Pathology of obstructive lung disease Flashcards
Give examples of obstructive airway diseases
chronic bronchitis(COPD), emphysema (COPD), asthma(type 1 hypersensitivity reaction
Why is the following: bronchiectasis, secondary tubersclulosis, lung cancer + inhaled foreign bodies not classified as an OAD?
There is localised obstruction. OAD causes obstruction in all the airways
FEV1 vs FVC
FEV1: forced expiratory volume of air eaving lung in the first second
FVC: final total amount of air expired
What is the normal FEV1 + FVC + their ratio?
- 70-80% of FVC
- 3.5-4L
- FVC= 5L
- FEV1:FVC is 0.7-0.8
What is the normal Peak expiratory flow rate? ( PEFR)
-Used to measure peak flow rate Normal 400-600L/min Normal range is 80-100% of best value -50-80% is a moderate fall <50% of best is marked fall
For obstructive Lung disease, state the changes in: PEFR, FEV1, FVC
PEFR: reduced
FEV1:reduced ( <70% of FVC)
FVC: reduced
Describe bronchial asthma
Type 1 Hypersensitivity of the airways
- mediated by degranulation of mast cells which is percipitated. The factors released by mast cells has affects on airway by:
1. Induction of acute inflammatory response in the airway (swelling)
2. causes bronchial smooth muscle to constrict - A combination leads to reduction in airway diameter. So, airflow limitation during attack of bronchial asthma.
- Patients will have symptoms of asthma and risk factors.
Is bronchial asthma/COPD reversible or irreversible?
- Reversible either spontaneously or as a result of medical intervention(drugs)
- Structural changes in airways which are irreversible by pharmacological intervention.
-COPD: irreversible but..
What is the main causes odf COPD ( chronic broncitis + emphysema)
- Tobacco smoking
- atmospheric pollution
- occupation: dust
- alpha-1-antiprotease(antritrypsin) deficiency
- age + suceptiblity
- men>women due to smoking/jobs
What is alpha-1-antiprotease(antritrypsin) deficiency?
-Rare cause of emphysema
Describe the FEV1 of a smoker compared to a non-smoker
FEV1 will decline with age(exposed to air pollution). In a smoker, it declines faster.
-But if you stop smoking it may be slightly reversible so FEV1 will decline slower depending on when you choose to stop smoking
What is the clinical definition of chronic bronchitis?
-cough productive sputum most days in at least 3 consecutive months for 2/+ consecutive years
What is complicated chronic bronchitis?
When yellow/mucopurulent(indicates infection) or FEV1 falls
State the morphological changes in chronic bronchitis
Large airways
- mucous gland hyperplasia
- Gobet cell hyperplasia = excess mucous prod.
- Inflammation and fibrosis (minor component)
Small airways (mainly contributes to airway reduction)
- Goblet cells appear ( not usually pressent)
- inflammation and fibrosis(more of an issue)
- initially inflammation is reversible which is why early smoking cessation improves symptoms
-narrowing of bronchioles is as a result of inlammation, mucous
What is emphysema?
-Increase in size of alveolar airspaces distal to the terminal bronchiole arising from either dilation / destruction of their walls WITHOUT FIBROSIS
State the forms of emphysema
- centriacinar
- panacinar
- periacinar
- scar ‘ irregular’ / ‘ bullous emphysema’
What is centriacinar emphysema?
- Loss of alveolar tissue in the middle of the acinus
- mainly caused by cigarrete smoking
- mainly affects apical parts of the lung
- begins with bronchiolar dilation, then eventually alveolar tissue is lost.
What is panacinar?
-wiping out of all the lung tissue
-linked with antitrypsin
deficiency
- can cause spaces in lungs ( blebs) or bulla(greater than 1cm)
What is periacinar emphysema?
- loss of tissue at edge of acinus ( acinar that are against pleura)
- blebs/bullous formation on edge of acinus
- leads to formation of blebs just underneath pleura. No complications unless it bursts>pneumothorax
What is bullous emphysema?
- excessive damage to alveolar structures to the point large alveolar spaces are formed
- hyper inflated lungs
Describe the pathogensis of emphysema
- Normally, in the lung, there is macrophages and neutrophils that produces enzymes that contain proteases, elastases to break down material.
-Everytime elastase is produced, anti-elastase(protease inhibitor) is also produced to prevent damage to the elastic framework lung.
-Tobacco smoke e
evokes an acute inflammatory reaction and causes immune cells to gather. It also inhibits anti-elastases which means tissue destruction occurs - There is repair mechanisms for elastin framework that are useless when you have emphysema.
-You can’t grow lung alveoli back again. It is irreversible.
Describe the pathogenesis of alpha 1 antitrypsin deficiency
- there is an absence in antitrypsin, so trypsin will lead to tissue destruction of alveoli
How can smoking lead to emphysema?
- more inflammatory cells in lungs
- induces elastases, and causes anti-elastases to now work. Repair mechanism is now poor.
- tissue destruction
How is COPD reversible?
-inflammation and smooth muscle tone respond to drugs
How does emphysema lead to airflow limitation?
- alveolar attachments; this gives a radial pull of the alveolar walls, hence maintaining the opening of airways.
- But when alveolar attachments is destroyed ( emphysema) and the terminal bronchioles is most likely to collapse
Why can COPD lead to hypoxaemia?
-Airway obstruction: leads to V/P msimatch ( V<p></p>
Why can COPD lead to hypoxaemia?
-Airway obstruction: leads to V/P mismatch ( V<p></p>
Why is COPD also classified as irreversible?
- Large airways
- Fibrosis
- partial collapse of airway wall on expiration
- All off this is does not respond to pharmacological intervention!
What is meant by cor pulmonale?
-hypertrophy of the right ventricle of the heart that occurs due to pressure overload. Results from disease affecting function/structure of lung.
Why can cor pulmonale lead to pulmonary hypertension?
- pulmonary vasoconstriction
- pulmonary arterioles ( muscle hypertrophy and intimal fibrosis)
- loss of capillary bed
- secondary polycythaemia
- bronchopulmonary arterial anastomoses
Long term consequences of COPD
Respiratory failure
Type 1: low O2, normal/low CO2( hypoxia and hypocapnia)
Type 2: low O2 and high CO2(hypoxia and hypercapnia)
Chronic hypoxia
pulmonary vasoconstriction>pul. hypertension
pul. hypertension > cor pulmonale
