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: b) Infection

a) Obstruction

Types of Lesions

1) Cylindroid – long tube like dilated 2) Fusiform3) 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. 1) Cor pulmonale 2) Metastatic brain abscess

Complications:
 

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 Cytokines

3)

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 eventually produce emphysema

may

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 middleaged 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 3) cyanosis COPD features

Thus they are called blue bloaters (cyanosed & edematous due to RHF) Longstanding COPD Cor Pulmonale RHF (right heart failure)

+ 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 α1AT.

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: 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

Smoking

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 scar). near the apex and

associated with scarring (e.g. old TB

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

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