Obstructive Airway

Diseases
Dr. Mehzabin Ahmed
 DIFFUSE PULMONARY DISEASES
There are two categories
Obstructive diseases: There is an increase in the resistance
to airflow because of partial or complete obstruction at
any level from trachea and larger bronchi to the terminal
and respiratory bronchioles The conditions include:
Chronic Bronchitis, Emphysema, Bronchial Asthma, and
Bronchiectasis.
Chronic Bronchitis & Emphysema are categorized as
COPD- chronic obstructive pulmonary disease
Restrictive diseases: There is decreased expansion of the
lung, with a reduced total lung capacity. There are
1) Chest wall disorders normal lungs
2) Acute / chronic interstitial and infiltrative diseases
BRONCHIECTASIS
 Definition: It is a chronic necrotizing infection of the
bronchi and bronchioles leading to or associated with
abnormal dilation of these airways.
 The dilation of the airways is permanent / irreversible.
 Causes of bronchiectasis
Bronchial obstruction: resulting from a tumor or foreign body or
occasionally impaction of mucus. The bronchiectasis is restricted or
limited to the obstructed lung segment. Diffuse obstruction in the
airways throughout the lung may be seen in cases of bronchial
asthma and chronic bronchitis.
Congenital / Hereditary diseases: This groups includes
 a) Congenital Bronchiectasis – Defect in the development of bronchi
 b) Cystic fibrosis
 c) Immuno deficiency states
 d) Immotile cilia and Kartageners syndrome
 Necrotizing Pneumonia: Most often due to M. Tuberculosis or
staphylococci or mixed infections.
Pathogenesis
 Two factors are implicated in the pathogenesis of a full fledged
bronchiectasis:
a) Obstruction b) Infection
 Types of Lesions
1) Cylindroid – long tube like dilated

2) Fusiform-

3) Saccular-
 Clinical Presentation
 Fever – sometime high depending on the pathogen
 Cough – Productive with copious amounts of foul smelling
sometimes bloody sputum.
 These symptoms are episodic and are precipitated by, upper tract
infection or pathogens.
 These episodes / paroxysms are most frequent when the patient
rises inthe morning as postural changes → drainage of pus into
bronchi.
 Obstructive ventilatory disturbances cause respiratory insufficiency
→ dyspnoea and cyanosis.
Complications:
 1) Cor pulmonale
 2) Metastatic brain abscess
Cut surface:
Cystic spaces- dilated
bronchioles with
necrotic debris in
their lumen
Diagnostic techniques

1) X-ray multiple air fluid levels may be seen especially in saccular

bronchectasis

2) Bronchography using a radioactive dye, CT Scan,

3) Sputum examination

4) Bronchoscopy

5) Pulmonary function tests

6) Sputum culture, skin testing, serology → asthmatic with

bronchiectasis suggests allergic bronchopulmonary Aspergillosis
Bronchial Asthma

Definition:

Chronic relapsing inflammatory disorder characterized by

hyperactive airways, resulting in reversible bronchoconstriction,

owing to increased reactiveness of the tracheo bronchial tree to

various stimuli
 It is the most common cause of recurrent breathlessness, cough and
wheeze.
 Obstruction in the small airways due to bronchospasm and mucus
plugging
 Agents that trigger the asthma:
 Exposure to allergens like dust, fur,etc.
 Infections- viral infections in children
 Occupational exposure to allergens
 Drugs- β-antagonists and aspirin
 Irritant gases- SO2, NO, ozone in smog
 Psychological stress
 Exertion
 Cold air
 Pathogenesis
 2 major events
 a) chronic airway inflammation
 b) bronchial hyper responsiveness
 In the airways
 Initial sensitization TH2 cells IL 4, 5

IgE by B cells
Mast cell growth (IL-4)
Eosinophil– activation and growth(IL-5)

Subsequent exposures Immediate IgE mediated response

Late phase reaction
 Mediators
 Mediators responsible for asthmatic response are divided based on the
clinical efficacy of inhibitors / antagonists. They are
 1) Bronchoconstrictors :

 Leukotrienes C4, D4, E4

 Acetyl choline
 2) Biogenic amines:
 Histamine (bronchoconstriction ),
 PGD2 (bronchoconstriction + vasodilation) and
 PAF- Aggregation of platelets + release of histamine and serotonin
 3) Cytokines
Clinical Presentation

 The onset of an asthmatic attack begins with dyspnoea and wheezing

lasting for upto several hours and then followed by prolonged
productive coughing.
 The symptoms may persist at a low level all the time or may be severe
when it is called “status asthmaticus”. In states asthmaticus – the
severe acute paroxysm may persist for days or weeks and may be so
severe that cyanosis, and even death may result due to impaired
ventilation. The sputum produced is copious, and stringy, thick often
appearing as casts.
Investigations
 1) Sputum – Eosinophils, Charcot – Leyden crystals, Curshmann’s
spirals
 2)  Blood- Eosinophilia- increased number of eosinophils

Complication
 In severe forms of asthma, the progressive hyperinflation may
eventually produce emphysema
 Superimposed bacterial infectious – results in Chronic persistent
bronchitis, Bronchiectasis & Pneumonia
 Cor pulmonale and heart failure - rarely
Chronic Bronchitis
 It is common in smokers and urban dwellers. In long standing
cases it can
1)  Be associated with obstruction
2) Causes cor pulmonale and Heart Failure
3)  Causes metaplasia and dysplasia
Definition
Persistent cough with sputum production for 3 month in 2
consecutive years
Simple chronic bronchitis: Hyperreactive airways with bronchospasm
and wheezing
Obstructive chronic bronchitis: Chronic airflow obstruction usually
with emphysema in smokers
Pathogenesis
 Depends on 2 factors:

1) Chronic irritation by inhaled substance

2) Microbiologic infections

 Any sex or age can be affected but is more common in middle-

aged men 4-10 times more common in heavy smokers.

 Infections (viral bacterial) are responsible for acute exacerbations

and for maintaining the chronic bronchitis rather than initiating it.
Cigarette smoke:
 1) Interferes with ciliary action of the respiratory epithelium
 2) Direct damage
 3) Inhibit the ability of the bronchial and alveolar leucocytes to
clear up infection
Narrowing of bronchioles is due to:
 1) Goblet cells metaplasia
 2) Mucus plugging
 3) Inflammation
 4) Fibrosis
 Clinical Presentation

Patients with chronic bronchitis give a history of

 Dyspnoea on exertion in long standing cases
 Persistent productive cough with copious sputum
 Recurrent infection with abundant purulent sputum

Persistent smoking causes:

1) hypercapnia
2) hypoxemia COPD features
3) cyanosis
Thus they are called blue bloaters (cyanosed & edematous due to RHF)

Longstanding Cor Pulmonale RHF (right heart failure)

COPD + Acute intercurrent bacterial infection

Death

Diagnostic Procedures:

1) Pulmonary function tests: total lung capacity & residual volume are
increased in emphysema & decreased in chronic bronchitis

2) X-ray

3) Blood gas analysis

 Emphysema
Definition: It is the abnormal permanent enlargement of airspaces
distal to the terminal bronchiole, accompanied by destruction of
their walls, without obvious fibrosis.
 Enlargement of airspaces, without destruction the walls is called over
inflation.
Classification of Emphysema
 Emphysema is typed according to the anatomic distribution with the
lobule, into 4 major types:
 1) Centriacinar- central and proximal parts of the acini – common in
smokers
 2) Panacinar- The acinus is uniformly enlarged - in patients with α1 -
AT deficiency
3) Paraseptal-Distal portions of the acini are involved close to the
pleura- seen adjacent to areas fibrosis, scarring or atelectasis
4) Irregular
Pathogenesis

 The imbalance in the protease – antiprotease mechanism plays a

central role in the pathogenesis resulting in alveolar wall

destruction. Principle protease is elastase and antiprotease is α1-

AT.

 Elastase is produced by neutrophils principally and also by

macrophages, mast cells, pancreases and bacteria.

In smokers:

1) ↑ Number of PMN and macrophages in their alveoli: Smoking

causes ↑ PMN recruitment by IL – 8, Nicotine

2) Smoking stimulates release of elastase from PMN

3) Smoking enhances elastolytic proteases from macrophages which can

digest α1 AT

4) Oxidants in cigarette smoke + O2 free radicals from PMN → inhibit α

1
AT

Clinical Presentation:

 Dyspnea, cough, wheezing, weight loss

 Clinical Presentation
1) Dyspnoea:
Appears after atleast 1/3 of the functioning parenchyma is in
capacitated and is progressive
The chest is barred shaped and the patient sits with a lunched posture
as if trying to squeeze the air out. Patient in advanced cases may over
ventilate and may be well oxygenated, called pink puffers.
2) Cough: If associated bronchitis is present. In advanced case, it is slight.
3) Wheezing may be present
4) Weight loss
5) Death may be due to
Respiratory acidosis and coma
RHF due to cor - pulmonale
Pneumothorax resulting in collapse of the lung
Other Types of Emphysema:
1)      Compensatory Emphysema:
Dilation of alveoli and no destruction of septal walls. It is
hyperexpansion, in response to loss of lung parenchyma elsewhere.
2)      Senile Emphysema:
Over distended, voluminous lungs in the aged as a result of changes in
the normal proportionate size of alveolar ducts and alveoli. The ducts
become larger and alveoli smaller.
There is no destruction or loss of elastic tissue.
3)      Obstructive inflation:
Trapping of air in the lung due to an obstruction resulting in over
inflation. The obstruction may be by a tumor or a foreign body.
Bullous Emphysema:
 Any form of emphysema that
produces large sub-pleural bullae
(bubble like lesion).

> 1cm diameter, when inflated.

Common near the apex and

associated with scarring (e.g. old TB
scar).
 They may rupture and result
pneumothorax.
 Interstitial Emphysema:
Entry of air into the connective tissue stroma of lung, mediastinum
or subcutaneous tissue. Alveolar tears may cause emphysema
into the connective tissue stroma of the lung.

These occur when there is cough in presence of obstruction

resulting in increased pressure, in the alveolar sacs.

E.g. whooping cough, bronchitis (in children), obstruction due

to foreign body, tumor or clots, artificial ventilation
(tracheostomy), sudden inhalation of irritant gases