Week 9: Airway Patency, Obstructive and Restrictive Lung Diseases Flashcards

1
Q

Explain the equal pressure point (using expiration) and what a negative transmural pressure gradient is

A

 During expiration the driving pressure (alveolar pressure – atmospheric pressure) reduces along the airways due to frictional airway resistance  Because of this, at some point, this driving pressure reduces so much that the pressure outside [pulmonary pressure] = intra-airway pressure. It is as this point that is the Equal pressure point (EPP)  Anywhere above this EPP will result in a negative transmural pressure gradient (when the pressure outside the airway [pulmonary pressure] is greater than the pressure inside the airway) which will result in collapse and/or compression of the airway (only if they don’t have cartilage)

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2
Q

Explain how EPP causes the collapse of airways in emphysema.

A
  • Patients lose their lungs radial traction (Is the elastic and type 4 collagen that helps pull the airways open) - Meaning their airway is going to narrow (not pulled open as much anymore) - This results in increased airway resistance - As the person is now feeling out of breath, they start doing more forced breathing - This increases the pulmonary pressure (pressure outside, from muscles forced breathing), that when combined with the increased airway resistance (from loss of radial traction) results in the EPP dropping below the cartilage supported zone collapsing more and more airways during expiration
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3
Q

What are obstructive diseases and what will they result in (in terms of TLC and FRC etc…)

A

an increase in airway resistance

  • Vital capacity will decrease (this is the maximum amount of air a person can expel after maximum inhalation)
  • There will be increased total lung capacity, increased residual volume (amount of air remaining after lungs have fully exhaled), increased functional residual capacity (air present in the lungs are passive expiration) – due to gas trapping
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4
Q

What is the diagnostic spirometry test that is used to diagnose obstructive and restrictive diseases?

A
  • FEV1 : FVC ratio
  • FEV1 (the amount of air you can blow out in 1 second) divided by,
  • forced vital capacity (the max someone can expel from their lungs after max inhalation)
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5
Q

What are restrictive diseases and what do they result in (in terms of TLC, FRC etc….)

A

restrictive diseases is a decrease in lung compliance

  • Restrictive diseases will result in;
  • Decreased VC
  • Decreased TLC, RV, FRC
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6
Q

Explain the FEV1 / FVC in restrictive vs obstructive pulmonary disease

A
  • In obstructive disease, patient’s airway resistance is increased, dropping the EPP out of the cartilage supported zone, collapsing the airways. It then takes longer for patients to completely exhale their vital capacity meaning there FEV1/FVC will be reduced
  • In restrictive disease, lung compliance drops, making it harder and harder to inflate the stiffened lung meaning they are going to have less than 80% of the lung capacity compared to their predicted (for their age, height, gender, ethnicity)
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7
Q

Define what FEV1 and FVC mean

A
  • FEV1 (the amount of air you can blow out in 1 second) divided by,
  • forced vital capacity (the max someone can expel from their lungs after max inhalation)
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8
Q

What effect does fibrosis and emphysema have on lung compliance and why?

A
  1. Fibrosis of the lungs;
    - Is characterised by a decrease in lung compliance, they become stiff
    - This is caused by an increase in collagen fibres within the lung
    - Thus, we need a large pressure to maintain a moderate volume
  2. Emphysema of the lungs;
    - Is characterised by an increase in lung compliance making the lung overly stretchy
    - This is caused by the breakdown of collagen and elastin within the lung
    - Whilst the lung may be easier to stretch (which reduces the cost of breathing) the surface area is diminished reducing the ability of the lung to exchange gas (meaning they have to increase minute ventilation to get enough alveolar ventilation to satisfy their metabolic need) – they have to breath more often to get gas diffusion occurring in their lung.
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9
Q

What is emphysema?

A
  • Is a condition characterised by the enlargement of the air spaces distal to the terminal bronchiole, and by the destruction of the walls of the alveolar (it is a presumptive diagnosis in a living person)
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10
Q

What are the major causes of emphysema? (main two)

A
  • Smoking
  • Air pollution
  • Occupational hazards (mining, asbestos)
  • Bacterial infections
  • Some genetic factors
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11
Q

Explain the pathogenesis of emphysema:

A

The destruction of the alveolar walls is caused by something known as the protease-antiprotease mechanism

  • Within the lung, there is a balance between the proteases (breaks stuff down) and antiproteases. It is when this balance is shifted that destruction occurs
  • The two sides of this balancing act within the lungs are;

1. Elastase (derived from neutrophils)

  • which digests elastin and type 4 collagen (is our protease)
  • These are very important in providing the structural integrity of the lung (particularly alveolar wall strength

2. Alpha 1 antitrypsin

  • Is our Anti-protease

Causes of the imbalance:

Some sort of stimulation (such as smoking) can cause an increase in number of neutrophils

It can also increase the amount of elastase in the neutrophil

Stimulated Neutrophils also release O2 free radicals which inhibit alpha 1 antitrypsin activity

You can also have low alpha 1 antitrypsin levels due to genetic cause

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12
Q

Explain the smoking effects on emphysema

A
  • Smokers have a greater number of neutrophils within their alveoli (as the production of neutrophils is stimulated by smoking)
  • Smoking stimulates the release of elastase from neutrophils (neutrophils also contain a greater number of elastase compared to non-smoker neutrophil)
  • The oxidants that are present in cigarette smoke also inhibits alpha 1 antitrypsin activity
  • The O2 free radicals released from the increased neutrophils also inhibits alpha 1 antitrypsin activity
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13
Q

What is a summary of the effects of emphysema (x3)

A
  • Destruction of the alveolar tissue, especially the septa (the walls)
  • Inflammation of the bronchioles due to inhalation of airway pollutants
  • Loss of radial traction (which leads to airway collapse leading to gas trapping)
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14
Q

What clinical manifestations of emphysema

A
  • Some patients may also develop a barrel shaped chest, due to over inflation of the lungs (caused by gas trapping)
  • Decreased surface area for gas exchange
  • Airway collapse due to loss of radial traction
  • In a patients x-ray with emphysema, what you will notice is an overinflated lung, and lowered flattened diaphragm (usually sits around the 5th intercostal space)
  • Increased Functional Residual Capacity
  • Increased Residual volume
  • Increased TLC
  • Decreased FEV1
  • Decreased Vital Capacity
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15
Q

What are the 3 types of emphysema?

A
  1. Centriacinar emphysema
    - Is the destruction of the central parts of the lobe, without damaging the alveolar
    - This results in reduced airflow to the alveolar, as the bronchioles etc. are collapsed
    - Most common in the upper regions, and then spreads downwards
  2. Panacinar emphysema
    - Is a form of emphysema that destroys the entire region of the lungs
    - The terminal airways and the alveolar space is destroyed
    - Shows no regional preference
  3. Alpha 1 antitrypsin deficiency
    - Is the genetic form of emphysema, resulting in reduced alpha 1 antitrypsin levels
    - This results in destruction of the lower lobes (then moving upwards)
    - Usually, in a non-smoker this wouldn’t be evident until 40 years of age
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16
Q

What are some treatments of emphysema

A
  • Cessation of smoking
  • Inhaled bronchodilators (beta -agonists and anticholinergics)
  • Corticosteroids
  • Anti-tussives (dextromethophans, codeine)
  • Expectorants (bromhexine)
  • O2 therapy
  • Antibiotics and antiviral agents
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17
Q

What are 4 restrictive diseases

A
  1. Diffuse interstitial pulmonary fibrosis
    - This is characterised by the fibroblasts down laying far too much collagen in the interstitium of alveolar walls
    - Patients with this end up with multiple air filled cystic pouches
    - This increases the thickness of the respiratory membrane, making gas diffusion far more difficult
    - It is also known as honey comb lung
  2. Pulmonary fibrosis
    - Treatment is so hard as there are a number of mechanisms that cause this disease
    - It is a disease characterised by the scarring and stiffening of alveolar
  3. Pneumothorax
    - Is a restrictive disease involving the pleura and chest wall
    - Basically, a pneumothorax is a loss of negative pressure within the pleura cavity, when the chest then expands, the lungs do not move with it
    - This negative pressure is affected by air that enter the pleural space or chest wall (usually a penetrating injury)
    - There are a number of different types of pneumothorax;
  4. Scoliosis
    - This is a restrictive condition that is caused by a problem with the neuromuscular and skeletal elements that relate to ventilation
    - Scoliosis is a lateral curvature of the spine and kyphosis (hunchback) to posterior curvature
    - In this disorder, the lung function itself is ok, but there instead there is a curvature of the spine which affects the ability of the ribs / diaphragm to move to inflate the lung
    - This causes areas of lung compression, with resulting V / Q inequalities
    - There is an increase cost of breathing because of the abnormally formed ribs
    - There may also be increased pulmonary artery bed on the compressed side (leading to pulmonary oedema
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18
Q

What is a pneumothorax

A
  • Is a restrictive disease involving the pleura and chest wall
  • Basically, a pneumothorax is a loss of negative pressure within the pleura cavity, when the chest then expands, the lungs do not move with it
  • This negative pressure is affected by air that enter the pleural space or chest wall (usually a penetrating injury)
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19
Q

what are 4 types of pneumothorax

A
  1. Spontaneous
    - Are caused by the rupturing of the surface of the lung near the apex
    - It is commonly the bullae that rupture due to their lack of structural support
    - These are usually small, and fix themselves slowly over time
  2. Closed
    - Is when there is no penetration of the chest (spontaneous pneumothorax is an example of this)
  3. Open
    - Is when there is a penetration of the chest wall
    - This allows air into the pleural space, causing a loss of negative pressure causing the lung to collapse
  4. Tension
    - Is an open pneumothorax, that by complete chance, when they draw air in it comes through the opening, and when they exhale the wound closes over sealing the chest
    - This means that air is continuously drawn into the body cavity and is not released
    - This is quite serious and can result in impeded blood flow, tracheal deviation, heart is pushed over, and you can put so much pressure on the heart is causes a heart attack
20
Q

What is a neuromusclar respiratory disease

A
  • Are those respiratory diseases caused by impairment of the respiratory muscles or their nerve supplies
21
Q

What test do you mainly look at for restrictive lung disease and what value should it be over

A

measured FVC / predicted vc

healthy lung should be over 80%

22
Q

What test do you mainly look for in obstructive lung disease and what normal value should it be?

A

FEV1 / FVC

value should be higher than 80% in a health lungs

23
Q

would you expect the resistance to airflow in a small airway, such as the broncioles increase or decrease during inspiration?

A

decrease - the airways dilate due to expansion of surrounding tissue during inspiration

24
Q

Would you expect the resistance to airflow in small airway, such as the bronchiole to increase or decrease during expiration?

A

Increase - compression of airway to to increase in pulmonary pressure during expiration

25
Q

Where is the EPP in a normal airway

A

in bronchi

26
Q

in the obstructed airway, where is the equal pressure point located during forced expiration?

A

In bronchioles - this is because you have a faster decrease in pressure (due to obstruction, narrowing of the airways) - friction costs higher

This means that these airways are suceptible to collapse as they do not contain cartilagneous support.

27
Q

How is forced experiatory volume affected by obstruction of the airways, both in terms of the amount expired in one second, and as a percentage of the forced vital capacity?

A

Both FEV1 / FVC are reduced

28
Q

how does maximum expiratory flow rate vary with lung volume?

A

expiratory flow rate will increase in lung volume due to elastic recoil

29
Q

How is the relationship between expiratory volume and flow rate affected by obstructive lung disease

A

mainly a significant decrease in flow rate (FEV1) - emphysema, FVC doesnt really drop

30
Q

How can someone with obstructive air disease compensate for airflow demands associated with exercise?

A

Hyperinflation - breathing at higher lung volumes (inflated lungs with shallow breathing) –> this will decrease the amount of collapsed airways –> further decreasing trapped gases as not collapsing lung as much

31
Q

Does a normal person, or someone with obstructive airway disease have a greater total lung capacity?

A

people with obstructive disease compensate by developing increased lung volume – also they have trapped gases in their lungs

32
Q

What does emphysema do to the

mechanical support?

gas exchange?

expansion and contration of the lungs with inspiration and expiration?

A

decrease - due to decrease radial traction

decrease - due to a decrease in surface area

reduced energetic cost for inspiration –> increase compliance

reduced expiratory time —> less elastic recoil, collapsed airways on expiration

33
Q

Why does a bullae predispose an individual to a pneumothorax?

A

bullae rupture –> can get air in pleura

34
Q

Why do emphysema patients have a normal PaO2 and PaCO2? - NOTE: this is only at the beginning of emphysema

A

Hypernoea - use of rapid short breaths in order to maintain blood gases at normal levels

35
Q

would anti-oxidants be likely to have a beneficial effect in individuals with a genetic predisposition to emphysema?

A

no - these patients lack a1 -antitrpsin

36
Q

Both emphysema and fibrosis show alterations in the lung parenchyma. Why is emphysema considered obstructive while pumonary fibrosis is considered restrictive?

A

emphysema—airways collapse during expiration due to loss of radial traction and increase reliance on forced expiration (thus increase in airway resisitance

in fibrosis –> radial traction may be excessive and therefore decrease in lung compliance

37
Q

how is a pneumothorax treated?

A

remove air from chest cavity –> use a neddle and syringe which is inserted into chest wall

38
Q

what is pleura effusion and how does it cause dyspnoea?

A

fluid entering the lungs rather than air in pleural space. If significant enough these reduce movement of chest on affected side and therefore makes it harder to breath.

39
Q

would you expect to measure a decrease in FVC in a patient with restrictive lung condition?

A

yes due to a decrease in lung compliance - this is the one thing which unities all restrictive diseases

40
Q

would you expect to measure a decrease in FVC in obstructive lung disease?

A

no, increase airway resistance charactersises obstructive conditions, this increases expiratory time but does not decrease FVC

41
Q

what is indicated by the appearance of a concave shape in the flow volume loop between FEF 25% and FEF 75%

+ can you calculate FEV1 from in the volume flow loop graph (its in the answers)

A

decrease in epiratory flow rate from smaller airways indicating airway obstruction in some ariways

No as time is not represent on either axis, FEV1 cannot be calculated directly from a flow volume loop

42
Q

Why are increased neutrophils consistent with COPD?

A

INcreased neutrophils are associated with inflammation such as from inhaling pollution, smokin, bacterial infection

43
Q

Why can chronic bronchitis lead to hypoxia in the general body(just basically a dercrease in Hb saturation)

A

Mucus gland hypertrophy and mucus accumulation - leads to airway obstruction –> increasesa airway resistance, reversal of transmural pressure gradient and gas trapping which decreases P1 = decrease

PAO2 = increase V/Q mismatch

This leads to a decrease in diffusion of O2 and increase in A-a gradient = decrease PaO2

(NOTE: A-a gradient is the PaO2 - PaCO2)

44
Q

Why can emphysema lead to hypoxia in the general body(just basically a dercrease in Hb saturation)

A

elastase reduced –> decrease radial traction –> increase airway resistance, airway obstruction and reversal transmural pressure gradient and gas trapping which decreases P1 -> increases V/Q mismatch

also decrease SA

This decreases diffusion of O2 and increases A-a gradient = decrease PaO2

(NOTE: A-a gradient is the PaO2 - PaCO2)

45
Q

What is the mechanism of

decongestant

antitussive

A

nasal mucosal vasconstrictor –> decrease mucous production

heterogeneous class of ocmpounds the inhibit cough through either a central or peripheral mechanism, or a mixture of the two

46
Q

what is the mechanism of

mucolytic

expectorant

A

breakdown the chemical structure of mucus, decrease mucus viscosity and elasticity and promote clearance

Increase hydration of mucus