BRONCHIAL ASTHMA -I Dr Ashutosh Ojha Reader ,Medicine
BRONCHIAL ASTHMA-IDr Ashutosh OjhaReader ,Medicine
Plan Defn Prevalence Etiology Precipitating Factors Pathology History Symptoms Clinical Features Investigtions
Definition of AsthmaAsthma is a chronic inflammatory disorder ofthe airways characterized by1. Airway hyper responsiveness to a wide
range of stimuli2. Airflow limitation that is usually reversible
either spontaneously or with treatment3. Inflammation of bronchi with Eosinophils,
T lymphocytes and mast cells
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
Etiology Two factors are involved in development
1. Atopy & allergy
2. Bronchial hyperresponsiveness
PRECIPITATING FACTORS
1. Atopy & allergy1. Atopy – a group of disorders(including
Asthma & hay fever) which appear to1. Run in families2. Have Wealing skin reactions to common
Environmental allergens3. Have circulating antibody that could be
transferred to the skin of non sensitizedTerm best used for individuals who readilydevelop IgE antibodies to Env Ag2. Allergens – are similar to those in rhinitis
ALLERGENS CAUSING ASTHMA:
1. Faecal particles of house Dust mites
2. Cockroach antigens3. Pollen grains4. Fungal spores – aspergillus
fumigatus5. Furry pets6. Birds7. Occupational sensitizers - Lab8. Food preservatives (sodium
metabisulphite)9. Coloring agents (Tartarazine)10. Chinese sauce (monosodium
glutamate)
2. Bronchial hyperresponsiveness
BPT with Methacholine - constriction
Full dilatation Usual Hyper response
Precipitating factors2. Occupational1. Non IgE Isocynates –
varnish/spray paint2. IgE related
1. Animals/Ab- Labs2. Flour – mill/bakers3. Enzymes - detergents
3. Non Specific Factors1. Cold air & exercise
1. Occurs after exercise2. Histamine released due to
desiccation of secretion2. Air pollution, dust, vapors,
fumes3. Emotion 4. Infections
1. Drugs 1. NSAIDS – aspirin/Indocid
1. 5% of Asthmatics2. Associated nasal polyps3. COX 1 inhibition
reduced PGE24. Susceptibles over
production of LTC4 occurs by E, Mast cells
2. Beta blocker1. No direct muscle
sympathetics2. Parasympathetic
antagonism by epinephrine Via ß2
3. ß2 block in asthmatics
Pathogenesis Asthma is a inflammatory disease Pathogenesis is complex and involves
Inflammatory cells Mediators Vascular leakage
Two key components1. Inflammation – Th2 T cell driven IgE synthesis2. Remodelling
1. Inflammation Key cells are(number increased)1. Mast cells- mediators act on muscle &
vessels. IL 4, IL 91. Histamine2. PGD23. LTC4
2. Eosinophils1. Attracted to airways by IL3, IL 5 2. Prime eosinophil for increased secretion
3. Macrophage & lymphocytes
Th 2 hypothesis
T lymphocytes may differentiate into 1. Th1( γ interferon, IL 2, IL 12) - Infections2. 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
Th2 HYPOTHESIS OF ASTHMA
In Asthma Th2 cytokines (IL-4, IL-5, IL-13) Th1 cytokines (IFN, IL-12,IL 2)
IgE-mast cells, eosinophils,
mucus gland hyperplasia
IL- 4IL-13 IL- 5
ASTHMA IS A Th2 DISEASE
Smooth muscleContraction
Mucus glandsHyper secretion
HISTAMINE
Mast cell
AN ALLERGIC DISORDER
2. Remodelling Alters the structure and functions of airways.1. Epithelium
1. Ciliated epithelium damaged, metaplasia2. Increased goblet cells3. More vulnerable to infections
2. Epithelium basement membrane1. Deposition of repair collagens below basement
membrane2. Fibroblast proliferation
3. Smooth muscle1. Hyperplasia2. Contract easily & stay contracted3. Contract too much & too easily on least provocation
Remodelling
Pathology
History
1. H/O atopy/ allergy2. Recurrent nocturnal
awakenings3. Food/drug intake4. Past severe attacks5. Family history
Symptoms Principal symptoms1. Cough2. Wheeze3. Episodic SOB4. Chest tightness
SYMPTOMS WORST IN NIGHT
Physical Examination Usually appear pink Tachypnoea Tachycardia. Accessory muscles of respiration The expiratory phase prolonged Expiratory wheeze Beware the silent chest
InvestigationsI. PFT
1. PEFR – first 2 ms, best for monitoring, occupational asthma
1. L/Min, > 4002. > 20% diurnal variation on 3 days/week for 2
weeks3. Monitor BD
2. Spirometry FEV1 – 15% reversibility. Absent1. Remission2. Chronic severe asthma3. On long acting dilators
3. Exercise tests – children. 6 min exercise on TMT, HR >160/min – FEV1 decrease > 15%
Investigations4. BPT – contraindicated if FEV1 <
1.5L PD20 – 20% fall in FEV1 Less for asthmatics (11 umol)
II. Blood & sputum eosinophiliaIII. Chest X ray
I. Over inflationII. PneumothoraxIII. ABPA
IV. Skin prick testsV. ECG
Differential Diagnosis
1. Bronchiolitis2. Pneumothorax3. Cardiac asthma 4. Epiglottitis 5. Croup
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