COPD Flashcards

1
Q

What two pathological mechanisms produce COPD?

A

Chronic bronchitis and emphysema

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2
Q

What do chronic bronchitis and emphysema have in common?

A
  • they both cause chronic airway obstruction, breathlessness and exercise intolerance
  • both are caused by smoking and often occur together
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3
Q

What happens to inhaled carbon?

A

Inhaled carbon is ingested by macrophages and can persist in the lung for many years.

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4
Q

Severe COPD can cause what?

A

Respiratory failure and death

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5
Q

Why is asthma not classed as COPD?

A

Because the obstruction is reversible.

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6
Q

How is airway obstruction measured clinically?

A

Using spirometry

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7
Q

What characterises COPD/ COAD?

A

COPD is characterised by persistent, largely irreversibly obstruction to airflow in the lungs.

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8
Q

What the is the forced expiratory volume?

A

It is the volume of air breathed out when breathing as fast and hard as possible following a maximal inspiration.

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9
Q

When should the majority of lung volume be expelled when looking at FEV?

A

In the first second

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10
Q

Describe the spirometry trace of a COPD patient.

A

In a COPD patient, the air is expelled much more slowly and FEV is also lower meaning that a larger volume of air remains in the lung.

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11
Q

What is chronic bronchitis?

A

Persistent inflammation of the bronchi

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12
Q

What is the cause of chronic bronchitis?

A

Chronic bronchitis is caused by inhaled irritants such as tobacco smoke that damage the mucosa —> persistent inflammation –> hyper section of mucus as an adaptive response to chronic irritation of the mucosa. –> excess mucus causes a cough productive of sputum.

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13
Q

What is the clinical definition of chronic bronchitis?

A

Sputum productive cough for at least three months in at least two consecutive years

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14
Q

What are the sources of intraluminal bronchial mucus?

A

Sub coal mucous glands and goblet cells of the respiratory epithelium

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15
Q

What makes chronic bronchitis an obstructive disorder?

A

The narrowing of bronchi and bronchioles produced

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16
Q

What factors contribute to the narrowing of bronchi and bronchioles in chronic bronchitis?

A
  • hyper trophy of goblet cells and enlargement of mucous glands –> increased mucus in the lumen
  • inflammatory oedema of the wall
  • thickened smooth muscle/ hyper reactivity of bronchial walls
17
Q

What factors cause bronchoconstriction ?

A
  • parasympathetic nerve activity
  • histamine
  • cigarette smoke
  • exercise
  • aspirin
18
Q

Chronic damage to bronchial epithelium can result in metaplasia. What type of metaplastic epithelium results?

A

The normal bronchial epithelium changes to stratified squamous epithelium. This is called squamous metaplasia.

19
Q

Describe the presentation of chronic bronchitis.

A
  • patients with chronic bronchitis have a cough by definition
  • failure in gas exchange –> exercise intolerance
    -breathlessness but respiratory drive is insufficient and fail to ventilate lungs sufficiently
    -hypoxia and carbon dioxide retention –> cyanosis
    BLUE BLOATERS.
  • as air passes through narrowed airways it produces abnormal sounds (crackles and wheezes) heard through a stethoscope.
20
Q

Why does chronic bronchitis predispose to infection?

A

Because of the excess mucus stagnating in the airways allows pathogen to settle especially if the smoking has damaged the mucociliary escalator. This is called an infective exacerbation of chronic bronchitis.

21
Q

If the bronchi become infected what happens to the sputum?

A

It changes from grey in colour to yellow or green.

22
Q

What are the commonest bacteria to cause infection in chronic bronchitis?

A

Streptococcus pneumoniae and haemophilus influenzae

23
Q

What happens if the infection spreads to adjacent alveoli?

A

It causes bronchopneumonia.

24
Q

What does chest infection refers to?

A

An infective exacerbation of chronic bronchitis or pneumonia.

25
Q

Why does hypoxia produce cyanosis?

A

Reduced haemoglobin is blue. Cyanosis indicates an increased concentration of deoxygenated haemoglobin in the blood.

26
Q

What is emphysema?

A

Abnormal enlargement of air spaces distal to terminal bronchioles due to destruction of the walls of respiratory bronchioles and alveoli.

27
Q

What is the principal cause of emphysema?

A

Damage due to cigarette smoke

28
Q

Much of what we know about the pathogenesis of emphysema can by explained by…

A

The protease/ antiprotease imbalance hypothesis

29
Q

Describe the protease/ antiprotease imbalance hypothesis

A

In emphysema, there is destruction of alveolar and respiratory bronchial walls by proteases that are derived from activated neutrophils and macrophages. These neutrophils and macrophages are part of the inflammatory reaction to tobacco smoke. In normal individuals, proteases are inactivated by antiprotease enzymes such as alpha 1- antitrypsin. This prevents the proteases from acting where they are not required.

In smokers, the normal balance between protease and antiprotease activity is upset because:

  • huge amounts of proteases are released from activated inflammatory cells
  • free radical production by tobacco smoke inactivates antiproteases reducing their effect

The excess protease activity in smokers allow proteases to act on the structural proteins of the respiratory airways. Neutrophil elastase is particularly important, destroying the elastin in the alveolar walls and reducing the elastic recoil.

30
Q

Why can individuals with alpha- 1 antitrypsin deficiency can acquire emphysema early and from just air pollution?

A

Because they lack the important anti protease even modest insults to the lung result in protease activity that cannot be inactivated.

31
Q

Why is there an obstructive component to emphysema?

A

Normally, elastin in alveolar walls keeps small airways open. In emphysema, the loss of alveolar walls particularly elastin, amuses loss of radial traction on small airways. Therefore small airways collapse during expiration causing expiratory obstruction to airflow.

32
Q

Describe the clinical features of asthma.

A
  • Emphysema causes exercise intolerance associated with marked breathless
  • patients normally use accessory muscles to breathe
  • the vigorous respiratory efforts tend to maintain oxygenation so patients are not cyanotic. “Pink puffer”
  • because obstruction to airflow tends to occur as the small airways collapse during expiration, patients typically try to keep the airways open as long as possible by pursing their lips to breathe out. This maintains a small positive pressure within the lungs tending to keep alveoli open.
  • patients may have a cough but there is no excess of sputum do cough is non- productive
  • the chest is often expanded (barrel chest) possibly as a result of chronic hyperventilation associated with outflow obstruction
  • patients often have a low BMI as continuous respiratory effort uses energy
  • not associated with chest infections
33
Q

Severe emphysema can produce what?

A

Bullae

34
Q

What are Bullae?

A

Bullae are air filled sacs just below the visceral pleura.

35
Q

If Bullae rupture, what complication is likely to occur?

A

Pneumothorax

36
Q

Compare and contrast chronic bronchitis and emphysema

A
  • both are caused by smoking
  • chronic bronchitis shows chronic inflammation of bronchi and bronchioles while in emphysema there is dilatation of respiratory bronchioles and alveoli
  • chronic bronchitis is characterised by excess mucus, inflammatory swelling of bronchial walls and smooth muscle hyper reactivity while emphysema is characterised by destruction of walls of respiratory bronchioles and alveoli
  • blue bloaters vs pink puffers
  • chronic bronchitis can cause infective exacerbations while emphysema can lead to pneumothorax due to ruptured Bullae