Lung pathology 2

Obstructive Lung Diseases

Dr.G.Bhanu prakash , www.gims-org.com,www.usmletutor.org

1.Chronic Bronchitis
• It is defined clinically as the presence of
productive cough for At least 3 months in at least
2 consecutive yrs in absence of any other
identifiable cause.
• The most important initiating agent is smoking
resulting in airways irritation leading to mucus
hypersecretion, the latter may cause airways
obstruction. Infection plays a secondary role
particularly in maintaining chronic bronchitis and
are also responsible for the acute exacerbations.
Dr.G.Bhanu prakash , www.gims-
org.com,www.usmletutor.org

• Histologic features Include chronic lymphocytic
infiltration of the airways and submucosal gland
hypertrophy. There is also increase in Reid index
(it is the ratio of the thickness of the mucus gland
layer to the thickness of the wall. The bronchial
epithelium may also have squamous metaplasia
and dysplasia.
• clinical features: Late onset of dyspnea with
productive cough(copious sputum), recurrent
infections, hypoxemia and mild cyanosis (BLUE
BLOATERS). Long standing chronic bronchitis can
cause cor pulmonale (right sided heart failure due
to pulmonary hypertension).

2.Emphysema
It is abnormal permanent enlargement of the air
space distal to terminal bronchioles and is
associated with destruction of their walls.
• Most imporant etiological agent for emphysema
is smoking which causes inflammation in airways
resulting in increased neutrophils and
macrophages. These inflammatory cells release
elastase responsible for destruction of lung
tissue resulting in emphysema.


• Normally, the pulmonary tissue destruction by
elastase is prevented by the presence of anti-
elastase activity which is primarily due to α1- AT
(with minor contribution from secretory
leukoprptease inhibitor in bronchial mucus and
α
serum 1- macroglobulin). So any increase in
neutrophils (usually in smokers) or deficiency of
α1-AT would contribute to development of
emphysema. Characteristically, there is loss or
reduction of elastic recoil of the lung.

• α1-AT is synthrsized in the liver. The normal
α1-AT phenotype is PiMM. The abnormal
phenotype is PiZZ which is associated with α1-
AT deficiency and development of emphysema at
earlier age and greater severity.+


Emphysema

Centriacinar Panacinar Distal acinar Irregular


ntriacinar Panacinar Distal acinar

ement of •Involvement of the •Distal part of acinus is
part of acinus entire acinus affected with sparing of
aring of alveoli . proximal part of acinus
•Seen with α1-AT
n smokers . deficiency • Seen in smokers .
y more sever in •Occurs more •Involvement of lung
obes (due to severely in lower adjacent to pleura
deficiency of lobes at base of lung
•Associated with the
1-AT to this less (due to lower lung
development of
d region). distribution of

• Clinical features: progressively increasing
dyspnea, weight loss, late onset of cough with
scanty sputum. The patient is non- cyanotic,
uses accessory muscle of respiration and shows
pursed lip breathing.(PINK PUFFERS)
• Management: Cessation of smoking and use of
bronchodilators is the mainstay of the
management.
Mnemonic:
 emPhysema had letter P (and not B). So Pink
Puffer.
Chronic Bronchitis has letter B(and not P) so blue
Bloater.

3.Asthma
Hyperactivity of the airways resulting in reversible
bronchoconstriction and air flow obstruction on
exposure to some external stimuli is called
asthma.
ASTHMA

Extrinsic asthma Intrinsic asthma


Extrinsic asthma Intrinsic asthma

ype I hypersensitivity •Viral pulmonary infection
action • Cold
• Inhaled irritants
Commoner type of asthma
• Stress
Positive family history • Exercise
erum IgE levels are • Drug induced (most
evated commonly by aspirin
ingestion)
• Negative family history
• Serum IgE levels are norma

• Pathogenesis: Primary exposure of an allergen
causes T H2 cell dominated inflammatory
response resulting in IgE production and
eosinophil recruitment (called sensitization).
Exposure to the same allergen causes cross
linking of IgE bound to IgE receptors on mast
cells in the airways which cause opening up of
epithelial cells due to released mediators.
• Antigens then cause activation of mucosal mast
cells and eosinophils and this along with
neruonal reflexes (subepithelial vagal
receptors)cause bronchospasm, increased
vascular permeability and mucus production
(Acute or immediate response).

• Later on, leukocytic infiltration causes release of
more mediators and damage to the epithelium
(late Phase Reaction). Eosinophils in airways
release major basic protein which causes
epithelial damage and more airways constriction.
• Leukotrienes C4, D4, E4 and acetylocholine have
definite role in bronchoconstriction whereas
agents like histamine, PGD2 and platelet
activating factor (PAF) may also role in the
features of the disease.


• In intrinsic asthma, aspirin causes shift of the
arachidonic acid metabolism towards the
lipoygenase pathway resulting in formation of
the bronchoconstrictor leukotrienes.
• Virus induced inflammation lowers the threshold
of the subepithelial vagal receptors to irritants.
• Exercise causes loss of water and heat from the
respiratory tract. The water loss causes mucosal
hyperosmolarity which stimulates release from
the mast cells. This explains the pahtogenesis of
exercise induced asthma.

• Important fact:
IL- 13 gene polymorphism is strongly associated
with bronchial asthma. ADAM-33 is another gene
causing proliferation of smooth muscle cells and
fibroblasts in bronchi resulting in bronchial
hyperreactivity and subepithelial fibrosis.


• Clinical features:
Acute asthmatic attack is characterized wheezing,
cough and severe dyspnea.
• Morphology:
 The most stroking macroscopic finding is
occlusion of the bronchi and bronchioles by
mucus plugs.
Histologically, there are numerous eosiphils,
Charcot leyden crystalsQ (composed of eosinophil
membrane protein called as galectin-10) and
Curschmann spirals Q (whorls of shed airways
epithelium). Dr.G.Bhanu prakash , www.gims-

 Structural changes in the bronchial wall called
“airway remodelling” is characterized by presence of
eosiphilic inflammation and edema of bronchial
walls, increased size of submucosal glands,
hypertrophy of bronchial wall smooth muscle and
deposition of subepithelial collagen in the bronchial
wall. Individual epithelial cells presents in the
sputum of the patients are called Creola bodies.
 Management is done with bronchodilators and
corticosteroids (for details, refer to the review of
pharmacology by the same authors.


4. Bronchiectasis
• Abnormal permanent airways dilation resulting
from chronic necrotizing infection is called
bronchiectasis.
Cause

Bronchial Necrotizing
Congenital Miscellaneous
Obstruction pneumonias
Tumor Cystic fibrosis Mycobactrium SLE
Kartagener syndrome Staph. aureus Rheumatoid
Foreign body arthritis
(triad of Bronchiectasis+
Aspergillus
Situs inversus+ sinusitis) Post
Influenza virus trasplanation

• Obstruction and infection are the chief
contributors to the damages of airways wall
associated with destruction of smooth muscle
and elastic tissue fibrosis and further dilation of
bronchi.


• Clinical features:
Chronic cough, fever, foul smelling sputum
production, recurrent pulmonary infection,
sinusitis and immune deficiencies.
It usually affects vertical air passages of the lower
bilaterally with involvement of left side more
frequent than right.
The dilated bronchi can be followed directly out
to the pleural surfaces. There is usually presence
of inflammatory cell in the walls of bronchi and
bronchioles which may also exhibit squamous
metaplasia. Dr.G.Bhanu prakash , www.gims-

• Complications include massive hemoptysis,
amyloidosis, visceral abscess and cor
pulmonale.
• Management is done by chest physiotherapy,
natural drainage, bronchilators and
antibiotics. High Resolution CT scan (HRCT) is
the best investigation for the detection of
bronchiectasis.


Lung pathology 2

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