pathology of obstructive lung disease Flashcards

1
Q

types of airway obstruction

A

localised obstruction of a large airway e.g. tumours, inhaled foreign bodies, scarring diseases and TB obstructive airway disease generalised small airway obstruction

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2
Q

obstructive airway diseases

A

chronic bronchitis emphysema (above 2 are collectively known as COPD) asthma mechanism of obstruction is different in each case

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3
Q

define FEV1

A

forced expiratory volume of air exiting the lung in the first second of this exercise

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4
Q

FVC

A

final total amount of air expired

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5
Q

normal values for FEV1 and FVC

A

FEV1 is usually about 70-80% of FVC normal FEV1: 3.5-4L normal FVC: 5L FEV1: FVC ratio: 0.7-0.8

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6
Q

what is predicted FVC based on

A

age sex height

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7
Q

how can obstructive lung disease be demonstrated

A

spirometry peak expiratory flow rate (PEFR)

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8
Q

PEFR

A

instantaneous maximum air flow that can be achieved compromised in patients with airflow limitation

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9
Q

normal and abnormal PEFR values

A

normal 400-600L/min normal range is 80-100% of best value 50-80% of best is moderate fall <50% of best is marked fall

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10
Q

how are values altered in obstructive lung disease (PEFR, FEV1, FVC)

A

airflow limitation reduced PEFR reduced FEV1 FVC may be reduced (can be normal but takes longer to achieve) FEV1 is less than 70% of FVC

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11
Q

bronchial asthma: type I hypersenstivity in the airways

A

specific Ige, drugs, chemicals, stress, cold - precipitate mast cell degranulation factors released by mast cells impact on the airways smooth muscle contraction and mucosal inflammation - reduction in lumen cross sectional area airflow limitation during asthma attack

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12
Q

bronchial asthma

A

reversible airway obstruction either spontaneously or as a result of medical intervention bronchial smooth muscle contraction and inflammation can be modified by drugs structural changes in chronic asthmatics may be irreversible by pharmacological intervention

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13
Q

aetiology of chronic bronchitis and emphysema

A

chronic inhalation of irritants: SMOKING, atmospheric pollution, occupation (dust) alpha-1-antiprotease deficiency (very rare cause) effect of age men > women, increasing in developing countries

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14
Q

effect of age and susceptibility to chronic bronchitis and emphysema

A

older = more likely to suffer if you have been exposed to air pollution some people are more susceptible to the damaging effects of air pollution than others

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15
Q

why do men suffer more than women from chronic bronchitis and emphysema

A

generally tend to smoke more and/or are occupied in jobs which are more likely to expose them to atmospheric pollution

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16
Q

clinical definition of chronic bronchitis

A

cough productive of sputum most days in at least 3 consecutive months for 2 or more consecutive years (excludes TB, bronchiectasis etc) clinically may be confused with chronic bronchial asthma

17
Q

what is complicated chronic bronchitis

A

mucopurulent - yellow sputum (acute infective exacerbation) or when FEV1 falls

18
Q

morphological changes in chronic bronchitis in large airways

A

mucous gland hyperplasia goblet cell hyperplasia inflammation and fibrosis is a minor component and occurs when the process becomes more chronic

19
Q

morphological changes in chronic bronchitis in small airways

A

goblet cells appear (method of adaptive protection) inflammation and fibrosis in longstanding disease

20
Q

why does XS mucus production occur in chronic bronchitis

A

defence mechanisms to protect the airway from the harmful substances being inhaled

21
Q

pathological definition of emphysema

A

increase beyond the normal in the size of airspaces distal to the terminal bronchiole arising either from dilation or destruction of their walls and WITHOUT obvious fibrosis

22
Q

define acinus

A

everything beyond the terminal bronchiole gas exchange region in the lung

23
Q

forms of emphysema

A

relate to where in the acinus is the alveolar tissue lost CENTRIACINAR (most important, associated with cigarette smoking) panacinar periacinar scar: irregular, bullous emphysema

24
Q

centriacinar emphysema

A

loss of alveloar tissue in the middle of the acinus around the respiratory bronchiole and alveolar ducts

begins with bronchiolar dilation

then alveolar tissue is lost

primarily affects the apex of the lung

25
panacinar emphysema
less common but very severe huge areas of lung tissue disappear
26
periacinar emphysema
less common loss of tissue at the edge of acinus, particularly those up against the pleura
27
define bulla
emphysematous space \>1cm
28
define bleb
often used to describe emphysematous spaces just underneath the pleura, usually found in the upper lobe of the lung no functional consequences can burst and lead to spontaneous pneumothorax
29
what is different about the inflation of lungs in emphysema on a CXR
lungs appear hyperinflated suffer less airflow limitation by keeping more air in the lungs
30
pathogenesis of emphysema
SMOKING protease - anti-protease imbalance angeing alpha-1-antitrypsin deficiency
31
anti-protease and protease activity in the normal individual
homeostatic balance between anti-elastase and elastase so damage to the individual doesnt occur neutrophils and macrophages are present if they are needed, use elastase to break down material elastin framework in alveolar tissue is maintained by anti-elastases repair mechanisms (elastin synthesis) isn't very effective - damage from emphysema can't be repaired
32
anti-protease and protease activity in alpha-1-antitrypsin deficiency
lack of full complement of protective enzymes elastase activity increases tissue can't be repaired unprotected elastase activity leads to tissue destruction and emphysema
33
anti-protease and protease activity in smokers
reduced anti-elastase activity increased elastase activity increased neutrophils and macrophages which contribute to increased elastases reduced repair mechanisms and elastin synthesis tissue destruction and emphysems
34
is airflow obstruction in COPD reversible
generally NO however, most airflow limitation isn't reversible with pharmacological intervention however there may be a reversible component
35
mechanisms of airway obstruction in COPD
large airways: little contribution by glands and mucous small airways: largest contribution to airflow limitation; smooth muscle tone (twitchy and hyper-reactive) and inflammation (increase in smooth muscle tone)respond to pharmacological intervention, fibrosis, partial collapse of airway wall on expiration in emphysema, loss of alveolar attachments is most important and this cannot be treated with drugs
36
loss of alveolar attachments in emphysema
radial pull around the terminal bronchioles are lost terminal bronchioles are no longer held open these are the ones affected in centriacinar emphysema
37
reduced respiratory drive in COPD
[CO2] in CSF is the primary driver of breathing body becomes habituated to elevated CO2 level, responds less to high levels of H+ kidney tries to compensate but eventually can't cope in end stage COPD, patients rely entirely on oxygen to drive breathing but breathe less and less due to reducing sensitivity to hypoxia - become cyanosed and edematosed (R heart failure) some patients remain very sensitive to hypoxia and breathe rapidly