1. Asthma is characterised by chronic airway inflammation and increased airway hyper- responsiveness leading to symptoms of wheeze, cough, chest tightness.

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Asthma is characterised by chronic airway inflammation and increased airway hyper-responsiveness leading to symptoms of wheeze, cough, chest tightness and dyspnoea.

It is characterised functionally by the presence of airflow obstruction which is variable over short periods of time, or is reversible with treatment.

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The prevalence of asthma increased steadily over the latter part of the last century in countries with a Western lifestyle and is also increasing in developing countries.

Current estimates suggest that 300 million people world-wide suffer from asthma and an additional 100 million may be diagnosed with asthma by 2025.

In childhood, asthma is more common in boys, but following puberty females are more frequently affected.

The socio-economic impact of asthma is enormous, particularly when poor control leads to days lost from school or work, hospital admissions and, for some patients, a premature death.

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Dietary intake may be important. Milk fat and antioxidants such as vitamin E and selenium may protect against the development of asthma in children; however, in other studies early exposure to cows' milk protein has been linked to the development of atopy and asthma.

higher levels of Lactobacillus in the gut may protect against the development of atopic disease.

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The increase in asthma may also be linked to the rise of obesity in Western society through mechanical mechanisms such as gastro-oesophageal reflux.

Shared genetic traits modification of the immune system by diet, or

alteration of airway responsiveness by hormones are, however, alternative explanations.

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In some circumstances the appearance of asthma relates to the use of medications.

Beta-adrenoceptor antagonists (β-blockers-even when administered topically as eye drops) may induce bronchospasm.

Aspirin and other non-steroidal anti-inflammatory drugs are associated with asthma in about 10% of patients. This is believed to reflect a shift in the metabolism of arachidonic

acid from the cyclo-oxygenase pathway generating prostaglandins, towards the lipo-oxygenase pathway generating cysteinyl leukotrienes.

Aspirin-sensitive asthma is often associated with rhinosinusitis and nasal polyps

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extrinsic Intrinsic(cryptogenic)

External factor identifiable No such factor

Serum shows high levels of IgE &IgG

No raised Ab levels but increased eosinophils present ,aspirin sensitivity, & presence of nasal polyp

Atopic manifestations may be present

No atopy

Dermatological and respiratory s/s show a see-saw relationship

Not associated with skin s/s

Positive family history present

Affects persons of 10-15 yrs Affects persons over 40 yrs

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Causes House dust Pollen Fungi Animal hairs Insect scales Fumes and drugs food Infection with respiratory syncitial virus Exercise induced asthma Exposure to cold

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Once sensitization occurs these antigens release chemical mediators from the mast cells by interacting with the IgE molecules on their surface- Type 1 hypersensitivity reaction-immediate asthmatic paroxysm

Some times type 3 hypersensitivity reaction also occurs and it is mediated by IgG –delayed paroxysm

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The inhalation of an allergen in a sensitised atopic asthmatic patient results in a two-phase bronchoconstrictor response .

The inhaled allergen rapidly interacts with mucosal mast cells via an IgE-dependent mechanism, resulting in the release of mediators such as histamine and the cysteinyl leukotrienes with resulting bronchoconstriction.

In persistent asthma a chronic and complex inflammatory response ensues, which is characterised by an influx of numerous inflammatory cells, the transformation and participation of airway structural cells, and the secretion of an array of cytokines, chemokines and growth factors

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Airflow limitation Usually reverses spontaneously or with treatment

Airway hyper-reactivity Exaggerated bronchoconstriction to a wide range of non-specific stimuli, e.g. exercise, cold air

Airway inflammation :Eosinophils, lymphocytes, mast cells, neutrophils; associated oedema, smooth muscle hypertrophy and hyperplasia, thickening of basement membrane, mucous plugging and epithelial damage

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With increasing severity and chronicity of the disease, remodelling of the airway occurs, leading to fibrosis of the airway wall, fixed narrowing of the airway and a reduced response to bronchodilator medication

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  Typical symptoms include recurrent episodes of breathlessness wheezing, cough. chest tightnessCommon precipitants include exercise, particularly in cold weather, exposure to airborne allergens pollutants viral upper respiratory tract infections (beware the cold that 'goes

to the chest' or takes more than 10 days to clear).

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Moderately severe cases the patient is orthopneic,cyanosed, and accessory muscles of respiration are active

Ineffective cough with tenacious mucoid expectoration

Pulse rapid BP normal or elevated Pulsus paradoxus in severe cases

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Chest expansion diminished ie,less than 2cm during attack.

Expiratory wheeze heard all over the chest. Patients with mild intermittent asthma are usually

asymptomatic between exacerbations which occur during viral respiratory tract infections or after exposure to allergens.

In persistent asthma the pattern is one of chronic wheeze and breathlessness

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a diurnal pattern, symptoms being worse in the early morning.

Particularly when asthma is poorly controlled, symptoms such as cough and wheeze disturb sleep and have led to the use of the term 'nocturnal asthma'.

Cough may be the dominant symptom in some patients and the lack of wheeze or breathlessness may lead to a delay in reaching the diagnosis of so-called 'cough-variant asthma'.

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Occupational asthma is now the most common form of occupational respiratory disorder and accounts for around 5% of all adult-onset asthma.

This should be considered in all adult asthmatics of working age, particularly if symptoms improve during time away from work, e.g. weekends or holidays.

Atopic individuals and smokers appear to be at increased risk.

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Early diagnosis and removal from exposure leads to a significantly improved prognosis and may result in cure.

The recognition of occupational asthma has important medico-legal implications and should prompt screening of the workplace and other employees .

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The diagnosis of asthma is made on the basis of a compatible clinical history combined with the demonstration of variable airflow obstruction

Eosinophilia Sputum reveals eosinophils. Sputum shows eosinophils, mucus plugs and curschmann’s spirals. Purulent sputum indicative of respiratory infection. Culture reveals the infecting organisms Pulmonary function tests Compatible clinical history plus either/or: FEV1 ≥ 15% (and 200 ml) increase following administration of a

bronchodilator/trial of corticosteroids > 20% diurnal variation on ≥ 3 days in a week FEV1 ≥ 15% decrease after 6 mins of exercise  

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Acute asthma is accompanied by hyperinflation, lobar collapse may be seen if mucus has occluded

a large bronchus. Flitting infiltrates, on occasion accompanied by

lobar collapse, suggest asthma complicated by allergic bronchopulmonary aspergillosis (ABPA).

An HRCT scan may be useful to detect bronchiectasis

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  An elevated sputum or peripheral blood eosinophil

count may be observed. The serum total IgE is typically elevated in atopic

asthma. Skin prick tests are simple and provide a rapid

assessment of atopy. Measurement of allergen-specific IgE.

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 Induced sputum and exhaled breath allow the non-invasive assessment of airway inflammation and may prove useful in the diagnosis of asthma and assist in the monitoring of disease activity.

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Achieve and maintain control of symptoms Prevent asthma exacerbations Maintain pulmonary function as close to normal as

possible Avoid adverse effects from asthma medications Prevent development of irreversible airflow limitation Prevent asthma mortality Patient education Avoidance of aggravating factors

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PEF 33-50% predicted (< 100 l/min) SpO2 < 92% or PaO2 < 8 kPa (60 mmHg) (especially if

being treated with oxygen) Normal PaCO2 Silent chest Cyanosis Feeble respiratory effort Bradycardia or arrhythmias Hypotension Exhaustion Confusion Coma

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PEF 33-50% predicted (< 200 l/min) Respiratory rate ≥ 25/min Heart rate ≥ 110/min Inability to complete sentences in 1 breath

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Bronchitis Bronchiectasis Pulmonary fibrosis

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