Asthma Flashcards
Asthma
• Chronic Inflammatory condition; Commonly starts between 3-5yrs; May worsen or improve
• Presents as Wheeze, Chest Tightness, Cough and SOB; Often worse at night
• Comprises Reversible Airflow limitation, Airway Hyperresponsiveness and Bronchial
Inflammation (due to T cells, Mast cells, Eosinophils, Oedema Smooth Muscle Hypertrophy,
Matrix Deposition, Mucus plugging and Epithelial damage)
o Chronic Asthma might be accompanied by irreversible airflow limitation as a result of
large and small Airway Remodelling and Mucus Impaction
• More common in developed countries; More frequent with individuals adopting
‘Westernised’ Lifestyle ?Environmental Factors
Occupational Asthma
Exposure to potential sensitizers
o Extrinsic – Atopic individuals (Sensitive to common inhalant allergens); Childhood
asthma often accompanied by Eczema (Atopic Dermatitis)
o Intrinsic – Middle age presentation; Sensitization to Occupational allergens,
Intolerance to NSAIDs or β-blockers
Prognosis
Improves after early childhood but might return in young adulthood; Airway
inflammation is present continuously from first onset; Airway remodelling accelerates decline
o Mandate early use of controller drugs, Environmental measures from first onset
Pathogenesis: Allergen specific IgE
Link between serum IgE and prevalence of Asthma and Airway
Responsiveness; Environmental and Genetic factors
o Genes controlling production of Cytokines – Affecting longevity of Eosinophils and
Mast cells and IgE Production, Interleukins
Pathogenesis: Environmental
Early childhood exposure to allergens and Maternal smoking
o Hygiene Hypothesis – Growing up in ‘dirtier’ environment allows immune system to
develop immune tolerance to allergens
o Exposure to bacterial cell wall components stimulate TLRs on Immune and Epithelial
cells to direct response away from Th2 (Allergic) to Th1 and Treg (Protective)
response – Implicated in tolerance of antigens
▪ Also implicated in Rhinitis although Pollens less implicated in Asthma
▪ Most Allergic Asthmatics sensitized to house-dust mite allergens; Other
sources include Cockroach allergy, Furry pets, Aspergillus spores
Pathogenesis: Airway Hyperresponsiveness
Characteristic feature of Asthma; Influenced by allergic mechanism as well as Airway Inflammation and Tissue Remodelling
o Demonstrated by Methacholine/Histamine Challenge Test – Graded based on
Provocation Dose/Concentration required to produce 20% fall in FEV1 (PD/PC50 FEV1)
o Patients with clinical symptoms of asthma respond to low doses of Methacholine
o Other tests include Exercise testing, Cold dry air, Mannitol or Hypertonic Saline;
correlated between with Symptoms and Diurnal PEFR variation
o NB: Some patients react to Methacholine at higher doses e.g. Asthma of extreme
exertion, Post viral infection wheeze/cough, Seasonal wheeze, Allergic Rhinitis
Precipitating Factors
Occupational sensitizers (LMW – Haptens or Direct activation, HMW –
Specific IgE), Cold Air, Exercise, Pollutants, Diet, Emotions, Drugs (e.g. NSAIDS, β-blockers)
o COX-1 blockade associated with overproduction of Cysteinyl Leukotrienes
Investigation of Asthma
• Peak Expiratory Flow Rate (PEFR) measurement on waking,
prior to taking Bronchodilators and before bed after taking
Bronchodilator to demonstrate Diurnal variation
• Spirometry – Useful, assesses reversibility; Diagnosed if
15% improvement in PEFR or FEV1 after Bronchodilator
administration; Less reversible if in remission or severe
• Carbon Monoxide Transfer Test is normal in Asthma
• Exercise and other provocation tests – Tests for Airway
Hyperresponsiveness, should not be performed in patients
with poor lung function (FEV1 <1.5L) or history of Brittle Asthma
• Corticosteroid Trial – Prednisolone 30mg daily for 2 weeks, measure Lung Function before
and after; Substantial reversal (>+15% FEV1); Exhaled NO can be used to measure efficacy
• FBC – Eosinophilia; Sputum Eosinophils more diagnostic
• CXR – Helpful in ruling out Pneumothorax or Pneumonia
• SPT and Serum Specific IgE (If patient on Antihistamines), Allergen Provocation Test for
suspected occupational asthma
Management of Asthma
• Avoiding causative allergens (e.g. Pets, Moulds, Foodstuffs); Little evidence in controlling
House mites; Smoking cessation, NSAID avoidance if indicated (COX-2 Inhibitors are suitable)
• Self-Asthma Monitoring with PEF meters
• Use of controller therapy (e.g. Inhaled Corticosteroids) and rescuer therapy (Short Acting
Bronchodilators) to relieve breakthrough symptoms
o Once Asthma brought under control for at least 2-3 months, Reassess dose
• β2 Agonists – Relaxation of Bronchial Smooth Muscle; Effective for relieving symptoms but do
not correct underlying airway inflammation; Short acting (Salbutamol) or Long acting
(Salmeterol); LABA should never be used alone but in combined with inhaled steroids
o Increasing use of Inhalers =a sign of progressive disease
• Non-selective Muscarinic Antagonists (e.g. Ipratropium) – Useful for exacerbations
• Inhaled Corticosteroids – Regular persistent symptoms (even mild) need regular Inhaled
Corticosteroids; Beclomethasone most widely used
o SE: Oral Candidiasis (5%), Osteoporosis (less common than Oral Steroids), Retardation
of short-term growth in children
o Should be stepped down if Asthma comes under control
o Asthmatics who smoke less responsive to inhaled Corticosteroids; Additional therapy
(e.g. LTRAs, Theophylline) required
• Oral Corticosteroids can be combined with low dose weekly Methotrexate or Ciclosporin can
significantly reduce the amount of Prednisolone required
• Cysteinyl Leukotriene Receptor Antagonists (LTRAs) – Inhibition of Cys LT1 Receptor (e.g.
Montelukast) – 4-week trial recommended before decision to continue or stop
o Should be tried in patients uncontrolled on low/medium dose Inhaled Steroids
• Monoclonal Antibodies (Omalizumab = Anti-IgE) – Downregulation of Mast Cell and Basophil
activity, given subcutaneously every 2-4 weeks; Others include Infliximab (Anti-TNF) and
Lebrikizumab (Anti-IL3)
Severe Attack
Unable to complete sentences
RR >25, PR >110, PEF 33-50% predicted
Life-Threatening Attack
Silent chest, Cyanosis, Weak respiratory effort
PEF>33%, Bradycardia/Hypotension, Coma
ABG shows RF, with Resp Acidosis (CO2
retention)
Management of Acute Severe Asthma
• Arterial Blood Gases and Pulse Oximetry – Very
Severe Life-Threatening attack if Hypercapnia,
Severe Hypoxaemia (PaO2<8 kPa) despite O2,
Low and falling Arterial pH
• Nebulised SABA, Nebulised SAMA; CXR TRO
Pneumothorax and Pneumonia etc; IV
Hydrocortisone; IV Salbutamol and/or
Magnesium Sulfate in very severe cases
• Ventilation required for patients refractory to
medical therapy
• More severe cases should be kept in hospital 2-5
days for SpO2 monitoring and PEF
• Bronchial Thermoplasty – Reduction of Airway
Smooth muscle mass
Brittle Asthma (Catastrophic Sudden Severe)
• Sudden Life-Threatening attacks despite being
well controlled between attacks
• Optimisation of standard therapy, Emergency
supplies of medications on person, Oxygen and
Resuscitation/Nebuliser equipment at work/home, 0.3mg Adrenaline Epi-Pens, Prednisolone
60mg Tablets and alert bracelet
• Attend hospital upon developing wheeze; Direct admission to ICU
Precipitants of Asthma Attacks
- Allergens – Pollen, Pets, Mould, HDM, Food Allergens
- Chemical and Mechanical Irritants – Smoking, Acid Reflux in GORD, Atmospheric conditions,
- Upper Respiratory Tract Infections
- NSAIDs (Ibuprofen, Aspirin), Beta Blockers, ACE Inhibitors
Management of Asthma (Based on BTS Guidelines 2016)
• SABA alone, if infrequent, short-lived asthma with normal lung function
o Offer Low Dose Inhaled Corticosteroid if frequent (e.g. 3 times a week or more, or
causing nocturnal waking) or uncontrolled with SABA Monotherapy
• Offer LABA in combination with ICA as next step
• Continue LABA+ICS if effective; if Partial Response, raise ICS dose
o If No Response, stop LABA+ICS and consider others (LTRA, SR Theophylline, LAMA)
• Subsequent steps involve further add-on therapy, increased ICS dose and Specialist Referral
