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Published byDamian Webb Modified over 9 years ago
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Dr. Shaikh Mujeeb Ahmed Assistant Professor AlMaarefa College
Bronchial Asthma IMS 423 BLOCK Dr. Shaikh Mujeeb Ahmed Assistant Professor AlMaarefa College
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Intended Learning Outcomes
Describe pathophysiology of Bronchial asthma Enumerate the predisposing factors for asthma Describe the clinical features of asthma Interpret the spirometry results lab results and correlate with severity of the disease.
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Epidemiology According to epidemiological studies asthma affects 1-18% of population of different countries.
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What is Asthma? Asthma is a chronic inflammatory disease of the airways characterized by variable recurring symptoms, air flow obstruction, and bronchial hyper responsiveness. Asthma is a disease that affects the lungs. It causes repeated episodes of wheezing, breathlessness, chest tightness, and nighttime or early morning coughing. If someone has asthma, he or she has it all the time, but asthma attacks will occur only when something bothers the lungs. We know that if someone in the family of a person with asthma has asthma, other family members are more likely to have it too. In most cases, we don’t know what causes asthma, and we don’t know how to cure it; however, it can be controlled. Asthma can be controlled by knowing the warning signs of an attack, staying away from things that trigger an attack, and following the advice from a healthcare provider. 4
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Airway obstruction Episodic wheezing Difficulty breathing,
Chest tightness, and Cough that often is worse at night and in the early morning.
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Types of Asthma Extrinsic – initiated by type I hypersensitivity
Atopic Intrinsic – Non immune mechanisms Respiratory tract infections Exercise, Ingestion of aspirin, Emotional upset, and Exposure to bronchial irritants such as cigarette smoke.
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Some allergens which may cause asthma
Spittle, excrements, hair and fur of domestic animals House-dust mites which live in carpets, mattresses and upholstered furniture Plant pollen Dust of book depo-sitories Pharmacological agents (enzymes, antibiotics, vaccines, serums) Food components (stabilizers, genetically modified products)
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Etiology & Pathogenesis
Early phase response Late phase response
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Etiology & Pathogenesis
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Extrinsic (Atopic) Asthma
Allergen Mast cells release inflammatory mediators WBCs enter region and release more Type I hypersensitivity Mast cells’ inflammatory mediators cause acute response within 10–20 minutes Airway inflammation causes late phase response in 4–8 hours
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Role of T lymphocytes T - Lymphocytes TH 1 - Lymphocytes
B - Lymphocytes Plasma Cells Ig G & Ig M Ig E
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Intrinsic (Nonatopic) Asthma
Respiratory infections Epithelial damage, IgE production Exercise, hyperventilation, cold air Loss of heat and water may cause bronchospasm Inhaled irritants Inflammation, vagal reflex Aspirin and other NSAIDs Abnormal arachidonic acid metabolism
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Aspirin and other NSAIDs
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Airway Obstruction in Asthma
inflammatory airway mediators inflammation increased epithelial impaired airway injury mucociliary responsiveness function bronchospasm edema airflow limitation
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Pathologic anatomy Macroscopic changes:
viscous mucous/ mucopurulent phlegm airway dyskinesia with zones of spastic contraction and paralytic expansion of bronchi obstruction of airway lumen lung emphysema, pneumosclerosis RV and RA hypertrophy and dilation
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Microscopic changes: Bronchial wall infiltration with mast cells, eosinophils, basophils and T-lymphocytes Edema of mucous and submucous tunics Destruction of bronchial epithelium Hypertrophy of bronchial smooth muscles, Hyperplasy of submucous glands Microvessels dilation
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Muscles cells Ciliated Goblet cells Bronchial glands Cartilage Bronchioles (section)
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Mucosal edema Mucus secretion increase Muscle contraction Asthma
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Risk Factors for Developing Asthma
Genetic characteristics Occupational exposures Environmental exposures Risk Factors for Developing Asthma 21
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Diagnosing Asthma: Medical History
Symptoms Coughing Wheezing Shortness of breath Chest tightness Symptom Patterns Severity Family History Diagnosing Asthma: Medical History 23
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Diagnosing Asthma Troublesome cough, particularly at night
Awakened by coughing Coughing or wheezing after physical activity Breathing problems during particular seasons Coughing, wheezing, or chest tightness after allergen exposure Colds that last more than 10 days Relief when medication is used Diagnosing Asthma 24
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Diagnosing Asthma Wheezing sounds during normal breathing
Hyperexpansion of the thorax Increased nasal secretions or nasal polyps Atopic dermatitis, eczema, or other allergic skin conditions Diagnosing Asthma
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Diagnosing Asthma: Spirometry
Test lung function when diagnosing asthma Diagnosing Asthma: Spirometry 26
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Spirometry Measurement of Forced expiratory volume (FEV1 )
forced vital capacity (FVC) FEV1/VC Peak Expiratory Flow rate (PEFR)
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Pulmonary Function Tests
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Reversibility Test
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Inhalational challenge test
Administration of sequential increasing conc. of either histamine , methacholine or mannitol.
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Diurnal variation in PEFR
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Exercise induced Asthma
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Allergic skin testing X-ray chest Induced sputum differential eosinophil count - >2% FENO
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Management Asthma is extremely common and causes considerable morbidity. The aims of treatment are to: Abolish symptoms Restore normal or best possible lung function Reduce the risk of severe attacks Enable normal growth to occur in children Minimize absence from school or employment.
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This involves: patient and family education about asthma
patient and family participation in treatment avoidance of identified causes where possible use of the lowest effective doses of convenient medications to minimize short-term and long-term side-effects.
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Control of extrinsic factors
Measures must be taken to avoid causative allergens such as the house-dust mite, moulds and certain food stuffs (e.g eggs ,checolate), particularly in childhood. Active and passive smoking should be avoided, as should beta-blockers in either tablet or eye drop form. Individuals intolerant to aspirin may benefit by avoiding salicylates and should avoid NSAIDs.
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50% of individuals sensitized to occupational agents may be cured if they are kept permanently away from exposure. The remaining 50% continue to have symptoms that may be as severe as when exposed to materials at work, especially if they were symptomatic for a long time before the diagnosis was made. This emphasises: the importance of the rapid identification of extrinsic causes of asthma and their removal wherever possible (e.g. occupational agents, family pets) once extrinsic asthma is initiated, it may become self-perpetuating possibly by non-immune mechanisms.
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Drug treatment The mainstay of asthma therapy is the use of therapeutic agents delivered as aerosols or powders directly into the lungs The advantages of this method of administration are that drugs are delivered direct to the lung and the first-pass metabolism in the liver is avoided; thus lower doses are necessary and systemic unwanted effects are minimized. Both national and international guidelines have been published on the stepwise treatment of asthma based on three principles:
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Asthma self-management with regular asthma monitoring using peak flow meters and individual treatment plans discussed with each patient and written down. The appreciation that asthma is an inflammatory disease and that anti-inflammatory (controller) therapy should be started even in mild cases. Use of short-acting inhaled bronchodilators (e.g. salbutamol and terbutaline) only to relieve breakthrough symptoms. Increased use of bronchodilator treatment to relieve increasing symptoms is an indication of deteriorating disease.
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Drugs used in asthma Quick relief medication
short acting β2 agonist (salbutamol, terbutaline) oral steroids Anticholinergic agents Long-acting relief/disease controllers - Long-acting β2 agonists - salmeterol, formoterol - Sodium cromoglicate (mast cell stabilizer) - Leukotriene modifiers Other agents with bronchodilator activity Theophylline preparations
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Steroid-sparing agents
- Methotrexate - Ciclosporin - Gold - Intravenous immunoglobulin - Anti-IgE monoclonal antibody - Omalizumab
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Asthma severity classification
Clinical course, severity Daytime asthma symptoms Nighttime awakenings FEV1, PEF Intermittent < 1 /week 2 and < /month >80% predicted. Daily variability < 20% Mild persistent 1 /week but not daily > 2 /month >80% predicted. Daily variability – 20-30% Moderate persistent Daily > 1 /week > 60 but < 80% predicted. Variability>30%. Severe persistent Persistent, which limit normal activity <60% predicted. Variability > 30%.
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Level of Asthma control
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Managing Asthma: Peak Expiratory Flow (PEF) Meters
Allows patient to assess status of his/her asthma Persons who use peak flow meters should do so frequently Many physicians require for all severe patients
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Managing Asthma: Peak Flow Chart
People with moderate or severe asthma should take readings: Every morning Every evening After an exacerbation Before inhaling certain medications Managing Asthma: Peak Flow Chart Source: “What You and Your Family Can Do About Asthma” by the Global Initiative For Asthma Created and funded by NIH/NHLBI
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A stepwise approach to the management of asthma
Step 1: Occasional use of inhaled short-acting β2-adrenoreceptor agonist bronchodilators Step 2: Introduction of regular ‘preventer’ therapy Step 3: Add-on therapy Step 4: Poor control on moderate dose of inhaled steroid and add-on therapy: addition of a fourth drug Step 5: Continuous or frequent use of oral steroids
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Acute severe asthma Patients with acute severe asthma typically have:
inability to complete a sentence in one breath respiratory rate ≥ 25 breaths per minute tachycardia ≥ 110 beats/min (pulsus paradoxus, is not useful as it is only present in 45% of cases) PEF < 50% of predicted normal or best.
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Features of life-threatening attacks are:
a silent chest, cyanosis or feeble respiratory effort exhaustion, confusion or coma bradycardia or hypotension PEF < 30% of predicted normal or best (approximately 150 L/min in adults).
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Treatment of severe asthma
At home The patient is assessed. Tachycardia, a high respiratory rate and inability to speak in sentences indicate a severe attack. If the PEFR is less than 150 L/min (in adults), an ambulance should be called. (All doctors should carry peak flow meters.) Nebulized salbutamol 5 mg or terbutaline 10 mg is administered. Hydrocortisone sodium succinate 200 mg i.v. is given. Oxygen 40-60% is given if available. Prednisolone 60 mg is given orally.
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At hospital The patient is reassessed. Oxygen 40-60% is given.
The PEFR is measured using a low-reading peak flow meter, as an ordinary meter measures only from 60 L/min upwards. Measure O2 saturation with a pulse oximeter. Nebulized salbutamol 5 mg or terbutaline 10 mg is repeated and administered 4-hourly. Add nebulized ipratropium bromide 0.5 mg to nebulized salbutamol/terbutaline. Hydrocortisone 200 mg i.v. is given 4-hourly for 24 hours.
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terbutaline 1.5-5.0 μg/min, or magnesium sulphate 1.2-2 g over 20 min.
Prednisolone is continued at 60 mg orally daily for 2 weeks. Arterial blood gases are measured; if the Paco2 is greater than 7 kPa, ventilation should be considered. A chest X-ray is performed to exclude pneumothorax. One of the following intravenous infusions is given if no improvement is seen: salbutamol 3-20 μg/min, or terbutaline μg/min, or magnesium sulphate g over 20 min.
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Arterial blood gases should always be measured in asthmatic patients requiring admission to hospital. Pulse oximetry is useful in monitoring oxygen saturation during the admission and reduces the need for repeated arterial puncture. Features suggesting very severe life-threatening attacks are: a high Paco2 > 45 severe hypoxaemia Pao2 < 60 despite treatment with oxygen a low and falling arterial pH.
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A Public Health Response to Asthma: Interventions
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