pathology of obstructive lung disease

Question 1

types of airway obstruction

Answer 1

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

Question 2

obstructive airway diseases

Answer 2

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

Question 3

define FEV1

Answer 3

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

Question 4

FVC

Answer 4

final total amount of air expired

Question 5

normal values for FEV1 and FVC

Answer 5

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

Question 6

what is predicted FVC based on

Answer 6

age sex height

Question 7

how can obstructive lung disease be demonstrated

Answer 7

spirometry peak expiratory flow rate (PEFR)

Question 8

PEFR

Answer 8

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

Question 9

normal and abnormal PEFR values

Answer 9

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

Question 10

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

Answer 10

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

Question 11

bronchial asthma: type I hypersenstivity in the airways

Answer 11

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

Question 12

bronchial asthma

Answer 12

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

Question 13

aetiology of chronic bronchitis and emphysema

Answer 13

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

Question 14

effect of age and susceptibility to chronic bronchitis and emphysema

Answer 14

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

Question 15

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

Answer 15

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

Question 16

clinical definition of chronic bronchitis

Answer 16

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

Question 17

what is complicated chronic bronchitis

Answer 17

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

Question 18

morphological changes in chronic bronchitis in large airways

Answer 18

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

Question 19

morphological changes in chronic bronchitis in small airways

Answer 19

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

Question 20

why does XS mucus production occur in chronic bronchitis

Answer 20

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

Question 21

pathological definition of emphysema

Answer 21

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

Question 22

define acinus

Answer 22

everything beyond the terminal bronchiole gas exchange region in the lung

Question 23

forms of emphysema

Answer 23

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

Question 24

centriacinar emphysema

Answer 24

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

Question 25

panacinar emphysema

Answer 25

less common but very severe

huge areas of lung tissue disappear

Question 26

periacinar emphysema

Answer 26

less common

loss of tissue at the edge of acinus, particularly those up against the pleura

Question 27

define bulla

Answer 27

emphysematous space >1cm

Question 28

define bleb

Answer 28

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

Question 29

what is different about the inflation of lungs in emphysema on a CXR

Answer 29

lungs appear hyperinflated

suffer less airflow limitation by keeping more air in the lungs

Question 30

pathogenesis of emphysema

Answer 30

SMOKING

protease - anti-protease imbalance

angeing

alpha-1-antitrypsin deficiency

Question 31

anti-protease and protease activity in the normal individual

Answer 31

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

Question 32

anti-protease and protease activity in alpha-1-antitrypsin deficiency

Answer 32

lack of full complement of protective enzymes

elastase activity increases

tissue can’t be repaired

unprotected elastase activity leads to tissue destruction and emphysema

Question 33

anti-protease and protease activity in smokers

Answer 33

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

Question 34

is airflow obstruction in COPD reversible

Answer 34

generally NO

however,

most airflow limitation isn’t reversible with pharmacological intervention

however there may be a reversible component

Question 35

mechanisms of airway obstruction in COPD

Answer 35

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

Question 36

loss of alveolar attachments in emphysema

Answer 36

radial pull around the terminal bronchioles are lost

terminal bronchioles are no longer held open

these are the ones affected in centriacinar emphysema

Question 37

reduced respiratory drive in COPD

Answer 37

[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