Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Semester 3 - respiratory > 3. Disorders of Ventilation and Lung Mechanics > Flashcards

3. Disorders of Ventilation and Lung Mechanics Flashcards

1
Q

what is the conducting portion of the respiratory tract?

A 
Nasal cavity
Pharynx
Larynx
Trachea
Primary bronchi
Secondary bronchi
Bronchioles
Terminal bronchioles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the respiratory portion of the respiratory tract?

A

Respiratory bronchioles
Alveolar ducts
Alveoli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what do lungs need to overcome to expand?

A
  • Elastic properties of alveolar walls

* Surface tension of alveolar fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what does expiration need to overcome?

A

– Need to overcome airways resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

define elastance

A

Elastance is a measure of elastic recoil = the tendency of something that has been distended to return to its original size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

defien complliance

A

Ease at which an elastic structure can be stretched

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the relationship between compliance and elastic recoil (measured in elastance)?

A

Inversely proportional

In tissues with a high compliance (easier to stretch), the elastic recoil is less
In tissues with a low compliance, elastic recoil (tendency to return to original size) is high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

define lung elasticity

A

Lung Elasticity represents mechanical properties of the lungs to be expanded (distended) by pressures surrounding or inflating the lungs, and to collapse as soon as pressures disappear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which factors affect lung compliance? State their relationship to compliance/how they affect compliance

A

Connective tissue surrounding alveoli - inversely prop (bcs the more elastic fibres –> increase in elastic recoil, meaning decrease in compliance).

Alveolar fluid surface tension - inversely prop (bcs increase in surface tension, meaning decrease in compliance).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

If there is an increase in surfactant, what effect would this have on compliance? Why?

A

Increase in compliance bcs decrease in surface tension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does “connective tissue surrounding alveoli tissue” and “alveolar fluid surface tension” affect elastic recoil?

A

•Directly related to connective tissue surrounding
alveoli - elastic fibers including elastin & collagen
and other matrix elements within the lung
parenchyma
•Directly related to alveolar fluid surface tension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what does ventilation depend on?

A

balance between compliance and elastic recoil

airway resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what does airway resistance depend on?

A 
– Surface tension within airways
– Diameter airways
• Mucous in airways
• Pulmonary pressure gradients
• Radial Traction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does the structure of a bronchus compare to the structure of a bronchiole?

A

How does the structure of a bronchus compare to the structure of a bronchiole?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Bronchioles have no cartilage.

How do they stay open in expiration?

A

• Due to Radial traction (outward tugging
action) of the surrounding alveolar walls
on bronchioles
• Prevents collapse of bronchioles during
expiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why would bronchioles collapse during expiration?

A

intra pulmonary pressure high pushing on bronchioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why is airway obstruction worse in expiration than inspiration?

A

Negative pressure in pleural space during inspiration helps to keep lower airways open whereas in expiration the pressure is positive which exacerbated narrowing of intra-thoracic airways.

Bronchioles don’t have rigid cartilage islands to oppose those (positive) pressures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is Atelectasis?

A

Lung collapse - Inadequate expansion of air spaces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Is atelectasis reversible?

A

-Yes, except for CONTRACTION ATELECTASIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Give 3 causes of atelectasis?

A

Impaired pulmonary surfactant production
Compression (causing collapse)
Obstruction (causing collapse)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Explain how impaired pulmonary surfactant production leads to atelectasis (lung collapse)?

A

Alveoli collapse due to increased surface tension so can’t expand to ventilate lungs. Decreases compliance so lungs can’t expand and so collapse.

alveoli never expand in the first place or only partially expand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Explain how compression can lead to atelectasis (lung collapse)? Give 3 examples of things that can cause this compression?

A

Air in pleural cavity (pneumothorax)
Fluid in pleural cavity (pleural effusion)
Tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Explain how obstruction of airways leads to atelectasis (lung collapse). what is the name of this type of atelectasis?

A

Resorption collapse: due to obstruction of a large airway (e.g. Lung cancer, mucous plugs)
– Airway obstructed; air downstream of
blockage slowly absorbed into blood stream
– Alveoli collapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How does atelectasis cause impaired respiratory function?

A

• Alveoli not ventilated

– So can’t participate in gas exchange –> impaired oxygenation and CO excretion.

• Collapsed alveoli more suggestible to lung infection

including pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is interstitial lung disease?

A

an umbrella term used for a large group of diseases characterized by Thickening of pulmonary interstitium, fibroblast proliferation, collagen deposition, and, if the processremains unchecked, pulmonary fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

is the thickening of pulmonary interstitium reversible?

A

sometimes reversible – sometimes not - depends - scarring due to increased collagen and pulmonary fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is the common final pathway for interstitial lung disease if not reversible, or if reversible but cause not diagnosed,?

A

lung fibrosis –Early detection/treatment key to preventing irreversible progression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what does the interstitium contain?

A
  • elastin fibres
  • collagen fibres
  • Fibroblasts
  • Matrix substance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the interstitial space (in the lungs) and when is this space apparent?

A

Potential space between alveolar cells and the capillary basement membrane. Only apparent in disease states when it may contain fibrous tissue, cells or fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How does interstitial lung disease/pulmonary fibrosis impair GE?

A

Affects both movement of air in airway (stiffer) and diffusion of gases :

Fewer alveoli and caps bcs replaced by scar tissue. Increased space btwn cap and alveoli .

Thickened alveolar capillary membrane means diffusion distance increases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

interstitial lung disease can follow?

A

• Specific exposure - e.g., asbestos, drugs, mouldy hay etc
OR
• Autoimmune-mediated inflammation
OR
• Unknown injury (e.g., idiopathic pulmonary fibrosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Give causes of interstitial lung disease, including - occupational, treatment related (iatrogenic), autoimmune, immunological causes.

A 
• Idiopathic - IPF
• Occupational 
- coal miners lung (pneumoconiosis), 
- farmers lung (mouldy hay), 
- asbestos
• Treatment related - radiation/chemo, methotrexate, nitrofurantoin
• Autoimmune - SLE, RA
• Immunological - sarcoidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How is compliance affected in interstitial lung disease?

A

Reduced - lungs are stiff so harder to expand

34
Q

How is elastic recoil of lungs affected in interstitial lung disease? What effect does interstitial lung disease have on the size of the lungs?

A

Elastic recoil of the lungs is increased - the resting lung volume is smaller than normal – but RATE of airflow not impaired

35
Q

what type of defect will be seen on spirometry for interstitial lung disease

A

‘Restrictive’ type of ventilatory defect on spirometry

36
Q

What effect does interstitial lung disease have vital and inspiratory capacity?

A

Reduced.

37
Q

Why are the airways not narrowed in interstitial lung disease?

A

Fibrous tissue exerts an outward ‘pull’ (known as

radial traction) on the small bronchioles keeping airways open

38
Q

What effect does interstitial lung disease have on diffusion distance?

A

Increases diffusion distance, effect is greater on oxygen than CO2 which is more soluble

39
Q

What are the symptoms of interstitial lung disease?

A

– Dry cough
– Dyspnoea on exertion progressing to at rest
– Fatigue
– Typically gradual, insidious progression

40
Q

What are the signs of interstitial lung disease?

A
  • decreased lung excursion on palpation
  • bi-basal end inspiratory lung crackles
  • Finger clubbing
  • Small pleural effusions
  • tachypnoea (increased respiratory rate),
  • tachycardia
  • reduced chest movement (bilaterally),
41
Q

What is Functional residual capacity?

A

the volume of air in the lungs at the end of a quiet expiration

42
Q

summarise the effect of fibrous lung tissue

A 
With fibrous tissue in the lung interstitium
• Lungs  are stiff and hard to expand
• Lung elastic recoil is increased
• and the lung volume is smaller 
• Compared with normal lungs
43
Q

in interstitial lung disease explain why lungs are harder to expand but can still be recoiled

A

• The lungs are stiffer and harder to expand, since
collagen fibres are less stretchy than elastin fibres.
• Therefore, lung compliance is reduced.
• The elastic recoil of the lungs is increased. The term
elastic recoil is not limited to the recoil of elastin fibres,
but by the tendency of BOTH elastin and collagen fibres to return to their original size when stretched)

44
Q

what is asbestosis

A

form of interstitial lung disease caused by asbestos exposure

45
Q

WHat is hypersensitivity pneumonitis

A

Another cause of interstitial lung disease is untreated
- an immunologically mediated lung disease caused by repetitive inhalation of antigens; most new cases arise from residential exposures, notably to birds – “bird fancier’s lung.”

46
Q

What is neonatal respiratory distress syndrome?

A

Caused by deficiency of surfactant in premature babies, particularly those less than 30 weeks old

47
Q

when does the fetus begin producing surfactant?

A

starts at 24 – 28 weeks gestation;

• increasing amounts by 32 weeks

48
Q

What happens in RDS due to lack of surfactant?

A
  • Insufficient surfactant à high surface tension
  • This makes the lungs harder to expand at birth; lung expansion at birth is incomplete;
  • some alveoli remain collapsed (airless); no gas exchange occurs in these alveoli
  • The lung is stiff - lung compliance is low
  • Increased effort is required to breathe – respiratory difficulty
  • Results in impaired ventilation
49
Q

What are the sign of RDS?

A 
Ø Grunting,
Ø Nasal flaring,
Ø Intercostal and subcostal retractions
Ø Rapid respiratory rate (tachypnoea)
Ø Cyanosis
50
Q

What is the treatment for RDS?

A

Surfactant replacement via an endotracheal

tube, and supportive treatment with oxygen and assisted ventilation

51
Q

Why do intercostal recessions occur in RDS?

A

Increases surface tension in alveoli make them hard to expand, they also have increased elastic recoil so interpleural pressure becomes more negative, especially during end of inspiration. This causes a pull on the intercostal and subcostal spaces pulling them inwards.

52
Q

compare RDS and diffuse pulmonary fibrosis

A

Both have stiff lungs
Both decreased compliance and increased elastic
recoil
Different underling mechanisms - First due to insufficient surfactant production whereas second due to increase in elastin fibres and collagen leading to fibrosis of lungs and smaller resting volume.

53
Q

what is COPD

A

• Clinical syndrome characterised by chronic respiratory symptoms with associated pulmonary
abnormalities – all conditions share impaired airflow that is not fully reversible – classic definition encompasses two medical conditions
– Chronic bronchitis
– Emphysema
– Above two conditions actually co-exist

54
Q

What is pre-COPD?

A

Airflow impaired but no clinical symptoms yet and “normal spirometry” - but at very high risk for developing COPD in the next 5 years.

55
Q

What is chronic bronchitis?

A

inflammation of the bronchi and bronchioles due to chronic exposure to irritants

56
Q

What happens to level of mucus in chronic bronchitis and what does this cause?

A

Hypersecretion from goblet cells and submucosal glands, causes narrowing of the airways

57
Q

What happens to cilica in chronic bronchitis?

A

Reduced, therefore mucus not cleared properly.

58
Q

what does hypersecretion of mucus and reduction of cilia cells in chronic bronchitis result?

A

– airflow limitation/obstruction by luminal obstruction of small
airways – worse on expiration
– epithelial remodelling,
– alteration of airway surface tension predisposing to collapse

59
Q

What criteria need to be met to diagnosis chronic bronchitis?

A

cough productive sputum > three months of the

year for > one year

60
Q

What is emphysema?

A

Loss of elastin and breakdown of alveolar walls
causing increased lung compliance, decreased elastic recoil, narrowing of small airways (non-reversible) and loss of alveolar surface area

61
Q

Describe the pathophysiology of emphysema

A

(Smoking) —-> inflammatory cells accumulate—-> release elastase and oxidants——> destroy alveolar walls and elastin –> decrease elastic recoil (therefore increase compliance).

62
Q

What is the effect of destruction of alveolar walls and reduced elastic recoil in emphysema?

A

Destruction : 1 big alveolus instead one lots of little ones. Leads to large air spaces and reduced SA for GE. Reduces RADIAL TRACTION so bronchioles collapse during expiration (positive pressures).

Reduced recoil : air enters bronchiole but it collapses during expiation so trapped air —> stale air.

63
Q

What causes barrel chest in emphysema?

A

• At rest the lungs are hyper-inflated, (i.e. more
expanded than normal), due to the loss of elastic recoil
Air trapping
Imbalance of chest wall recoil (same) vs lung recoil (decreased).

64
Q

What effect does emphysema have on the level of the diaphragm?

A

Diaphragm normally at the level of 5th rib anteriorly, will be below that in emphysema

65
Q

What happens to the diameter of small airways in emphysema?

A

Narrowed, loss of elastic fibres so reduced radial traction

66
Q

summarise effects on lung elastic recoil and compliance in emphysematous COPD

A

Lungs have increased compliance and are easier to expand

Lung elastic recoil is decreased and the lung volume is increased compared with normal lungs - stale air not fresh

67
Q

what type of ventilatory defect is seen on Spirometry in emphysema?

A

onstructive

68
Q

Emphysema vs pulmonary fibrosis

A

Emphysematous Dominant COPD
• Loss of elastic tissue
• Increased compliance & reduced elastic recoil
• Hyper inflated: Barrel chest
• Small airways collapse in expiration (loss of radial traction)
• Air trapping (because of obstruction and ↓recoil)
• Obstructive pattern on spirometry testing

Pulmonary Fibrosis
• Increase of fibrous tissue
• Less compliant - Stiff - harder to expand
• Smaller lungs
• Decreased functional residual capacity and other lung volumes
• No airway obstruction
• Restrictive disease on Spirometry testing

69
Q

What is asthma?

A

Chronic inflammatory process, causes airway narrowing

70
Q

How is the airways narrowed in asthma?

A

Due to bronchial smooth muscle contraction, thickening of airway walls by mucosal oedema and excess mucus production which can partially block the lumen

71
Q

What is pneumothorax?

A

A disorder where air enters the pleural space, with
loss of pleural seal and lung collapse

  • If the chest wall or the lung is breached,
  • A communication is created between pleural space and atmosphere
  • Air flows from atmosphere (higher pressure) à into the pleural cavity (lower pressure)
  • Until the pleural pressure = atmospheric pressure
72
Q

Why does the lung collapse in pneumothorax?

A

Pleural seal is broken, and the elastic recoil of the lung causes it to collapse towards the hilum, as the negative pleural pressure and outward recoil of
the chest wall can no longer counteract it.

73
Q

What are the symptoms of emphysema?

A

Shortness of breath, reduced exercise tolerance, cough

74
Q

What initiates the cough reflex?

A

irritation of mechano- and/or chemoreceptors in the respiratory epithelium.

75
Q

Outline coughing reflex

A

Initiated by irritation of mechano- and/or chemoreceptors in the respiratory epithelium.

  • Deep inspiration
  • The glottis is closed by vocal cord adduction
  • Strong contraction of the expiratory muscles (abdominal muscles, internal intercostal muscles) which builds up intrapulmonary pressure
  • Sudden opening of the glottis causes an explosive discharge of air.
76
Q

Define a cough

A

Cough is an explosive expiration of air from the lungs

77
Q

Where is the cough reflex coordinated from in brain?

A

Cough centre in Medulla oblongata

78
Q

define Anatomical dead space

A

The volume of air in the conducting airways

79
Q

define Alveolar dead space

A

air in alveoli which do not take part in gas exchange

These are alveoli which are not perfused or are damaged

80
Q

define Physiological dead space

A

Anatomical dead space + Alveolar dead space

Semester 3 - respiratory (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions