pathology of obstructive lung disease Flashcards
types of airway obstruction
localised obstruction of a large airway e.g. tumours, inhaled foreign bodies, scarring diseases and TB obstructive airway disease generalised small airway obstruction
obstructive airway diseases
chronic bronchitis emphysema (above 2 are collectively known as COPD) asthma mechanism of obstruction is different in each case
define FEV1
forced expiratory volume of air exiting the lung in the first second of this exercise
FVC
final total amount of air expired
normal values for FEV1 and FVC
FEV1 is usually about 70-80% of FVC normal FEV1: 3.5-4L normal FVC: 5L FEV1: FVC ratio: 0.7-0.8
what is predicted FVC based on
age sex height
how can obstructive lung disease be demonstrated
spirometry peak expiratory flow rate (PEFR)
PEFR
instantaneous maximum air flow that can be achieved compromised in patients with airflow limitation
normal and abnormal PEFR values
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
how are values altered in obstructive lung disease (PEFR, FEV1, FVC)
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
bronchial asthma: type I hypersenstivity in the airways
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
bronchial asthma
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
aetiology of chronic bronchitis and emphysema
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
effect of age and susceptibility to chronic bronchitis and emphysema
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
why do men suffer more than women from chronic bronchitis and emphysema
generally tend to smoke more and/or are occupied in jobs which are more likely to expose them to atmospheric pollution
clinical definition of chronic bronchitis
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
what is complicated chronic bronchitis
mucopurulent - yellow sputum (acute infective exacerbation) or when FEV1 falls
morphological changes in chronic bronchitis in large airways
mucous gland hyperplasia goblet cell hyperplasia inflammation and fibrosis is a minor component and occurs when the process becomes more chronic
morphological changes in chronic bronchitis in small airways
goblet cells appear (method of adaptive protection) inflammation and fibrosis in longstanding disease
why does XS mucus production occur in chronic bronchitis
defence mechanisms to protect the airway from the harmful substances being inhaled
pathological definition of emphysema
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
define acinus
everything beyond the terminal bronchiole gas exchange region in the lung
forms of emphysema
relate to where in the acinus is the alveolar tissue lost CENTRIACINAR (most important, associated with cigarette smoking) panacinar periacinar scar: irregular, bullous emphysema
centriacinar emphysema
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

panacinar emphysema
less common but very severe
huge areas of lung tissue disappear

periacinar emphysema
less common
loss of tissue at the edge of acinus, particularly those up against the pleura

define bulla
emphysematous space >1cm
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
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
pathogenesis of emphysema
SMOKING
protease - anti-protease imbalance
angeing
alpha-1-antitrypsin deficiency
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
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
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
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
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
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
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