Pathology of Obstructive Lung Disease

Question 1

Contrast the management of asthma with strategies for management of COPD.

Answer 1

asthma and COPD both have similarities in inhaled therapy- bronchodilators.

COPD:

• smoking cessation services
• pulmonary rehabilition
• nutritional support
• pyschological support
• inhaled therapy

Question 2

Describe the major pathological feature of the common obstructive lung diseases, asthma, chronic bronchitis and emphysema and their complications (including hypoxic cor pulmonale).

Answer 2

in obstructive lung disease…

• Airflow limitation
• FEV1 is reduced
• FVC may be reduced
• FEV1 is <70% of FVC
• PEFR is reduced

Question 3

Define chronic bronchitis

Answer 3

• Defined clinically by cough productive of sputum most days in at least 3 consecutive months for 2 or more consecutive years.

Question 4

Define emphysema

Answer 4

• An abnormal increase in the size of airspaces distal to the terminal bronchiole (last conducting tube) either because of dilatation or from destruction of their bronchial walls.
• HYPER inflated lungs- because it keeps the airways open thus having more air their lungs
• Destruction of alveolar wall tissue, reduces surface area for gas exchange to take place.

Question 5

Forms of emphysema

Answer 5

• Centra-acinar:
  o Affects the top of the lung, holes
  o Begins with dilatation of the bronchiole
  o Then alveolar tissue is lost
• Pan-acinar:
  o Wiping out ALL of the lung tissue
  o BULLA which is an emphysematous space >1cm
  o Bleb is BULLA spaces just beneath the pleura

Question 6

Pathogenesis of Emphysema

Answer 6

• Smoking causes Protease-Antiprotease imbalance
• Ageing
• Alpha-1-antitrypsin deficiency
• Normal individual:
  o Production of elastase for Alveoli, there needs to be an anti-elastase so there is a safe elastic framework in the lungs.
• Emphysema patients do not have all of these protective enzymes.
  o Anti-elastase is absent in alpha 1 antitrypsin deficiency
• Smoking:
  o Too much elastase but insufficient anti-elastase leads to tissue destruction

Question 7

pathogenesis of COPD

Answer 7

• MOST of the obstruction in airways is not reversible, but there is a reversible component
• Most airway limitation results from obstruction of the SMALL airways.
  o Increase in smooth muscle tone
  o Inflammation respond to the same drugs as in Asthma however in the airways of chronic bronchitis there is also FIBROSIS. NO drug can treat fibrosis.
  o Emphysema- we cannot regrow our alveolar walls, there is no drug to do this. We LOSE OUR ALVEOLAR ATTACHMENTS
   When we expire, we do not collapse because of the alveolar walls have elastic tissue acts like “tent poles”. Keeps the airway open.
   In emphysema, the tent poles are gone and we lose the pull of the terminal bronchiole. FLOPPY airways -> airflow limitation.

Question 8

Abnormal Pulmonary Gas exchange- recap.

Answer 8

• Normal PaO2 10.5 – 13.5 kPa
• Normal PaCO2 4.8 – 6.0 kPa

Respiratory Failure
• Type I PaO2 <8 kPa (normal or low PCO2)

• Type II PaCO2 >6.5 kPa (usually low PaO2)

Question 9

Describe the term ‘s_h_u_n_t_’._ _

Answer 9

• Blood passes from the right side of the heart to the left side of the heart without contacting ventilated alveoli.
• Severe bronchopneumonia
• Lobar pattern with large areas of consolidation

Question 10

Know the difference between anatomical, alveolar and physiologic dead space.

Answer 10

Anatomic dead space describes the volume of air that does not take part in gas exchange.

physiologic, dead space refers to the portion of the air that reaches gas exchange regions of the lung, but does not receive enough BLOOD FLOW for gas exchange to occur

Alveolar dead space alveoli which have little or no blood flow through them. Alveolar is ventilated but not perfused, so as a result, no gas exchange can occur.

Question 11

complications of COPD

Answer 11

• cor pulmonale
• anemia
• recurrent pneumonia
• depression
• pneumothorax
• respiratory failure
• polycythaemia

Question 12

describe cor pulmonale

Answer 12

Right-sided heart failure (heart disease secondary to lung disease)

It is caused by chronic hypoxia and subsequent vasoconstriction in pulmonary vasculature which causes pulmonary hypertension and right-sided heart failure.

Question 13

describe “blue bloaters”

Answer 13

in severe Chronic bronchitis, reduced respiratory drive.

-Gradually the body begins to realise that it cannot cope with poor ventilation.
o Central chemoreceptors are sensitive to H ions in CSF is the primary drive for regulating arterial PCO2.
o There is a loss of respiratory drive because they have become insensitive to hypoxia.

Question 14

describe pink puffers

Answer 14

in severe emphysema, increased respiratory drive

• breathing like crazy, responding to hypoxia

Question 15

why does hypoxaemia occur in COPD patients?

Answer 15

• reduced respiratory drive
• loss of alveolar surface area
• airway obstruction
• ventilation/perfusion imbalance
• shunt