Flashcards in RM Week 9 Deck (44):
Why does driving pressure reduce along the airways?
Due to frictional airway resistance
Describe equal pressure point
When the extra airway pressure equals intra airway pressure.
In a normal airway, where is the equal pressure point located during forced expiration?
In upper cartilagenous airways
In obstruction, where does the equal pressure point move to?
Smaller, collapsible airways closer to the alveoli. Eg. The bronchioles.
What does resistance to airflow depend on?
The number of parallel pathways present. Hence why medium sized airways actually provide more resistance to flow than the numerous dividing small airways
When would an airway collapse?
When the pressure inside the airways is less than the pressure outside the airways
Why are smaller airways more susceptible to flow related airway collapse than the larger?
Because the larger airways have cartilaginous support when smaller airways have not got structural rigidity
Which type of diseases involve an increase in airway resistance?
Which type of diseases involve a decrease in lung compliance?
What would you expect the % to be for FEV1/FVC in obstructive conditions?
Less than 80%
List a condition where lung compliance is decreased?
Fibrosis.Lungs stiffen and need a large pressure to maintain a moderate volume
Why is it not a good thing that emphysema patients have high lung compliance?
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.
Lost two examples of copd?
Emphysema and chronic bronchitis
What is asthma classified as?
Variable obstructive pulmonary airway disease VOPD/VOAD
What is the most plausible hypothesis to account for the destruction of the alveolar walls in emphysema
Protease- antiprotease mechanism
Describe the Protease- antiprotease mechanism ?
Alveoli wall destruction results from an imbalance in the number of proteases and anti proteases in the lung (more proteases)
List some major causes emphysema
Smoking, air pollution, occupational hazards, bacterial infections
What gene is defective for the genetic emphysema ?
Gene Z- results in a alpha1 antitrypsin deficiency which is a protease inhibitor. Without it, it increases action of proteases.
Name the principle protease responsible for emphysema
Where is the largest amount of protease elastase derived from?
What does elastase digest?
Lung tissue, type for collagen (which is important in maintaining alveolar wall strength)
Apart from releasing elastase , what do neutrophils also release to contribute to emphysema?
Oxygen free radicals that inhibit the action of alpha-1 antitrypsin
True or false : smokers have greater numbers of neutrophils in their lung alveoli?
True. Smoking also stimulates neutrophils to release elastase
What does smoking do to macrophages?
Enhances the elastolytic protease activity in the macrophages
Name the two main types of emphysema?
Centriacinar and panacinar
Describe Centriacinar Emphysema?
Destruction is limited the central parts of the alveoli and peripheral alveolar ducts Alveoli may escape unscathed.
Where is Centriacinar Emphysema most markedly seen in the lung (which part)
The upper lobe
Describe Panacinar Emphysema?
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.
What are Bullae?
Local areas of hyper inflation in the lung.
List some clinical manifestations of emphysema?
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.
What happens to your FVC in emphysema?
It is increased
What happens to your residual volume in emphysema?
It is increased
What happens to you too long capacity in emphysema?
It is increased
What happens to your FEV1 in emphysema?
It is decreased.
List some treatments for emphysema?
Cessation of smoking, bronchodilators (baiter agonists and anticholinergics), corticosteroids, antitussives (Stopping coughing), expectorant's, oxygen therapy, antibiotics and anti-viral agents.
Describe diffuse interstitial pulmonary fibrosis?
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.
What eventually happens in pulmonary fibrosis?
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.
Describe a pneumothorax?
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
What are the two types of pneumothorax?
Spontaneous and tension pneumothorax
Describe a spontaneous pneumothorax?
Cause by the rupture of small Bullae /blens on the surface of the lung near the apex.
Describe a tension pneumothorax?
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.
What is scoliosis?
A lateral curvature of the spine
How does scoliosis effect pulmonary function?
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