
Histologically,
there is enlargement of mucus secreting glands of the trachea and main bronchi.
Major increase is in the size of the mucous glands with raised goblet cell No.
The
thickening is assessed by the Reid index = ratio of thickness of mucous
gland layer to the gap btw surface epithelium and cartilage
•
Squamous
metaplasia or dysplasia may occur
•
Severe
bronchiolar narrowing may occur by goblet cell metaplasia, mucus plugging,
inflammation and fibrosis referred to as bronchiolitis fibrosa obliterans.
•
Complications
include cor pulmonale, metaplasia and dysplasia.
•
BRONCHIAL ASTHMA
•
Is a dx xrised by increased responsiveness of the
tracheobronchial tree to various stimuli potentiating paroxysmal constriction
of the bronchial airways
•
Attacks of broncho-spasm suddenly trigger severe
attacks of dyspnoea and wheezing
•
Status asthmaticus may prove fatal
•
Types and pathogenesis of asthma
•
A) Atopic or allergic asthma
-Is
mediated by type I hypersensitivity reaction
-Is
the most common type of asthma
-positive
family history of atopy is present
-IgE
levels are usually elevated
Mediators of allergic asthma:
a)
10 mediators include-histamineàbronchospasm by
direct and cholinergic
reflex
-Eosinophil
and Neutrophil chemotactic factors
b)
20 mediators include
-leukotrienes
(C4, D4 & E4) prolonged bronchoconstriction
-prostaglandin
D2 (PGD2) and PAF
Late phase reaction; second wave of
mediators released by basophils, PMN, and eosinophils attracted by chemotactic
factors from mast cells
•
B) Non-atopic asthma
•
Most commonly triggered by respiratory viruses
rather than bacteria
•
Serum IgE is normal
•
Is thought to be due to hyper irritability of the
bronchial tree
C) Drug induced
asthma
•
Example in this group is aspirin. This drug is
thought to interfere with arachidonic acid derivatives
D) Occupational asthma
•
Is stimulated by fumes, organic and chemical dust,
gases, penecillins, etc
•
Is thought to be directly induced or via IgE
•
Morphology
of asthma
•
Pulmonary
over distension because of hyperinflation
•
Bronchial
tenacious mucus plugs
•
Curschman’s
spiral and charcot-laden crystals
•
BM
thickening
•
Oedema
and inflammation of bronchial walls
•
Prominence
of eosinophils in the cellular infiltrate
•
Hypertrophy
of bronchial wall muscle
Clinically varies with severity of
attacks and the complications
•
BRONCHIECTASIS
•
This is a chronic necrotising infection of the
bronchi and bronchioles leading to or associated with abnormal permanent
dilatation of the airways
•
Is charaterised by cough, fever, expectoration of foul
smelling sputum
•
Conditions associated with bronchiectasis
•
A) bronchial obstruction as in FB,
tumours, mucus impaction, can complicate diffuse obstructive airway disease
•
B) Congenital or hereditary conditions
•
Congenital bronchiectais
•
Cystic fibrosis
•
Intralobar sequestration of lung
•
Immunodeficiency statesàheightened
susceptibility to infection
•
Immotile cilia and Kartigener’s syndrome
* C)
Necrotising pneumonia
•
Aetiopathogenesis
•
Obstruction-àinfectionàbronchial wall
destructiondilatation
•
Morphology
•
Gross morph.
-usually affects lower lobes
bilaterally particularly those air passages that are most vertical
-may be localised in local obstruction
Most severe lesions are found in the
more distal bronchi and bronchioles
-air way dilatation may reach up to 4X
the normal size
-
patterns
of dilatation include cylindrical, fusiform and saccular
-
The
dilated channels can be traced to the sub-pleura
-
Varying
degrees of emphysema and atelectasis are present.
•
Morph.
Continua.
•
Microscopy:
-intense acute and chronic inflammatory
exudation within the walls of the bronchi and bronchioles with epithelial
desquamation and extensive areas of necrotising ulceration
-squamous metaplasia
-lung abscess may form
-chronic stages may lead to fibrosis of
bronchial and peribronchiolar wall
•
Pathology of lung tumours
•
A variety of benign and malignant tumours may arise
in the lungs but the vast majority are carcinomas
•
90%-95% are bronchogenic carcinomas
•
5% are bronchial carcinoids
•
2%-5% are mesenchymal and other miscellaneous
neoplasms
•
20 lung cancers can come from anywhere as
the lung performs a filter-like fuction (universal recipient….)
•
CARCINOMA OF THE LUNGS
(bronchogenic carcinoma)
(bronchogenic carcinoma)
•
Lung cancer is currently the most frequently
diagnosed major cancer in the world and the most common cause of cancer
mortality worldwide…western world
•
Carcinoma of the lung occurs most often between the
ages of 40 and 70 years
•
Bronchogenic carcinoma refers to carcinoma arising
from the bronchial mucosa
•
The prognosis is poor
•
Aetiology and pathogenesis
A- Tobacco smoking. There is
little doubt about the positive relationship between T smoking and bronchogenic
carcinoma (BC)
-There
is statistical evidence between daily smoking, tendency to inhale, duration of
smoking, the number of cigarettes per day and the risk of developing BC
-there
is 10X increase risk to average smokers compared to non-smokers and risk rises
up to 60 fold in smokers of >40 cigarettes/day
-clinically
there are atypical cytological changes in the respiratory mucosa of 96.7% of
smokers
-experimentally,
0ver 1200 substances have been counted in cigarette smoke many of which are
carcinogens
-initiators
and promoters have been discovered in the cigarette smoke
•
Aetiol. & P continua.
•
B-Industrial hazards. All forms of radiation
increase the risk of cancer. Example is the Hiroshima atomic bomb
-asbestos,
nickel, chromates, coal, mustard gas, arsenic, beryllium and iron increase the
risk of devt. of cancer
•
C-Air pollution. Urban factor, it has been observed
that BC is commoner among city dwellers probably smoking related
•
D-Genetic factors. Occasional familial clustering
has suggested a genetic predisposition
•
E-Scarring. Some BC (adenocarcinomas) have been
observed to arise in the vicinity of scars (?scar cancer)
•
A
& P contin.
•
Molecular genetics. Gene amplification such as c-myc
amplification and l-myc amplification are associated with particularly
aggressive tumours.
-Mutational
inactivation of p53 and Rb genes are common in small cell lung carcinoma
-all
small cell lung carcinomas have deletion of 3p14-25 where 3 distinct tumour
suppressor genes reside
-k-ras
mutations are found in 30% of adenocarcinomas
•
HISTOLOGICAL CLASSIFICATION OF LUNG CARCINOMAS
•
1 Squamous
cell carcinoma 35%-50%.
•
2 Adenocarcinoma
(bronchial derived and bronchiolo- alveolar).
•
3 Small
cell carcinoma.
a)
oat cell carcinoma
b)
intermediate cell or polygonal cell carcinoma
c)
combined
•
4 Large
cell carcinoma
•
5 Combined
squamous cell and adenocarcinoma
•
6 MiscellaneousàMesothelioma
•
Morphology
•
BC arises most often in and about the hilus of the
lung
•
75% take origin from the 1st, 2nd,
and 3rd order bronchi
•
Small % arises from the periphery of the alveolar
septal cells or terminal bronchioles
•
Begins as a small area of cis, then fungates,
ulcerates or penetrates the bronchial wall
•
Most are gray-white and firm on cut section
•
Areas of haemorrhage and necrosis may be present
•
Extension to pleura and pericardium may occur
•
Spread is to the trachea, bronchi, and lymph nodes
•
Distant metastasis is through the blood and
lymphatics with high predilection for adrenals (50%)
•
SqCC
•
Most commonly found in men
•
Most commonly asociated with smoking and produces
keratin microscopically
•
Tends to spread locally and metastasise somewhat
later than the other forms
•
Adenocarcinoma
•
Equal sex incidence
•
More peripherally located
•
80% mucin positive
•
Less frequently associated with smoking
•
Sometimes associated with areas of scarring
•
Small cell carcinoma
•
Highly malignant and the most aggressive of all BCs
•
Cells are generally small with little cytoplasm and
occasionally lymphocyte-like
•
No glands or squamous differentiation
•
EM shows dense-core neurosecretary granules in some
of the tumours
•
Also has strong relationship with cigarette smoking
•
Is the most common pattern associated with ectopic
hormone production
•
Large
cell carcinoma
•
Larger and more polygonal cells
•
Probably represents some undifferentiated SCCs and
adenocarcinomas
•
Malignant giant cells may be present
•
Secondary
pathology
•
Partial obstruction may lead to emphysema
•
Complete obstruction may lead to atelectasis
•
Impaired drainage of the airways may lead to acute
suppuration, ulceration or bronchiectasis
•
Pulmonary abscesses may form
•
Superior venacaval syndrome may occur
•
Horner’s syndrome may develop (enopthalmos,
ptosis, anhidrosis and miosis)
•
Pancoats tumour may develop. (Horner’s
syndrome + pain along the
distribution of the ulnar nerve)
*Pericarditis and pleuritis may occur
•
Staging
of lung cancer
It is important for comparison of treatment results from different centres
It is important for comparison of treatment results from different centres
Ocult carcinoma-Bronchopulmonary secretions
contain malignant cells but no other evidence of cancer
Stage I T</= 3 cm with or without involvolvement
of
ipsilateral LNs (T1 No
Mo, T1 N1 Mo)
T > 3 cm but no LN involvement (T2 No
Mo)
Stage II T > 3 cm with involvement of ipsilateral
LNs (T2
N1 Mo)
Stage III T of any size with
invasion of pleura and adjacent structures or involving contralateral
mediastinal LNs or showing
distant metastasis
•
Clinical features
•
It
is insiduous but aggressive
•
Seen
mostly in the 6th decade of life usually with 7/12 symptoms of cough
(75%), wt loss (40%), chest pain (40%), dyspnoea (20%) and sometimes discovered
by its 20 spread
•
Despite
advances in high tech early diagnosis, 5-year survival is in the range of 9%
•
Adenoca
and SCC tend to remain localised longer and have a slightly better prognosis
•
Small
cell carcinomas are surgically un-resectable at the time of diagnosis
•
Paraneoplastic
syndromes may occur
•
Paraneoplastic syndromes seen in pts with BC
•
Some
of these syndromes antidate the BC
•
ADHà hyponatremia, mainly in small
cell carcinoma
•
ACTHà Cushing’s syndrome, mainly in
small cell carcinoma
•
Parathormone
or PGEà hypercalcaemia
mainly in SCC
•
Calcitoninà hypocalcaemia
•
Gonadotropinsà gynaecomastia
•
Serotoninà carcinoid syndrome, most
probably from carcinoid tumours
•
Other systemic manifestations of BC include:
•
Myopathy
•
Peripheral neuropathy
•
Acanthosis nigricans
•
Leukemoid reaction
•
Hypertrophic osteoarthropathy
•
Apical lung cancers can lead to:
a)
Horner’s syndrome = enopthalmos, ptosis, anhidrosis and
miosis
b)
Pancoat’s tumour = Horner’s syndrome + pain along the
distribution of the ulnar nerve
•
Other forms of pulmonary carcinomas
•
Bronchoalveolar carcinoma: this forms 1.1-9% of lung
cas and occurs in pts in their 3rd decade of life. The tumour occurs
well out of the pulmonary parenchyma and has equal sex distribution. Overall
survival rate is about 25%
•
Bronchial carcinoid. Seen about 1-5% of lung cancer
cases. It is locally invasive with occasional metastasis and most of the pts
are <40 years of age. May occur as part of MEN syndrome. The tumour rarely
exceeds 3-4 cm. Clinically may lead to carcinoid syndrome.
•
Lung diseases caused by air pollution
(pneumoconiosis)
•
These include:
•
Anthracosis due to exposure to coal dust
•
Silicosis due to exposure to silica dust
•
Asbestosis due to exposure to asbestos
•
Beryllosis due to exposure to beryllium
•
Siderosis due to exposure to iron
•
Stannosis due to exposure to tin oxide
•
Baritosis due to exposure to barium sulfate
These diseases have in common the
ability to cause diffuse pulmonary fibrosis due to the tissue reaction to the
presence of mineral dusts. Other chemical fumes, vapours and organic dusts are
also known to cause pulmonary fibrosis
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July 11, 2015
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