Obstructive and Restrictive Pulmonary Disease Flashcards
What happens to overall size of the lungs in obstructive disease compared to a normal lung?
It gets bigger. This is due to air getting trapped prior to breathing in (after breathing out in the previous breath)
What happens to overall size of the lungs in restrictive disease?
The reduced compliance of the lung prevents it from inflating as much as it should thus making it smaller overall.
What is FVC?
The maximum amount of air that can be forced out after taking the deepest breath possible.
What is FEV1?
Amount of air that can be expired forcefully in 1 second.
What happens to FEV1:FVC ratio in obstructive lung disease?
It is decreased due to slower expelling of air from the lungs as a result of the obstruction.
FVC is typically normal in obstructive lung disease or it can be slightly decreased (probably due to trapping of gas)
Examples of Obstructive Lung Diseases:
Chronic bronchitis (mucous gland hypertrophy, hyperplasia, and hypersecretion)
Bronchiectasis (airway dilation and scarring)
Asthma (Smooth muscle hypertrophy and hyperplasia, mucous secretion and inflammation)
Emphysema (Air space enlargement and wall destruction)
Bronchiolitis (inflammatory scarring and partial obliteration of bronchioles)
What is asthma?
A chronic inflammatory disorder characterised by hyper-responsive airways. (people become overly-reactive to stimuli reversibly undergoing bronchospasm/bronchoconstriction
What are the types of asthma and their subtypes?
Extrinsic asthma: Atopic asthma, Drug-induced asthma, and Occupational asthma
Intrinsic asthma: Non-atopic asthma
What is atopic asthma?
Allergic asthma which is caused by type I IgE mediated hypersensitivity reaction. This is often triggered by allergens such as dust, pollen, infections and animal hair.
What is non-atopic asthma?
Asthma that isn’t triggered by allergic reactions. (negative allergen tests and aren’t always associated with family history, typically overlaps with bronchitis and mostly in people who smoke)
What are the symptoms of asthma?
Severe dyspnoea with wheezing which lasts for several hours or more and subsides naturally or responds to bronchodilators.
What is the mortality rate of asthma?
0.2% per annum
What is the condition in which asthma fails to subside for days/weeks called? What can this condition cause?
Status asthmaticus which can cause respiratory failure and death
How is asthma treated?
Prevention of asthma attacks are the mainstay of treatment
Is childhood asthma permanent?
No it may resolve with adulthood in approximately 50% of people
What happens in people with asthma?
Classic atopic asthma is associated with excessive type 2 helper T cells releasing IL-5, IL-13, and IL-4 and IL-3
In asthmatics what does IL-5 trigger?
Eosinophil activation
In asthmatics what does IL-13 trigger?
Mucus production
In asthmatics what do IL-3 and 4 trigger?
Mast cells degranulate
What are the phases of an asthma reaction? What happens during these phases?
Early phase (bronchoconstriction, increased mucous production, and vasodilation)
Late phase (Inflammatory mediators stimulate epithelial cells to produce chemokines and recruiting of Th2 cells and eosinophils which amplifies inflammatory response)
What happens to lung tissue in response to repeated infection?
Airway remodeling as a result of smooth muscle hypertrophy, mucous gland hypertrophy, and increased collagen deposition.
This has often already occured by the time the patient shows up in clinic
What happens histologically to lung tissue in asthma?
Mucus plugging of bronchi
Focal necrosis of epithelium
Eosinophilic inflammation
Oedema of bronchial walls
Thickening of epithelial basement membrane
Hypertrophy of bronchial mucous glands
Hypertrophy of smooth muscle of bronchial wall
The formation of Charcot-Leyden Crystals
Curschmann’s spirals
What are Charcot-Leydin Crystals?
Crystals that form from reaction between eosinophil granules and proteins
What are Curschmann’s spirals?
Casts of airways formed by mucin and cell debris
What is emphysema?
Abnormal permanent enlargement of airspaces distal to terminal bronchiole (just before the alveoli) WITHOUT obvious fibrotic damage
What abnormal lung changes does emphysema result in?
Trapping of air in dilated airspaces and loss of elastic recoil of the lungs (when breathing out) due to damage of parenchyma
What causes emphysema?
2 main causes:
Smoking / air pollution / industrial exposure and accumulation of neutrophils + macrophages in respiratory bronchioles
Genetic predisposition (most common in alpha1-antitrypsin deficiency)
How is damage caused in emphysema?
Acinar (physical) damage + Chronic inflammation + Protease (in neutrophils + macrophages in lung) / anti-protease activity (bronchial mucus)
What does smoking do to lungs that causes emphysema?
It inhibits alpha1 antitrypsin and other antiproteases.
The result is those proteases accumulate causing damage to the lining of the bronchioles in addition to the action of inflammation without being inhibited by the antiproteases.
Where does antitrypsin get produced?
Typically in the liver so cirrhosis of the liver in infancy means there can be severe emphysema in early adult life
How common is homozygous alpha1-antitripsin deficiency? What does this do to levels of antitrypsin and what is the resulting effect?
1 in 7000 adults
10% of normal level of antitrypsin which causes cirrhosis of the liver in infancy and severe emphysema in early adult life