pathophysiology of bronchial asthma f
DESCRIPTION
pathology of bronchial asthmaTRANSCRIPT
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PATHOPHYSIOLOGY OF BRONCHIAL ASTHMA
MODERATOR RESOURCE FACULTY PRESENTERProf. G.P. Rauniyar DR. Santosh Upadhyaya Bimal Khadka
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OBJECTIVES
• PATHOPHYSIOLOGY OF BRONCHIAL ASTHMA
• MODEL FOR ALLERGIC ASTHMA
• MORPHOLOGY OF BRONCHIAL ASTHMA
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DEFINITION
ASTHMA is a chronic inflammatory disorder of the airways that causes:
– recurrent episodes of wheezing, breathlessness, chest tightness
– cough, particularly at night and/or in the early morning.
Inflammation causes an increase in airway responsiveness to a variety of stimuli
Patients with asthma experience disabling attacks of severe dyspnea, coughing, and wheezing triggered by sudden episodes of bronchospasm. Rarely, a state of unremitting attacks, called status asthmaticus.
Attacks triggered by
– Exercise
– Cold
– Exposure to an allergen
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intermittent,
mild persistent,
Moderate persistent, and
severe persistent asthma.
Based on frequency and severity of symptoms, categorized into:
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Typically asthma is categorized into
• 1. Extrinsic
• 2. Intrinsic
• Other categorisation according to agents or events that trigger bronchoconstriction are:-
• a) seasonal
• b) exercise induced
• c) drug induced
• d) occupationl induced e) asthmatic bronchitis to smokers
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TYPES
• Atopic
• Non-atopic
• Drug-induced
• Occupational
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ETIOLOGY
• Genetic Predisposition To Type I Hypersensitivity Reaction
• Acute And Chronic Airway Inflammation
• Bronchial Hyperresponsiveness
• Childhood infections eg. Respiratory Syncytial Virus
• Allergen exposure eg. Pollens, Animal Dander
• Indoor Pollution
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pappa
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ATOPIC ASTHMA
• most common• begins in childhood• triggered by environmental antigens such as
dusts, pollens, animal dander, and foods• positive family history of atopy
• asthmatic attacks are often preceded by allergic rhinithypersensitivity
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MEDIATORS RESPONSIBLE
1ST GROUP: role in bronchospasm is clearly supported by pharmacological interventions
• e.g. leukotrienes C4,D4,E4, acetylcholine 2nd GROUP:- have potent asthma like effects but their actual clinical
role appears to be minor on the basis of lack of efficacy of potent antagonists or synthesis inhibitors
• e.g. histamine, prostaglandin D2, PAF 3RD GROUP:- whose specific antagonists are not available and even their role
in asthma is not clear
• e.g. IL-1, TNF, IL-6, chemokines, nitric oxide, bradykinin , endothelins ,neuropeptides..
•
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NON ATOPIC ASTHMA
• Triggered by respiratory tract infections
• viruses:-rhinovirus, para influenza
• positive family history of atopy is uncommon
• no associated allergies
• serum ige level normal
• skin test negative
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PATHOGENESIS
Virus, SO2, O3, NO2
Infect respiratory mucosa
Inflammation
lowers the threshold of subepithelial vagal receptors to irritants
Hyperreactivity of epithelial layer
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DRUG INDUCED ASTHMA
Aspirin sensitive asthma :
recurrent rhinitis and nasal polyps.
• aspirin triggers asthma by:
• inhibiting the cycloxygenase pathway of arachidonic acidmetabolism without affecting the lipoxygenase route,this tipping the balance towards elaboration of the bronchoconstrictor leukotrienes
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OCCUPATIONAL ASTHMA
• stimulated by fumes(plastics), organic and chemical dusts(wood,cotton, platinum), gases(toluene) and other chemicals(formaldehyde, penicillin products).
underlying mechanism is type I hypersensitivity reactions
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MORPHOLOGY OF BRONCHITIAL ASTHMAGROSS:-
• lungs are overdistended due to overinflation
• small areas of atelectasis can be seen
• occlusion of bronchi and bronchioles by thick tenacious mucous plug:- most striking finding.
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MORPHOLOGY:-HISTOLOGICAL
mucous plugs contain whorls of shed epithelium which give rise to well known CURSCHMANN’S SPIRALS
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numerous eosinophils and CHARCO LEYDEN CRYSTALS are present
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Muscle hypertrophy
Sub basement membrane fibrosis
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SUMMARY:
Allergen Irritant
cell activation
cytokine
cellular infiltration
cytokine/ mediator
Airway inflammation & Obstruction
ASTHMA
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THANK YOU...