Obstructive Airway Diseases Flashcards
A. What is an obstructive airway disease?
A disease in the airways that has an impact on respiration
A. What is a restrictive airway disease?
A disease in the lungs that leads to problem with respiration.
A. Give some examples of obstructive airway disease
Asthma, chronic bronchitis and emphysema. The latter being part of COPD.
ACO - Asthma and COPD overlap syndrome.
A. What are the causes of airway obstruction within a COPD or asthma patient?
Muscle constriction of smooth muscle can lead to lumen shrinkage of the airways.
Alveolar walls can be lost.
A. What is emphysema?
A lung condition in which the alveoli are damaged, resulting in large air spaces when the alveoli rupture
A. What are the three points of the asthma triad?
T2 airway inflammation (eosinophil is usually the effector)
Airway hyper responsiveness
Reversible airflow obstruction
A. Describe the way in which asthma symptoms progress.
- Broncho-constriction - brief symptoms
- Chronic airway inflammation - exacerbations of airway hyper-responsiveness.
- Airway remodelling - fixed airway obstruction with laying down of collagen tissue
A. What are the hallmarks of remodelling in asthma?
- Thickening of the basement membrane.
- Collagen deposition in the submucosa
- Hypertrophy of the smooth muscle.
A. Describe the process of type 2 inflammation in asthma.
- Allergen comes into contact with airway epithelium.
- Thymic stromal lymphoproteins are released and bind to dendritic cells.
- This complex then moves to the lymph node.
- This leads to the differentiation of T cells into TH2 cells which produces the cytokine, IL-5, which is chemotactic for eosinophils.
- It also interacts with B cells to produce cytokines IL-4 and IL-13, and release IgE which interacts with mast cells (to release histamine) and basophils (to release leukotriene D4)
- The leukotriene D4 will attract eosinophils and cause goblet cells to produce mucous.
A. Name factors that, if present, will lead to type 2 inflammation in asthma.
Presence of cytokines (IL4/5/13)
Raised total or specific IgE
Blood/sputum eosinophilia
Raised FeNO
A. Describe the inflammatory cascade in asthma.
We would treat the top of the cascade first.
- Inherited or acquired factors e.g. allergens such as pets.
- Eosinophilic inflammation e.g. anti inflammatory medication such as corticosteroids.
- Mediators and Th2 cytokines e.g. antihistamines, monoclonal antibodies
- Twitchy smooth muscle e.g. bronchodilators
A. Name some triggers for asthma exacerbations.
Allergens - animal dander, pollens etc. Exercise Viral infection Smoke Cold Chemicals Drugs - NSAIDs, beta blockers
A. Describe the clinical syndrome of asthma.
Episodic symptoms Diurnal variability. Non-productive cough/wheeze Triggers - allergens, exercise etc. Associated T2 comorbitities Reversible Family history
A. What are some associtated T2 comorbidities of asthma?
Allergic rhino conjunctivitis Chronic rhino sinusitis with nasal polyps Atopic dermatitis Eosinophilic esophagitis Urticaria
A. How will asthma be diagnosed?
History and examination
A. What tests can be used to diagnose asthma?
Diurnal variation of peak flow rate
Reduced forced expiratory ratio (<75%)
Reversibility to inhaled salbutamol (>15%)
Provocation testing
A. Describe the MULTICOMPONENT disease process of COPD.
The inhalation of noxious particles or gases via smoking leads to -
Mucociliary dysfunction
Inflammation
Tissue damage.
This leads to the development of obstruction and the ongoing progression of the disease.
A. What are some of the characteristics of COPD?
Exacerbations - worsening of the disease
Reduced lung function - particularly on expiration.
A. What are some of the symptoms of COPD?
Breathlessness
Worsening quality of life
A. What are some of the features of COPD within the lungs?
Mucous hypersecretion (chronic bronchitis)
Emphysema - disrupted alveolar attachments
Obliterative bronchiolitis - mucosal and peribronchial inflammation and fibrosis.
A. Describe the process of COPD.
- Individual continually inhales cigarette smoke.
- This activates alveolar macrophages to produce chemotactic factors, cytokines (IL-8)etc.
- This releases neutrophils.
- These release damaging proteases.
- This then results in emphysema, chronic bronchitis and reduction in airflow.
A. Describe chronic bronchitis
This is chronic neutrophilic inflammation (20% of patients also have eosinophilic inflammation).
It results in mucous hyper secretion, mucociliary dysfunction, altered lung biome (increase in gram -ve bacteria), smooth muscle spasm/hypertrophy.
It is partially reversible.
A. Describe emphysema.
This is alveolar destruction.
This results in impaired gas exchange, loss of bronchial support.
This is irreversible.
A. Describe the clinical syndrome of COPD.
Chronic symptoms Smoking related. Non-atopic - not caused by allergens Daily productive cough Progressive breathlessness Frequent infective exacerbations Chronic bronchitis and emphysema
A. What is the chronic cascade in COPD?
- Progressive fixed airflow obstruction.
- This results in impaired alveolar gas exchange.
- This can lead to type 2 respiratory failure.
- This causes pulmonary hypertension that is stimulated by hypoxia.
- This leads to right ventricular hypertrophy/failure.
- Ultimately, this caused death.
A. What is ACO?
This is an asthma COPD overlap syndrome.
This occurs in COPD patients who have blood eosinophilia >300/ul
These patients respond better to inhaled steroids.
It may be difficult to distinguish from asthmatic smokers.
A. Describe the non-pharmalogical management of COPD.
Smoking cessation.
Immunisation against infections
Physical activity
Oxygen for 15 hours a day
A. Describe the pharmacological management of COPD.
LABA/LAMA combo
ICS/LABA combo
ICS/LABA/LAMA combo
B. Name some effort dependent pulmonary function tests.
Forced expiratory volumes
Flow rates
B. Name some effort independent pulmonary function tests.
Relaxed vital capacity
Exhaled breath nitric oxide
impulse oscillometry
B. Name some gas diffusion pulmonary function tests.
CO transfer factor
Arterial blood gases @ rest
SaO2 during exercise
B. How does restrictive lung diseases present in spirometry?
The FEV1 and FVC will be reduced proportionately therefore there will be a normal FEV1:FVC ratio.
B. How does COPD present in spirometry?
The patient won’t reach a normal FVC due to gas trapping.
The FEV1 will be below 75%.
B. How does asthma present in spirometry?
The FVC will be normal.
The FEV1 will be below 75%.
