Asthma Flashcards
Define asthma?
Asthma is a heterogeneous disease, usually characterised by chronic airway inflammation. It is defined by the history of respiratory symptoms such as wheeze, shortness of breath, chest tightness and cough that vary over time and in intensity, together with variable expiratory airflow limitation
What is the epidemiology of asthma?
Asthma is a global disease
•Prevalence vary from country to country and within geographical areas within a country.
•5.4% of Nigerians are asthmatic by current estimates
•Approximately 10–12% of adults and 15% of children affected
•WHO/GINA estimates that, up to 300 million people around the globe suffer from asthma
•In developing countries where the prevalence of asthma had been much lower, there is a rising prevalence, which is associated with increased urbanization.
•It can present at any age, with a peak age of 3 years.
•In childhood it has a male-to-female ratio of 2:1 until puberty when the male-to-female ratio becomes 1:1
Classification of asthma
Which one has a late onset?
•Extrinsic – implying a definite external cause
•Intrinsic – when no causative agent can be identified
•Extrinsic asthma occurs most frequently in atopic individuals who show positive skin-prick reactions to common inhalant allergens such as dust mite, animal danders, pollens and fungi
•Intrinsic asthma often starts in middle age (‘late onset’)
Risk factors of asthma: Endogenous Factors
Genetic predisposition
Atopy
Airway hyperresponsiveness
Gender
Ethnicity
Obesity
Early viral infections
Risk factors of asthma: Environmental Factors
Indoor and outdoor allergens: Early childhood exposure to allergens such as house dust mite, fungal spores, cockroach antigens (indoor) and pollen (outdoor).
Occupational sensitizers such as e.g. isocyanates, epoxy resins and wood dust
Passive smoking (esp. maternal cigarette smoking)
Diet
Paracetamol
What is atopy? And what does it consist of?
Atopy is used to describe a group of disorders (such as asthma, allergic rhinitis and atopic dermatitis) that run in families, have characteristic whealing skin reactions to common allergens in the environment and have circulating allergen-specific IgE.
What are some asthma triggers?
•Allergens
•Upper respiratory tract viral infections
•Exercise and hyperventilation
•Cold air
•Sulfur dioxide and irritant gases
•Drugs (β blockers, aspirin)
•Stress
•Irritants (household sprays, paint fumes)
•Enclosed space
•High altitude
Pathogenesis of asthma
- Inhalation of an allergen in a sensitised atopic asthmatic patient results in a bronchoconstriction
•The inhaled allergen rapidly interacts with mucosal mast cells via an IgE-dependent mechanism, resulting in the release of mediators such as histamine and the cysteinyl leukotrienes which lead to bronchoconstriction. - •A full spectrum of inflammatory cells, however, are involved in the pathogenesis of asthma.
•Epithelial and smooth muscle cells are also capable of releasing inflammatory mediators rather than acting solely as passive targets.
•All of these cells are also involved in the initiation of asthma in non-atopic patients. - •Eosinophils are characteristically present in increased numbers in the airway.
•These cells release bioactive lipid mediators and oxygen radicals; their granules also contain toxic basic proteins
•The number of airway macrophages is also increased in asthma - •Microvascular leakage is also a feature and may be triggered by many inflammatory mediators.
•This results in plasma exudation into the lumen of the airways, contributing to mucous plugging, decreased mucociliary clearance, release of kinins and complement fragments and oedema of the airway wall. - As a result of the ongoing airway inflammation, therefore, the asthmatic airway wall is thickened by;
–oedema,
–cellular infiltration,
–increased smooth muscle mass and;
–hypertrophy of mucus-secreting glands - With increasing severity and chronicity of the disease, remodeling of the airway occurs, leading to;
–fibrosis of the airway wall,
–fixed narrowing of the airway and;
–a reduced response to bronchodilator medication.
Inflammatory cells
Mast cells
Eosinophils
Th2 cells
Basophils
Neutrophils
Platelets
Inflammatory cells
Mast cells
Eosinophils
Th2 cells
Basophils
Neutrophils
Platelets
Structural cells
Epithelial cells
Sm muscle cells
Endothelial cells
Fibroblast
Nerves
Mediators
Histamine
Leukotrienes
Prostanoids
PAF
Kinins
Adenosine
Endothelins
Nitric oxide
Cytokines
Chemokines
Growth factors
Effects of mediators
Bronchospasm
Plasma exudation
Mucus secretion
AHR (airway hyperresponsiveness)
Structural changes
CLINICAL FEATURES
•Asthma is characterised by recurrent episodes of exacerbations, attacks or flare-ups.
•Patients are asymptomatic in between flare-ups.
•Acute asthma or asthma flare-ups consist of episodes of progressively worsening symptoms and a decrease in lung functions from the patients usual status.
•Symptoms are usually worse during the night
Use of accessory muscles and inability to talk in sentences or even in phrases may or may not be present, depending on the severity of the flare-up.
•These signs and symptoms are accompanied by a reduction in lung function as measured by FEV1, Peak expiratory flow rate (PEFR), PaO2, PaCO2, and arterial oxygen saturation (SaO2)
Signs and symptoms
Symptoms include;
–breathlessness,
–cough,
–wheeze, and;
–chest tightness.
•The signs include;
–agitation,
–tachypnoea, and;
–tachycardia
-respiratory distress
If chronic asthma
-barrel shaped chest
How do you categorize acute asthma or asthma exacerbations or flare ups?
–Mild;
–Moderate;
–Severe,
–Life-threatening or;
–Near fatal
Clinical features of ACUTE MILD ASTHMA
•Breathlessness While walking
•May be agitated
•Tachypnoea
•End expiratory wheeze
•Peak expiratory flow rate (PEFR) ≥ 70%
•Prompt relief from Short Acting Beta Agonist, SABA (+/- steroid)
Clinical features of ACUTE MODERATE ASTHMA
•Breathless at rest
•Usually agitated
•Tachypnoeic
•Wheezes through out exhalation
•Pulse rate: 100 – 109b/min
•Pulsus paradoxus may be present (10-25mm Hg)
•PEFR 50-69% of best or predicted.
•Relief from repeated doses of steroid.
Clinical features of ACUTE SEVERE ASTHMA
•Breathless at rest
•Usually agitated
•Unable to complete sentences (usually a word at a time)
•Tachypnoeic with a RR often ≥25c/min
•Use of accessory muscles of respiration
•Loud inspiratory and expiratory wheeze
•Pulse rate ≥110b/min
•Pulsus paradoxus >25mmHg (only present in 45% of cases)
•PEFR <50%
•Arterial blood gas (ABG) analysis shows;
–Hypoxemia (PaO2 <8Kpa) and;
–Low PaCO2 (<6.0 Kpa) due to hyperventilation
•SaO2 <92%
CF of LIFE THREATENING ASTHMA?
•Dyspnoeic at rest
•Drowsy or confused
•cyanosed
•Feeble respiratory effort with a RR <12c/min
•Silent chest
•Bradycardia or hypotension
•PEFR <33% of predicted
•ABG shows PaO2 <8Kpa, PaCO2 Normal or <6.oKpa
•SaO2 <92%
CF of NEAR FATAL ASTHMA
•Elevated PaCO2 (>6.oKpa)
•Low pH<7.2
•Together with other features of life threatening asthma
•Requires mechanical ventilation
How to use spirometer to investigate asthma?
Spirometry confirms airflow limitation with;
a reduced FEV1 and FEV1/FVC ratio (normally >0.75–0.80 in adults).
Variability of airflow limitation is confirmed by;
Positive bronchodilator reversibility test which implies an increase in FEV1 of >12% and >200 mL from baseline, 10–15minutes after 200–400 mcg of inhaled short-acting β2-agonist (usually salbutamol) or;
Significant increase in lung function after 4 weeks of anti-inflammatory treatment which implies an increase in FEV1 by >12% and >200 mL (or PEFR by >20%) from baseline after 4 weeks of oral corticosteroids (OCS) (prednisone or prednisolone 30–40 mg daily), outside respiratory infections.
These tests are diagnostics for asthma
Other investigations include;
Peak expiratory flow rate (particularly when unstable)
Skin-prick tests
Exercise test
Histamine or methacholine bronchial provocation test,
Occupational exposure test
Elevated sputum or peripheral blood eosinophil count
An increased serum level of total or allergen-specific IgE
Chest X-ray: There are no diagnostic features of asthma on the chest X-ray, although hyperinflation is characteristic during an acute episode or in chronic severe disease.
Arterial blood gas pressures (PaO2 and PaCO2) are important in the management of patients with acute severe asthma
What is the drug treatment of asthma?
Controller (preventer) medications
Used for regular maintenance treatment.
Reduce airway inflammation
Make airways less reactive to triggers
Control symptoms,
reduce future risks of exacerbations and decline in lung function.
What are the two categories of drug treatment of asthma?
- Controller (preventer) medications
Used for regular maintenance treatment.
Reduce airway inflammation
Make airways less reactive to triggers
Control symptoms,
reduce future risks of exacerbations and decline in lung function. - Relievers: All are bronchodilators
Relax the muscles of the wall of the airways during attack e.g. inhaled salbutamol
Examples include;
Inhaled short acting B2 agonists (SABA) e.g salbutamol
Anticholinergics e.g ipratropium bromide
Theophylline
Examples of Controller medications
- Inhaled corticosteroids (ICS) e.g. beclometasone, budesonide, fluticasone
- Leukotriene modifiers e.g. montelukast, zafirlukast, zileuton
3 Long-acting inhaled β2-agonists (LABA) e.g. salmeterol, formoterol
- Systemic glucocorticosteroids e.g prednesolone
- Theophyllines
- Cromones e.g. Sodium cromoglicate
- Anti-IgE e.g. Omalizumab
- Steroid sparing drugs e.g. Methotrexate, cyclosporin A, azathioprine
Reliever/ rescuer medications
All are bronchodilators
Relax the muscles of the wall of the airways during attack e.g. inhaled salbutamol
Examples include;
Inhaled short acting B2 agonists (SABA) e.g salbutamol
Anticholinergics e.g ipratropium bromide
Theophylline
Combination drugs
Combination of Salmeterol and fluticasone
Combination of formoterol and budesonide
Used both as a reliever and a controller because formoterol has a rapid onset of action
Stepwise treatment of chronic asthma
Step 1: As-needed low dose ICS/formoterol
OR
Low-dose ICS taken whenever SABA is taken
Step 2: Daily low-dose ICS plus as-needed low dose ICS/formoterol
Step 3: Combination low dose ICS/formoterol as both maintenance and reliever treatment
Step 4: Combination medium dose ICS/LABA plus as-needed low dose ICS/formoterol
Step 5: Combination high dose ICS/LABA with or without add-on therapy such as tiotropium, anti IgE etc.
Management of severe acute asthma
SOS-Salbutamol, Oxygen, Steroids (hydrocortisone, prednisolone)
Oxygen
High doses of inhaled β2-adrenoceptor agonists
Systemic corticosteroids
Regular PEFR recordings should be made to assess for response.
Continuous monitoring of oxygen saturation by pulse oximetry is valuable in all patients to help assess response
Mechanical ventilation may be necessary esp in life threatening and near fatal asthma
What is Samter’s Triad?
This condition is characterized by the following three key features:
1. Asthma
2. Nasal polyps
3. Aspirin/NSAID sensitivity – Symptoms worsen after taking aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen.
Complications of Asthma
Type 1 respiratory failure (causing cyanosis)
Hernia
Side effects of drugs
Pneumothorax
What is the LABA that also acts as a reliever?
Formoterol can also act as a reliever due to its rapid onset on action
