Asthma

Assistant professor Dr Lamya Abd

Alkarem
Consultant physician , MRCP
Member of Royal College of Physicians London,
Edinburgh, Glasgow
 Objectives

 1. Definition of asthma
 2. Epidemiology and scope of the problem
 3. Pathogenesis
 4. Clinical presentation at various stages
 5. A practical approach to diagnosis
 6. Acute and long term management outlines
 7. Future perspectives
 ASTHMA
 Definition: is a chronic inflammatory disorder of
the airways, in which many cells and cellular
elements play a role.
 Asthma is characterised by
❖ chronic airway inflammation
❖ increased airway hyper-responsiveness
 leading to symptoms of wheeze, cough
(particularly at night and in the early morning),
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 either
spontaneously or with treatment.
 Epidemiology
 The prevalence of asthma increased steadily in
Western lifestyle and in developing countries.
 Current estimates suggest that 300 million people
world-wide suffer from asthma
 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.
 Epidemiology
 Although the development and course of the
disease, and the response to treatment, are
influenced by genetic determinants, the rapid
rise in prevalence implies that environmental
factors are critically important in the
development and expression of the disease.
 To date, studies have explored the potential
role of indoor and outdoor allergens, microbial
exposure, diet, vitamins, breastfeeding,
tobacco smoke, air pollution and obesity
 but no clear consensus has emerged.
 Pathophysiology
 The inhalation of an allergen in a
sensitised atopic asthmatic patient
results in a two-phases
bronchoconstrictor response .
 A- 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
 Pathophysiology

 B- In persistent asthma : a chronic and

complex inflammatory response ensues
 Characterised by an influx of numerous
inflammatory cells, the transformation
and participation of airway structural
cells
 the secretion of cytokines, chemokines
and growth factors
 CARDINAL PATHOPHYSIOLOGICAL
FEATURES OF ASTHMA
1-Airflow limitation Usually reverses spontaneously
or with treatment
2- Airway hyper-reactivity (AHR)
Exaggerated bronchoconstriction to a wide range
of non-specific stimuli, e.g. exercise, cold air
3- Airway inflammation
 Eosinophils, lymphocytes, mast cells, neutrophils
 Associated oedema
 Smooth muscle hypertrophy and hyperplasia
 Thickening of basement membrane
 Mucous plugging and epithelial damage.
 Pathophysiology
 Other factors are likely to be important
including the
❖behaviour of airway smooth muscle
❖ the degree of airway narrowing
❖ the influence of neurogenic mechanisms.
 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
 Clinical features
 Asthma is not a uniform disease but a dynamic
clinical syndrome with a variety of features.
 Typical symptoms include recurrent episodes
of wheezing, chest tightness, breathlessness
and cough.
 Common precipitants include
❖exercise
❖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).
 Clinical features
 Asthma characteristically displays a diurnal pattern,
with symptoms and PEF (peak expiratory flow) being
worse in the early morning.
1- Mild Asthma ; patients with intermittent attacks and
are usually asymptomatic between exacerbations.
 exacerbations occur during viral respiratory tract
infections or after exposure to allergens.
2- Persistent Asthma: the pattern is ongoing
breathlessness and wheeze, but these are variable,
with symptoms fluctuating over the course of one day,
or from day to day or month to month.
 Particularly when asthma is poorly controlled,
symptoms such as cough and wheeze disturb sleep
therefore, we use of the term 'nocturnal asthma'. '
 Clinical features
3- 'cough-variant 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.
4- Medications induced asthma: In some
circumstances the appearance of asthma relates
to the use of medications.
❖Beta-adrenoreceptor antagonists (β-blockers-
even when administered topically as eye drops)
may induce bronchospasm.
❖ oral contraceptive pill, cholinergic agents and
prostaglandin F2α.
❖Betel nuts contain arecoline, which is structurally
similar to methacholine and can aggravate
asthma.
 Clinical features
❖ 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; The classical
patient is female and presents in middle age
with asthma, rhinosinusitis and nasal polyps.
 Clinical features
 Aspirin-sensitive patients may also report
symptoms following
❖ alcohol (in particular, white wine) and
❖ foods containing salicylates like Almonds.
Apples, Apricots, Berries, Cherries, Coffee,
Cucumbers and pickles, Grapes and raisins.
 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
 Clinical features
5- Occupational asthma is now the most common
form of occupational respiratory disorder
 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.
 Early diagnosis and removal from exposure leads
to a significantly improved prognosis and may
result in cure.
 Clinical features

 The recognition of occupational asthma

has important medico-legal implications
 should prompt screening of the
workplace as other employees may also
have developed the disease.
 INVESTIGATIONS
A- Pulmonary function tests

 The diagnosis of asthma is made on the

basis of a compatible clinical history
combined with the demonstration of
variable airflow obstruction .
 Pulmonary function tests and Peak flow
meters are inexpensive and widely
available
 Provide a simple and straightforward
method of confirming the diagnosis.
 Investigations
1- PEFM ( peak expiratory flow meter)
Ideally patients should be instructed to record
peak flow readings after rising in the morning
and before going to bed
 A diurnal variation in PEF (the lowest values
typically being recorded in the morning) of
more than 20% is considered diagnostic and
the variability provides some indication of
disease severity
 A trial of corticosteroids (e.g. 30 mg daily for 2
weeks) may be useful in documenting the
improvement in PEF
 Investigations: Spirometry
2-The measurement of FEV1 and VC by
spirometry allows the demonstration of
airflow obstruction
 Following the administration of a
bronchodilator, confirms the diagnosis
when a 15% (and 200 ml) improvement in
FEV1 is noted .
 Spirometry is also particularly helpful in
monitoring the severity of airflow
obstruction in patients with impaired lung
function
 Investigations

3-AHR (Airway Hypersensitivity)

 Enhanced bronchoconstriction (AHR) to
a variety of direct and indirect stimuli
including exercise, cold air, dusts, smoke
and chemicals such as histamine and
methacholine, is an integral part of the
definition of asthma
 helpful in patients presenting with
normal lung function
 Investigations

4- Exercise
 For patients whose symptoms are
prominently related to exercise, an
exercise test may be followed by a drop
in PEF or FEV1 .
 MAKING A DIAGNOSIS OF
ASTHMA
Compatible clinical history plus either/or:
1) FEV1 ≥ 15% (and 200 ml) increase
following administration of a
bronchodilator/trial of corticosteroids
2) > 20% diurnal variation on ≥ 3 days in a
week for 2 weeks on PEF diary
3) FEV1 ≥ 15% decrease after 6 mins of
exercise
.
 INVESTIGATIONS
B- Radiological examination
 Radiological examination is generally
unhelpful in establishing the diagnosis
 May point to alternative diagnoses.
 Acute asthma is accompanied by
hyperinflation, and 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)
 INVESTIGATION
C- Measurement of allergic
status
 An elevated sputum or peripheral blood
eosinophils count may be observed
 Serum total IgE is typically elevated in
atopic asthma.
 Skin prick tests are simple and provide a
rapid assessment of atopy.
 Similar information may be provided by the
measurement of allergen-specific IgE
 The diagnosis of
occupational asthma
 can be particularly difficult
 Two-hourly recordings of peak flow,
preferably including a period of time away
from work, may establish the diagnosis but
are often difficult to undertake .
 Bronchial provocation tests with the
suspected agent may be required.
 Skin prick tests or the measurement of
specific IgE may confirm sensitivity to the
suspected agent.
 Assessment of airway
inflammation
 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.
 THE GOALS OF ASTHMA
MANAGEMENT
 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
 Encouraging patients to take responsibility for
control of their disease should lead to improved
clinical outcomes.
 Patient education should begin at the time of
diagnosis and be revisited in subsequent
consultations.
 Patients (or their carers) should be taught about
the relationship between symptoms and
inflammation
 The importance of key symptoms such as
nocturnal waking
 The different types of medication
 The use of PEF to guide management decisions.
 Written action plans may prove helpful in
developing these skills.
 Avoidance of aggravating
factors
 Cold air
 Exercise
 Emotion
 Allegen: house dust mite, pollen
 Infection
 Smoking
 Pollution
 NSAID
 B blockers
Stepwise management of stable asthma

 MART( maintenance and relieving therapy)

British Thoracic Society BTS& SIGN Guidelines
 A stepwise approach to the
management of asthma
Step 1: mild intermittent asthma
❖ symptoms less than once a week for 3 months
❖ fewer than two nocturnal episodes/month),
 Occasional use of inhaled short-acting β2-
adrenoreceptor agonist bronchodilators as
required basis
 However, many patients, and their physicians,
under-estimate the severity of asthma and
these patients should be carefully supervised.
 A history of a severe exacerbation should lead
to a reclassification of the patient's condition
as persistent asthma.
 Step 2: Introduction of
regular preventer therapy
 Patient has experienced an exacerbation
of asthma in the last 2 years
 Regular anti-inflammatory therapy
(preferably inhaled corticosteroids-ICS)
should be started +inhaled β2-agonists
taken on an as required basis
 uses inhaled β2-agonists three times a week
or more
 reports symptoms three times a week or
more
 is awakened by asthma one night per
week.
 Step 3: Add-on therapy
1. Add inhaled long-acting β2 agonist (LABA)
2. Assess control of asthma:
Good response to LABA - continue LABA
Benefit from LABA but control still inadequate-
continue LABA and increase inhaled steroid
dose to 800 mcg/day
No response to LABA
 stop LABA and increase inhaled steroid to 800
mcg/ day.
 If control still inadequate
 Institute trial of other therapies,
❖leukotriene receptor antagonist
❖ SR theophylline
 Step 4 : Persistent poor
control
Consider trials of:
increasing inhaled steroid up to 2000
mcg/day
addition of a fourth drug
 e.g. leukotriene receptor antagonist,
 SR theophylline,
 β2 agonist tablet
 STEP 5: Continuous or frequent
of oral steroid

 Use daily steroid tablet in lowest dose

providing adequate control
 Maintain high dose inhaled steroid at
2000 mcg/day*
 Consider other treatments to minimise
the use of steroid tablets
 Refer patient for specialist care