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Respiratory and Cardio > Airflow obstruction > Flashcards

Airflow obstruction Flashcards

1
Q

Diagnosis of airflow obstruction is done using a

A

Spirometer

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2
Q

Shape of obstructive in a flow diagram:

A

Can see a ‘dent’

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3
Q

Shape of restrictive in a flow diagram:

A

Smaller/all reduced

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4
Q

Normal FEV1/FVC

A

> 75%

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5
Q

Abnormal FEV1/FVC

A

<70%

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6
Q

Why might an airway be narrowed?

A

Mucus
Hypertrophy of bronchial smooth muscle
Breakdown of alveolar walls so airways collapse

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7
Q

Ex of conditions in which airway is obstructed by mucus:

A

Infection (acute bronchitis)

Chronic bronchitis

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8
Q

Ex of condition in which bronchial smooth muscle hypertrophies

A

Asthma

COPD

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9
Q

Ex of condition in which alveolar walls break down

A

Emphysema

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10
Q

Asthma is an example of what time of hypersensitivity reaction?

A

Type 1

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11
Q

Asthma is reversible/irreversible

A

Reversible

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12
Q

What does ‘reversible airflow obstruction’ mean?

A

Reversible with time or bronchodilators

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13
Q

Asthma is characterised by:

A
  • Reversible
  • Airway inflammation
  • Hyperactivity of airway
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14
Q

Airway hyperactivity =

A

Increased tendency to spasm

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15
Q

How to diagnose asthma:

A

Hx - should be variable airway narrowing (bad periods which are self-limiting)
- Demonstrate variability using PF monitoring/bronchodilator reversibility studies/treatment trials

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16
Q

What increase of FEV1 in response to a bronchodilator is diagnostic of asthma?

A

> 15%

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17
Q

Bronchial hyperreactivty study =

A

Give a substance like histamine, mannitol etc.

Measure drop in FEV1

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18
Q

What kind of variation does peak flow have?

A

Diurnal

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19
Q

What can be given to an asthmatic to help them recognise exacerbations or when they need to use treatment?

A

Peak flow monitor

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20
Q

How can we find eosinophilia?

A
  • Sputum eosinophila

- measure exhaled NO

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21
Q

Exhaled NO is a marker for

A

Eosinic airway inflammation

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22
Q

FENO =

A

Fraction exhaled nirtic oxide

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23
Q

Triggers for asthma:

A 
Dust 
Air pollution
Pet dander
Foods: peanuts, wheat
Chemicals
Pollen
Mould
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24
Q

What dominate asthmatic inflammation?

A

Th2 cells

eosinophils

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25
Q

Th1 t cells

A

promote cell immunity

IgG

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26
Q

Th2 cells

A

Enhance mast cells, eosinophils and IgE

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27
Q

What type of immunoglobulin to Th2 cells stimualte the production of

A

IgE

28
Q

Name some cytokines released by Th2

A

IL-4

IL-5

29
Q

IL-4 =

A

IgE

Mast cells

30
Q

Mast cells release

A

Histamine
Leukotrienes
Prostaglandin

31
Q

IL-5 =

A

Eosinophils

32
Q

Eosinophils release

A

Histamine

Leukotrienes

33
Q

“A genetic tendency to develop allergic diseases” =

A

Atopy

34
Q

3 conditions a person with atopy is likely to develop

A

Asthma
Allergic rhinitis
Atopic dermatitis

35
Q

What are drug developers now interested which attract eosinophils to the airways?

A

IL-5

36
Q

Acute airway change in asthma =

A 
Smooth muscle contraction
Sensory nerve action
Mucus hypersectrion
Plasma leakage
Oedema
Inflammatory infiltrate
37
Q

Chronic airway changes in asthma:

A

Subepithelial fibrosis

Smooth muscle hypertrophy

38
Q

Chronic airway changes occur when

A

Asthma is ongoing, untreated, cannot be suppressed

39
Q

2 conditions under the COPD umbrella:

A

Chronic bronchitis

Emphysema

40
Q

In comparison to asthma, COPD is

A

Non-reversible
Doesn’t respond to bronchodilators/steroids
Doesn’t markedly change

41
Q

Air becomes what in COPD

A

Trapped

42
Q

What increases in COPD?

A

Expiatory residual volume/ total lung capacity

43
Q

Emphysema is based on … Chronic bronchitis is based on ….

A

Emphysema = structural changes

Chronic bronchitis = clinical symptoms

44
Q

What happens in emphysema

A

Alveoli are damaged, elastin broken down
Lose elasticity, enlarge
Septa breakdown
Difficult for lungs to recoil - collapse on expiration

45
Q

What causes the breakdown of elastin in emphysema?

A

Inflammatory reaction - release leukotrienes, IL-8, TNF-a and proteases

46
Q

What usually stops airways collapsing in expiration?

A

Elastic recoil/elastin

47
Q

Most common pattern of emphysema associated with smoking =

A

Centrilobar

48
Q

Panacinar emphysema is associated with =

A

Alpha-1 antitrypsin deficiency

49
Q

What is alphae 1-antritrypsin?

A

A protease inhibitor which protects alveoli from unintended collateral damage from macrophages

50
Q

What can happen with a paraseptal emphysema?

A

Pneumothorax

51
Q

What can be seen on imaging in emphysema?

A

Bollous

52
Q

Bollous =

A

Presence of abnormally large air space surrounded by relatively normal lung tissue

53
Q

Chronic bronchitis definition:

A

Productive cough for at least 3 months/year for 2 consecutive years

54
Q

What happens in chronic bronchitis?

A 
Mucus gland hypertrophy
Goblet cell hyperplasia
Smooth muscle hypertrophy
Inflammatory cells infiltrate
Excess mucus
55
Q

What inflammatory cells are involved in chronic bronchitis?

A

Neutrophils and lymphocytes

56
Q

risk factors for COPD:

A 
Smoking
Occupational
Passive smoke/cannabis
Chronic asthma
Biofules 
Familial (alpha 1 antitrypsin deficiency)
57
Q

What is released by alveolar macrophages to clean up debris?

A

Proteases

58
Q

Blue bloaters =

A

Chronic bronchitis

59
Q

Pink puffers =

A

Emphysema

60
Q

Shape of chest in emphysema can be

A

Barelled - due to air trapping

61
Q

V/Q < 1 =

A

Perfusion is higher than ventilation

62
Q

What can happen when perfusion is higher than ventilation?

A

pO2 falls
pCo2 increases
Pulmonary vasoconstriction

63
Q

Consequences of pulmonary vasocontriction

A

Pulmonary hypertension –> cor pulmonale

64
Q

Cor pulmonale =

A

Right sided heart failure

65
Q

What happens in bronchiectasis?

A

Bronchial dilation

Chronic sputum production

66
Q

What does cronchiectasis increase?

A

Infections

67
Q

What does bronchiectasis resemble clinically?

A

COPD

Asthma

Respiratory and Cardio (14 decks)

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