pathology of bronchial Asthma summary of the lecture Define bronchial asthma, classify it and list the triggers for attacks of intrinsic and extrinsic bronchial asthma. Explain the pathogenesis of asthma and resulting effects.

1. Bronchial
Objective
10 – 15 min 15 Slides Apirl 25, 2018
Asthma

2. What’s Asthma?What’s the coronary circulation?
10 – 15 min 15 Slides Apirl 25, 2018
Objective
Define bronchial asthma, classify it
and list the triggers for attacks of intrinsic and extrinsic bronchial asthma.
Explain the pathogenesis of asthma and resulting effects.

3. What’s Asthma?

4. A chronic airway disease characterized by
episodes of reversible airway obstruction,
bronchial hypersensitivity, and bronical
inflammation.
Definition

5. The hallmarks of this disease are:
- Intermittent reversible airway obstruction.
- Chronic airway inflammation.
- Bronchial smooth muscle hypertrophy/hyperplasia.
- Mucus gland hypertrophy/hyperplasia and their secretion.
Definition

6. Drug-induced
Non-AtopicAtopic
Occupational
Clinical
Classifications
AtopicNon-Atopic

7. - The commonest type.
- Arising in childhood.
- type-I hypersensitivity.
- Associated with other types of atopy.
- Environmental triggers (dusts, pollen, animals, food, infections, others).
Atopic
Clinical
Non-Atopic

8. - No evidence of atopy.
- No family history.
- Associated with respiratory viral infection and
air pollutants.
Non-Atopic
Atopic
Drug-induced

9. ----------------→ Arachidonic ----------------→ Inflammatory mediators.
ygenaseCycloox
Lipoxygenase
NSAIDs
Phospholipase A2
Drug-induced
Non-Atopic

10. - The best example is aspirin.
- The exact mechanism is unknown.
- Other drugs still unknown.
Drug-induced
Occupational

11. Some environmental jobs are associated with
exposure to some irritant substances as fumes,
chemicals, & gas.
Those irritant substances will induce asthma.
Occupational
Drug-induced

12. Stimuli
(through APC)
Pathogenesis

13. TH2 lymphocytes Epithelial cells Mast cells
(re-exposure)
Pathogenesis
Eosinophils

14. TH2 lymphocytes Epithelial cells Mast cells
IL-4 → IgE production
IL-5 → Eosinophils
activation
IL-13 → IgE & mucus
production
Eotaxin→ Eosinophils
activation &
recruitment
(re-exposure)
Histamine & IL-5 →
Eosinophils activation,
bronchospasm, &
mucus secretion
Pathogenesis

15. -----------------------------------------------------------------→
-----------------------------------------→
---→---→----→
---→
Eotaxin
Activations &
degranulation
IL-4 IgE-ab IL-5
IL-5
TH2
Stimuli
B Mast
EosinophilAPC
Epi.
Pathogenesis

16. Early phase Late phase
Pathogenesis
Early phaseLate phase

17. Within 10 minutes of exposure.
This phase characterized by prominent
bronchoconstriction.
Direct vagal receptors activation, Edema
Bronchial smooth muscle & Mucus gland hypertrophy/hyperplasia
Early phase
Pathogenesis
Late phase

18. Within 4 hours of exposure.
This phase characterized by predominant
tissue damage and inflammation
especially eosinophils.
Late phase
Early phase

19. Sources
Advisor >
Dr. AlKhamiss.
Websites >Robbins 9th > QuMed >
• Asthma. SlideShare