BRONCHIAL

ASTHMA
BY

DR JUMBO J
Associate Prof/Consultant Physician
NDU,WILBERFORCE ISLAND,BAYELSA STATE

1
INTRODUCTION
 Asthma has puzzled and confused
physicians from the time of
Hippocrates to the present day.
 The word “asthma” comes from a
Greek word meaning “panting”, but
reference to asthma can also be
found in ancient Egyptian, Hebrew
and Indian medical writings.

2
 There were clear observations of
patients experiencing attacks of
asthma in the 2nd century, and
evidence of disordered anatomy in
the lung as far back as the 17th
century.

3
 Asthma is a common chronic disease
 Commoner in males before puberty
 Male preponderance changes to female
preponderance during adolescence
 Asthma presenting in middle age occur
slightly more in females than males

4
How common is asthma?
 Asthma is a global disease
 The prevalence of asthma vary from
country to country,regions and
geographical areas within a country.
 WHO/GINA estimates that up to 334M
people around the world are affected
and this global prevalence is expected
to increase to 400M by 2025.

5
 Suggested reasons for the increasing
prevalence of bronchial asthma are
1. Improve knowledge and diagnosis of
bronchial asthma
2. Increased rural to urban migration
3. Increase in air pollution
4. Increase in smoking
5. Reduced childhood infections(HYGIENE
HYPOTHESIS).
6
How common is Asthma?

 Mean prevalence of clinical asthma

in W/A is 5.7%.
 North Africa is 2.9%
 5.4% of Nigerians are asthmatic
Highest prevalence of asthma in
Africa is in S/A-Prevalence rate of
8.1%.
7
What is asthma?

The Global Initiative for Asthma (2017), after

various modifications defined Asthma as follows:
Asthma is a heterogeneous disease usually
characterized by chronic airways
inflammation. It is defined by the history of
respiratory symptoms such as wheeze,
shortness of breath, chest tightness and
cough that vary over time and in intensity,
together with variable expiratory airflow
limitations.

International Consensus report on diagnosis asthma

8
What is asthma?

Primary care definition:

Asthma is characterized by the periodic
occurrence of one or more of the following
symptoms established by a patient’s
medical history: wheezing, dyspnoea or
coughing,chest tightness combined with
one or more of the following objective
criteria: reversible airway obstruction or
clinical peak flow variability of more than
20%.
9
Asthma mortality
 It is estimated that about one of 250 deaths globally
is due to asthma. Mortality in developing countries is
higher.
Causes:
 Sub-sensitivity to asthma
 Delay in seeking medical care
 Inadequate access to health care
 Increased incidence of viral infection
 Over use of beta-agonist medications
 Poor management of acute severe asthma
 Increase in air pollution

10
What causes asthma?
 Predisposing Factors:
-Allergy :tendency to produce
abnormally high level of IgE in
response to exposure to
substances in the environment.
-Hereditary: strong family
history.
11
 Any potential risk factor must
eventually interact with an
underlying, genetically determined
pathway to result in the
manifestation of disease. A number
of different exposures interact with
various genetic backgrounds in a
range of racial or ethnic groups will
eventually result in changes in the
12
 incidence of asthma as a result of
changes in pathways involving atopy,
airway inflammation, airway
hyperresponsiveness, or other still
unknown factors

13
 In a large proportion of patients,
asthma starts in the first years of life.
New-onset asthma also occurs during
puberty and later in adulthood, but
many cases of asthma in adults
represent the reappearance of
symptoms in persons who were
transiently free of problems during
adolescence and young adulthood..
14
 Some Substances are capable of
stimulating the immune system to
react by producing specific IgE
antibodies.
 When exposed to such an allergens,the
T-lymphocytes-Th2-Cytokines---act on
B-lymphocytes and Plasma cells and
stimulate them to produce specific IgE.

15
 Th2 lymphocytes that produce
interleukin 4, 5, 9 and 13 are
increased in the airway in asthma.
Inflammatory cells are attracted to
the airway by chemokines and then
bind to adhesion molecules on the
vessel endothelium. From there, they
migrate into the local tissue.

16
Sensitization occurs and on exposure to
the allergens again inflammatory
process is triggered by cell mediators
from mast cells activated by the rxn
b/w the allergen and lgE.
Mediators are also produced by
macrophages,lymphocytes and
Eosinophils.

17
 The inflammatory allergic response
consist of
- Constriction of smooth muscles
-Mucus secretion
- Fluid leakages
-Oedema of the bronchial wall
Mucosa becomes thickened,inflammed
and oedematous.
18
Causal Factors
 Indoor Allergens:House dust
mites(beddings,carpets and
rugs)
,moulds,animals(cats,dogs,rats),ins
ects(cockroaches).
 Outdoor Allergens:Pollens,mould.
 Workplace exposures to chemicals.

19
Cats are the most problematic domestic
pet for people with
asthma.

20
Swimming is the exercise least likely to
provoke exercise-induced
asthma.

21
Contributing Factors
Indoor air pollution:
Environmental tobacco smoke
Cooking and/or heating biomass fuel
Outdoor air pollution
Acute Respiratory Infection
particularly
due to respiratory syncytial virus

22
 Obesity is a major cause of morbidity
that has been increasing in
prevalence over the past few
decades. There is increasing evidence
relating body-mass index to the
prevalence and incidence of asthma
in both children and adults.

23
 Studies have examined dietary
intakes of fruits, vegetables, cereals
and starches, various fatty acids,
vitamin A, vitamin C, vitamin E,
minerals (sodium, magnesium,
copper, zinc, and selenium), and
antioxidants for possible associations
with asthma.

24
Protecting Factors
 Living in rural areas, on a farm in contact
with livestock(Hygiene Hypothesis).
 Exposure during the first yrs of life to
domestic pets. It may be that early
exposure helps in maturation of the
immune system
 Having older siblings or being exposed in
early life to older children(Hygiene
Hypothesis).

25
 Prolonged exclusive breastfeeding
was once thought to protect against
allergic diseases,including asthma,
but this is no longer thought to be the
case.

26
Trigger Factors
 These are factors that are capable of triggering
attack and they include:
 Irritants:smoke from wood ,household
aerosols,vehicle pollution,tobbacco smoke
 AcuteBacterial and Viral infection in upper
and lower airways,in both children and adults.
 Chronic infestation with helminths may also
confer protection, but short-lived episodes of
infestation may exacerbate atopic disorders.

27
 Exercise
 Weather changes
 Gastro-oesoghageal reflux dx
 Pregnancy,menstruation
 Stress and emotional situations
 Drugs: Aspirin,NSAIDs,B-blockers.

28
 Types of Asthma
 Childhood onset: Most asthma starts in
childhood, usually on an atopic
background. Tends to have significant
variability and identifiable precipitants.
 Adult onset: Often a relapse of earlier
asthma, but may have initial onset at any
age. Often more persistent with fewer
obvious precipitants except infection
29
 Nocturnal Asthma: Common in all
types of asthma, related to poor
overall control and increased reactivity.
 Cough-variant Asthma: Cough is a
common symptom and may precede
airflow obstruction. Asthma should be
considered as the cause of chronic
unexplained cough.

30
 Exercise-induced: Common
precipitant, exercise may be the only
significant precipitant in children.
 Brittle Asthma
Type 1: chaotic uncontrolled asthma
with very variable peak flow.
Type 2: sudden severe deterioration
from a background of good control.
31
 Aspirin-sensitive Asthma: May be
associated with later onset and nasal
polyps.
 Occupational Asthma. Occupational
asthma forms a subset where there is
an identifiable cause which may work
through an irritant or immunological
trigger.

32
Clinical Features
 The 4 cardinal symptoms of asthma
are: cough,breathlessness,chest
tightness and wheeze.
 These symptoms are none specific but
are episodic,worse at night and early
hours of the morning.
 Symptoms that disappear either
spontaneously or after taking
bronchodilators.
33
 A hx of coughing spells not explained
by other causes.
 Symptoms brought on by a variety of
factors such as dust ,cold air , sudden
changes in the weather ,frying oil
odours etc.
 A pt with a personal hx of
allergies(rhinitis,conjuctivitis,pharyngiti
s and eczema)or a family hx.
34
35
 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

36
Barnes PJ
Why is asthma often worse at night?

 Cause not fully established (may involve effects of

increased vagal tone, decreased epinephrine, cortisol
and increased histamine at night)

 Exposure to allergens in the bedroom (dust mites)

 Delayed allergic response

 Chronic sinus problems and/or post-nasal drip

 GERD

37
Why is asthma often worse at night?

 Airway cooling at night (↓ in body temp)

 Sleep apnea – brief repetive cessation of

breathing during sleep by URT obstruction

 increased nighttime airway hyperreactivity

decreased mucocilliary activity

 Airway inflammation is also increased at night

→ airway narrowing (cause is not known)
38
Diagnosing and classifying
asthma
 Pulmonary Function Test:
-Spirometry is useful esp in assessing
reversibility.A reversibility of >15%.
FEV1 <80%predicted value and FEV1/FVC
ratio <70% establishes the diagnosis.
- Peak Expiratory Flow(PEF) is useful in
diagnosis.A variability of >20% is
significant.

39
 Exercise Test :An exercise test may consist of
baseline peak flow measurements,then 6 minutes
of vigorous supervised exercise such as running,
followed by peak flow measurements for 30
minutes afterwards. 6min walk on treadmill >15%
decrease in PEF.
 Cold air challenge, isocapnoenic hyperventilation
 Skin Test to identify allergens
 Allergen provocation tests
 Histamine or methocholine bronchial provocation
test –Hyperresponsiveness.

40
 Chest X-Ray:Normal in most cases.
Useful in exluding
chest infection and complication such
as pneumothorax.Features of
hyperinflation may be seen but is
rare.

41
How is asthma classified?
According to British Thoracic Society (BTS)
step 1 – includes ‘trivial’ and potential. Asthma that can
be controlled adequately by intermittent treatment, taken
as needed.
step 2 – asthma that is adequately controlled by regular
inhaled anti-inflammatory treatment (usually inhaled
steroids)
step 3 – asthma that is adequately controlled by regular
inhaled anti-inflammatory treatment + regular inhaled
long-acting β2 –agonists.
step 4 – asthma that requires step 3 treatment together
with additional therapies
step 5 – asthma that requires chronic oral steroid
treatment.

42
 ‘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

43
GINA Guidelines 1998
44
 Modern view of asthma
Allergen

Macrophage/
dendritic cell Mast cell

Th2 cell Neutrophil

Eosinophil
Mucus plug
Epithelial shedding
Nerve activation

Subepithelial
fibrosis
Plasma leak
Sensory nerve
Oedema activation
Vasodilatation Cholinergic
Mucus New vessels reflex
hypersecretion
Hyperplasia Bronchoconstriction
Hypertrophy / hyperplasia

45

Barnes PJ
Asthma Inflammation: Cells and Mediators

46
Source: Peter J. Barnes, MD
Inflammatory processes

47
Asthma - an inflammatory
disease

48
‘Clinical’ exacerbation

PEF

Mild attack

Acute severe
attack

Exacerbation

Days

49
 Levels of Asthma Control
Partly controlled Uncontrolle
Characteristic Controlled (Any present in any
week)
d

Daytime None (2 or More than

symptoms less / 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 More than
“reliever” any week
less / week) twice / week
treatment
< 80% predicted
Lung function
Normal or personal best (if
(PEF or FEV1)
known) on any day
One or more / year 1 in50any
Exacerbation None
week
Treatment objectives

 No chronic symptoms

 No asthma attacks

 No emergency visits

 Minimal need for quick relief (as needed) ß2-

agonist

51
Treatment objectives

 Maintain normal physical activity including

exercise

 Maintain lung function as close to normal as

possible

 Minimal (or no) adverse effects from medicine

52
Goals of asthma treatment

 Prevent chronic and troublesome

symptoms

 Maintain (near-) normal pulmonary

functions

 Maintain normal activity levels

53
Goals of asthma treatment

 Prevent recurrent exacerbations of

asthma

 Provide optimal pharmacotherapy

with minimal or no adverse effects

 Meet patients’ and families’

expectations
54
Definition of well-controlled asthma

 Asthma symptoms twice a week or less

 Rescue bronchodilator use twice a week

or less

 No nighttime or early morning awakening

55
Definition of well-controlled asthma

 No limitations on exercise, work, or

school

 Well controlled asthma by patient and

physician assessment

 Normal or personal best PEF or FEV1

56
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

57
Simplified guidelines for the pharmacotherapy of
asthma(Step ladder management)
Step 1: Short-acting β-agonist as needed (indicated for all
patients)

Step 2: Low-dose ICSs, leukotiene modifiers, theophylline,

cromolyn, or nedocromil

Step 3: Low-dose/medium-dose ICSs plus inhaled LABA or

medium-dose ICSs; low-dose/medium-dose ICSs
plus either leukotriene modifier or theophylline

Step 4 High-dose ICSs and LABA plus systemic cor

ticosteriods if needed (consider monoclonal anti-IgE)

58
 Levels of Asthma Control
Partly controlled Uncontrolle
Characteristic Controlled (Any present in any
week)
d

Daytime None (2 or More than

symptoms less / 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 More than
“reliever” any week
less / week) twice / week
treatment
< 80% predicted
Lung function
Normal or personal best (if
(PEF or FEV1)
known) on any day
One or more / year 1 in59any
Exacerbation None
week
Pharmacological treatments

Eight types of drugs : -

 Β2 agonist (short acting)
 Corticosteriods
 Cromogens
 Β2 agonist (long acting)
 Theophyllines
 Anticholinergic drugs
 Leukotriene receptor antagonists
 Other drugs (anti IgE, antibodies to TNFα)
60
 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

61
Non-pharmacological treatment

 Homeopathy
 Yoga
 Hypnosis
 Acupuncture
 Chiropractic
 Bronchial thermoplasty

62
 ‘Growing out’ of asthma Over half
the children whose wheezing is
infrequent will be free of symptoms
by the time they are 21 years old, but
of those with frequent, troublesome
wheezing only 20% will be symptom
free at 21, although 20% will be
substantially better.

63
 In 15% of patients, asthma becomes
more troublesome in early adult years
than it was in childhood.
 Asthma is less likely to go into
remission in patients with a strong
family history of atopy or a personal
history of other atopic conditions, low
respiratory function, onset after the
age of 29 and frequent attacks.
64
ACUTE SEVERE ASTHMA
 Acute Severe Asthma is an asthmatic
exacerbation that is severe enough to
persist despite the pts optimum use of
his or her conventional medications
and necessitate RX in an emergency
room.
Features:
-Inability to complete a sentence in
one breath
65
- RR>25/min
- Tachycardia>110/min
- PEF<50% predicted normal or best.
Features of life threatening
attacks
are:
-A silent chest,cyanosis,feeble resp
effort,exhaustion,confusion,coma
66
-Bradycardia,hypotension.
-PEF<30% predicted or best.
Treatment :
The first line mgt is summarized in
the acronym SOS.
S-Salbutamol(bronchodilator,
nebulized )dose 2.5-5mg.Repeat
every 20-30min.
67
O-Oxygen 40-60% continously via nasal
cannula or face mask.
S-Steroid, oral prednisolone 40-60mg,
iv Hydrocortisone 200mg 4-6 hourly
may also be given.If pt does not
respond, Second line mgt: -iv
Aminophyline 5-7.5mg/kg as a start
dose given slowly over 20-30 mins, then
0.5mg/kg as an infusion.
68
-Nebulized Ipratropium bromide
0.5mg can be added.
-iv Mgso4 1.2-2g over 20 mins.
Monitor pt with -PEF
- Measure oxygen saturation with
pulse oximeter
-Arterial blood gases.

69
REFERENCES
Global initiative for Asthma, Global Strategy for Asthma management and prevention NIH publication NO. 02-
3659 2007 (update).
Erhabor G.E, Agbroko S.O, Bamigboye P; Awopeju O.F. of prevalence of asthma symptoms among university
students 15-35years of age in OAU Ile-Ife, Osun State, Nigeria Journal of Asthma 2006; 43: 161-164.
John Rees. Global Prevalence of Asthma BMJ 2006; 332: 767-771
Falade AG, Olawuyi F, Osinnusi K, Onadeko BO. Prevalence and severity of symptoms of asthma, allergic
rhinoconjuctivitis and atopic eczema in secondary school children in Ibadan. ISAAC study. East Afr Med J

1998; 75:695-698
Kathryn D. Convers, Raymond G. Slavin. (2014) Attitudes toward allergy: what do the pediatricians think?. Annals of Allergy, Asthma & Immunology
113, 544-548
CrossRef

Strachan DP, Butland BK, Anderson HR. Incidence and prognosis of asthma and
wheezing illness from early childhood to age 33 in a national British cohort. BMJ
1996;312:1195-1199
CrossRef | Web of Science | Medline
2. Schaub B, von Mutius E. Obesity and asthma, what are the links? Curr Opin
Allergy Clin Immunol 2005;5:185-193
CrossRef | Web of Science | Medline

70
 3. Supichaya Pojsupap, Klevis Iliriani, Tatiana Zorub Assis Loreto Sampaio, Katie O’Hearn,
Thomas Kovesi, Kusum Menon, James Dayre McNally. (2014) Efficacy of high-dose vitamin D in
pediatric asthma: a systematic review and meta-analysis. Journal of Asthma, 1-9
CrossRef
 4. Fengying Zhang, Jingqing Hang, Buyong Zheng, Li Su, David C. Christiani. (2014) The
changing epidemiology of asthma in Shanghai, China. Journal of Asthma, 1-6
CrossRef
 Yazdanbakhsh M, Wahyuni S. The role of helminth infections in protection from atopic
disorders. Curr Opin Allergy Clin Immunol 2005;5:386-391
CrossRef | Web of Science | Medline
 van Strien RT, Engel R, Holst O, et al. Microbial exposure of rural school children, as assessed
by levels of N-acetyl-muramic acid in mattress dust, and its association with respiratory health.
J Allergy Clin Immunol 2004;113:860-867
CrossRef | Web of Science | Medline

 Eder W, von Mutius E. Hygiene hypothesis and endotoxin: what is the evidence? Curr Opin
Allergy Clin Immunol 2004;4:113-117
CrossRef | Medline
 Nathan R.A., Sorkness C.A. Kosinki M, et al. Development of the Asthma Control J. Allergy Clin.
Immunol 2004; 113 59-65.

71
THANK YOU FOR THE ATTENTION

72