ASTHMA

for
MBBS
 ASTHMA
OLD NEW

• Asthma is a heterogenous
• Chronic inflammmatory disease usually characterized
disorder of the airways. by chronic airway
• Involving many cells and inflammation. It is defined
cellular elements. by a history of respiratory
• Leading to airway hyper- symptoms such as cough,
responsiveness. wheeze, dyspnoea, chest
tightness that vary of time
• Variable airflow
and in intensity, together
obstruction. with variable airflow
• Completely reversible limitation (GINA 2016).
spontaneously/treatment.
Asthma – a global healthcare issue
• Asthma is a worldwide problem
– WHO estimates, 235 million people suffer from asthma
– it occurs in all countries regardless of level of development. Over 80%
of asthma deaths occurs in low and lower-middle income countries
– Asthma is under-diagnosed and under-treated, creating a substantial
burden to individuals and families.
– There are an estimated 250,000 annual worldwide deaths from
asthma
• Over the last 40 years there has been a sharp increase in the
global prevalence, morbidity, mortality, and economic burden
associated with asthma
• Asthma prevalence is expected to increase by 50% every
decade.
 How common is asthma?

 Mean prevalence of asthma in North Africa is estimated at

3.9%.

 Prevalence of clinical asthma in West Africa is 5.7%

 5.4% of Nigerians are asthmatic by current estimates

 Highest prevalence of asthma in Africa is in the Southern

Africa – mean prevalence rate of 8.1% of the population

4
 How common is asthma?

 Asthma is very common at all ages and is becoming more

common in children and adults especially in the last 20-30
years.

 Reason is uncertain but related to;

exposure to smoking
indoor and outdoor pollution
genetic susceptibility
diet

5
 Who gets asthma?

 Asthma may occur at any age but usually starts in childhood.

 Peaks at age 5, mid-teenage years and aged 40-50 years

 Atopy occurs more commonly in boys; asthma symptoms

more common in boys

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 Who gets asthma?

 Undoubtedly a genetic component exists.

 But asthma is not an inherited disorder.

 Asthma does run in families (family with strong history of
allergies and atopy).
 Concordance of asthma in monozygotic twins is much greater
than in dizygotic twin

 A child born to two atopic parents has about 66% chance of

developing one or more atopic phenotypes (33% risk if born
to one atopic parent).

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 Who gets asthma?

 Genes controlling Il -3,4,5 etc=mast cell dev./Ige production&

are associated with development of asthma and atopy.

 Twin studies suggested a genetic factor confers susceptibility

to asthma.

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 A strong environmental component is contributory-
exposure to antigens- coackroach, pets, aspergillus
fumigatus, house dust mite (dermatophagoides
pteronisis), helminths.
 Viral infecions-Rhinoviruses.
 Industrial pollutants-fumes and smokes from
hydrocarbons.
 Various high- and low-molecular-weight compounds
(eg, insects, plants, latex, gums, diisocyanates,
anhydrides, wood dust, and fluxes; associated with
occupational asthma)
• Aspirin or nonsteroidal anti-inflammatory
drug (NSAID) hypersensitivity, sulfite
sensitivity.
• Use of beta-adrenergic receptor blockers
 PATHOGENESIS:

• Complex ,poorly understood.

• Allergic asthma most studied/understood.
• Hallmark is chronic Inflammation = occurs in
the bronchi in response to allergens and
other inducers.
• Cells, Mediators, Nerves are activated by
several mech.
• Remodelling.
• Airway inflammation in asthma may represent
a loss of normal balance between two
"opposing" populations of Th lymphocytes.
• Two types of Th lymphocytes have been
characterized: Th1 and Th2.
• Th1 cells produce interleukin (IL)-2 and IFN-α,
which are critical in cellular defense
mechanisms in response to infection.
• Th2, in contrast, generates a family of
cytokines (IL-4, IL-5, IL-6, IL-9, and IL-13) that
can mediate allergic inflammation.
• In asthmatics the Th2 response
dominates>>inflammation(chronic,
acute ,subacute)
 Airflow limitation
• Airflow obstruction can be caused by a variety
of changes, including acute
bronchoconstriction, airway edema, chronic
mucous plug formation, and airway
remodeling.
• Acute bronchoconstriction is the consequence
of immunoglobulin E-dependent mediator
release upon exposure to aeroallergens and is
the primary component of the early asthmatic
response.
• Airway edema occurs 6-24 hours following an
allergen challenge and is referred to as the
late asthmatic response.

• Chronic mucous plug formation consists of an

exudate of serum proteins and cell debris that
may take weeks to resolve.
• Airway remodeling is associated with
structural changes due to long-standing
inflammation and may profoundly affect the
extent of reversibility of airway
obstruction(fixed airways).
• Airway obstruction causes increased
resistance to airflow and decreased expiratory
flow rates.
• These changes lead to a decreased ability to
expel air and may result in hyperinflation.
Asthma Inflammation: Cells and
Mediators

Source: Peter J. Barnes, 18

MD
• Mast cells-↑in epith, smooth muscle, mucus
glands.
• Mediators-histamine, LTCs,growth factor.
• Eosinophils- large numb. in bronchial walls.
• Dendritic cells-present allergens to
lymphocytes =release of cytokines to attract
mast cells , eosinophils.
• Promotion of Th2 phenotype(Inflammation)
 remodelling
• Remodelling-alteration in structure/function of
elements of bronchial wall.
• Epith- metaplasia- increase in goblet cells& expression
of NO2.
• Basement membrane- collagen deposition, matrix
proteins etc=fibrosis.
• Smooth muscle- hyperplasia=increased contractile
property.
• Nerve endings- transmit stimuli to & fro brain-
bronchoconstriction.
 INDUCERS
Allergens, Chemical sensitisers,
Air pollutants, Virus infections

INFLAMMATION

Airway
Hyperresponsiveness Airflow Limitation

TRIGGERS SYMPTOMS
Allergens, Cough Wheeze
Exercise Chest tightness
Cold Air, SO2 Dyspnoea
Particulates

Barnes PJ 21
Inflammation and bronchoconstriction: a
two-part problem

Damaged airway passage wall Inflammation

Normal airway Airway inflammation

and bronchoconstriction
Diagnosis of asthma

 history and pattern of symptoms

 physical examination
 measurements of lung function

• - reversibility test
• - diurnal variability
 evaluation of allergic status

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Is it asthma?

 symptoms - vary over time and in severity:


Cough, wheeze, breathlessness

chest tightness
 symptoms occur or worsen at night or after
exposure to trigger
 colds “go to the chest” or take >10 days to clear

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Ask about triggers
Symptoms can occur or worsen in the presence of:

Allergens Others
 animal dander  exercise
 dust mites  viral infection
 pollen  smoke
 Fungi, moulds  changes in temperature
 Cockroaches  strong emotional expression
 aerosol chemicals
 drugs (NSAIDs, ß-blockers)

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What is difference between trigger and an allergen?

 All allergens are triggers but not all triggers are allergens

 A trigger is any substance that is capable of inducing or

exacerbating asthma. e.g. Cold air, exercise and viral upper
respiratory tract infections.

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What is difference between trigger and an allergen?

 An allergen is a special form or type of trigger that induces

allergic asthma. E.g. cat dander, pollen and house dust
mites.

 An allergic reaction or allergy describes a type of immune

response to external agents in which the response itself
causes harm or damage to the body.

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P/E & INV

• WHEEZE(RHONCHI)
• HYPERINFLATION
• PR,RR, CYNOSIS
• PEF or FEV
• ABG,OXIMETRY
• CXR
• ALLERGY SKIN TESTING
• BRONCHIAL CHALLENGE- METHACHOLINE, HISTAMINE
Reversible and variable airflow limitation

 Reversibility of airways’ obstruction

 increased PEF >15% 15-20 minutes after inhaling ß 2-
agonist
 FEV 15% or 200ml increase after 2weeks oral
steriod(prednisolone 30mg/day.)

 Variability of airways’ obstruction

 PEF varies between morning and evening
>20% in patients taking bronchodilator
>10% in patients not taking bronchodilator

 Exercise-induced airways’ obstruction

 decreased PEF >15% after 6 minutes of exercise 29
CLASSIFCATION of asthma

• EXTRINSIC/INTRINSIC
• FREQUENCY/DURATION OF SYMPTOMS- Intermittent, Persistent
• AGE- Childhood Or Adult Onset
• OCCUPATIONAL
• EXERCERBATION PRONE
• ASPIRIN INDUCED
 ‘Clinical’ classification of severity

Clinical features before treatment

Symptoms Night-time PEF
symptoms

STEP 4 Continuous <60% predicted

Severe Limited physical Frequent
persistent Variability >30%
activity
STEP 3 Daily >60% - <80%
Moderate Use 2-agonist daily >1 time a week predicted
persistent
Attacks affect activity Variability >30%
STEP 2
>1 time a week >80% predicted
Mild persistent
but <1 time a day >2 times a month
Variability 20-30%

STEP 1 <1 time a week

Intermittent >80% predicted
Asymptomatic and <2 times a month
normal PEF between Variability <20%
attacks

31
GINA Guidelines 1998
DIFFERENTIAL DIAGNOSIS

• COPD
• ALVF/CCF
• HYPERVENTILATION SYNDROME
• OSA
• GERD
• CHAURG-STRAUSS SYNDROME
• FB INHALATION
• ILD
• TUMOURS
• PULMONARY EMBOLISM
• OTHER CAUSES OF COUGH/BREATHLESSNESS
 Asthma impacts patients’ lifestyles

50 48 48
47
46
45

40
Percentage of respondents

35 33
answering 'yes' (%)

30

25 24

20

15

10 9

0
Night or early Bother, Restriction of Using reliever Prevents you Social life Affects sex life
morning irritation, sporting medication > from trying restrictions
awakening frustration activities 2 days/week new sporting
activities

1. Bellamy D et al. Primary Care Respir J 2005; 14: 252–258.

 Asthma restricts activities in adults and
children

60
% of patients surveyed

50

40
Adults
30
Children
20

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1. Neffen H et al. Pan American J Public Health 2005; 17:191–197..

 Patients live in fear of asthma symptoms

“Anxiety-
provoking” “Scary”

• A quarter of patients over 65 described their asthma as “life-threatening”, and

27% of those over 55 described it as “frightening”
• 1 in 5 patients view their asthma as potentially fatal
• Many patients restrict their activities because of their fear of asthma
symptoms

“Living on a
”Stressful” knife edge”

1. Asthma UK. Living on a knife edge. May 2004.

MANAGEMENT OF ASTHMA
Management of asthma

 Inflammation is a hallmark of asthma.

 Most important advance in the treatment of asthma

 Widespread use of corticosteroids – ‘gold standard’ for

asthma treatment

37
 Asthma is a two component disease:
complementary effects of long-acting 2-agonist/
corticosteroid combination therapy

Smooth Airway
LABA muscle inflammation/ ICS
dysfunction remodelling

 • Bronchoconstriction
• Inflammatory cell infiltration/ 
activation
 • Bronchial hyper-reactivity • Mucosal oedema 
 • Hyperplasia • Cellular proliferation 
 • Inflammatory-mediator release • Epithelial damage 
• Basement-membrane thickening 

Symptoms\exacerbations
1. Johnson M. Proc Am Thorac Soc 2004; 1: 200–206.
 The goal of asthma management:
guideline-defined control

• The Global Initiative for Asthma (GINA) defines clinical control of

asthma as:1

• No (twice or less/week) daytime symptoms

• No limitations of daily activities, including exercise
• No nocturnal symptoms or awakening because of asthma
• No (twice or less/week) need for reliever treatment
• Normal or near-normal lung function
• No exacerbations

1. Global Initiative for Asthma (GINA): Global strategy for asthma management and prevention. Revised Edition 2007.
 Goals of asthma treatment

 Prevent chronic and troublesome symptoms

 Maintain (near-) normal pulmonary functions

 Maintain normal activity levels

40
 DEFINITIONS
• Severity – intrinsic intensity of dx. activity or
intensity of rx. req. to achieve good control.
• Control – degree to which rx. can eradicate or
ameliorate features of asthma and reduce risks.
• Exacerbations- events which become sufficiently
severe enough to mandate a change in therapy
or req. urgent therapy.*hospitalization, ER visit,
use of systemic steroids*
 Goals of asthma treatment

 Prevent recurrent exacerbations of asthma

 Provide optimal pharmacotherapy with

minimal or no adverse effects

 Meet patients’ and families’ expectations

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Treatment strategy

 Identify and avoid triggers that make asthma worse

 Achieve control by selecting appropriate medication

 Treat asthma attacks promptly and effectively

 Educate patients to manage their condition

 Monitor and modify asthma care to maintain effective long-term

control

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 Pharmacological treatments

Eight types of drugs : -

 Β2 agonist (short acting)-salbutamol,TERBUTALINE, ALBUTEROL
 Corticosteriods-HYDROCORTISONE,PREDNISOLONE,TRIAMCINOLONE
 Cromogens-CROMOLYN,
 Β2 agonist (long acting)-SALMETEROL, FORMETEROL
 Theophyllines-AMINOPYLLINE, THEOPYYLLINE
 Anticholinergic drugs-IPRATRPIUM
 Leukotriene receptor antagonists- MONTELUKAST,ZAFIRLUKAST
 Other drugs (anti IgE, antibodies to TNFα)

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 Pharmacological therapy

Controllers
Relievers  Inhaled corticosteroids
 Inhaled fast-acting  Inhaled long-acting 2-agonists
2-agonists  Inhaled cromones
 Inhaled anticholinergics  Oral anti-leukotrienes
 Oral theophyllines
 Systemic  Oral corticosteroids
glucocorticosteriods  Systemic glucocortisteriods
 Theophyline  Anti IgE (Omalizumab),
 Short acting oral β2
 Anti TNFα (etanercept)
agonist
 Interferon-α,
 Anti-interlerukin 13

45
 COMBINATION ICS+LABA(CONTROLLERS)

• FLUTHICASONE +SALMETEROL dpi (SERETIDE)

• FLUTHICASONE +SALMETEROL MDI (ESIFLO OR SALMEFLO)
• BUDESONIDE +EFORMETEROL (symbicort)
 STEPS
• DIAGNOSIS
• CLASSIFICTION (FOR INITIATION OF THERAPY)
• INITIATE AT APPROPRIATE STEP usuALLLY 2.
• FOLLOW UP 4WEEKS- ASSESS CONTROL, ADJUST MEDICATION, COMPLIANCE,
EDUCATE.

• FOLLOW UP 4-12WEEKS.
 Levels of Asthma Control
Partly controlled Uncontrolle
Characteristic Controlled (Any present in any
week)
d

Daytime None (2 or less / More than

symptoms week) twice / week
Limitations of
None Any 3 or more
activities
features of
Nocturnal partly
symptoms / None Any controlled
awakening asthma
Need for rescue / present in
None (2 or less / More than
“reliever” any week
week) twice / week
treatment
< 80% predicted or
Lung function
Normal personal best (if
(PEF or FEV1)
known) on any day
One or more / year 1 in any
Exacerbation None
week 49
 Assessment of symptom control:
The Asthma Control Test
Asthma control involves:
• No (twice or less/week) daytime
symptoms
• No limitations of daily activities,
including exercise
• No nocturnal symptoms or
awakening because of asthma
• No (twice or less/week) need for
reliever treatment
• Normal or near-normal lung
function
• No exacerbations

© 2002, by QualityMetric Incorporated.

Asthma Control Test is a trademark of QualityMetric Incorporated.
"US English version modified for use in UK"
 The Asthma Control Test
• The ACT questionnaire asks patients to report, for the
previous 4 weeks, on:1
– Limitations to activities
– Shortness of breath
– Night-time awakening
– Use of rescue medication
– Perception of control

• Completion of the ACT results in a potential score of

between 5 and 25; a score of ≤19 indicates uncontrolled
asthma1

• An ACT score of 20 or above is optimal for confirming

asthma control2

1. Lai CKW et al. Eur Respir Rev 2006; 15: 24–29. 2. Schatz M et al. J Allergy Clin Immunol 2006; 117: 549–556.
Current status of asthma control: a vicious
circle

Patient Physician
Acceptance of asthma symptoms as Acceptance of a certain level of
part of their usual life: under-report symptoms for their asthmatic patients
Trust in their physicians to accurately As patients do not complain,
assess their condition and give them assumption that patients are well
the best treatment enough controlled
 Acute asthma(exercabtions)
• Increase in severity of symptoms requiring
intervention.
 Types of exercabations
Type 1 Type 2
• Slow onset >6hrs-days • Sudden <6hrs
• F>M • M>F
• Trigger-URTI • Allergens
• Severe obstruction • Bronchospasm
• Slow response to rx • Rapid response to rx
• Hosp. admisssion req. • Less hosp adm.req.
 ACUTE SEVERE ASTHMA
• DIAGNOSTIC CRITERIA.
• UNABLE TO SPEAK IN SENTENCES
• PR≥110
• RR≥25
• PEFR ≤ 50% EXPECTED/PERSONAL BEST
• PULSUS PARADOXUS
• HYPOXIA
• SILENT CHEST
• CONFUSION
• BRADYCARDIA
• RESPIRATORY ARREST
 High risk groups
• Hx near fatal asthma.
• 3ED visits/2hospitalizations in the last 1yr.
• Using/having used oral steroids.
• NOT on ICS
• Psychiatric illness/co-morbidities.
• Non-compliance
• Excessive>2canisters of SABA/month.
• Low socioeconomic status.
 ASSESEMENT
• Duration/severity of symptoms.
• Risks.
• Current medication.
• RR,PR,PEF,O2 sat,cxr?
 TREATMENT
Oxygen high conc.40- 60%
Nebulised salbutamol 5-10mg q 15-20min or continous.
Nebulised ipratropium 500mcg q 30min
Spacer device-SALBUTAMOL/IPRATROPIUM 4-20 PUFFS PER HR.
IV route
Steroids I.V hydrocortisone200-500MG 6HRLY OR
Oral PREDNISOLONE 40-60MG DLY ×5-10DAYS OR
i.v. Metyl prednisolone
IVF as needed –DO NOT OVERLOAD
Monitor PEF 15-30min.
 Reasseess @1hr
• IMPROVING-CRITERIA MODERATE
• CONTINUE RX 1-3HRS.
• GOOD RESPONSE:
• normal P/E
• PEF>70% predicted/personal best(PB).
• Normal saO2>90%
• Sustained for at least 1hr AFTER LAST RX.
• Disch on medications.
• NO improvement @1hr:
• Continue treatment & Monitoring
• ADD IPRATROPIUM (if not already on it)+MG

• ASSESS @ 1-2HRS:GOOD ,PARTIAL ,POOR/NO

RESPONSE.
 Partial response
• Persisting signs.
• PEF <60% predictted/PB.
• O2 sat not improved.
• Continue rx/monitoring= ED/hospital ward.
 Poor response

• Severe symptoms.
• Drowsy, confused, arrythmias, myocardial
ischaemia.
• PEF<30%.
• RESP FAILURE.pCO2<45mmHg,pO2>60mmHg.
• SaO2<90%.
 ICU
• Life threatening features.
• Worsening PEF
• Exhaustion/poor resp. effort
• Resp.failure.
 Additional therapy.

2nd line
Magnesium sulphate 1-2g i.v over 30mins.
Aminopylline i.V 5mg/kg loading, 0.5mg/kg/hr
infusion in 500mls n/saline or 5%dextrose if
no response to above.
3rd line
Heliox =helium/oxygen mixture.
Epineprine. 0.5-1mg sc
 NOT USEFUL/HARMFUL
• SEDATIVES
• MUCOLYTICS/COUGH SYRUPS-WORSEN COUGH
• CHEST PHYSIO-DISCOMFORT
• OVERHYDRATION
 DISCHARGE
• Off nebulizer/relivers =24hrs.
• On ICS+LABA
• PEF =80% predicted.
• Minimal dly variation in PEF.
• Education.
• Follow up within 2 weeks.
 COMPLICATIONS
• Pneumothorax ,mediastenum,subcut.
emphysema.
• Atelectasis
• Myocardial infarction.
• Lactic acidosis.
• Anoxic brain damage
• Drug toxicity theophyilline.
 SPECIAL SITUATIONS
• PREGNANCY- TREAT PROMPTLY ANY
EXERCABATION.
• OBESITY- WEIGHT LOSS.
• SURGERY – OPTIMIZE RX. NEAR NORMAL PEF.
• OCCUPATIONAL ASTHMA- CHANGE
JOBS./SPECIALIST CARE
• GERD-PROTON PUMP INHIBITORS.
 PREVENTION
• TOBACCO SMOOKE-AVOID
• SENSITIZERS-FOOD,CHEMICALS-AVOID
• HOUSE DUST MITE- WASH SUNDRY,IRON LINENS,NO
CARPETS,ENCASE PILLOWS MATRASSES.
• ANIMAL FUR-AIR FILTERS,REMOVAL OF ANIMALS.
• COAKROACH- CLEAN HOME,SPRAY PESTICIDES.
• OUTDOOR POLLEN –INDOORS
• INDOOR- AVOID DAMP CONDITION
 PROBLEMS
• Health care providers-availability/knowledge.
• Facilities
• Cost
• Loss to follow up.
• THANKS