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PATHOPHYSIOLOGY OF
BRONCHIAL ASTHMA
MODERATOR RESOURCE FACULTY PRESENTER
Prof. 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
acid
metabolism 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 ASTHMA
GROSS:-
• 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...

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Pathophysiology of bronchial asthma f

  • 1. PATHOPHYSIOLOGY OF BRONCHIAL ASTHMA MODERATOR RESOURCE FACULTY PRESENTER Prof. G.P. Rauniyar DR. Santosh Upadhyaya Bimal Khadka
  • 2. OBJECTIVES • PATHOPHYSIOLOGY OF BRONCHIAL ASTHMA • MODEL FOR ALLERGIC ASTHMA • MORPHOLOGY OF BRONCHIAL ASTHMA
  • 3. 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
  • 4.  intermittent,  mild persistent, Moderate persistent, and severe persistent asthma. Based on frequency and severity of symptoms, categorized into:
  • 5. 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
  • 6. TYPES • Atopic • Non-atopic • Drug-induced • Occupational
  • 7. 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
  • 9. 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
  • 10.
  • 11. 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..
  • 12. 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
  • 13. PATHOGENESIS  Virus, SO2, O3, NO2  Infect respiratory mucosa  Inflammation  lowers the threshold of subepithelial vagal receptors to irritants  Hyperreactivity of epithelial layer
  • 14. DRUG INDUCED ASTHMA  Aspirin sensitive asthma :  recurrent rhinitis and nasal polyps. • aspirin triggers asthma by: • inhibiting the cycloxygenase pathway of arachidonic acid metabolism without affecting the lipoxygenase route,this tipping the balance towards elaboration of the bronchoconstrictor leukotrienes
  • 15. 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
  • 16. MORPHOLOGY OF BRONCHITIAL ASTHMA GROSS:- • 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.
  • 17. MORPHOLOGY:-HISTOLOGICAL  mucous plugs contain whorls of shed epithelium which give rise to well known CURSCHMANN’S SPIRALS
  • 18. numerous eosinophils and CHARCO LEYDEN CRYSTALS are present
  • 19.
  • 20.
  • 21. Muscle hypertrophy Sub basement membrane fibrosis
  • 22. SUMMARY: Allergen Irritant cell activation cytokine cellular infiltration cytokine/ mediator Airway inflammation & Obstruction ASTHMA