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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