Part 1 of Asthama Lecture for Final Year MBBS students Definition, Pathophysiology, Pathology, History, Symptoms, Signs , Investigation. also see Part2

1. BRONCHIAL ASTHMA-I
Dr Ashutosh Ojha
Reader ,Medicine

2. Plan
 Defn
 Prevalence
 Etiology
 Precipitating Factors
 Pathology
 History
 Symptoms
 Clinical Features
 Investigtions

3. Definition of Asthma
Asthma is a chronic inflammatory disorder of
the airways characterized by
1. Airway hyper responsiveness to a wide
range of stimuli
2. Airflow limitation that is usually reversible
either spontaneously or with treatment
3. Inflammation of bronchi with Eosinophils,
T lymphocytes and mast cells

4. Prevalence
 One of the most commonest Chronic Diseases,
affecting 4 to 5 % of the population.
 Developed countries have highest prevalence
 Prevalence is increasing specially in 2nd
decade
where 10 – 15% may be affected.
 20% of work force may have occupational
asthma

5. Etiology
Two factors are involved in development
1. Atopy & allergy
2. Bronchial hyperresponsiveness
PRECIPITATING FACTORS

6. 1. Atopy & allergy
1. Atopy – a group of disorders(including
Asthma & hay fever) which appear to
1. Run in families
2. Have Wealing skin reactions to common
Environmental allergens
3. Have circulating antibody that could be
transferred to the skin of non sensitized
Term best used for individuals who readily
develop IgE antibodies to Env Ag
2. Allergens – are similar to those in rhinitis

7. ALLERGENS CAUSING ASTHMA:
1. Faecal particles of house Dust
mites
2. Cockroach antigens
3. Pollen grains
4. Fungal spores – aspergillus
fumigatus
5. Furry pets
6. Birds
7. Occupational sensitizers - Lab
8. Food preservatives (sodium
metabisulphite)
9. Coloring agents (Tartarazine)
10.Chinese sauce (monosodium
glutamate)

8. 2. Bronchial
hyperresponsiveness
BPT with Methacholine - constriction
Full dilatation Usual Hyper response

9. Precipitating factors
2. Occupational
1. Non IgE Isocynates –
varnish/spray paint
2. IgE related
1. Animals/Ab- Labs
2. Flour – mill/bakers
3. Enzymes - detergents
3. Non Specific Factors
1. Cold air & exercise
1. Occurs after exercise
2. Histamine released due to
desiccation of secretion
2. Air pollution, dust, vapors,
fumes
3. Emotion
4. Infections
1. Drugs
1. NSAIDS – aspirin/Indocid
1. 5% of Asthmatics
2. Associated nasal polyps
3. COX 1 inhibition reduced
PGE2
4. Susceptibles over
production of LTC4
occurs by E, Mast cells
2. Beta blocker
1. No direct muscle
sympathetics
2. Parasympathetic
antagonism by
epinephrine Via ß2
3. ß2 block in asthmatics

10. Pathogenesis
 Asthma is a inflammatory disease
 Pathogenesis is complex and involves
 Inflammatory cells
 Mediators
 Vascular leakage
 Two key components
1. Inflammation – Th2 T cell driven IgE
synthesis
2. Remodelling

11. 1. Inflammation
Key cells are(number increased)
1. Mast cells- mediators act on muscle &
vessels. IL 4, IL 9
1. Histamine
2. PGD2
3. LTC4
2. Eosinophils
1. Attracted to airways by IL3, IL 5
2. Prime eosinophil for increased secretion
3. Macrophage & lymphocytes

12. Th 2 hypothesis
 T lymphocytes may differentiate into
1. Th1( γ interferon, IL 2, IL 12) - Infections
2. Th2( IL3,4,5,13) – IgE response from B cells +
+
 In infancy a shift from in utero Th2 bias to
Th1 occurs to fight infections
 Reduction in infection allows Th2 bias to
persist & directs immune system towards
allergic type of response

13. Th2 HYPOTHESIS OF ASTHMA
In Asthma
−↑ Th2 cytokines (IL-4, IL-5, IL-13)
−↓ Th1 cytokines (IFNγ, IL-12,IL 2)
IgE-mast cells, eosinophils,
mucus gland hyperplasia
IL- 4
IL-13
IL- 5
ASTHMA IS A
Th2 DISEASE

14. Smooth muscle
Contraction
Mucus glands
Hyper secretion
HISTAMINE
Mast cell
AN ALLERGIC DISORDER

15. 2. Remodelling
Alters the structure and functions of airways.
1. Epithelium
1. Ciliated epithelium damaged, metaplasia
2. Increased goblet cells
3. More vulnerable to infections
2. Epithelium basement membrane
1. Deposition of repair collagens below basement
membrane
2. Fibroblast proliferation
3. Smooth muscle
1. Hyperplasia
2. Contract easily & stay contracted
3. Contract too much & too easily on least provocation

16. Remodelling

17. Pathology

18. History
1. H/O atopy/ allergy
2. Recurrent nocturnal awakenings
3. Food/drug intake
4. Past severe attacks
5. Family history

19. Symptoms
Principal symptoms
1. Cough
2. Wheeze
3. Episodic SOB
4. Chest tightness
SYMPTOMS WORST IN NIGHT

20. Physical Examination
 Usually appear pink
 Tachypnoea
 Tachycardia.
 Accessory muscles of respiration
 The expiratory phase prolonged
 Expiratory wheeze
 Beware the silent chest

21. Investigations
I. PFT
1. PEFR – first 2 ms, best for monitoring,
occupational asthma
1. L/Min, > 400
2. > 20% diurnal variation on 3 days/week for
2 weeks
3. Monitor BD
2. Spirometry FEV1 – 15% reversibility. Absent
1. Remission
2. Chronic severe asthma
3. On long acting dilators
3. Exercise tests – children. 6 min exercise on
TMT, HR >160/min – FEV1 decrease > 15%

22. Investigations
4. BPT – contraindicated if FEV1 <
1.5L
 PD20 – 20% fall in FEV1
 Less for asthmatics (11 umol)
II. Blood & sputum eosinophilia
III.Chest X ray
I. Over inflation
II. Pneumothorax
III.ABPA
II. Skin prick tests
III.ECG

23. Differential Diagnosis
1. Bronchiolitis
2. Pneumothorax
3. Cardiac asthma
4. Epiglottitis
5. Croup

24. THANK
YOU