asthma.pptx

Respiratory module Lecture3: Asthma Dr. ali baay 1  Objectives define asthma and describe the nature of the air flow obstruction in asthma. describe, in outline, the pathophysiology of asthma. describe the major precip...

Respiratory module Lecture3: Asthma Dr. ali baay 1  Objectives define asthma and describe the nature of the air flow obstruction in asthma. describe, in outline, the pathophysiology of asthma. describe the major precipitating factors for asthmatic attacks. describe the symptoms and signs of asthma and their pathophysiological basis. describe the tests used to assess the condition of a patient suspected of asthma, and how they are interpreted. describe, in outline, the principles of treatment of asthma.  Definition It is a chronic inflammatory disorder of the airways in susceptible individuals, with widespread but variable airflow obstruction and an increase in airway responsiveness to a variety of stimuli. Obstruction is often reversible, either spontaneously or with treatment.  Epidemiology Asthma is: Increasing in prevalence More common in the developed world Increasing in populations who move from developing  developed countries 5.4 million people in the UK current receive treatment – 1.1 million children < 4.3 million adults Genetic risk Sensitisation to airborne allergens – House Dust Mite – Pollens – Air pollution – Tobacco smoke (Pre-/post natal exposure, active) – Hygiene hypothesis Pathophysiology  Pathophysiology Asthma is a chronic inflammatory process driven by Th2 cells Macrophages process and present antigens to T lymphocytes. This ‘activates’ T cells, with TH2 cells being preferentially activated. TH2 cells release cytokines, which attract and activate inflammatory cells, including mast cells and eosinophils. TH2 cells also activate B cells, which produce IgE Typically, in a sensitized atopic asthmatic, exposure to antigen results in a 2 phase response consisting of an immediate response (reaching maximum in about 20 minutes) followed by a late phase response ( 3 – 12 hours later).  1. The immediate response is an example of type 1 hypersensitivity. It is caused by interaction of the allergen & specific IgE antibodies, leading to mast cells degranulation and release of mediators (histamine, tryptase, prostaglandin D2 and leukotriene) which cause bronchial smooth muscle contraction → bronchoconstriction. 2. The Late phase response is an example of type IV hypersensitivity. It is complex, involving the full spectrum of inflammatory cells, including eosinophils, mast cells, lymphocytes, & neutrophils, which release an array of mediator and cytokines, which cause airway inflammation. The eosinophils release Leukotriene C4 and other mediators, some of which are toxic to epithelial cells, and causes shedding of epithelial cells. (Eosinophils are very sensitive to steroid therapy).  Pathology The air way inflammation causes reduced airway calibre (airway narrowing) due to: Mucosal swelling (oedema) due to vascular leak. Thickening of bronchial walls due to infiltration by inflammatory cells Mucous over production; the mucus is also abnormal- it is thick, tenacious & slow moving. The cough is therefore usually dry or only productive of scanty, white sputum. In severe cases many airways are occluded by mucus plugs. Smooth muscle contraction The epithelium is shed and is incorporated into the thick mucus  Long term poorly controlled asthma, can lead to airway remodelling some of which may not be fully reversible. The changes include: 1. hypertrophy & hyperplasia of smooth muscle, 2. hypertrophy of mucus glands 3. thickening of the basement membrane  Effect of airways narrowing causes wheezing & other clinical features of asthma results in an obstructive pattern on Spirometry (↓ FEV/FVC ratio < 70% ) & typical flow volume loops; which shows reversibility with bronchodilators, or over a period of time air trapping with increased residual volume  Effect on gas exchange: Airway narrowing leads to reduced ventilation of the affected alveoli → this causes a ventilation / perfusion mismatch in the affected area. Hyperventilation of better ventilated areas of the lung cannot compensate for the hypoxia, but can compensate for CO2 retention by increased breathing out of CO2.  In mild to moderate asthma – the picture is one of ↓pCO2 and ↓pO2 = type 1 respiratory failure In severe attacks = extensive involvement of airways (fewer unaffected areas where hyperventilation wash out CO2), and exhaustion (which limits respiratory effort), limits the amount of CO2 which can be breathed out, leading to a rise in CO2 Thus the blood gas analysis reveals ↑pCO2 and ↓pO2 = type 2 respiratory failure Therefore increasing pCO2 is a sign of life threatening Asthma. (Disease is severe & extensive and patient is exhausted--- these patients often require assisted ventilation)  Triggers of Asthma cold air allergens - pollen, animals (animal hair/dander), house dust mite faeces exercise emotional distress fumes - Car exhaust, cigarette smoke, perfumes chemicals - Isocyanates and acid anhydrides (varnish/paint) drugs - NSAIDS and beta blockers Because of airway hyper-responsiveness, non- allergic stimuli like cold air & fumes can also trigger attacks.  Symptoms of asthma Wheeze High pitched, expiratory sound Wheeze originates in airways which have been narrowed by compression or obstruction In asthma the wheeze is of variable intensity and tone (Polyphonic) Cough Often worse at night (Lack of sleep, poor performance at school) Exercise induced (Decreased participation in activities) Dry cough Breathlessness With exercise Chest Tightness Variable Airflow Obstruction  Examination Inspection Chest – Normal (common) – Scars, deformities – Hyper-expansion (Barrel Chest) General health – Eczema, hay-fever – Lethargy – Can they speak? Room – Meds – Charts Percussion Hyper-resonant Auscultation Polyphonic wheeze  Tests used to assess the condition of a patient suspected of asthma Spirometry – Flow Volume Loop Low PEFR Low FEV1/FVC Ratio >12% or 200 cc increase in FEV1 following salbutamol Allergy Testing Skin prick to aero-allergens, e.g. cat, dog, HDM Blood IgE levels to specific aero- allergens Chest X-Rays Performed to exclude other diseases/inhalation of foreign body/pneumothorax  Treatment Education Educate patients to correctly recognise their symptoms, to use their medication timely, use services appropriately and to develop their own Personal Asthma Action Plan.  Treatment Primary Prevention Stop smoking Fresh air Reduce exposure to allergens /triggers Weight Loss vaccination  Treatment Pharmacological Treatment Drug treatment using the BTS (British Thoracic Society) stepwise approach. 3classes of drugs available : - Bronchodilators: to dilate the airways i.e. symptomatic - Anti-inflammatory: to suppress the inflammation - Biological drugs: reduce dis. Activity - The forms of drugs either oral form ,injection ,inhaler or nebulizer  Oral  Bronchodilator as aminophylline or B agonist : rich in side effects with limited use  Anti-inflammatory : oral steroid & leukotriene modifier  Montelukast Indications Duration Side effects  Injection rich in side effect with use in the emergency state only  Nebulizer benefits vs. uselessness  Inhalar Drugs Device Forma  Acute attacks of asthma It is vital to assess patients for features of acute severe asthma which requires immediate treatment and hospitalisation. Treatment of acute severe asthma includes  O2 treatment : high flow high concentration up to 100%  nebulised B2 agonists and ipratropium delivered in oxygen  intravenous steroids followed by a short course of high dose oral prednisolone.  Other drugs such as magnesium sulphate and aminophylline may also be required.  Patients with features of life threatening asthma need ITU management and may require ventilation. anks for Listening