Pathophysiology of bronchial asthma f

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

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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

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...