Session 2: Some Disorders of Ventilation and Lung Mechanics Flashcards

1
Q

Give some common disorders of ventilation and lung mechanics.

A

Interstitial lung disease

Respiratory distress syndrome in the new born

Emphysema

Asthma

Pneumothorax

Hypoventilation

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2
Q

Explain the relationship between compliance and elastic recoil.

A

It’s an inverse relationship.

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3
Q

Bronchioles have no cartilage. How do they stay open in expiration?

A

Due to something called radial traction.

This is the outward tugging actiong of the surrounding alveolar walls on bronchioles.

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4
Q

Briefly explain what interstitial lung disease is.

Also give the cause.

A

This is the thickening of the pulmonary interstitium. A lot of collagen is layed down in the interstitium.

There are over 200 different types of the disease and causes.

However the common final pathway almost always result in the same thing: lung fibrosis.

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5
Q

Is interstitial lung disease reversible?

A

Sometimes, sometimes not.

It depends on what kind and how early it was detected/treated.

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6
Q

Give a some common causes of interstitial lung disease.

A

Asbestos

Coal workers pneumoconiosis

Radiation

Rheumatoid arthritis

Sarcoidosis

Exterernal alleric alveolitis

Fibrosing alveolitis

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7
Q

Which lung is healthy?

A

The left lung.

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8
Q

What does pulmonary interstitium contain?

A

Elastin fibres

Collagen fibres

Fibroblasts

Matrix substance

In interstitial lung disease there is a lot more collagen fibres.

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9
Q

Explain the pathophysiology of interstitial lung disease.

(Consequences of the disease)

A

The lungs become stiffer and harder to expand since the collagen fibres are less stretchy than elastin fibres.

Lung compliance is reduced.

Elastic recoil of the lungs is increased.

Smaller lungs

On examination chest expansion is reduced.

Also thicking of the alveolar walls increases the distance oxygen has to diffuse from alveolar air to the blood and vice versa. Less efficient gas exchange.

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10
Q

Why are the lungs smaller in interstitial lung disease?

A

Because of the increased elastic recoil creating a netforce inwards since the chest recoil of the muscles still stay the same.

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11
Q

Symptoms of interstitial lung disease.

A

Shortness of breath

Reduced exercise tolerance

Dry cough

Fatigue

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12
Q

Signs of interstitial lung disease.

A

Tachypnoea

Tachycardia

Reduced chest movement (bilaterally)

Coarse crackles

Pleural effusions

Finger clubbing

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13
Q

How can you examine the reduced chest movement of interstitial lung disease.

A

If you put your hands on their back with your thumbs touching. In a normal lung as they take a deep breath your thumbs should separate.

If they don’t, this is a sign.

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14
Q

What happens to compliance in interstitial lung disease?

A

It is greatly reduced.

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15
Q

Explain Respiratory distress syndrome in new born.

A

It comes down to insufficient amount of surfactant.

Surfactant is produced by type II pneumocytes in increasing quantities from 32 weeks’ gestation.

RDS is therefore caused by deficiency of surfactant in premature babies, particularly those less than 30 weeks old.

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16
Q

Pathophysiology of RDS in new born.

A

Without the surfactant the surface tension in the fluid lining of the alveoli will be high.

This makes the lungs harder to expand at birth. Since lung expansion is incomplete and due to the absence of surfactant some alveoi remain collapsed and some existing ones start to collapse. There is no gas exchange in these alveoli.

Lungs are stiffer and harder to expand which means compliance is low.

This means more effort is needed to breathe sufficiently.

Impaired ventilation.

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17
Q

Signs of RDS in new born.

A

Cyanosis

Grunting

Intercostal and subcostal recession.

Nasal flaring

Tachypnoea

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18
Q

Treatment of RDS of the new born.

A

Surfactant replacement via an endotracheal tube

Supportive treatment with oxygen and assisted ventilation.

19
Q

Classic definition of COPD encompasses two medical conditions.

Which?

A

Chronic bronchitis

Emphysema

20
Q

Which part of the airways/lungs is affected in COPD?

A

From bronchi to bronchioles.

21
Q

Pathophysiology of chronic bronchitis.

A

There is mucus hypersecretion from goblet cells and submucus glands.

There is also reduced cilia which means that the mucus is not cleared effectively and can lead to mutliple infections.

Airflow is limited and obstructed.

Epithelial remodeling.

Parts of airways tend to collapse because of increased surface tension.

22
Q

Clinical diagnosis of chronic bronchitis.

A

Cough productive sputum over three months of the year for over one year.

23
Q

Common cause of emphysema (and COPD).

A

90% of cases of COPD and emphysema are due to smoking.

Inhaled cigarette smoke results in the breakdown of elastin fibres and alveolar walls.

24
Q

Pathophysiology of emphysema.

A

Loss of elastin fibres due to the cigarette smoke.

Higher compliance since there is less elastin and less elatic recoil.

The reduction of elastic recoil disturbs the net balance between elastic recoil (inwards) and chest recoil (outwards).

This causes the lungs to be hyperinflated.

The small airways are narrowed.

25
Q

Why are the small airways narrowed?

A

Due to the loss of elastic fibres which exert an outwards pull (the radial traction) on the small bronchioles.

Radial traction is reduced and this increases airways resistance.

26
Q

Signs of emphysema.

A

Barrel chest due to the hyperinflation.

27
Q

How is the airways resistance increased in chronic bronchitis?

A

Increased mucus production in bronchitis ‘fills’ the bronchi causing obstruction.

28
Q

Symptoms of emphysema.

A

Shortness of breath and reduced exercise tolerance.

29
Q

Causes of emphysema not due to smoking.

A

Alpha-1 antitrypsin deficiency which is inherited.

Alpha-1 antitrypsin is an anti-proteinase.

If alpha-1 antitrypsin is not produced this leads to an imblanace in proteinases and antiproteinases. This leads to destruction of elastin in early age and signs usually show early on as well.

30
Q

What is asthma?

What triggers it?

A

A chronic inflammatory process.

May be triggered in susceptible individuals by allergic and/or non-allergic stimuli.

31
Q

Pathophysiology of asthma.

A

The inflammation leads to airway narrowing due to bronchial smooth muscle contraction.

There is also thickening of airways walls by mucosal oedema and excess mucus production which can partially block the lumen.

All of this greatly increases airway resistance. This makes it much harder to inspire.

32
Q

What is a pneumothorax?

A

The presence of air in the pleural space.

33
Q

Explain how a pneumothorax can come about, and why.

A

The intrapleural pressure is always less than the atmospheric pressure.

This intrapleural pressure along with the pleural seal makes the visceral pleura of the lungs stick to the chest wall (parietal pleura.

However if an opening is created which means that the pleural space can communicate with the outside. This will cause air to quickly flow into the pleural cavity down the pressure gradient until equilibrium is reached (intrapleural pressure = atmospheric pressure).

This causes the pleural seal to be broken and the elastic recoil of the lung is not affected by the chest wall recoil anymore. The lung will collapse towards its hilum.

34
Q

Give some causes of pneumothorax.

A

Trauma to chest like a stab.

Spontaneous rupture of a weak area of the lung.

Insertion of central venous catheter via the subclavian vein (higher incidence) or the internal jugular vein (lower incidence).

35
Q

Is pneumothorax simply a collapsed lung?

A

No, lung collapse is not synonymous with pneumothorax because there are other causes of lung collapse.

36
Q

Fancier word for lung collapse.

A

Atelectasis

37
Q

Briefly explain atelectasis.

A

Incomplete expansion of the lungs or collapse of previously inflated lung.

This produces areas of relatively airless pulmonary parenchyma.

38
Q

Main types of atelectasis.

A

Neonatal atelectasis

Compression atelectasis

Resportion atelectasis.

39
Q

What is compression atelectasis?

A

Whenever significant volumes of air or fluid accumulate in the pleural cavity.

40
Q

Common causes of compression atelectasis.

A

Pneumothorax or pleural effusion.

41
Q

What is resorption atelectasis?

A

Complete obstruction of airways which means that over time air is resorbed from the alveoli and they will collapse.

42
Q

Causes of resorption atelectasis.

A

Bronchial carcinoma

Excessive mucuous secretion and failure of clearance. (Can happen after surgery with an inability to cough, cystic fibrosis, severe asthma attacks)

Foreign body (common in children which inhale something)

43
Q

Causes of hypoventilation.

A

Incorrect neural output. Impulses originating in the respiratory centre needs to reach the respiratory muscles via spinal pathways and nerves.

Malformed bony thorax

Respiratory muscles weakness of any cause

Severe thoracic wall deformities

Very stiff lungs (high compliance)

Severe airway obstructions.