Dr. Ramesh-Asthma ppt

Category: Education

Presentation Description

Asthma is one of chronic and frequently occurring disease in now a days......so i am here to educate the people foe awareness of asthma to readers........


Presentation Transcript

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BY: Dr. B . RAMESH P harm D (MBA) 1-SEM ….AIHA-HYD ASTHMA 1 drrameshhealth2@gmail.com




ANOTOMY OF LUNGS: 3 drrameshhealth2@gmail.com

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Defination: :

Defination: Asthma is a chronic inflammatory disease of small airways of the lungs. It characterized by intermittent airway narrowing and airflow obstruction that leads to symptoms of wheezing and shortness of breath. 6 drrameshhealth2@gmail.com


TYPES: 1. Extrinsic asthma (Allergic or atopic asthma) 2. Intrinsic asthma (Non allergic or non-atopic asthma) 7 drrameshhealth2@gmail.com

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Extrinsic asthma: It is initiated by IgE -sensitised mast cells on the mucosal surface. Mast cells on degranulation release mediators like histamine, leukotriens, prostaglandins and PAF for eosiniphils & neutrophils which causes the bronchoconstriction, oedema, mucus hypersecretion. Intrinsic asthma: This type of asthma develops later in adult life & normal serum levels of IgE. There are no recognisable allergens but about 10% of patients become hypersensitive to drugs. The symptoms triggered by non allergic factors such as viral infection, irritants. 8 drrameshhealth2@gmail.com

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EPIDEMIOLOGY: It has been estimated that about 4% of the British and American population is reported to suffer asthma. Mortality rate is estimated approximately 0.4 per 1,00,000 in America and about 1500 deaths per annum in UK. It may occurs in all ages but nearly 50% of cases develop at <10 years of age. 2:1 male-female ratio is observed in children and in adults, both sexes are affected equally. 10 drrameshhealth2@gmail.com


ETIOLOGY: One of the most common trigger factors is the allergen found in the faeces of the house dust mite, which is almost universally present in carpets and soft furnishing. Pollen from grass can lead to seasonal asthma. Drug induced asthma can be severe and the most common causes are β-blockers and prostaglandin synthetase inhibitors. Viruses such as Respiratory syncytial virus (RSV), rhinovirus, influenza and parainfluenza can cause asthma. 11 drrameshhealth2@gmail.com

What substances trigger asthma?:

What substances trigger asthma? Type of Substance Examples Allergens Pollens, moulds, house dust mites, animals(dander, saliva & urine) Industrial chemicals Hair sprays, manufacture aluminium, epoxy resins. Foods Egg, wheat, nuts, sea food, dairy products. Other industrial triggers Wood or grain dust, cotton dust , cigarette smoke Medications Aspirin, anti-inflammatory drugs, prostaglandin synthetase inhibitors & β -blockers Miscellaneous Cold air, hyperventilation, emotion or stress. 12 drrameshhealth2@gmail.com


PATHOPHYSIOLOGY: Various allergens , viruses, industrial chemicals stimulate the production of IgE antibodies. These IgE antibodies sensitise various cells like Mast cells, eosinophils, epithelial cells, macrophages and activated T- lymphocytes cause the release of the inflammatory mediators which play an important role in causing asthma. These cells act on the airways to cause inflammation . These inflammatory mediators play a role in causing the main features of asthma: marked hypertrophy and hyperplasia of bronchial smooth muscle, mucus gland hypertrophy leading to excessive mucus production and air way plugging , airway oedema, acute bronchoconstriction and impaired mucociliary clearance. 13 drrameshhealth2@gmail.com

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Figure 13-2. The immunologic mechanisms in asthma. 14 drrameshhealth2@gmail.com

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Allergen Mast cell Activated T-lymphocytes Eosinophil Virus, endotoxin , particulates Epithelial cells Macrophages Neutrophil Air way inflammation Bronchospasm Airflow limitation, oedema, mucous and plugging Respiratory symptoms Airway hyperresponsive EXTRINSIC INTRINSIC Hist,PG , leuko -tries 15 drrameshhealth2@gmail.com

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Mast cell components are released as a result of an IgE antibody mediated reaction on the surface of the cell. Histamine and other mediators of inflammation are released from mast cells. Ex: Leukotrienes, bradykinin, adenosine, prostaglandins as well as various chemotactic agents that attract esinophils and neutrophils. 16 drrameshhealth2@gmail.com

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Epithelial damage results and thick viscous mucus is produced that cause further deterioration in lung function. In asthma patients there is an increase in the size of bronchial glands and goblet cells that produce mucus. Mucociliary clearance is also decreased due to inflammation of epithelial cells. 17 drrameshhealth2@gmail.com

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Clinical manifestations of asthma::

Clinical manifestations of asthma: Cough Wheezing, a whistling sound Dyspnoea Chest tightness Sneezing & runny nose Itchy and inflamed eyes 19 drrameshhealth2@gmail.com


Diagnosis Forced Expiratory Volume (FEV) Forced Vital Capacity (FVC) Peak Expiratory Flow Rate (PEFR) 20 drrameshhealth2@gmail.com

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FEV: This measured by means of lung function assessment apparatus such as spirometer. The patient inhales as deeply as possible and then exhalels forcefully and completely into a mouth piece connected to a spirometer and it measures the first second of exhalation. FVC: It assess the maximum volume of air exhaled with maximum effort after maximum inspiration. The FEV 1 is usually expressed as a % of the total volume of air exhaled, and is reported as the FEV 1 /FVC ratio. This ratio is useful and highly reproducible measure of the capabilities of the lungs. Normal individuals can exhale at least 75% of their total capacity in 1 second. Any reduction indicates a deterioration in lung performance 21 drrameshhealth2@gmail.com

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Asthma patient Normal patient FEV 1 FVC 22 drrameshhealth2@gmail.com

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PEFR : It can be measured by peak flow meter . It gives slightly less reproducible results than the spirometer but has the advantage that the patient can do regular tests at home with hand-held meter. The PEFR can be used to assess the improvement or deterioration in the disease as well as the effectiveness of treatment. 23 drrameshhealth2@gmail.com

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Risk factors:

Risk factors Smoking Pollen Genetic factor Exposure to chemicals Chronic bronchitis Allergic rhinitis 25 drrameshhealth2@gmail.com


MANAGEMENT NON PHARMACOLOGICAL TREATMENT: Patient education and the teaching of self management skills should be the cornerstone of the treatment program. Avoidance of known allergenic triggers can reduce symptoms Patients with acute severe asthma should receive supplemental oxygen therapy. Smoking cessation 26 drrameshhealth2@gmail.com


PHARMACOLOGICAL THERAPY: 1. Bronhodilators: -- A) Sympathomimetics I) selective β 2 agonists-- Short acting : Salbutamol, Terbutaline Long acting: Salmeterol, Fenoterol, Formoterol II) Non selective agents – Adrenaline , Isoprenaline , Ephedrine B) Methyl xanthines- Theophylline, Aminophylline 2. Anti cholinergics: -- Ipratropium bromide, Atropine 3. Anti – Inflammatory agents: -- A) Systemic - Glucocorticoids, Hydrocortisone, Prednisolone B) Inhalational - Beclomethasone, Budesonide 4. Mast cell stabilizers– Disodium cromoglycete, Nedocromil 5. Leukotriene receptor antagonists:-- Montelukast , Zafirlukast 27 drrameshhealth2@gmail.com

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1. BRONCHODILATORS A) Sympathomimetics:-- I. Selective β 2 agonists Short acting :-Salbutamol, Terbutaline MOA: Adrenergic agonists stimulate β 2 receptors in the bronchial smooth muscles which in turn cause activation of adenylyl cyclase resulting in increased C AMP levels . This increased C AMP inhibit the release of inflammatory mediators resulting in bronchodilation. ADR: Muscle tremors, palpitation and nervousness, hypokalaemia. 28 drrameshhealth2@gmail.com

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Long acting: Salmeterol, fenoterol, formoterol Salmetrol have a slow onset of action but the effect remains for 12 hours. It is also used for prevention of nocturnal asthamatic aattacks. II. Non selective agents – Adrenaline , isoprenaline , ephedrine B) Methylxanthines:- Theophylline and aminophylline MOA: phosphodiesterase is the enzyme that degrades cyclic AMP . Methyl xanthines inhibit PDE and thereby enhance cAMP levels which bring about bronchodilation. cAMP PDE Methylxanthenes 5’AMP ADRs: Vomiting, insomnia, tremours, hypotension. 29 drrameshhealth2@gmail.com

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2. Anti cholinergics- - Ipratropium bromide, Atropine MOA: It relaxes bronchial smooth muscles and it also increase mucociliary clearance. ADRs: Dry mouth, constipation. 3. Anti – Inflammatory agents-- a) Systemic – Glucocorticoids, Hydrocortisone, prednisolone MOA: They suppress the inflammatory response to antigen antibody reaction and reduces mucosal oedema . Mainly they bind to steroidal receptors in the cytoplasm , drug receptor complex moves to the nucleus, binds to DNA which induces the synthesis of mRNA ., which results in decreased PG synthesis and leukotrienes . ADRs: Diabetes, immunosupression, cushing’s syndrome. b) Inhalational - Beclomethasone, Budesonide ADRs: Hoarseness of voice 30 drrameshhealth2@gmail.com

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4. Mast cell stabilizers – Disodium cromoglycete, Nedocromil MOA: It inhibits the degradation of mast cells & there by inhibits the release of mediators of inflammation ADRs: Throat irritation, rashes 5. Leukotriene receptor antagonists – Montelukast , Zafirlukast. MOA: They block the effects of leukotrienes and there by reduce mucosal oedema and relieve bronchospasm. They inhibit exercise induced and aspirin induced bronchospasm. ADRs: Headache, rashes, abdominal pain, diarrhoea. 31 drrameshhealth2@gmail.com

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Step-2 Regular preventer therapy Add inhaled steroid 200-800 µcg/day* 400 µcg is an appropriate starting dose for many patients Start a dose of inhaled steroid appropriate to severity of disease Step-1 mild intermittent Asthma Inhaled short-acting β 2 agonist as required Step wise management of Asthma in adults 32 drrameshhealth2@gmail.com

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Step-3 Add-on therapy Add inhaled long acting β 2 agonist (LABA) Assess control of asthma: good response to LABA- continue LABA Benefit from LABA but control still inadequate- continue LABA and Increase inhaled steroid dose to 800 µcg/day* No response to LABA-stop LABA and increase inhaled steroid to 800 µcg/day*. If control still inadequate, institute trial of other therapies, e.g. leukotriene receptor antagonist or SR theophylline Step-4 Persistent poor control Consider trials of: Increasing inhaled steroid up to 2000µcg/day* Addition of fourth drug e.g. leukotriene receptor antagonist, SR theophylline, β 2 agonist tablet Step-5 Continuous or frequent use of Oral Steroids Use daily steroid tablet in lowest dose providing adequate control Maintain high dose inhaled steroid at 2000 µcg/day* Consider other treatments to minimize the use of steroid tablets Refer patient for specialist care 33 drrameshhealth2@gmail.com


PATIENT COUNSELLING There are three main steps in the education of the asthamatic patient. 1) The patient should have an understanding of the action of each of the medicines they use. 2) The appropriate choice of inhalation device should be made and the patient educated to use them correctly. 3) An individualized action plan should be developed for each patient. 34 drrameshhealth2@gmail.com

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If a bronchodilator and maintenance medications are prescribed , the patient needs to use bronchodilator first wait for 5 min and then use the maintenance inhaler. Patient needs to shake the inhaler and wait app. 1 min between inhalations if multiple inhalations are prescribed. 35 drrameshhealth2@gmail.com

Questionz plzzzz!!??????:

Questionz plzzzz!!?????? 36 drrameshhealth2@gmail.com

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