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Asthma and COPD
Asthma - definition, epidemiology, pathophysiology, diagnosis, investigations, management, exacerbations, 'acute asthma' COPD - definition, epidemiology, pathophysiology, diagnosis, asthma vs COPD, management (pharmacological and non-pharmacological), exacerbations
Terms in this set (54)
What is the definition of asthma?
Chronic inflammatory disease of the airways - characterised by variability of symptoms and reversibility of airways obstruction
- airway hyper-responsiveness
What causes the airway obstruction?
Broncho-constriction, mucus hyper-secretion
What are the clinical symptoms?
Wheeze, chest tightness, cough, mucous production, shortness of breath
What might the reversibility of airways depend upon?
Can be spontaneous, may be due to treatment with beta-2 agonists/anti-inflammatory agents (corticosteroids)
What does the variable nature of asthma mean?
Most patients experience periods of good asthma control and periods of worsening symptoms
What does bronchial hyper-responsiveness lead to?
Episodes of coughing, wheezing, chest tightness, breathing difficulties
What can asthma exacerbations be triggered by?
Various stimuli such as allergens, infections, environmental factors, exercise
Why is the use of reliever and anti-inflammatory medicines often poorly maintained?
When the asthma is exacerbated, patients use reliever medication to control symptoms but don't also increase the anti-inflammatory medication - without this additional controller therapy, inflammation may increase leading to airway obstruction and possible ER treatment (often to be given oral steroids)
What factors induce asthma variability?
Allergens, cigarette smoke, respiratory infections, exercise, hyperventilation, weather changes, air pollutants (eg sulfur dioxide), some food/additives/drugs
What is the epidemiology of asthma?
300 million worldwide suffer with asthma - huge healthcare and social implications
Responsible for 1 in every 250 deaths worldwide
Approx 15% prevalence in Western world
What is asthma risk increased by?
Genetics, maternal smoking, viral infections in infancy, possible diet/breast-feeding/pre-term birth
Why might asthma be becoming more common?
Hygiene hypothesis, increase in house dust mite, pollution, poly-unsaturated fats in diet
What is the hygiene hypothesis?
The idea of the cytokine balance
- presence of older siblings, early exposure to daycare, viral infections, farm environment, TB - give Th1 CD4 protective immunity
- widespread AB use, Western lifestyle, urban environment, diet, aero-allergens - Th2 CD4 allergic diseases (including asthma)
What causes inflammation?
Antigen binds to IgE on the mast cell - causes degranulation (histamine) and membrane products (like leukotreines) - the mediators of inflammation
T cell (CD4) and IL-5, eosinophils
What inflammatory cells are involved in asthma?
Raised eosinophils, mast cells, T lymphocyte cytokines, macrophage cytokines and dendritic cells
Increased epithelium mediators, vascular leak, smooth muscle hypertrophy, mucus secretion
What is the pathophysiology of asthma?
Smooth muscle dysfunction - bronchoconstriction, hyper-reactivity, hyperplasia, inflammatory mediator release
Airway inflammation - inflammatory cells infiltration, mucosal oedema, cell proliferation, epithelial damage, basement membrane thickening
What are the causes of airway obstruction?
Broncho-constriction (smooth muscle)
Mucosal shedding, oedema
Airway re-modelling (thickened airways)
How is airway obstruction measured?
Peak flow meter, spirometry
How can asthma be diagnosed?
No one test alone is enough to make diagnosis
History is very important, use investigations to help confirm suspected diagnosis
How might asthma patients present?
History of intermittent and variable wheeze (tight chest), cough (sometimes with clear sputum), breathlessness
Worse on exertion and exposure to triggers (eg aerosols, cold air)
Symptoms tend to be worse at night and first thing
Possible history of atopy (rhinitis, eczema etc) or family history of asthma
Occupation - eg baker, paint sprayer
Symptoms improve with salbutamol in short term and steroids in the long term
What might become apparent upon clinical examination?
May be normal if not symptomatic (due to variability of symptoms); may reveal wheeze on auscultation
How might acute severe asthma or chronic asthma present?
Acute severe - accessory muscle use, tachypnoea, tachycardia, silent chest
Chronic - hyperinflated, reduced breath sounds, prolonged expiration
What investigations can be done for asthma?
Variability in PEFR (20% during the day)
Spirometry has significant reversibility with salbutamol (eg FEV1 improves by 200ml/15%)
Exercise testing or allergen provocation with pre/post spirometry
Skin prick tests
IgE in plasma, specific allergen (RAST)
Response to treatment with oral (2 weeks) or inhaled (8 weeks) of steroids
What are the asthma management guidelines?
No daytime symptoms
No night-time awakening due to asthma
No need for 'rescue' medication
No limitations on activity (including exercise)
Normal lung function (FEV1/PEF >80%)
Minimal side effects from medication
What are the consequences of lack of asthma control?
Development of chronic irreversible asthma
What closed questions might be really useful to gain insight into asthma?
Have you had any recent day-time asthma symptoms?
Have you needed your blue inhaler?
Do you ever wake up in the night due to asthma?
Have you had an attack or ER visit recently?
What medication is prescribed for asthma?
Inhalers (less often tablets, nebulisers and injections)
Inhaled steroids and bronchodilators - SAMA, SABA, LAMA, LABA
Inhaled steroid use - long term as a 'preventer'
Combination inhalers (ICS and LABA)
What is the step wise approach for asthma medication?
Step 1 - mild intermittent asthma - use short acting broncho-dilator (eg salbutamol) as a reliever
Step 2 - regular preventer therapy - inhaled corticosteroid (eg beclometasone dipropionate) as preventer
Step 3 - add on therapy - addition of long acting beta-2 agonist to ICS
Step 4 - addition of fourth drug - increase ICS or add other agents
Step 5 - oral steroids
What is the 'non-inhaler' treatment for asthma?
Steroids (for exacerbations or severe disease)
Aminophylline derivatives, monteleukast (anti-leukotriene), omalizumab (parenteral anti-IgE)
What questions need to be considered in difficult/poorly controlled asthma?
Are they using their inhaler - is the technique adequate?
Is the diagnosis correct (eg COPD) or are there other concomitant conditions (eg obesity)?
Is there exposure to a persistent trigger/allergen? Smoking, pollution, stress, occupation
Drugs? (NSAID, beta-blocker)
Do they have concomitant allergic rhinitis?
Why is compliance in asthma very poor?
Variable disease - don't like taking medication when feel okay, preventer doesn't help symptoms, fear that inhalers will stop working if over-used
What is the mortality in asthma?
>1000 deaths/year - about 20 under 16
90% are avoidable
What are the main reasons and risk factors for the mortality in asthma?
Poor compliance, under-recognition
Risk factors - race, psychiatric illness, low socio-economic class, smoking
What are asthma exacerbations?
A sustained worsening of symptoms usually accompanied by a fall in peak flow
If not due to viral illness (eg RSV, flu, adenovirus) or another precipitant - suggests poor asthma control
What should be assessed in acute severe asthma presentation?
Ability to talk, cyanosis, exhaustion
Heart and respiratory rates, oxygen saturation, BP
Breath sounds, degree of wheeze
Peak flow (as % of best) - <50% is severe, <33% is life threatening
CXR (look for pneumothorax)
ABGs to assess PaO2 and PaCO2 (normal/high CO2 is worrying!)
What is the treatment for severe asthma?
Help! High flow oxygen (15 L/min), steroids (PO, IV), nebulised bronchodilator
IV magnesium and aminophylline, intubation
What is the definition of COPD?
Chronic obstructive pulmonary disease, characterised by airflow obstruction that is not fully reversible
- progressive condition where lung function declines irreversibly, airflow obstruction associated with abnormal inflammatory response to noxious stimuli
Chronic inflammation throughout the airways, parenchyma, pulmonary vasculature - primarily COPD affects the lungs, also has systemic consequences
What is the initial cause of inflammation in COPD?
Inhalation of harmful particles and gases (particularly cigarette smoke)
In what way is COPD a multisystem disease?
Osteoporosis (RR 3.1), loss of fat-free mass (cachexia), type II diabetes, peptic ulcer disease, CV disease (RR 2.7), chronic renal impairment
What is the difference between chronic bronchitis, emphysema and COPD?
Chronic bronchitis - cough and sputum most days
Emphysema - abnormal, permanent dilation of the airways, distal to terminal bronchioles and destruction of their walls
COPD - umbrella term including different degrees of chronic bronchitis and emphysema
What is the aetiology (cause) of COPD?
Cigarette smoking (dose response)
Occupational (coal dust, silica, cadmium etc)
Biomass fuel emission
Nutrition - low vitamin C, E and antioxidants in diet
Birth weight, maternal smoking
What is the pathophysiology of COPD?
Inflammation of all airways, alveoli and pulmonary vasculature
Inflammatory exudate in airways
Inflammatory cells - neutrophils, macrophages, TNF-alpha/IL-8, CD8 lymphocytes
Increased goblet cells, mucus production
What is the mechanism of lung damage in COPD?
Protease/anti-protease imbalance and oxidative stress - leads to
- loss of alveolar attachments (small airway collapse)
- narrowed airway lumen (exudate, mucus)
- muco-ciliary dysfunction
Why is COPD described as multi-component?
Inflammation (respiratory pathogens like H influenzae, secrete lipo-oligosaccharide - inflammatory stimulus leading to increase in neutrophils, macrophages, eosinophils, T lymphocytes)
Mucociliary dysfunction (hypersecretion, inhibited ciliary activity)
Tissue damage (bacterial colonisation damages epithelial cells)
How do these 3 components interact?
Cause ongoing disease progression and obstructive airflow - leading to signs and symptoms of COPD (decline in lung function, exacerbations) - decline in health status
Destruction of alveolar support, loss of elastic recoil (small airway collapse), occlusion of lumen (mucus, inflammatory cells) - leads to airflow obstruction and reduced lung function (breathlessness and exacerbations)
What are the consequences of COPD?
Fixed airway obstruction, impaired gas exchange
Reduced exercise tolerance, progressive deconditioning and disability
Recurrent infections and exacerbations
Respiratory failure (chronically low oxygen levels)
What is the impact of COPD?
Growing problem worldwide - 5th leading cause of death in 1999, kills ~30,000/year
~900,000 diagnosed patients in UK - about 2 million undiagnosed cases
What is the age distribution in COPD?
Thought of as an elderly disease but 44% patients are below retirement age, 24% prevented from working by their disease (24 million working days lost annually due to COPD)
What is the direct cost of COPD to the NHS/year?
£492 million, accounts for ~1/8 of all emergency hospital admissions
In what patients should a diagnosis of COPD be considered?
Patients over 35, smokers or ex-smokers (20 pack years)
Symptoms - exertional breathlessness, chronic cough, regular sputum production, frequent winter 'bronchitis', wheeze
Evidence of airflow obstruction on spirometry
No clinical features of asthma
When should asthma be considered rather than COPD?
Previous history of asthma/atopy, strong family history of asthma
Significant variability in symptoms
>20% diurnal or day-day variability in PEFR, >400ml response to bronchodilators/steroids
Why should reversibility testing not be necessary to distinguish between COPD and asthma?
NICE guidelines state that history and symptoms should make it possible to distinguish
In terms of smoking, age, chronic productive cough, SOB, night time waking with SOB/wheeze, significant diurnal/day-day variability of symptoms; distinguish differential diagnosis between COPD and asthma
COPD - nearly all are smokers, rare to have symptoms <45, common to have chronic productive cough, persistent and progressive breathlessness, uncommon to have night-time waking with breathlessness/wheeze, uncommon to have symptom variability
Asthma - possibly smoker, often symptoms present <age 45, uncommon to have cough, breathlessness very variable, common to have night time waking and variable symptoms
Slide 19 bitches
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