The document discusses the etiology, pathophysiology, diagnosis and management of asthma. Some key points: - Atopic allergy and allergy to common inhalants like house dust mites, pollens and molds contribute to 75-85% of asthma cases. Occupational allergens can also cause asthma. - Pathophysiology involves airway smooth muscle contraction, epithelial secretions and inflammatory edema narrowing the airways. Early and late phase asthmatic reactions are mediated by IgE and inflammatory cells/mediators. - Diagnosis involves assessing symptoms, lung function tests like spirometry, allergy tests and inflammation markers. Severity is classified based on symptoms, lung function

1. Guided by : DR .Anusuya
Presented by : DR. Deepti Dewan

3. ETIOLOGY
 ATOPY AND ALLERGY: 75-85% of pts. With asthma have positive immediate
skin reactions to common inhalant allergens
 Most people with asthma are atopic and can be measured by skin tests or with
measurements of specific IgE, house dust mite allergens appear to be the most
common one ass. with asthma
 Allergens increases the severity of the disease
 Occupational asthma occurs due to allergens and sensitizers , some healthy
people exposed to these agents sensitization occurs and episodic wheeze is
present
 Intrinsic asthma people have higher levels of circulating IgE than non-asthmatic
population
 House mites, grass pollens, animal and moulds, Alternia alternate (fungus
causing leaf spot) ,climates ,surroundings.

4.  Predominant offending allergen :
 Delhi: Amaranthus , Cassia siamea,Ricinus, Brassica,
Imperata, Prosopis, Cenchrus, Cassia Occidentalis.
 Prosopis : Bikaner, Lucknow ,Varanasi
 Brassica : Bhopal, Kanpur
 Parthenium in Kohlapur

5.  Pollen allergy : particles greater than 10micron in diameter do not
penetrate the LRT. Ragweed and grass pollination. It is mainly season related
 Mould : mould spores smaller than pollen grains
 House dustmite: arachnoids related to ticks and spiders. ubiquitous living
in house dust and scales of skin shed by human. Commonest mite is
Dermatophagoides pteronssinus. High levels found in
mattresses,pillows,carpets, bed covers, clothes soft toys.
 Animal allergens: cat allergen is more likely to cause sensitisation than that
of dogs. Major cat allergen Fel d 1, which is a protein secreted by cat’s
salivary,sabeceous and lacrimal glands, this protein is stable and does not
lose its antigenic property for a month. A no. of epidemiological study
suggest close contact with a cat or dog in very early infancy reduces the
prevalence
 Cockroach allergen: imp. Species Blatella germanica and periplaneta
American
 Infection

6. PROVOCATEURS OF ASTHMA
The principal infection provacateurs of asthma in childhood during the
first 2years of life are rep. synctial virus (RSV), parainfluenza virus,
and rhinovirus. Exacerbate Mycoplasma pneumoniae, clamydia
pneumoniae
In recent years it is observed that some infections are protective of
bronchial asthma. viral infections can undoubtedly cause
deterioration of established asthma,viral or bacterial infections
during the first three years of life may serve a protective function
against the development of allergic diseases. Possibly they evoke a
Th-1- like protective response with the generation of IFN-gamma
and IL-2.
This high conc. Of Th1 cytokines could inhibit the release of Th2
cytokines thus tuning the mucosal immune response away from
allergen sensitisation

7. Drugs
 About 5-20% of adults with asthma will experience severe
and even fatal exacerbations of bronchoconstriction after
ingestion of aspirin or certain non-steroidal anti-
inflammatory drugs(NSAIDS)
 Apirin , Ibuprofen ,Indomethacin, Piroxicam, Sulindac,
Tolmetin, Naproxen, Fenoprefen, Meclofanamate,
Mefenamic acid, Diclofenac sodium.
 In these individuals ,ingestion of asspirin is followed
within 1-2 hours by the onset of bronchospasm
accompanied by urticaria and rhinitis

8. Exercise induced asthma
 EIA asthma of persons in whom exercise is predominant or even the
only trigger to airflow obstruction. EI bronchoconstriction is one
manifestation of asthmatic diathesis
 All people with asthma have airway hyperirritability that leads to
exercise-induced asthma if provocative stimulus-eucapnic voluntary
hyperventilation- is appropriately intensified
 It is the airway narrowing develops within2-3 minutes after cessation
of exercise. It reaches its peak about 5-10mins, after cessation of
activity and usually resolves spontnaeously in next 30-90 mins or
with few mins after administration of an inhaled beta adrenergic
bronchodilator.
 A rapid change to warm, moist air post-exercise tends to worsen the
development of airflow obstruction.
 Some pts. Who engage in continuous, repetitive exercise periods ,
EIA diminishes during a refractory period usually lasts 2hrs after an
exercise challenge.

9. EIA
 It is mainly due to smooth muscle contraction, thus its known as airflow-
induced bronchoconstriction (AIB) or exercise-induced bronchospasm(EIB)
 EIA is due to loss of heat or water or both, from the lung during exercise
resulting from hyperventilaion of air that is cooler and dryer than the
bronchial tree

10. Occupation and asthma
 It accounts for 10% adult onset asthma

11. Tartrazine and sulphite sensitivity
 It is a yellow dye commonly employed in food and
medications.
 Sulphiting agents is used to preserve foods and
beverages since ancient times, maintaining crisp and
fresh appearance of foods, prevents browning and
control microbial growth and spoilage

12.  Rhinitis and sinusitis
 GER: reflex vagal bronchoconstriction occurs secondary to
stimulation of sensory nerve fibres in lower oesophagus
 Psychological factors
 Pollution: passive smoking , diesel fumes ass. With
increased allergic responses. Tokyo Yokohama asthma.
Asthmatic smokers have higher soutum total cell and
neutrophil numbers and IL-8 concentrations compared to
asthmatic non smokers, sputum eosinophils and
eosinophil-cation-protein levels are higher in non smoking
sugesting a normalising effect of smoking on Th1/Th2
balance

13.  Endocrinal factors
 Genetics: molecular genetic linkage studies indicate
“atopy” genes locus is on chromosome 11

15. PATHOPHYSIOLOGY
 Three factors narrow airway caliber to limit the flow:
 Airway smooth muscle contraction
 Gland and epithelial secretions and exudation into the
airway lumen
 Inflammatory oedema and vasodilatation (hyperemia)

16. EARLY ASTHMATIC REACTION
 This early reaction is IgE dependent and is the result of IgE
binding to mast cells by its Fc portion and to specific
antigens by its F(ab) portion.
 When IgE-sensitized mast cells are exposed to antigen
against which the IgE molecule is directed, preformed and
newly generated mediators are released.
 These can be detected in the blood as they overflow into the
circulation, in bronchoalveolar lavage (BAL) fluid and as
metabolites in the urine and include histamine,
prostaglandin D2 , and leukotriene C4 from airway mast cells
,this early response is due to histamine.

17. LATE ASTHMATIC REACTION (LAR)
AND BRONCHIAL HYPERREACTIVITY
(BHR)
 The LAR is characterised by release of inflammatory
mediators into same fluids.
 The BHR is exaggerated bronchoconstriction of smooth
muscles and airway narrowing on exposure to small
quantity of non-allergic stimulant that usually does not
provoke such a reaction in normal subjects

18. Pathogenesis
 T-lymphocyte play a key role in asthmatic airway inflammation and
sensitisation.
 Two types of T-lymphocyte helper (Th)cells.
 Th 1 controls synthesis of Igs such as IgA and IgM whereas Th 2 controls
IgE production. There is balance between Th1/T2 switch.
 Exposure to an inducing factor sensitises T cells of a person wiith genetic
susceptibility with bronchial asthma, and it shifts th Th1/Th2 switch in
favour Th2 dominance.
 Once sensitised these Th2 cells get into airway mucosa and governs IgE
mediated responses of allergic reaction.
 Normal individual when a noxious allergic substance enters airway, IgA
released. However in a sensitised person IgE is released


19. PATHOLOGY
 Crystalline material consisting largely of major basic
protein derived from eosinophils granules (Charcot-
Leyden crystals) maybe present.
 Oedema,dense eosinophilic infiltration and epithelial
denudation in bronchial wall
 Airway samples obtained at open lung biopsy show
goblet cell hyperplasia, peribronchial smooth muscle
hypertrophy and apparent basement membrane
thickening
 Strips of epithalial cells Curschmann’s spirals, clumps of
cells (Creola bodies) or isolate metaplastic cells are
common

20. Clinical Presentation
 Wheezing,cough, white or clear sputum,chest tightness
 Flexural eczema
 In children evidence of hyperinflation of lungs with use
of accessory muscles , appearance of hunched shoulders
and “pigeon chest”
 Intensity of breath sounds in symptomatic asthma will be
reduced and expiratory phase is prolonged.

24. CLASSIFICATION
 Intrinsic and extrinsic asthma
 Late onset asthma
 Occupational asthma: and work aggravated asthma
 Nocturnal asthma
 Chronic asthma:
 Brittle asthma: intractable and persistent asthma resistant to
all conventional therapy
 Morning dippers: worsen symptoms during early hours of
night. In children attack is worse around 2am and in adults it
is variabe increasing slowly and rapidly from midnight

26. diagnosis
 Blood examination: patients have eosinophil count in the range of 5-
15%
 Sputum induction: no. of eosinophils are increased in induced
sputum
 Airway hyperresponsiveness: Methacholine or histamine challenge
test
 Chest Radiograph: hyperinflation in patient with ashma
 Skin prick test: sensitivity to a particular antigen can be identified by
injecting a small amount of allergens into the skin. Wheal and flare
appear at the site of injection of a sensitised allergen. Allergerns can
be identified by estimation of specific IgE im blood through
radioallergosorbent test (RAST)

27. ASSESMENT OF SEVERITY
 PEAK EXPIRATORY FLOW RATE (PEFR):
It represents maximal expiratory effort
performed after full inhalation. Its measured
using a peak flow meter. Personal best value is
highest recorded PEFR value of a person taken
over a few days during asymptomatic period.
The magnitude of variation between mornning and evening
PEFR values is called PEFR variability and is proportional to
the severity of asthma.
Another useful index is PEFR reversibility.
Salbutamol or terbutaline administered

28.  SPIROMETRY:
A ratio of FEV1 and forced vital capacity (FVC) less than 0.7 is
diagnostic of airway obstruction.
 LUNG VOLUMES AND DIFFUSING CAPACITY:
Lung vols. Such as residual volume and total lung capacity are
increased in a patient with asthma. Carbon Monoxide diffusing capacity
(DLCO) is either normal or increased in asthma patients but its increased
in COPD.
 OXIMETRY:
O2 saturation should be more than 90%
 ARTERIAL BLOOD GAS ANALYSIS
PaO2 decreases but PaCO2 normal, when latter increased
for assisted ventilation

29. Indices determining control of
asthma
 Day time symptoms less than twice per week.
 Short acting beta agonist (SABA) inhaler use less than twice per
week.
 Without an night symptoms
 Without limitation of activity
 Normal PEFR and FEV1
 controlled if indices fulfilled and no exacerbation in last one year.
 PARTLY CONTROLLED: if any of the indices are fulfilled and patient
did not have an exacerbation during last one yr.
 POORLY CONTROLLED: more than 3indices are more severe and pt.
had exacerbation in last one week

30. Management of asthma
 Patient education
 Identify and reduce exposure to risk factors
 THERAPEUTICS

33. Thank you.