Obstructive Airways Disease Flashcards
where is the problem in obstructive disease compared to restrictive disease?
Obstructive - airways
Restrictive - lungs
What is the obstructive airway syndrome? (3 factors) What is ACOS?
- asthma
- chronic bronchitis
- emphysema
ACOS: asthma/COPD overlap syndrome - COPD with reversability and eosinophilia who are steroid responsive, more reversably to salbutamol
What is the asthma triad?
- reversible airflow obstruction
- airway inflammation
- airway hyperresponsiveness
In asthma what do: -Bronchoconstriction -Chronic airway inflammation -airway remodelling Lead to?
Bronchoconstriction leads to brief symptoms
Chronic airway inflammation leads to exacerbations of airway hyperresponsiveness
Airway remodelling leads to fixed airway obstruction
What is seen in the: -basement membrane -Submucosa -Smooth muscle In the remodelling that takes place in asthma?
- Thickened basement membrane
- collagen deposition in the submucosa
- smooth muscle hypertrophy
Describe the four steps of the inflammatory cascade in asthma, where does:
- avoidance
- anti-inflammatory drugs: corticosteroids/cromones
- Anti-leukotriene/histamine, anti-IgE, anti-IL5
- Bronchodilators: B2-agonists, muscarinic antagonists
Fit in with this?
1: genetic predisposition and triggers (virus/allergen/chemical/nutrition)
- avoidance
2: eosinophilic inflammation
- anti-inflammatory
3: mediators and TH2 cytokines
- Anti-leukotriene/histamine
- Anti-IgE
- Anti-IL5
4: hyper-reactive smooth muscle
- bronchodilators
list some triggers assoc. commonly with asthma (10)
Allergens: animal dander, dust mites, pollens, fungi
Others: exercise, viral infection, smoke, cold, chemicals, drugs (NSAIDs/BBlockers)
What are the different clinical features for the clinical syndrome of asthma? (7)
- episodic symptoms and signs
- diurnal variability (nocturnal or early morning)
- non-productive cough/wheeze
- triggers
- assoc. atopy (eczema/conjunctivitis/rhinitis)
- FH asthma
- Wheezing due to turbulent airflow
What are the five aspects of asthma diagnosis?
1: history and examination
2: diurnal variation of peak flow rate
3: reduced forced expiratory ratio - FEV1/FVC < 75%
4: reversability to inhaled salbutamol
5: provocation testing = bronchospasm (exercise/histamine/methacholine/mannitol)
Describe the pathophysiology of COPD
Noxious particles or gases e.g. smoking lead to the activation of alveolar macrophages and neutrophils that release proteases which causes:
-mucociliary dysfunction
-inflammation
-tissue damage
(mucus hypersecretion, emphysema, mucosal and peribronchial inflammation and fibrosis)
which leads to the development of obstruction and ongoing disease progression to result in:
Characteristics - exacerbations/reduced lung function
Symptoms - breathlessness, worsening QOL
What are proteases normally counteracted by? what is the difference in the balance of this in COPD patients
- anti-proteases such as a1-antitripsin
- usually there is a balance between proteases and anti-proteases however in COPD there is an imbalance: either an increase in proteases or a decrease in anti-proteases
How is mucociliary function affected in COPD?
-COPD patients have recurrent resp. tract infection which damage the airway tissue leading to loss of ciliated cells
what is the difference between chronic bronchitis (6) and emphysema (4) in COPD
Chronic bronchitis:
- Chronic neutrophilic inflammation
- Mucus hypersecretion
- Mucociliary dysfunction
- Altered lung microbiome
- Smooth muscle spasm and hypertrophy
- Partially reversible
Emphysema:
- Alveolar destruction
- Impaired gas exchange
- Loss of bronchial support
- Irreversible
What are the 4 ways COPD is assessed? What indicates high risk?
- assess symptoms
- assess degree of airflow limitation using spirometry
- assess risk of exacerbations
- assess co-morbidities (IHD/HF)
2 exac. or more within the last year
or
FEV1<50% predicted
= indicators high risk
What are the 7 factors that make up the clinical syndrome of COPD
- chronic symptoms
- smoking
- non-atopic
- daily productive cough
- progressive breathlessness
- frequent infective exacerbations
- chronic bronchitis = wheezing
- Emphysema = reduced breath sounds
Describe how COPD leads to cor-pulmonale
Progressive fixed airflow obstruction Impaired alveolar gas exchange Respiratory failure: low PaO2 high PaCO2 Pulmonary hypertension Right ventricular hypertrophy/failure (i.e. cor pulmonale)
What is the difference between type 1 and type 2 respiratory failure?
Type 1 respiratory failure: hypoxaemia with low or normal carbon dioxide levels
Type 2 resp. failure: hypoxaemia with hypercapnia
describe the differences between asthma and COPD: smoker? allergic? onset? intermittant or chronic? productive or non productive cough? eosinophilic or neutrophilic inflamm? diurnal variability? -steroid response? bronchodilatory response FVC and TLCO changes Gas exchange normal or abnormal?
Asthma: Non smokers Allergic Early or late onset Intermittent symptoms Non productive cough Non progressive Eosinophilic inflammation Diurnal variability Good corticosteroid response Good bronchodilator response Preserved FVC and TLCO Normal gas exchange
COPD: Smokers Non allergic Late onset Chronic symptoms Productive cough Progressive decline Neutrophilic inflammation No diurnal variability Poor corticosteroid response Poor bronchodilator response Reduced FVC and TLCO Impaired gas exchange
What are the 6 risk factors for developing asthma?
Family history of atopic disease (e.g. asthma, eczema, allergic rhinitis, or allergic conjunctivitis)
Co-existence of atopic disease
Male sex (for pre-pubertal asthma) and female sex (for persistence of asthma from childhood to adulthood)
Bronchiolitis in infancy
Parental smoking, including perinatal exposure to tobacco smoke
Low birthweight and/or Premature birth
In COPD is there a higher or a lower residual volume than in normal lungs?
-higher
what is the treatment for COPD?
General management
smoking cessation advice annual influenza vaccination one-off pneumococcal vaccination
Bronchodilator therapy
a short-acting beta2-agonist (SABA) or short-acting muscarinic antagonist (SAMA) is first-line treatment for patients who remain breathless or have exacerbations despite using short-acting bronchodilators the next step is determined by the FEV1
FEV1 > 50%
long-acting beta2-agonist (LABA), for example salmeterol, or: long-acting muscarinic antagonist (LAMA), for example tiotropium
FEV1 < 50%
LABA + inhaled corticosteroid (ICS) in a combination inhaler, or: LAMA
For patients with persistent exacerbations or breathlessness
if taking a LABA then switch to a LABA + ICS combination inhaler otherwise give a LAMA and a LABA + ICS combination inhaler
Oral theophylline
NICE only recommends theophylline after trials of short and long-acting bronchodilators or to people who cannot used inhaled therapy the dose should be reduced if macrolide or fluoroquinolone antibiotics are co-prescribed
Mucolytics
should be 'considered' in patients with a chronic productive cough and continued if symptoms improve
Cor pulmonale
features include peripheral oedema, raised jugular venous pressure, systolic parasternal heave, loud P2 use a loop diuretic for oedema, consider long-term oxygen therapy ACE-inhibitors, calcium channel blockers and alpha blockers are not recommended by NICE
