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pathology of bronchial asthma
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PATHOPHYSIOLOGY OF BRONCHIAL ASTHMA
MODERATOR RESOURCE FACULTY PRESENTERProf. G.P. Rauniyar DR. Santosh Upadhyaya Bimal Khadka
OBJECTIVES
• PATHOPHYSIOLOGY OF BRONCHIAL ASTHMA
• MODEL FOR ALLERGIC ASTHMA
• MORPHOLOGY OF BRONCHIAL ASTHMA
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
intermittent,
mild persistent,
Moderate persistent, and
severe persistent asthma.
Based on frequency and severity of symptoms, categorized into:
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
TYPES
• Atopic
• Non-atopic
• Drug-induced
• Occupational
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
pappa
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
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..
•
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
PATHOGENESIS
Virus, SO2, O3, NO2
Infect respiratory mucosa
Inflammation
lowers the threshold of subepithelial vagal receptors to irritants
Hyperreactivity of epithelial layer
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
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
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.
MORPHOLOGY:-HISTOLOGICAL
mucous plugs contain whorls of shed epithelium which give rise to well known CURSCHMANN’S SPIRALS
numerous eosinophils and CHARCO LEYDEN CRYSTALS are present
Muscle hypertrophy
Sub basement membrane fibrosis
SUMMARY:
Allergen Irritant
cell activation
cytokine
cellular infiltration
cytokine/ mediator
Airway inflammation & Obstruction
ASTHMA
THANK YOU...