RM Week 9

Question 0

Describe equal pressure point

Answer 0

When the extra airway pressure equals intra airway pressure.

Question 1

Why does driving pressure reduce along the airways?

Answer 1

Due to frictional airway resistance

Question 2

In a normal airway, where is the equal pressure point located during forced expiration?

Answer 2

In upper cartilagenous airways

Question 3

In obstruction, where does the equal pressure point move to?

Answer 3

Smaller, collapsible airways closer to the alveoli. Eg. The bronchioles.

Question 4

What does resistance to airflow depend on?

Answer 4

The number of parallel pathways present. Hence why medium sized airways actually provide more resistance to flow than the numerous dividing small airways

Question 5

When would an airway collapse?

Answer 5

When the pressure inside the airways is less than the pressure outside the airways

Question 6

Why are smaller airways more susceptible to flow related airway collapse than the larger?

Answer 6

Because the larger airways have cartilaginous support when smaller airways have not got structural rigidity

Question 7

Which type of diseases involve an increase in airway resistance?

Answer 7

Obstructive diseases

Question 8

Which type of diseases involve a decrease in lung compliance?

Answer 8

Restrictive diseases

Question 9

What would you expect the % to be for FEV1/FVC in obstructive conditions?

Answer 9

Less than 80%

Question 10

List a condition where lung compliance is decreased?

Answer 10

Fibrosis.Lungs stiffen and need a large pressure to maintain a moderate volume

Question 11

Why is it not a good thing that emphysema patients have high lung compliance?

Answer 11

The lungs in emphysema do not require as much muscular work to inflate but they also have a decreased surface area due to alveolar destruction which means less gas diffusion and less elastic recoil. This means they need to increase expiratory effort.

Question 12

Lost two examples of copd?

Answer 12

Emphysema and chronic bronchitis

Question 13

What is asthma classified as?

Answer 13

Variable obstructive pulmonary airway disease VOPD/VOAD

Question 14

What is the most plausible hypothesis to account for the destruction of the alveolar walls in emphysema

Answer 14

Protease- antiprotease mechanism

Question 15

Describe the Protease- antiprotease mechanism ?

Answer 15

Alveoli wall destruction results from an imbalance in the number of proteases and anti proteases in the lung (more proteases)

Question 16

List some major causes emphysema

Answer 16

Smoking, air pollution, occupational hazards, bacterial infections

Question 17

What gene is defective for the genetic emphysema ?

Answer 17

Gene Z- results in a alpha1 antitrypsin deficiency which is a protease inhibitor. Without it, it increases action of proteases.

Question 18

Name the principle protease responsible for emphysema

Answer 18

Elastase

Question 19

Where is the largest amount of protease elastase derived from?

Answer 19

Neutrophils

Question 20

What does elastase digest?

Answer 20

Lung tissue, type for collagen (which is important in maintaining alveolar wall strength)

Question 21

Apart from releasing elastase , what do neutrophils also release to contribute to emphysema?

Answer 21

Oxygen free radicals that inhibit the action of alpha-1 antitrypsin

Question 22

True or false : smokers have greater numbers of neutrophils in their lung alveoli?

Answer 22

True. Smoking also stimulates neutrophils to release elastase

Question 23

What does smoking do to macrophages?

Answer 23

Enhances the elastolytic protease activity in the macrophages

Question 24

Name the two main types of emphysema?

Answer 24

Centriacinar and panacinar

Question 25

Describe Centriacinar Emphysema?

Answer 25

Destruction is limited the central parts of the alveoli and peripheral alveolar ducts Alveoli may escape unscathed.

Question 26

Where is Centriacinar Emphysema most markedly seen in the lung (which part)

Answer 26

The upper lobe

Question 27

Describe Panacinar Emphysema?

Answer 27

Distension and destruction of whole lobule. Shows no regional preference in the lung. It is however slightly more common in the lower lung. severe panacinar emphysema develops in patients that homozygous for the defective Z gene. This severe type results in destruction which begins in the lower lobes. It is usually evident by the age of 40 and occurs without any history of cough or smoking.

Question 28

What are Bullae?

Answer 28

Local areas of hyper inflation in the lung.

Question 29

List some clinical manifestations of emphysema?

Answer 29

Clinical signs do not usually appear until a third of the lung parenchyma is destroyed. Major problem is there is a decrease surface area for gas exchange and airway collapse can occur due to loss of radial traction of the alveoli. They can be progressive dyspnoea, cough or wheezing, development of a barrel shaped chest with prolonged expiration, the only reliable and consistent finding is a low forced expiration.

Question 30

What happens to your FVC in emphysema?

Answer 30

It is increased

Question 31

What happens to your residual volume in emphysema?

Answer 31

It is increased

Question 32

What happens to you too long capacity in emphysema?

Answer 32

It is increased

Question 33

What happens to your FEV1 in emphysema?

Answer 33

It is decreased.

Question 34

List some treatments for emphysema?

Answer 34

Cessation of smoking, bronchodilators (baiter agonists and anticholinergics), corticosteroids, antitussives (Stopping coughing), expectorant’s, oxygen therapy, antibiotics and anti-viral agents.

Question 35

Describe diffuse interstitial pulmonary fibrosis?

Answer 35

The thickening of the interstitium of the alveolar wall. Infiltration of lymphocytes and plasma cells, followed by fibroblasts that lay down thick collagen fibres into the alveolar wall.

Question 36

What eventually happens in pulmonary fibrosis?

Answer 36

Alveolar architecture is destroyed and scarring results in multiple air filled cystic spaces formed by dilated terminal and respiratory bundles. This is called a honeycomb lung.

Question 37

Describe a pneumothorax?

Answer 37

When area enters the plural space from the lungs or less commonly through the chest wall (if it is a penetrating injury). If air enters the intrapleural pressure space the lung will collapse and the ribs will spring outwards

Question 38

What are the two types of pneumothorax?

Answer 38

Spontaneous and tension pneumothorax

Question 39

Describe a spontaneous pneumothorax?

Answer 39

Cause by the rupture of small Bullae /blens on the surface of the lung near the apex.

Question 40

Describe a tension pneumothorax?

Answer 40

When air enters the pleural space during inspiration but can’t escape. It can impede Venus return, cause respiratory distress, tachycardia, tracheal deviation. Usually due to a laceration.

Question 41

What is scoliosis?

Answer 41

A lateral curvature of the spine

Question 42

How does scoliosis effect pulmonary function?

Answer 42

Has normal airway resistance. Can cause areas of lung compression, increases the V/Q inequality, increases work of breathing, increased pulmonary pressure due to restricted vascular beds in lung

Question 43

How does a neuromuscular disease affects the respiratory function?

Answer 43

Impairment of the respiratory muscles or then of supply. Generally results in dyspnoea and respiratory failure when the diaphragm is involved