Pm Bronchial Asthma

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    PRESENTED BYDr.ASHA V SASI2ND MD CR DEPT

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    Asthma is characterised by chronic airwayinflammation and increased airway hyper-

    responsiveness leading to symptoms of wheeze,cough, chest tightness and dyspnoea.

    It is characterised functionally by the presenceof airflow obstruction which is variable over

    short periods of time, or is reversible withtreatment.

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    The prevalence of asthma increased steadily over the

    latter part of the last century in countries with aWestern lifestyle and is also increasing in developingcountries.

    Current estimates suggest that 300 million people

    world-wide suffer from asthma and an additional 100million may be diagnosed with asthma by 2025.

    In childhood, asthma is more common in boys, butfollowing puberty females are more frequently

    affected. The socio-economic impact of asthma is enormous,

    particularly when poor control leads to days lost fromschool or work, hospital admissions and, for somepatients, a premature death. www.similima.com 3

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    Dietary intake may be important. Milk fat andantioxidants such as vitamin E and selenium may

    protect against the development of asthma inchildren; however, in other studies early exposure tocows' milk protein has been linked to the developmentof atopy and asthma.

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

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    The increase in asthma may also be linked to therise of obesity in Western society throughmechanical 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 asthmarelates to the use of medications.

    Beta-adrenoceptor antagonists (-blockers-even whenadministered topically as eye drops) may inducebronchospasm.

    Aspirin and other non-steroidal anti-inflammatory

    drugs are associated with asthma in about 10% ofpatients. This is believed to reflect a shift in the metabolism of

    arachidonic acid from the cyclo-oxygenase pathwaygenerating prostaglandins, towards the lipo-oxygenasepathway generating cysteinyl leukotrienes.

    Aspirin-sensitive asthma is often associated withrhinosinusitis and nasal polyps

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    extrinsic Intrinsic(cryptogenic)

    External factor identifiable No such factor

    Serum shows high levels of IgE &IgGNo raised Ab levels but increasedeosinophils present ,aspirinsensitivity, & presence of nasal

    polypAtopic manifestations may bepresent

    No atopy

    Dermatological and respiratory s/sshow 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 releasechemical mediators from the mast cells byinteracting with the IgE molecules on theirsurface- Type 1 hypersensitivity reaction-immediate asthmatic paroxysm

    Some times type 3 hypersensitivity reaction alsooccurs and it is mediated by IgG delayed

    paroxysm

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    The inhalation of an allergen in a sensitised atopicasthmatic 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 withresulting bronchoconstriction. In persistent asthma a chronic and complex

    inflammatory response ensues, which ischaracterised by an influx of numerous inflammatory

    cells, the transformation and participation of airwaystructural cells, and the secretion of an array ofcytokines, chemokines and growth factors

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    Airflow limitation Usually reversesspontaneously 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, mucousplugging and epithelial damage

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    With increasing severity and chronicity of thedisease, remodelling of the airway occurs,leading to fibrosis of the airway wall, fixednarrowing of the airway and a reduced responseto bronchodilator medication

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    Typical symptoms include recurrent episodes of breathlessness wheezing,

    cough. chest tightness

    Common precipitants include

    exercise, particularly in cold weather,

    exposure to airborne allergens pollutants

    viral upper respiratory tract infections (beware the coldthat 'goes to the chest' or takes more than 10 days toclear).

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    Moderately severe cases the patient isorthopneic,cyanosed, and accessory musclesof respiration are active

    Ineffective cough with tenacious mucoidexpectoration

    Pulse rapid BP normal or elevated

    Pulsus paradoxus in severe cases

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    Chest expansion diminished ie,less than 2cmduring attack.

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

    usually asymptomatic betweenexacerbations which occur during viralrespiratory tract infections or after exposureto allergens.

    In persistent asthma the pattern is one of

    chronic wheeze and breathlessness

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    a diurnal pattern, symptoms being worse in theearly 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 reachingthe diagnosis of so-called 'cough-variantasthma'.

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    Occupational asthma is now the mostcommon form of occupational respiratorydisorder and accounts for around 5% of alladult-onset asthma.

    This should be considered in all adultasthmatics of working age, particularly ifsymptoms 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 exposureleads to a significantly improved prognosisand may result in cure.

    The recognition of occupational asthma hasimportant medico-legal implications andshould prompt screening of the workplaceand other employees .

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    The diagnosis of asthma is made on the basis of a

    compatible clinical history combined with thedemonstration of variable airflow obstruction

    Eosinophilia Sputum reveals eosinophils. Sputum shows eosinophils, mucus plugs and

    curschmanns spirals. Purulent sputum indicative of respiratory infection. Culture reveals the infecting organisms Pulmonary function tests

    Compatible clinical historyplus 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 FEV

    1 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 bylobar collapse, suggest asthma complicated byallergic 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 inatopic 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 airwayinflammation and may prove useful in thediagnosis of asthma and assist in themonitoring 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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    Management Oxygen therapy Iv fluids

    HOMOEOPATHIC MANAGEMENT Respiration asthmatic(synthesis) Diseases asthma(Murphy) Respiration asthma(BBCR) Asthma bronchial(Phatak) Respiratory system asthma(Boericke)