Respiratory System

Question 1

Primary & Secondary Acelectasis

Answer 1

• Atelectasis in the newborn or primary atelectasis is defined as incomplete expansion of a lung or part of a lung.
• Pulmonary collapse or secondary atelectasis is the term used for reduction in lung size of a previously expanded and well aerated lung.

Question 2

Kinds of pulmonary collapse or secondary atelectasis?

Answer 2

1. Compressive collapse.
   
   • Pressure from outside causes compressive collapse e.g. by massive pleural effusion, haemothorax, pneumothorax, intrathoracic tumour, high diaphragm and spinal deformities.
   • Compressive collapse involves subpleural regions and affects lower lobes more than the central areas.
2. Obstructive/absorptive collapse.
   
   • Obstruction of a bronchus or many bronchioles causes absorption of oxygen in the affected alveoli followed by collapse
   • e.g. by viscid mucus secretions in bronchial asthma, chronic bronchitis, bronchiectasis, bronchial tumours and aspiration of foreign bodies.
   • Obstructive collapse is generally less severe than the compressive collapse and is patchy.
3. Contraction collapse.
   
   • This type occurs due to localised fibrosis in lung causing contraction followed by collapse.

Question 3

What are the main causes of pulmonary edema?

Answer 3

• Hemodynamic disturbances
  
  • The most common mechanism is the one attributable to increased hydrostatic pressure, as occurs in left-sided congestive heart failure.
  • It can also occur as a consequence of decreased plasma oncotic pressure.
• Direct increase in capillary permeability
  
  • The most common causes are infectious agents, inhaled gases, liquid aspiration, and drugs.
  • The edema results from primary injury to the vascular endothelium or damage to alveolar epithelial cells (with secondary microvascular injury).
• Lymphatic insufficiency
  
  • Lymphangitic carcinomatosis.
  • Fibrosing lymphangitis (e.g., silicosis).

Question 4

What are the pathologic features of pulmonary congestion and edema?

Answer 4

• Macroscopic features
  
  • Pulmonary congestion and edema are macroscopically characterized by heavy, wet lungs.
  • Long-standing pulmonary congestion causes brown induration of the lungs (the lungs are firm and brown), which predisposes to infection.
• Histologic features
  
  • The alveolar capillaries are engorged.
  • Proteinaceous material is located within the alveoli; it appears pink in the hematoxylin and eosin-stained specimens.
  • In long-standing cases of pulmonary congestion, numerous heart failure cells, as well as fibrosis and thickening of the alveolar walls, appear.

Question 5

Chronic obstructive pulmonary disease (COPD)

Answer 5

Chronic obstructive pulmonary disease (COPD) or chronic obstructive airway disease (COAD) are commonly used clinical terms for a group of pathological conditions in which there is chronic, partial or complete, obstruction to the airflow at any level from trachea to the smallest airways resulting in functional disability of the lungs i.e. they are diffuse lung diseases. The following 4 entities are included in COPD:

1. Chronic bronchitis
2. Emphysema
3. Bronchial asthma
4. Bronchiectasis

Question 6

What is chronic bronchitis?

Answer 6

Chronic bronchitis is defined clinically as persistent cough with sputum production for at least 3 months of the year, in at least 2 consecutive years.

Most important initiating agent in chronic bronchitis is smoking

Question 7

Reid index

Answer 7

Reid index is the ratio of the mucus gland layer thickness to the thickness of the wall between epithelium and cartilage.

Normal Reid index is 0.4 whereas its value increases in chronic bronchitis.

Question 8

Discuss the pathologic characteristics of chronic bronchitis.

Answer 8

Hyperemia, swelling, and bogginess of the mucous membranes are the main macroscopic features. They are frequently accompanied by excessive mucinous to mucopurulent secretions covering the epithelial surfaces. Heavy casts of secretions and pus occasionally fill the bronchi and bronchioles.

The typical histologic feature of chronic bronchitis is enlargement of the mucus-secreting glands of the trachea and bronchi. Increase in the size of the mucous glands is assessed by the ratio of the thickness of the mucous gland layer to the thickness of the wall between the epithelium and the cartilage (Reid index). The Reid index is normally 0.4.

Marked narrowing of bronchioles caused by goblet cell metaplasia also occurs, as do mucous plugging, inflammation, and fibrosis. In the most severe cases, obliteration of lumens (bronchiolitis obliterans) further aggravates the patient’s condition.

Question 9

What are the clinical features of chronic bronchitis?

Answer 9

• Late onset of dyspnea with productive cough (copious sputum), recurrent infections, hypoxemia and mild cyanosis (BLUE BLOATERS).
• Long-standing severe chronic bronchitis often results in cor pulmonale with cardiac failure.
• There is a persistent cough productive of copious sputum.
• When persistent for years, eventually dyspnea on exertion develops.
• In time, and usually with continued smoking, hypercapnia, hypoxemia, and mild cyanosis with other elements of COPD may appear.

Question 10

What is emphysema?

Answer 10

Emphysema is a condition of the lung in which abnormal permanent enlargement of the airspaces distal to the terminal bronchiole is accompanied by destruction of their walls, without obvious fibrosis. There are four main types of emphysema:

• Centriacinar (centrilobular)
• Panacinar (panlobular)
• Paraseptal (distal acinar)
• Irregular

Only the first two types cause clinically significant airflow obstruction. Centriacinar emphysema accounts for 95% of all cases and is far more common than the panacinar form or other rare forms of emphysema.

Question 11

Alpha-1 antitrypsin and Emphysema

Answer 11

• Normally, the pulmonary tissue destruction by elastase is prevented by the presence of anti-elastase activity which is primarily due to α1 -antitrypsin.
• Any increase in neutrophils (usually in smokers) or deficiency of a1 –AT would contribute to development of emphysema.
• Characteristically, there is loss or reduction of elastic recoil of the lung.
• a1 -AT is synthesizedinthe liver.
• The normala 1 -AT phenotype is PiMM.The abnormal phenotype is PiZZ which is associated with a1 -AT deficiency and development of emphysema at earlier age and greater severity.

Question 12

What are the main characteristics of different types of emphysema?

Answer 12

1. Centriacinar (centrilobular)
   
   • The central or proximal parts of acini, formed by respiratory bronchioles, are affected, whereas distal alveoli are spared.
   • The lesions are often localized and usually more severe in the upper lobes, particularly in the apical segments.
   • The walls of the emphysematous spaces often contain abundant black pigment.
   • It tends to occur in heavy smokers.
2. Panacinar (panlobular)
   
   • The acini are uniformly enlarged because the process affects all of the structures, from the respiratory bronchiole to the alveoli (the prefix pan refers to the entire acinus but not to the entire lung)
   • It tends to occur in the lower zones and in the anterior margins of the lung and is associated with a1-antitrypsin deficiency.
3. Paraseptal (distal acinar)
   
   • The proximal part of the acinus is normal, and the distal acinar portion is dominantly involved (more severe in the upper half of the lungs).
4. Irregular
   
   • It is almost invariably associated with scarring.
   • The acinus is irregularly involved.

Question 13

Emphysema; Clinical features

Answer 13

• 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)

Question 14

Define bronchial asthma and status asthmaticus.

Answer 14

Bronchial asthma is a chronic relapsing inflammatory disorder presenting with hyperreactive airways that cause episodic, reversible bronchoconstriction. The reaction is the consequence of increased responsiveness of the tracheobronchial tree to various stimuli. Patients experience unpredictable disabling attacks of severe dyspnea, coughing, and wheezing triggered by sudden episodes of bronchospasm. Between the attacks, virtually no symptoms occur, but in some people, chronic bronchitis or cor pulmonale supervenes.

In the most severe form of asthma, status asthmaticus, the severe acute paroxysm persists for days and even weeks, threatening the ventilatory function enough to cause severe cyanosis and even death.

Question 15

Asthma

Answer 15

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

Question 16

Asthma; Pathogenesis

Answer 16

1. Primary exposure of an allergen causes TH2 cell dominated inflammatory response resulting in IgE production and eosinophil recruitment (called sensitization).
2. 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.
3. Antigens then cause activation of mucosal mast cells and eosinophils and this along with neuronal reflexes (subepithelial vagal receptors) cause bronchospasm, increased vascular permeability and mucus production (Acute or Immediate response).
4. Later on, leukocytic infiltration causes release of more mediators and damage to the epithelium (Late Phase Reaction).
5. Eosinophils in airways release major basic protein which causes epithelial damage and more airway constriction.
6. Leukotrienes C4 , D4 , E4 and acetylcholine have definite role in bronchoconstriction whereas agents like histamine, PGD2 and platelet activating factor (PAF) may also have role in the features of the disease.

Question 17

Exercise induced asthma

Answer 17

Exercise causes loss of water and heat from the respiratory tract. The water loss causes mucosal hyperosmolarity which stimulates release of mediators from the mast cells. This explains the pathogenesis of exercise induced asthma.

Question 18

3 C’s of sputum findings in asthma;

Answer 18

Charcot leyden crystals

Curschmann spirals

Creola bodies