Asthma Flashcards
Definition
Chronic reversible airway disease characterised by REVERSIBLE AIRWAY OBSTRUCTION secondary to type 1 hypersensitivity reaction = inflamed bronchioles and mucus hypersecretion
- typically presents in children
Allergic/Eosinophilic asthma (70%) - allergens and atopy - IgE = EXTRINSIC
- Pollen, smoke, dust, mould, antigens
- consider genetics and hygiene hypothesis
Non-allergic/non-eosinophilic (30%) - cold air, exercise, stress, obesity = INTRINSIC
- may present later, harder to treat, associated with smoking (like COPD)
Epidemiology
Developed countries
5-15 years peak
Pre-pubertal = males
Persistent into adulthood = females
Risk factors (AA LENSS)
Atopy History (atopic triad)
- Atopic rhinitis
- Asthma
- Eczema
Antenatal factors
- maternal smoking
- viral infection during pregnancy
Low birthweight
Exposure to allergens - house dust mites, pollen, smoke
Not breastfed
Smoking around child
Somter’s triad
- nasal polyps
- asthma
- aspirin sensitivity (triggers prostaglandin production -> leukotriene production)
Aetiology (HAVOK)
Hx of eczema, atopic rhinitis and asthma
ADAM33
Viral - rhinovirus, influenza
Occupational
smoKe - Maternal smoking
Triggers
Infection,
Allergen,
Cold weather,
Exercise,
Drugs (Bb, Aspirin)
Pathophysiology
Environmental trigger (smoke)
The antigens are picked up by dendritic cells (APCs) + presented to Th2 cells
Excessive reaction to the allergens by Th2 cells
Release cytokines (IL4, IL5, TNF-a, leukotriene LTB4)
IL-4 triggers production of IgE antibodies = prime mast cells
Next time exposed to allergen, mast cells release granules containing histamine, leukotrienes (cause bronchoconstriction + more potent than histamine) + prostaglandins
IL-5 triggers eosinophils = release more cytokines
Signs
Reduced peak expiratory flow rate (PEFR)
Expiratory wheeze on auscultation
Hyper-resonance on percussion
Pulsus paradoxes (dip in BP during insp.)
Symptoms
Usually occur at day time but can night
Productive cough
Spiral mucus plugs + is worse at night
Wheeze,
Chest tightness,
Dyspnoea
Investigations
Spirometry
- FEV1 = reduced
- FVC = normal
- FEV/FVC < 0.7
FeNO3 - fractional exhaled nitric oxide (usually done + 17)
- Adults > 40 pbb
- Child > 35 pbb (only done in children with diagnostic uncertainty)
Bronchial challenge test = (histamine/methacholine) = trigger response
CXR = hyperinflated chest
FBC = increased eosinophils
Allergy testing
Peak expiratory flow rate < 20% variability
Bronchodilator reversibility
Asthmatics will have bronchodilator reversibility positive result if there has been an improvement in FEV1 by 12% or more + increase in at least 200ml volume post bronchodilator
Acute management (exacerbations) = OSHITME
- Oxygen
- Salbutamol nebulisers (SABA)
- ICS Hydrocortisone (IV) or oral prednisolone
- IV magnesium sulphate (MgSO4) bronchodilator
- IV theophylline
+/- Abx if infection is present
Long term treatment - Children
- SABA (Salbutamol)
- SABA + ICS (Salbutamol + budesonide)
- SABA + ICS + LTRA (Leukotriene receptor antagonist) = (Salbutamol + Budesonide + Montelukast
- SABA + ICS + LABA (Salbutamol + Budesonide + Salmeterol
CHECK INHALER TECHNIQUE AND COMPLIANCE AFTER 2.
Long term treatment - Adults
- SABA (Salbutamol)
- SABA + ICS (Salbutamol + Budesonide)
- SABA + ICS + LTRA (Salbutamol + Budesonide + Montelukast)
- SABA + low dose ICS + LABA
- consider stopping LTRA depending on response - SABA + MART +/- LTRA(maintenance and reliever therapy)
- Switch ICS + LABA with MART (combination of LABA and low dose ICS) - Increase dose of ICS in mart or change to moderate dose MIC + LABA
- SABA +/- LTRA
- one of the following:
* Increase ICS to high dose (NOT AS A MART)
* Trial additional drug = LAMA or theophylline
How does ICS work
Reduce inflammation by switching off pro inflammatory genes
How do LTRA work
Leukotrienes which are produced by mast cells cause inflammation secretion. Inhibition prevents symptoms
