Obstructive Lung Diseases (L17-18)

Question 1

When might respiratory failure occur?

2

Answer 1

When there is:

• Impaired Clearance of CO2 from the Lungs
• Impaired Absorption of O2 from the Air

Question 2

Describe Type I Respiratory Failure/Acute Hypoxaemic Respiratory Failure.

Answer 2

• Caused by a ventilation/perfusion mismatch

1. Arterial pO2 is low
2. Arterial pCO2 is normal or low

Question 3

Type I Respiratory Failure occurs with diseases that damage the lung.
Name them.

Answer 3

• Low ambient oxygen (high altitude)
• Pneumonia (parenchymal disease)
• Pulmonary Fibrosis
• Ventilation/Perfusion mismatch (pulmonary embolism)

Question 4

Describe Type II Respiratory Failure

Answer 4

• Caused by increased airway resistance due to reduced breathing effort, increased resistance to breathing or a decrease in the lung area available for gas exchange.

1. Arterial pO2 is low
2. pCO2 is high (Hypercapnia)

Question 5

List the most common causes of Type II Respiratory Failure.

Answer 5

• COPD
• Asthma
• Poliomyelitis
• Drug overdose
• Myasthenia gravis
• Motor neuron disease

Question 6

Define Obstructive Lung Disease.

Answer 6

A decrease in the exhaled air flow caused by acute or chronic narrowing or blockage of the airways causing increased resistance to airflow.

Question 7

Define Restrictive Lung Disease.

Answer 7

A decrease in the total volume of air that the lungs are able to hold. Often this is due to a decrease in the elasticity of the lungs or a problem related to the expansion of the chest wall during inhalation.

Question 8

What is the predominant cause of COPD?

Answer 8

Smoking.

Question 9

COPD Pathology:

Central Airways:
Bronchial gland hypertrophy and goblet cell metaplasia – results in excessive ___1___ production (chronic bronchitis).
___2___ metaplasia of airway epithelium, loss of cilia and cilia dysfunction, increased smooth muscle and connective tissue.

Peripheral Airways:
Bronchiolitis at an early stage. Pathological extension of goblet cells and ___2___ metaplasia in the peripheral airways. As the disease progresses there is fibrosis and increased deposition of ___3___.

Pulmonay Vasculature:
Pulmonary vasculature changes begin early in disease. Initially characterised by ___4___ of the vessel wall and endothelial cell dysfunction.
Followed by increased smooth muscle, infiltration of inflammatory cells and in advanced disease there is ___3___ deposition and destruction of the capillary bed.

Answer 9

1. Mucus
2. Squamous
3. Collagen
4. Thickening

Question 10

COPD is characterized by an increase in ___1___, macrophages, and T lymphocytes (especially ___2___) in various parts of the lung.
There may also be an increase in eosinophils in some patients, particularly during exacerbations.
These increases are brought about by increases in inflammatory cell recruitment, ___3___, and/or activation.
Many studies reveal a correlation between the number of inflammatory cells of various types in the lung and the severity of COPD.

Answer 10

1. Neutrophils
2. CD8+
3. Survival

Question 11

Describe the Inflammatory Cell Increases in COPD in the following:

Large Airways.

Small Airways.

Parenchyma.

Pulmonary Arteries.

Answer 11

Large Airways:

• Macrophages
• T lymphocytes (especially CD8+)
• Neutrophils (severe disease only)
• Eosinophils (in some patients)

Small Airways:

• Macrophages
• T lymphocytes (especially CD8+)
• Eosinophils (in some patients)

Parenchyma:

• Macrophages
• T lymphocytes (especially CD8+)
• Neutrophils (severe disease only)

Pulmonary Arteries:

• T lymphocytes (especially CD8+)
• Neutrophils (severe disease only)

Question 12

Inflammation is present in the lungs of ___1___ without a diagnosis of COPD. This inflammation is similar to, but less intense than, the inflammation in the lungs of patients with COPD. Thus, the inflammation characteristic of COPD is thought to represent an ___2___ of a normal, protective response to inhalational exposures.

Answer 12

1. Smokers

2. Exaggeration

Question 13

List the most common symptoms of COPD.

Answer 13

• Exertional Breathlessness
• Chronic Cough
• Regular Sputum production
• Frequent winter bronchitis
• Wheeze

They may also show:

• Weight loss
• Effort intolerance
• Waking at night
• Ankle swelling
• General fatigue

Question 14

The MRC dyspnoea scale is used to grade breathlessness.

Describe it from grade 1 (least severe) to grade 5 (most severe).

Answer 14

Grade 1: Not troubled by breathlessness except on strenuous exercise

Grade 2: Short of breath when hurrying or walking up a slight hill

Grade 3: Walks slower than contemporaries on level ground because of breathlessness, or has to stop for breath when walking at own pace.

Grade 4. Stops for breath after walking about 100 metres or after a few minutes on level ground.

Grade 5. To breathless to leave the house, or breathless when dressing, undressing.

Question 15

What is used to treat stable COPD?

4

Answer 15

• Bronchodilators
• Corticosteroids
• Mucolytics
• Antibiotics

Question 16

Clinically define Chronic Bronchitis.

Answer 16

A cough productive of sputum on most days for three months of the year for at least two consecutive years.

Question 17

What is the major consequence of chronic bronchitis?

Answer 17

Airway obstruction.

Question 18

What does Chronic Bronchitis lead to?

4

Answer 18

• Alveolar Hypoventilation
• Hypoxaemia
• Hypercapnia
• Type II Respiratory Failure

Question 19

Define Emphysema.

Answer 19

Permanent enlargement (dilation) of any part of the respiratory acinus (air spaces distal to the terminal bronchiole) with destruction of their walls (without scarring).

Question 20

Name the 2 main patterns of Emphysema.

Describe each.

Answer 20

Centriacinar (centrilobular)
- Is a result of the destruction of the respiratory bronchioles.

Panacinar (panlobular)
- Results from a more uniform destruction of all of the acinis and particularly affects the lower lungs.

Question 21

The main Emphysema pathogenesis theory is:
The proteinase-antiproteinase hypothesis.

Describe it.

Answer 21

Destruction of alveoli occurs due to the un-regulated activity of proteinase enzymes.

It is due to an imbalance of protease and the protease inhibitor a1-antitrypsin. Proteases (particularly Neutrophil Elastase) cause the breakdown of alveolar walls and collapse of small airways.

Question 22

Alpha -1 antitrypsin deficiency (AATD) is thought to be one of the most common genetic deficiencies in ___1___.

There are many different mutations in AAT but the most severe type is commonest in North West Europe. It occurs with a frequency of 1/___2___ in Scandinavia.

The most common form allele in the European population is M and two mutant alleles S and ___3___ account for most of the disease.

Answer 22

1. Caucasians
2. 1600
3. Z

Question 23

What is the classic presentation of patients with Emphysema?

Answer 23

Barrel-chested and dyspnoeic.

Question 24

The loss of elastic recoil and structural support due to Emphysema leads to what?
(3)

Answer 24

• Trapping of air in lungs
• Over inflated lungs
• Decreased rate of airflow on expiration

Question 25

Cyanosis, hypercapnia and cor pulmonale (enlargement of the right ventricle) occur _____ in Emphysema after progressive decline in lung function.

Answer 25

Late.

Question 26

Individuals with emphysema have reduced oxygen uptake despite an increase in ventilation.

Although they manage to maintain blood oxygenation by rapid respiration they feel breathless on the slightest exertion and become hypoxic (Type II respiratory failure).

Patients are known as ‘_____ _____’

Answer 26

Pink Puffers.

Question 27

Describe the pathology of Asthma.
(5)

This leads to?

Answer 27

• Mucosal Oedema
• Inflammatory cell infiltration (Eosinophils 5%-50%)
• Basement membrane thickening
• Goblet cell and submucosal gland hyperplasia.
• Hypertrophy and hyperplasia of the smooth muscle in the bronchial wall.
• Airway Obstruction
• Bronchial Muscle Constriction
• Airway Congestion

Question 28

In Asthma thick mucus plugs can block the bronchi and bronchioles.
What do the mucus plugs contain?

Answer 28

• Whorls of shed epithelium
• Eosinophils
• Charcot - Leyden Crystals

Question 29

Asthma is split into extrinsic and intrinsic asthma which is based on its cause.

Describe each type.

Answer 29

Extrinsic (allergic) asthma
- Caused by Type I hypersensitivity reactions on exposure to extrinsic allergen

Intrinsic asthma
- Non-immune trigger mechanism e.g. cold, stress, exercise, inhaled irritants (gases)

Question 30

Describe Obliterative bronchiolitis.

Answer 30

Obliterative bronchiolitis (OB) is an irreversible lung disease that occurs in children and adults after injury to the lower respiratory tract. There is concentric narrowing and distortion of the bronchiole walls caused by inflammation and fibrosis. The alveoli are not involved.

Question 31

Describe Non-smoking fixed obstruction.

Answer 31

There is evidence that in some non-smoking patients with asthma remodelling may occur that may finally result in fixed lung obstruction.

Question 32

Describe Viral wheeze.

Answer 32

Episodic attacks of wheeze triggered by viral colds are common in children aged between 1 and 5 years.

Question 33

Describe Allergic bronchopulmonary aspergillosis.

Answer 33

A hypersensitivity response to the fungus Aspergillus fumigatus. The subsequent damage to the bronchial wall causes (proximal) bronchiectasis. Repeated acute episodes left untreated can result in progressive pulmonary fibrosis.

Question 34

Describe Bronchiectasis.

Answer 34

Localized, irreversible dilation of part of the bronchial tree. Bronchi are dilated, inflamed, and easily collapsible, resulting in airflow obstruction and impaired clearance of secretions. Normally a result of infection.