This document provides information on bronchial asthma (BA), including: 1. BA is a chronic inflammatory disease of the airways characterized by variable and recurring symptoms of wheezing, coughing, chest tightness, and shortness of breath in response to triggers. 2. Pathogenesis involves chronic airway inflammation, intermittent airflow obstruction from bronchoconstriction and remodeling, and bronchial hyperresponsiveness. Principal cells involved are mast cells, eosinophils, and T lymphocytes. 3. Classification of BA severity is based on symptoms, nighttime symptoms, lung function measurements, and exacerbations. Clinical evaluation includes patient history, physical exam assessing respiratory distress, and tests to measure lung function such

1. Bronchial Asthma
Lecturer Pavlova J.M.

2. INTRODUCTION TO THE
RESPIRATORY TRACT

3. Normal lung

4.  The right and left main bronchi divide into
lobar bronchi.
 The lobar bronchi divide into
tertiary/segmental bronchi, each of which
supplies a bronchopulmonary segment.
 The segmental bronchi divide into primary
bronchioles which divide into terminal
bronchioles and then divide into
respiratory bronchioles, which go on to
divide into alveolar ducts.
 Each alveolar duct divides into five or six
alveolar sacs.
 The alveolar sacs are made up of alveoli.
The alveolus is the basic anatomical unit of
gas exchange in the lung.
 Beyond terminal bronchiole gas exchange
occurs
 The distal airspaces are kept open by
elastic tension in alveolar walls

5. Function of lungs
• Gas exchange (O2, CO2)
– Depends on compliance
(stretchability) of lungs
– Can only occur in alveoli that
are both ventilated and
perfused

7. Spirometer
 is an equipments used for measuring
the volume of air inspired and expired by
the lungs ( Pulmonary Function Tests)

8. Spirometry (pulmonary physiology)
• Forced expiratory volume (FEV1): volume of air blown
out forcibly in 1 second. A function of large airways.
Dependent on body size.
• Vital capacity (VC): total volume of expired air.
• Diffusing capacity or Transfer factor of the lung for
carbon monoxide (DLCO or TLCO): absorption of carbon
monoxide in one breath (gas exchange). It is dependent
on the concentration of blood haemoglobin, which has a
strong affinity for CO and it assesses the ability of the
lungs to exchange gas efficiently.

9. Definition
• According to the modern view, BA of any severity
is a chronic inflammatory disease accompanied
by hyper-responsiveness and hypersensitivity of
the bronchi.
• Clinical manifestations of the disease include
periodical expiratory or mixed dispnea (asphyxia)
due to obstruction of the airways caused by
constriction of the bronchi, excessive mucus
secretion, and pulmonary edema.

10. • At least 300 million patients worldwide suffer
from BA.
• In 2019 asthma affected approximately 262
million people and caused approximately
461,000 death
• In the Russian Federation, according to a
recent epidemiological study, the prevalence
of BA among adults is 6.9% , and among
children and adolescents – about 10%

12. ICD-10
J45 Asthma
• J45.0 Predominantly allergic asthma
• J45.1 Nonallergic asthma
• J45.8 Mixed asthma
• J45.9 Asthma, unspecified
J46 Status asthmaticus

13. • Asthma is a long-term inflammatory disease of
the airways of the lungs.
• It is characterized by variable and recurring
symptoms, reversible airflow obstruction, and
easily triggered bronchospasms.
• Symptoms include episodes of wheezing,
coughing, chest tightness, and shortness of
breath. These may occur a few times a day or a
few times per week.
• Depending on the person, asthma symptoms may
become worse at night or with exercise

14. Hygiene hypothesis
• The hygiene hypothesis attempts to explain the increased rates of asthma
worldwide as a direct and unintended result of reduced exposure, during
childhood, to non-pathogenic bacteria and viruses. It has been proposed
that the reduced exposure to bacteria and viruses is due, in part, to
increased cleanliness and decreased family size in modern societies.
Exposure to bacterial endotoxin in early childhood may prevent the
development of asthma, but exposure at an older age may provoke
bronchoconstriction. Evidence supporting the hygiene hypothesis includes
lower rates of asthma on farms and in households with pets.
• Use of antibiotics in early life has been linked to the development of
asthma. Also, delivery via caesarean section is associated with an
increased risk (estimated at 20–80%) of asthma – this increased risk is
attributed to the lack of healthy bacterial colonization that the newborn
would have acquired from passage through the birth canal. There is a link
between asthma and the degree of affluence which may be related to the
hygiene hypothesis as less affluent individuals often have more exposure
to bacteria and viruses.

15. Genetic
• Family history is a risk factor for asthma, with many different
genes being implicated. If one identical twin is affected, the
probability of the other having the disease is approximately
25%. By the end of 2005, 25 genes had been associated with
asthma in six or more separate populations, including GSTM1,
IL10, CTLA-4, SPINK5, LTC4S, IL4R and ADAM33, among
others.Many of these genes are related to the immune system
or modulating inflammation.
• Some genetic variants may only cause asthma when they are
combined with specific environmental exposures. An example
is a specific single nucleotide polymorphism in the CD14
region and exposure to endotoxin (a bacterial product).
Endotoxin exposure can come from several environmental
sources including tobacco smoke, dogs, and farms. Risk for
asthma, then, is determined by both a person's genetics and
the level of endotoxin exposure.

16. Medical conditions
• A triad of atopic eczema, allergic rhinitis and asthma is called atopy. The
strongest risk factor for developing asthma is a history of atopic disease; with
asthma occurring at a much greater rate in those who have either eczema or
hay fever. Individuals with certain types of urticaria may also experience
symptoms of asthma.
• There is a correlation between obesity and the risk of asthma with both having
increased in recent years. Several factors may be at play including decreased
respiratory function due to a buildup of fat and the fact that adipose tissue
leads to a pro-inflammatory state.
• Beta blocker medications such as propranolol can trigger asthma in those who
are susceptible. Cardioselective beta-blockers, however, appear safe in those
with mild or moderate disease. Other medications that can cause problems in
asthmatics are angiotensin-converting enzyme inhibitors, aspirin, and NSAIDs.
Use of acid suppressing medication (proton pump inhibitors and H2 blockers)
during pregnancy is associated with an increased risk of asthma in the child.

17. • Different individuals react to various factors in different ways. Most
individuals can develop severe exacerbation from a number of triggering
agents.
• Home factors that can lead to exacerbation of asthma include dust,
animal dander (especially cat and dog hair), cockroach allergens and
mold. Perfumes are a common cause of acute attacks in women and
children. Both viral and bacterial infections of the upper respiratory tract
can worsen the disease. Psychological stress may worsen symptoms – it
is thought that stress alters the immune system and thus increases the
airway inflammatory response to allergens and irritants.
• Asthma exacerbations in school‐aged children peak in autumn, shortly
after children return to school. This might reflect a combination of
factors, including poor treatment adherence, increased allergen and viral
exposure, and altered immune tolerance.

18. Factors affecting the development and
manifestations of BA
Domestic factors
• Genetic predisposition to atopy
• Genetic predisposition to bronchial
hyperactivity
• Gender (in childhood, BA develops more often
in boys; in adolescence and adulthood-in
women)
• Obesity

19. Factors affecting the development and
manifestations of BA
Environmental factors
• Allergens: house dust mites, pet allergens, cockroach
allergens, fungal allergens, plant pollen, fungal allergens
• Infectious agents (mainly viral)
• Professional factors
• Aeropollutants: ozone, sulfur and nitrogen dioxides, diesel
fuel combustion products, tobacco smoke (active and
passive smoking)
• Diet: increased consumption of highly processed foods,
increased intake of omega-6polyunsaturated fatty acid and
reduced intake of antioxidants (in the form of fruits and
vegetables) and omega-3polyunsaturated fatty acid (as part
of fatty acids varieties of fish)

20. Pathogenesis
• Asthma is the result of
chronic inflammation of
the conducting zone of
the airways (most
especially the bronchi
and bronchioles), which
subsequently results in
increased contractability
of the surrounding
smooth muscles.
• This among other factors
leads to bouts of
narrowing of the airway
and the classic symptoms
of wheezing.
• The narrowing is typically
reversible with or
without treatment.

21. • Other cell types
involved include: T
lymphocytes,
macrophages, and
neutrophils. There may
also be involvement of
other components of
the immune system
including: cytokines,
chemokines, histamine,
and leukotrienes
among others.

22. • Typical changes in the
airways include an
increase in eosinophils
and thickening of the
lamina reticularis.
• Chronically the
airways' smooth
muscle may increase
in size along with an
increase in the
numbers of mucous
glands.
Obstruction of the lumen of a bronchiole by
mucoid exudate, goblet cell metaplasia, and
epithelial basement membrane thickening in a
person with asthma.

24. BRONCHIAL ASTHMA
• It is a triad of:
1. intermittent and reversible airway obstruction
2. chronic bronchial inflammation with eosinophils
3. bronchial smooth muscle cell hypertrophy and hyper-
reactivity
• Primarily targets the bronchi and terminal bronchioles
• Most common chronic respiratory disease in children.
• More common in children than adults

25. Pathogenesis of Bronchial Asthma
complex and involves the following components:
1. Chronic airway inflammation
2. Intermittent airflow obstruction. Airflow
obstruction can be caused by a variety of
changes, including acute bronchoconstriction,
airway edema, chronic mucous plug formation,
and airway remodeling
3. Bronchial hyper-responsiveness causes
exaggerated bronchoconstriction. The degree of
airway hyper-responsiveness generally
correlates with the clinical severity of asthma.

26. Pathogenesis of Bronchial Asthma
Principal cells in asthma: mast cells, eosinophils,
epithelial cells, macrophages, and activated T
lymphocytes (TH2 subset) and neutrophils.
T lymphocytes play an important role in the
regulation of airway inflammation through the
release of numerous cytokines
The pathogenetic mechanisms have been best
studied in atopic asthma

27. Classification of BA by severity
Mild
Intermittent
Mild
Persistent
Moderate
Persistent
Severe
Persistent
Daily symptoms Symptoms < 1
times a week
or asymptomatic
between
exacerbations
Symptoms > 1
times a
week but <1
time a day
Daily use
of inhaled short-
acting
beta2-agonists.
Continual
symptoms.
Limited physical
activity
Nighttime
Symptoms
≤ 2 times a
month
> 2 times a
month
> 1 time a
week
Frequent
Asthma flare-ups
(exacerbations)
short periods Exacerbations
affect activity.
Lung Function PEF ≥80%
predicted,
PEF variability
<20%
PEF ≥80%
predicted
PEF variability
20-30%
PEF >60%-<80%
predicted
PEF variability
>30%
PEF ≤60%
predicted
PEF variability
>30%
Peak expiratory flow (PEF)

28. Clinical Evaluation of the Patient History
• Common respiratory symptoms in asthma
include wheezing, dyspnea, and cough.
• These symptoms often vary widely within a
particular individual, and they can change
spontaneously or with age, season of the year,
and treatment.
• Symptoms may be worse at night, and nocturnal
awakenings are an indicator of inadequate
asthma control.

29. • The classical description of bronchial asthma was given
in 1838 by G. I. Sokolsky.
• An attack of allergic asthma begins abruptly and
acutely and usually quickly subsides.
• Attacks of dyspnea developing against the background
of chronic infectious diseases of the respiratory ducts
(infectious-allergic asthma) are often not severe but
protracted.
• Attacks of dyspnea in bronchial asthma are quite
similar; they arise suddenly, gradually increase in
strength, and last from a few minutes to several hours
and even several days.
• A prolonged attack of asthma is called status
asthmaticus.
• Patients with uncomplicated bronchial asthma have no
complaints in the periods clear of attacks.

30. Complaints and history
• Typical complaints of patients are paroxysmal attacks of
expiratory dyspnea and cough especially after previous
contact with allergens or irritants.
• Attacks of asthma can be provoked by various odours, by
some foods and medicinal preparations.
• An attack of asthma can sometimes be provoked not by the
allergen itself but by memory of it or by remembrance of
the conditions under which the allergen acted in the past.
• Endogenic allergens causing attacks of asthma include
microbial antigens that are formed during various
inflammatory processes, such as sinusitis, chronic
bronchitis, chronic pneumonia, etc.
• Products of decomposition of microbes and tissue proteins
forming due to proteolytic process at the inflammatory
focus (especially in chronic infections of upper airways) can
act as allergens.

31. Symptoms
■ Cough with or without sputum (phlegm) production
■ Pulling in of the skin between the ribs when breathing (intercostal
retractions)
■ Shortness of breath that gets worse with exercise or activity
■ Wheezing
Emergency symptoms that need prompt medical help:
■ Bluish color to the lips and face
■ Decreased level of alertness, such as severe drowsiness or confusion, during an
asthma attack
■ Extreme difficulty breathing
■ Rapid pulse
■ Severe anxiety due to shortness of breath
■ Sweating
Other symptoms that may occur:
■ Abnormal breathing pattern --breathing out takes more than twice as long as
breathing in
■ Breathing temporarily stops
■ Chest pain
■ Tightness in the chest

32. Physical Examination
• It is important to assess for signs of respiratory distress,
including tachypnea, use of accessory respiratory
muscles, and cyanosis.
• On lung examination, there may be wheezing and
rhonchi throughout the chest, typically more
prominent in expiration than inspiration. Localized
wheezing may indicate an endobronchial lesion.
• Evidence of allergic nasal, sinus, or skin disease should
be assessed.
• When asthma is adequately controlled, the physical
examination may be normal. Signs of chronic
bronchitis, pneumosclerosis, and lung emphysema can
be revealed in such patients in periods clear of
paroxysms.

33. Survey
• During such an attack, the patient has to assume a
forced position; he usually sits in bed, leans against
his laps, his breath is loud, often whistling and noisy,
the mouth is open, the nostrils flare out.
• The veins of the neck become swollen during
expiration and return to norm during inspiration.
• At the peak of an attack, the patient begins coughing
with poorly expectorated thick and tenacious
sputum.
• The chest expands during an attack (to the size of the
chest during inspiration due to acute emphysema).
• Accessory respiratory muscles are actively involved in
the respiratory act.

35. Clinical finding
• Percussion of the lungs gives the bandbox sound, the lower
borders of the lungs are below normal, mobility of the
lower borders is sharply limited during both inspiration and
expiration. The borders of complete dullness of the heart
cannot be determined because of the acute inflation of the
lungs.
• Auscultation reveals many whistling rales against the
background of weakened vesicular respiration with a
markedly prolonged expiration. The whistling rales are
sometimes heard even at a distance.
• Tachycardia is usually observed.
• By the moment the attack reduced the sputum thins and
expectoration becomes easier: high and dry rales in the
lungs determined by auscultation decrease to give ways to
low buzzing and often moist nonconsonant rales of various
calibers; the attack of dyspnea gradually abates.

36. • X-ray examination during an attack of asthma
shows high translucency of the lung fields and
limited mobility of the diaphragm.
Hyperinflated
lung

37. Sputum analysis may reveal 40% to 60 %of eosinophils and often
Curschmann spirals (casts of the distal airways) and Charcot-Leyden crystals.
Coiled, basophilic plugs of
mucus formed in the lower
airways and found in sputum
and tracheal
Eosinophilic needle-shaped
crystalline structures.

38. Tests to measure lung function
■ Spirometry. This test estimates the narrowing of the bronchial tubes
by checking how much air the patient can exhale after a deep breath
and how fast he can breathe out.
■ Peak flow. A peak flow meter is a simple device that measures how
hard you can breathe out. Lower than usual peak flow readings are a
sign the lungs may not be working as well and that the asthma may be
getting worse.

39. • Spirometry detects FEV1 or PEF > 80% predicted,
PEF variability 20–30%.
• The level of bronchial obstruction increases during
provocative inhalation tests (allergens, irritants,
histamine, acetylcholine) and decreases after β-
adrenergic agonist inhalation.

40. Additional tests
■ Methacholine challenge. Methacholine is a known asthma
trigger that, when inhaled, will cause mild constriction of the
airways. If the patient reacts to the methacholine, he likely has
asthma. This test may be used even if your initial lung function
test is normal.
■ Imaging tests. A chest X-ray and high-resolution computerized
tomography (CT) scan of the lungs and nose cavities (sinuses)
can identify any structural abnormalities or diseases (such as
infection) that can cause or aggravate breathing problems.

41. Additional tests
■ Allergy testing. This can be performed by a skin test or blood test.
Allergy tests can identify allergy to pets, dust, mold and pollen. If
important allergy triggers are identified, this can lead to a
recommendation for allergen immunotherapy.
Positive wheel
and flare
reaction

42. Additional tests
■ Provocative testing for exercise and cold-
induced asthma. In these tests, the doctor
measures the airway obstruction before and
after the patient performs vigorous physical
activity or take several breaths of cold air.
■ Common blood test during attacks detects
moderate lymphocytosis and eosinophilia.
■ Physical, X-ray, and laboratory examinations
may reveal no changes except eosinophilia of
the blood at the periods clear of attacks.

43. COMPLICATIONS OF ASTHMA
 Airway remodeling: some persons with long standing asthma
develop permanent structural changes in the airway with a
progressive loss of lung function that increase airflow
obstruction and airway responsiveness.
 Superimposed infection i.e. pneumonia
 Chronic bronchitis (i.e.Asthmatic bronchitis: chronic bronchitis
with superimposed asthma)
 Emphysema AND pneumothorax
 Bronchiectasis
 Respiratory failure requiring intubation in severe
exacerbations i.e. status asthmaticus
 In some cases cor pulmonale and heart failure develop.

44. Some clinical variants of bronchial
asthma
• It has been divided into two basic types:
1. Extrinsic asthma.
2. Intrinsic asthma.
• Sometimes extrinsic and intrinsic can co-exist in the same patient

45. Extrinsic/ Allergic BA
• It is also known as allergic, immune mediated, atopic or reaginic
asthma.
• Bronchospasm is induced by inhaled antigens, usually in children
with a personal or family history of allergic disease (e.g., eczema,
urticaria, or hay fever).
• Atopic (allergic) asthma is the most common type and begins in
childhood
• Other allergic manifestation may be present: allergic rhinitis,
urticaria, eczema.
• Skin test with antigen is positive and results in an immediate wheel
and flare reaction
• Other family members are commonly also affected immune related
with the involvement of TH2 subset of CD4+ T cells

46. Allergic (extrinsic, occupational) bronchial
asthma
• - 2-15% of all asthmatics patients.
• Respiratory symptoms, and variable airflow
limitation and/or bronchial hyperresponsiveness
due to exposure in a particular place separate
from those outside the work/or living
environment.
• It should be considered in any case of adult-onset
asthma or worsening asthma.
• Allergic asthma characteristics are immediate and
last phase allergic reactions; indoor, outdoor
allergens, seasonal variation. It may be due to
chemicals, metals, dusts, pollens, insects, proteins.

47. Occupational bronchial asthma
• Occupational bronchial asthma is related to
industrial chemicals, animal plants and proteins.
• Respiratory symptomes intensify when a worker
returns from a weekend off or vacation.
• It is very common with cotton dust endotoxin in
byssinosis, also in sawdust, hemp, or any factory
processing raw materials

48. Nonallergic (intrinsic) bronchial
asthma
• Nonallergic (intrinsic) bronchial asthma is related
to upper respiratory infection, purulent rhinitis,
sinusitis, cold air, odors (tobacco smoke),
perfumes, household cleaning agents,
insecticides, fresh paint, air pollution, GERD
(gastro-esophageal reflux disease).

49. • Mixed bronchial asthma is combination of allergic
and nonallergic bronchial asthma.
• Exercise induced bronchial asthma: Contributing
factors are hard exercise (>80% max heart rate for
>6-8 min), cold air, low humidity (dry air), airborne
particles (allergens, dust, irritants, auto exhaust,
commercial pollutants like sulfur, dioxide, nitrogen
dioxide, ozone).
• Exacerbation of exercise induced bronchial asthma
may be due to respiratory infections, fatigue,
emotional stress, athletic overtraining (especially
running > cycling >swimming)

50. • Aspirin induced bronchial asthma is characterized by
bronchial hypersensitivity and hyperresponsiveness
to acetylsalicylic acid and to most of other non-
steroid anti-inflammatory drugs (NSAID).
• Aspirin triad (including acetylsalicylic acid sensitivity,
chronic nasal polyps, asthma) is very typical.
• Cough variant asthma are seen in 40% of those who
present with isolated chronic nonproductive cough
with normal chest X-ray.
• These patients need in spirometry examination to
precise the level of bronchial obstruction.
Aspirin induced bronchial asthma

51. Diagnosis
• Diagnosis of bronchial asthma is based on clinical
picture of paroxysmal syndrome of bronchial
obstruction confirmed by data of spirometry
demonstrating reversible airway obstruction.
• Bronchial asthma should be considered in anyone
who wheezes (whistling rales); it is the likeliest
diagnosis when typical paroxysmal wheezing
starts in childhood or early adulthood and is
interspersed with asymptomatic intervals.
• A family history of allergy or asthma can be
elicited from most asthmatics.

52. • The diagnosis of asthma is established by demonstrating
reversible airway obstruction. Reversibility is traditionally
defined as a 15% or greater increase in FEV1 after two puffs
of a β-adrenergic agonist.
• When the spirometry results are normal at presentation,
the diagnosis can be made by showing heightened airway
responsiveness to challenges with histamine, acetylcholine,
or isocapnic hyperventilation of cold air.
• Positive wheal-and-flare reactions to skin tests can be
demonstrated to various allergens, but such findings do not
necessarily correlate with the intrapulmonary events.
• Sputum and blood eosinophilia and measurement of serum
IgE levels are also helpful but are not specific for asthma.
• Chest roentgenograms showing hyperinflation are also
nondiagnostic.

53. Management of asthma
General principals:
• The long-term goals of asthma management are
risk reduction and symptom control
• The aim is to reduce the burden of the patient
and to reduce their risk of asthma-related death,
exacerbations, airway damage and medication
side-effect
• Assessment of a patient with asthma includes not
only symptom control, but also the patient’s
individual risk factors and comorbidities
• Medication:

55. Medications for asthma treating
2 reliever choices across asthma severity
• Track 1, with low dose inhaled corticosteroids
(ICS) as the reliever, is the preferred approach
• Track 2, with short-acting betta2-agonist
(SABA) as the reliever, is an alternative
approach

56. Preferred
therapy
As needed
low dose ICS
or SABA
Preferred
therapy:
Daily low dose
ICS or as needed
low dose ICS-
SABA
Other controller
options: Daily
leukotriene
receptor
antagonism
(LTRA)
Preferred therapy:
low dose ICS-LABA
Other controller
options: medium
dose ICS or low
dose ICS+LTRA
Preferred therapy:
medium dose ICS-
LABA
Other controller
options: high dose
ICS, add-on
tiotropium or add-
on LTRA
Preferred
therapy: high
dose ICS-LABA
Refer for
phenotypic
assessment
Other controller
options: low
dose OCS but
consider side
effect
Symptoms
less than twice
a month
Symptoms
twice a month
or more but less
than daily
Symptoms
most days or
waking with
asthma
once a week or
more
Symptoms
most days or
waking with
asthma
once a week or
more or low lung
function
STEP 5

57. Patient’s education
Every patient should also be trained in essential
skills and guided asthma self-management
including:
• Asthma information
• Inhaler skills
• Adherence
• Written asthma action plan
• Self-monitoring of symptoms and/or peak flow
• Regular medical review

58. Non-pharmacological treatment
■ Removal of allergens (especially pets with feathers or fur)
■ Structured patient education: improved self-management
leading to better symptomatic control, reduction of the number
of asthma attacks and emergency situations, improved quality
of life, and improvement in various other parameters of
disease course including days taken off from school or work
and days spent in hospital
■ Physical training (reduction of asthma symptoms, improved
exercise tolerance, improved quality of life, reduced
morbidity)
■ Respiratory therapy and physiotherapy (e.g., breathing
techniques, pursed-lip breathing)
■ Smoking cessation (with medical and non-medical aids, if
necessary)
■ Psychosocial treatment approaches (family therapy)
■ For obese patients, weight loss