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Asthma . By Alice Keyte ajk1g10@soton.ac.uk. DAPSICAMP. Definition Aetiology Pathophysiology Signs and Symptoms Investigations Complications Alternative Dx Management Prognosis. Definition. WHAT IS ASTHMA?
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Asthma By Alice Keyte ajk1g10@soton.ac.uk
DAPSICAMP Definition Aetiology Pathophysiology Signs and Symptoms Investigations Complications Alternative Dx Management Prognosis
Definition • WHAT IS ASTHMA? • Chronic Inflammatory airway disease of the large airway, characterised by variable, reversible, widespread airway obstruction and hyper-responsiveness. • GINA – Global Initiative for Asthma • http://www.ginasthma.org/
Chronic Asthma • Periodic/episodic asthmatic symptoms: • Cough • Chest tightness • Wheezing • Seasonal (allergy to pollens) and Diurnal variation
Aetiology of Atopic Asthma Polygenic inheritance (genes encoding cytokines, T-cell receptor, IgE receptor, MHC). MZ twin concordance 20-60% and first degree relatives with asthma increases risk by 10x Atopyalso has a genetic basis.
Aetiology Immune system is Th2 primed during fetal life and early childhood which promotes allergic sensitisation. Higher antigen dose and repeated exposure promotes Th2 responses. Histamine gives allergic symptoms. IgE becomes important as patient develops asthma. Repeated exposure causes immune cells to reside in tissues and become hypersensitive. Viral infections in early life facilitates sensitisation by damaging the epithelial surface.
Triggers • Cold air • Exercise • Allergens (pets, house dust mite, pollens) • Non-specific irritants (cigarette smoke)
Pathophysiology • Factors contributing to obstruction: • smooth muscle constriction (leukotriene mediated) • oedema due to increased vascular permeability (leukotriene mediated) • mucus hyper-secretion (leukotriene mediated) • dead epithelial cells sloughed off by eosinophil toxins • Tissue infiltration with immune cells (due to chemoattractant release)
Damage to epithelial barrier means asthmatics are more likely to get LRTI following URTIs. Permanent remodelling occurs, giving smooth muscle hyperplasia, hypertrophy, thickening of BM.
Signs and Symptoms CLINICALLY: Cough Chest tightness Wheezing Dyspnoea (short of breath)
How Well Controlled Are You? • 3 Questions by Royal College of Physicians: • Have you had difficulty sleeping because of your asthma? • Have you had your usual asthma symptoms during the day time? • Has your asthma interfered with your usual activities?
Examination • Frequently normal in chronic asthma • Hyperinflation – if had asthma for many years • Wheezes: • Expiratory • Diffuse (all over the chest) • Polyphonic (musical) • Signs of atopy (associated signs of asthma): • Eczema • Conjunctivitis • Allergic rhinitis
Diagnosis • Not always easy • Important to exclude: • Inhaled foreign bodies, CF in children • Carcinoma, pulmonary oedma (HF) in adults
Alternative Dx • Atypical Symptoms: • Cough without wheeze • Voice disturbance • Lack of airways obstruction on spirometry • No variation (suggests COPD or HF) • No relief with B2 agonist • PMH: • Cardiac disease (MI, hypertensive) • Smoking history • Exam: • Any signs other than wheeze (crackles, bronchial breathing) • Tar staining • Features associated with cardiac disease (peripheral oedema)
Alternative Dx • CONDITIONS: • COPD • Heart Failure • Bronchiectasis • GORD • Pulmonary fibrosis • Large airway obstruction (rare) • Obliterative bronchiolitis
Main Tests • SPIROMETRY • PEFR (Peak Expiratory Flow Rate) • PEFR variability (>20%) – someone who’s uncontrolled • Bronchodilator responsiveness • Steroid responsiveness • Methacholine or histamine challenge (give and see bronchoconstriction)
Management • 3 goals of treatment: • Control of asthma symptoms • Prevent exacerbations (single cause of morbidity and mortality) • Preservation of normal lung function (reduce airway remodelling as = decline in lung function)
Acute Severe Asthma • O SHIT – first thing you do. • MOVE – do for anyone acutely unwell • M – monitor (3 lead cardiac monitoring, BP, pulse oximetry) • O – oxygen • V – venous access (drugs, fluids) • E – ECG
Assess Severity - history • Will be difficult to get a history so make it CONCISE! • Determine if AT RISK OF GOING TO ITU • Risk factors: • Previous ITU stay • Previous mechanical ventilation for asthma • Previous hospital admission for asthma (recent) • Exclude anaphylaxis
Assess Severity - Examination RED = pre-terminal signs to be aware of! GCS HR BRADYCARDIA BP RR Cyanosis Exhaustion Chest expansion (air in and out) SILENT CHEST Pneumothorax (complication of asthma) EXCLUDE ANAPHYLAXIS
Assess Severity - Investigations SpO2% (<92%) PEFR - may be too unwell, try and find out their best – now as a % of their best (<33% predicted) ABG – if signs of hypoxemia + sats <92 (PaO2 <8kPa) CXR if indicated (pneumothorax, pneumonia) Beta blockers should not be prescribed to asthmatics
BTS Guidelines http://www.brit-thoracic.org.uk/document-library/clinical-information/asthma/btssign-guideline-on-the-management-of-asthma/ MODERATE ACUTE SEVERE LIFE THREATENING
Treatment • O SHIT! (sit them up) 1. O – Oxygen 2. S – Salbutamol (nebulised, often, back to back) 4. H – Hydrocortisone (if can take oral – prednisolone 30/40mg depending on size) 3. I – Ipratropium Bromide (inhibit parasympathetic NS = increase intracellular cyclic AMP = broncodilation. Nebulised back to back with salbutamol ) 5. T – Theophylline / Magnesium sulphate (take senior advice!) • MONITOR frequently (1/2 hr – 1hr obs) • Things can change rapidly
Prognosis • The prevalence of asthma is rising. Possible reasons for this are: • Increased detection • Improved living standards and fewer childhood infections (hygiene hypothesis) • Change in indoor environment (central heating increases dust mite exposure)
Education Important Exams! Compliance issues with inhaled therapies
OSCE’s • Inhaler + Spacer Technique • Peak Flow Technique • Look in the green unofficial guide to passing OSCEs for step to step guides.
Questions 1. Outline treatment strategies for an acute exacerbation of asthma Nebulised – Salbutamol, Ipratropium Bromide IV – Steroids, Methyl Xanthines, MgSO4