Brainscape's Knowledge GenomeTM

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


See full index

Respiratory System & CVS Physiology Year 1 > Pathology Of Obstructive Lung Disease > Flashcards

Pathology Of Obstructive Lung Disease Flashcards

1
Q

What percentage of the FVC if FEV1 in healthy patients?

A

70 - 80 %

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

What is the normal volume of FEV1?

A

3.5 - 4L

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

What is the normal volume of FVC?

A

5L

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

What is the normal peak expiratory flow rate?

A

400-600L/min

Normal range is 80-100% of predicted value.
Moderate fall is 50-80%
<50% is a marked fall

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

What happens in obstructive lung disease?

A

Airflow limitation, Peak expiratory flow rate is reduced, FEV1 is reduces and less than 70%, FVC may be reduced.

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

What is asthma?

A

It is airflow limitation due to bronchial constriction, the reduction in the luminal cross section area in the small airways in the lungs (smooth muscles).

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

What are the two effect that are made from mast cell granules?

A
  • Inducing inflammation by attracting a number of inflammatory cell types in to the airways leading to swelling and oedema within the bronchial mucosa
  • direct effect on bronchial smooth muscle leading it to constrict.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the aetiology of chronic bronchitis and emphysema?

A
  • Smoking
  • Atmospheric pollution
  • Alpha-1-protease (emphysema)
  • Age and susceptibility
  • Men > Women
  • Increasing in developing countries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the clinical definition of chronic bronchitis?

A

The patient has a cough productive of sputum most days in at least 3 consecutive months for 2 or more consecutive year.

Complicated chronic bronchitis when sputum turns mucopurulent (yellow or green) or FEV1 falls

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

What happens to the large airways during chronic bronchitis?

A

Mucous glands get bigger, number of goblet in the surface respiratory epithelia increases, inflammation and fibrosis.

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

What happens to the small airways during chronic bronchitis?

A

Goblets cells appear, inflammation and fibrosis in long standing disease.

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

What is the pathological definition of emphysema?

A

Increase beyond the normal in the size of the airspaces distal to the terminal, bronchial arising either from dilatation or from destruction of their walls and without obvious fibrosis.

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

What is acinus?

A

The gas exchange tissue part of the lung, everything distal to the terminal bronchiole.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is centriacinar acinus?

A

The loss of of lung tissue is concentrated around the middle of the acinus.

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

What is panacinar acinus?

A

It takes out large areas of the lungs,

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

What is periacinar acinus?

A

Loss around the edges of the acinus.

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

What is bleb?

A

It is used to describe spaces underneath the plasma.

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

What is the pathogenesis of emphysema?

A
  • Smoking
  • Protease - Antiprotease imbalance
  • Ageing
  • Alpha-1-antitrypsin deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the main mechanisms of airways obstruction in COPD?

A
  • change in large airways has little contribution.
  • inflammation in the small airways leads to change in the smooth muscle tone.
  • In emphysema the loss of alveolar attachments is the most common factor
  • fibrosis - partial collapse of airways on expiration.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do the small airways remain open?

A

The intrathoracic pressure increase causes them to want to collapse but the radial pull and counterbalance from these elastic structures pulling the small airways open.

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

What is pulmonary arteriolar vasoconstriction?

A

When alveolar oxygen tension falls, can be localised effect, all vessels constrict if there is hypoxaemia.

22
Q

What is chronic cor pulmonale?

A

A respiratory disorder results in high blood pressure in the pulmonary arteries (pulmonary hypertension).

23
Q

Why do patients with hypoxia cor pulmonale get pulmonary hypertension?

A
  • Pulmonary vasoconstriction
  • Pulmonary arterioles
  • Loss of capillary bed
  • Secondary polycythaemia
24
Q

What is used to predict FVC?

A

Age, sex and height

25
Q

Besides FEV1/FVC ratio how else can an obstructive lung disease be demonstrated?

A

Peak expiratory flow rate

26
Q

What causes the decrease in diameter size in bronchial asthma?

A

Degranulation of mast cells and smooth muscle contraction (both reversible by use of drugs or spontaneously)

27
Q

What type of hypersensitivity is bronchial asthma?

A

Type I

28
Q

What physical substances obstruct airways in chronic asthma?

A

Oedema, mucus, plasma exudation

29
Q

What is the effect of smoking on alpha-1-antiprotease (antitrypsin)?

A

Malfuntion of antitrypsin (alpha-1-antiprotease) -= emphysema or COPD

30
Q

What is the result of anti trypsin deficiency?

A

Neutrophil elastase is free to break down elastin, which contributes to the elasticity of the lungs. Antitrypsin would normally It protect tissues from enzymes of inflammatory cells, especially neutrophil elastase

31
Q

How does FEV1 change with age?

A

Reduces

32
Q

What does chronic bronchitis exclude?

A

TB Bronchiecstasis These may be confused with asthma

33
Q

What is acute exacerbation of COPD?

A

Sudden worsening of COPD symptoms (shortness of breath, quantity and colour of phlegm) that typically lasts for several days. It may be triggered by an infection with bacteria or viruses or by environmental pollutants. Infection is most common cause (75%)

34
Q

How does the frequency of exacerbations change as the COPD progress?

A

Exacerbations become more and more frequent

35
Q

What are the morphological changes in the large airways in chronic bronchitis?

A

Mucous gland hyperplasia Goblet cell hyperplasia Inflammation and fibrosis (minor component)

36
Q

What are the morphological changes in small airways in chronic bronchitis?

A

Goblet cells appear inflammation and fibrosis in long standing disease

37
Q

What is centriacinar emphysema?

A

Most common type of pulmonary emphysema mainly localized to the proximal respiratory bronchioles with focal destruction and predominantly found in the upper lung zones. This is because most material inhaled ends up here - max inflammation and destruction occurs here

38
Q

What is a secondary pulmonary lobule?

A

The subsegment of lung supplied by three to five terminal bronchioles and separated from adjacent secondary lobules by intervening connective tissue (interlobular septa)

39
Q
  • What is panacinar emphysema?
A

Emphysema affecting all parts of the secondary pulmonary lobule, typically involving the inferior part of the lung and often asociated with a α1-antitrypsin deficiency.

40
Q

What is bulla?

A

Emphysematous space greater than 1 cm

41
Q

What portion of COPD is reversible?

A

Smooth muscle tone and inflammation.

42
Q

What are the normal reference ranges of PaO2 and PaCO2?

A

PaO2 10.5 - 13.5kPa, PaCO2 4.8 - 6.0kPa

43
Q

What are the two types of respiratory failure?

A

Type I PaO2 <8kPa (PaCO2 normal or low)

Type II PaCO2 >6.5kPa (PaO2 usually low)

44
Q

What are the common causes of hypoaxaemia?

A

Ventilation/perfusion imbalance, Diffusion impairment, Alveolar Hypoventilation, Shunt

45
Q

How does COPD involve V/Q mismatch, aveolar ventilation, diffusion impairment and shunt?

A

Airway obstruction, Reduced Respiratory Drive, Loss of alveolar surface area, Shunt only during acute infective exacerbation

46
Q

Why does pneumonia cause hypoxaemia?

A

Ventilation / perfusion abnormality (mismatch) - some ventilation of abnormal alveoli just not enough, Shunt - No ventilation of abnormal alveoli

47
Q
  • What is the most common cause of hypoxaemia clinically?
A

Low V/Q

48
Q
  • What is the normal percent of blood that is shunted?
A

2-4%

49
Q

What is the effect of hypoventilation of PaCO2 and PaO2?

A

Hypoventilation increases PACO2, and thus increases PaCO2

•Increase in PACO2 decreases PAO2, which causes PaO2 to fall

50
Q

What causes physiological pulmonary vasoconstriction?

A

When alveolar oxygen tension falls

51
Q

How is physiological pulmonary vasoconstriction protective?

A

Do not send blood to alveoli short of oxygen

52
Q

What is Type I hypersensitivity?

A

Type I hypersensitivity disease relating the degranulation of mast cells in the airways which release a number of chemical factors from mast cell granules.

Respiratory System & CVS Physiology Year 1 (58 decks)

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