asthma .pptx

asthma .pptx

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  ASTHMA
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  • Asthma isa chronic inflammatory disorder involving the airways in the lungs. • Asthma is a condition in which your airways narrow and swell and may produce extra mucus. • This can make breathing difficult and trigger coughing, a whistling sound (wheezing) when you breathe out and shortness of breath. • It is hyper-responsive to various stimuli which results in narrowing of airways, bronchial secretion, mucosal oedema and mucous plugging.
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  • Epidemiology/Incidence: • Asthmais one of the major non-communicable diseases. • It was estimated that more than 339 million people had Asthma globally in 2016. It is a common disease among children. • Most asthma-related deaths occur in low- and lower-middle income countries. • According to WHO estimates, there were 417,918 deaths due to asthma at the global level and 24.8 million DALYS (Disability-adjusted life years) attributable to Asthma in in 2016. • The strongest risk factors for developing asthma are inhaled substances and particles that may provoke allergic reactions or irritate the airways. • Medication can control asthma. Avoiding asthma triggers can also reduce the severity of asthma.
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  Etiology • Stimuli: • Allergens:pollen grain, house dust, mite. • Viral infection, Respiratory tract infection • Psychological factors (stress, anxiety, crying) hard laughter or • Occupational exposure (e.g. Chemical, irritant, flour, etc.) • Exercise • Exposure to irritants (like strong odors, chemical, fumes) • Environmental exposure (weather change, cold air, cigarette smoke) • Drugs eg. NSAIDS, b-blocker Drug which induces the hypersensitivity reaction
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  SYMPTOMS The most commonsymptom of asthma is • wheezing, a squealing or whistling sound made when you breathe. • Coughing, especially at night, • Tightness in the chest • Dyspnea- shortness of breath, breathing difficulty • anxiousness or panic, fatigue • Inflammatory changes in airway, hyperplasia of airways • Impaired mucocilliary clearance. hypertrophy and
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  • CLASSIFICATION:- Accordingto severity, asthma is classified by national institute of health as: TYPE CHARACTERISTICS Intermittent Most people have this type of asthma, which doesn’t interfere with daily activities. Symptoms are mild, lasting fewer than two days per week or two nights per month Mild persistent The symptoms occur more than twice a week — but not daily — and up to four nights per month. Moderate persistent The symptoms occur daily and at least one night every week, but not nightly. They may limit some daily activities. Severe persistent The symptoms occur several times every day and most nights. Daily activities are extremely limited.
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  PATHOPHYSIOLOGY • Major ContributingProcesses • 1.Airway obstruction:- • Mainly due to bronchoconstriction, airway wall edema, mucus plug formation, smooth muscle cell hypertrophy and hyperplasia etc. • 2.Airways hypersensitivity • It’s an exaggerated response to certain stimuli like virus, drugs, environmental factors, allergen etc. which results in to increase in a level of inflammatory mediators which results in to airway obstruction and causes asthma.
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  • 3.Airway inflammation:- •It’s a crucial to development of asthma. • It occurs due mainly to the activation of the inflammatory cells like mast cell, T-cell, macrophages, eosinophil, and etc. which secretes the inflammatory mediators and influences the airway directly. • 4.Airway remodeling:- • It can result from persistent inflammation. • The resulting damage can yield permanent airway abnormality because of sub-basement membrane collagen deposition and fibrosis.
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  • ThereAre SeveralEvents ThatAre Occur InAsthma: 1. Triggering:- 2. Signaling:- 3. CellActivation:- 4. Tissue Stimulation and Damage:- • THE EFFECT OF ALL ABOVE MECHANISM WILL RESULTS IN EITHER 1. Early or phase of asthmatic response 2. Late phase of asthmatic response. OR: It may be results in to chronic asthma.
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  • 1). EARLYASTHMATIC RESPONSE:- (Seen within a minutes.) ANTIGEN Bind to IgE present on mast cell surface Mast cell degranulation Release of histamine, PGD2, LTC4, LTD4, PAF, etc Bronchoconstriction
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  • 2). LATEASTHMATICRESPONSE:- (Seen within an hrs.) Which cause release of PAF, LTC4, major basic Protein etc. and finally cause inflammation and Increase bronchial hyper-responsiveness. activation of neutrophil, eosinophil, & macrophage Submucosal edema & increase Bronchial hyper- responsiveness. Here Th1 produces IL-2 & INFγ while Th2 cell Produces IL-2, -5,-8 Release of LTB4, PAF, Via mast cell degranulation. Bound to APC like T-helper CD4+ cell present on the surface of the lymphocytes. Bound to mast cell By IgE present on Surface of mast cell. ANTIGEN
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  • 3) CHRONICASTHMA:-(responseare seen even after days) ANTIGEN Bound toAPC like T-helper CD4+ cell on lymphocyte Release of IL-3,-5 & GM-CSF (Granulocyte- macrophage colony-stimulating factor) Sensitize the pre-eosinophil (bone-marrow) & so, finally After maturation, it releases the PAF, LTC4, cytokines, etc. Finally epithelial cell damage, mucus hyper secretion, and Causes hyper responsiveness.
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  Diagnosis 1. lung functiontest • FEV: Forced expiratory spirometer. volume is measured by • FEV1: Expiratory volume in 1 second it is expressed as % the total volume of air exhaled. • FVC: Forced vital capacity - maximum volume of air exhaled after maximum inspiration. • FEV1/FVC ratio is used generally for measurement of lung function.
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  2. Peak Expiratoryflow rate: (PEFR) • Flow is measured at the various interval: 1 hr, 2 hr, 3, 4… etc. 3. Measuring partial pressure of oxygen and carbon dioxide in arterial blood. • Reference range: PaO2: 12-16 kPa, PaCO2: 4.6 – 6 kPa. 4.pH range: 7.35 – 7.45 – used to identify inflammation. It increases in inflammation. 5. Concentration of HCO3- in serum: (22-28 mmol/l) 6. Antibody detection
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  Treatment • Antiasthmatic drugs: I.Bronchodilators • A. β2 Sympathomimetics: Salbutamol, Terbutaline, Bambuterol, Salmeterol, Formoterol, Ephedrine. • B. Methylxanthines: Theophylline (anhydrous), Aminophylline, Choline theophyllinate, Hydroxyethyl theophylline, Theophylline ethanolate of piperazine, Doxophylline. • C. Anticholinergics: Ipratropium bromide, Tiotropium bromide.
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  II. Leukotriene antagonists •Montelukast, Zafirlukast. III. Mast cell stabilizers • Sodium cromoglycate, Ketotifen. IV. Corticosteroids • A. Systemic: Hydrocortisone, Prednisolone and others. • B. Inhalational: Beclomethasone Budesonide, Fluticasone propionate, Ciclesonide. V .Anti-IgE antibody - Omalizumab dipropionate, Flunisolide,