BRONCHIAL ASTHMA AND COPD:

features of diagnosis and

treatment
 Anatomy of the lower
respiratory tract
Trachea
Main bronchi
Left
Bronchioles
Right

Bronchi
rigid due to Acinus
C- shaped
cartilage rings Alveoli

Acinus

Capillaries

Epithelium Alveolar space Alveoli

Capillaries
 Structure of the lower
respiratory tract
Trachea and main bronchi Bronchioles
Smooth muscle

Connective tissue

Cartilage
Mucous

Respiratory mucosa
Slime
Cilia
Secretory cells Epithelium
Ciliated cells

basement membrane
Submucosal layer
 Bronchial asthma

Global strategy for the

treatment and
prevention of
bronchial asthma
( GINA – 200 7 )
 Bronchial asthma is a chronic inflammatory
disease of the respiratory tract.

 Chronic inflammation causes a concomitant

increase in airway hyperresponsiveness, leading
to recurrent episodes of wheezing, shortness of
breath, chest tightness, and coughing, especially
at night and in the early morning.
 These attacks are associated with bronchial
obstruction, which is reversible either
spontaneously or with treatment.

GINA, 200 7
Prevalence of bronchial asthma

 Prevalence in children ranges from 0 to 30%.

The highest prevalence is in Australia, New
Zealand and England.

 There has been an increase in the prevalence

of asthma in adults, but it is not as dramatic
as in children.

 The prevalence of asthma in adults is higher

among women than among men.
 Prevalence
Frequency per 1000 population bronchial asthma

80
70 For all ages
60 0–4
5–14
50
15- 34
40 35– 64
thir 65+
ty
20
1980 1981 – 831984 – 861987 – 891990 – 921993 – 94
10

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In developed countries, living in
cities is associated with a
higher prevalence of asthma-
like symptoms
(hygiene hypothesis).

GINA, 200 7
 Factors leading to the
development of asthma
Patient-related factors
- Genetic (eg, genetic predisposition to atopy, airway
hyperresponsiveness)
- Obesity
- Floor

External factors
- Allergens
- domestic (house dust mites, fur-covered animals, substances released
during cooking, mushrooms, etc.)
- external (pollen, mushrooms)
- Infections (mostly viral)
- Occupational allergens
- Tobacco smoking (active, passive)
- Air pollution
- Diet
GINA, 200 7

GINA, 200 7
Internal factors (congenital)
Atopy is the production of increased amounts of IgE in
response to exposure to external allergens)

AD in children and adults is often found in association with

atopy , which is defined as the production of excessive
amounts of immunoglobulin E ( IgE ), designed to bind to
environmental allergens such as house mites, animal
proteins, pollen, and fungi.
Internal factors (congenital)

Sexual characteristics
In childhood, boys suffer from asthma more
often than girls.
The difference between the sexes
disappears after 10 years, when the
diameter/length ratio of the bronchi
becomes the same.
During puberty and beyond, bronchial
asthma develops more often in girls.
Triggers of bronchial asthma:
infections

ARVI Sinusitis Bronchitis

or bronchus and
olitis
 Triggers of bronchial asthma:
inhalant allergens
Animal
House dust dander
Furniture
materials

Pollen

Fungal House dust mite

allergens

Feather
pillow Cockroaches
both indoors and outdoors
Triggers of bronchial asthma:
inhaled irritants
Tobacco smoke, Cold
including passive air
smoking

Industrial rubber,
chemicals, metals Air pollution
Poorly ventilated room
heaters
 Triggers of bronchial asthma
Medicines Food Exercise stress
Aspirin allergens

Beta blockers (including Sulfites

eye drops) (food additives)
Pathophysiology of the airways
in bronchial asthma

Epithelium Mucosal surface

Submucosal gland
duct

basement
membrane

Blood vessel

Allergen- Smooth muscle

immunoglobulin
complex E
Hypersecretion of Contraction of smooth muscles
mucus leads to bronchospasm

Increased vascular
permeability leads
to edema
Allergen Pathogenesis of bronchial asthma:
Allergen-IgE clinical manifestations
complex

Release of mediators
mast cell
Airways

Norm Early asthmatic Late asthmatic Chronic

response (minutes): response (watch): illness
bronchospasm, inflammation, swelling, (months):
vasodilation epithelial damage chronic inflammation,
basement
membrane fibrosis
Pathogenesis of bronchial asthma

 Inflammation of the airways in asthma is characterized

by an increase in the number of activated eosinophils,
mast cells, macrophages and T-lymphocytes in the
mucous membrane and lumen of the bronchial tree.

In parallel with the chronic inflammatory process,

bronchial damage stimulates a repair process, leading
to structural and functional changes called airway
remodeling.

GINA, 200 7
Components of bronchial obstruction:

 Airway hyperresponsiveness
 Swelling of the bronchial wall
 Chronic mucus obstruction
 Remodeling of the bronchial wall.
 Classification of bronchial asthma.

By etiology:
- Allergic (atopic, exogenous)
- Non-allergic (infection-dependent, endogenous)
- Aspirin asthma (nasal polyposis, intolerance to
NSAIDs, asthma attacks)
 Classification of bronchial asthma
by severity
T severe persistent asthma
• Constant symptoms • Physical activity is limited
• Frequent exacerbations by manifestations of bronchial asthma
• Frequent nighttime symptoms • PSV is less than 60% of expected
• Fluctuations in PEF more than 30%
Moderately severe persistent asthma
• Daily symptoms: flare-ups disrupt activity and • Daily intake of  2 - short-acting
sleep agonists
• Nighttime asthma symptoms occur more than • PSV 60-80% of due
once a week • PSV fluctuations 20-30%
Mild persistent asthma
• Symptoms once a week or more often, • Nighttime asthma symptoms occur
but at least once a month more than twice a month
• Exacerbations may interfere with activity • PSV more than 80% of expected
and sleep • PSV fluctuations 20-30%
And intermittent asthma
• Symptoms less than once a week • No symptoms and normal
• Short exacerbations of the disease lung function between exacerbations
(from several hours to several days) • PSV more than 80% of expected
• Nocturnal symptoms 2 times a month or less often • Fluctuations in PEF less than 20%
 Criteria for determining the severity of
bronchial asthma

 Frequency of daytime symptoms

 Frequency of night symptoms
 Frequency and severity of exacerbations
 FEV indicators (FEV 1 and PSV values as a percentage of the
required values)
 Variability of FER parameters (FEV 1 and PEF)
 Extent of therapy and response to treatment
 GINA, 200 7
Asthma control levels
characteristics Controlled Partially uncontrollable
controlled

Daytime None (or < 2 per > 2 per week Presence of three
symptoms week) or more signs of
partially controlled
Activity Limit none any asthma in any
week
Night symptoms none any

Emergency drug None (or < 2 per > 2 per week

needs week)

Lung functions normal < 80% of

expected

exacerbation none 1 or more per 1 during any week

year
Clinical picture of bronchial
asthma
 The face becomes puffy, and
during the exhalation phase,
swelling of the neck veins
may be observed.

 The chest seems to freeze in

the position of maximum
inspiration. The act of
breathing involves auxiliary
respiratory muscles, which
help overcome existing air
resistance.
Criteria for diagnosing bronchial
asthma
 History and symptom assessment
 Clinical examination
 Pulmonary function test
 Spirometry
 Peak flowmetry
 Assessment of allergological status
 Scarification, intradermal tests, prick test
 IgE antibodies in blood serum
 X-ray of the lungs
 ECG
 Clinical blood test
 Sputum analysis
Objective status during an asthma attack

 With percussion lungs

 boxed percussion sound
 downward displacement of the lower borders of the
lungs
 a sharp restriction of their lung mobility
 Auscultation of the lungs
 Vesicular breathing is weakened
 Lots of whistling sounds

Percussion and auscultation of the heart

 The diameter of absolute dullness of the heart
decreases significantly
 muffled tones, tachycardia, accent of 2 tones over the
pulmonary artery.
Instrumental diagnosis of bronchial
asthma

UAC. Eosinophilia and leukocytosis

In sputum analysis. Increased viscosity,
eosinophils, Courshman spirals, Charcot-
Leyden crystals
X-ray of the lungs in a direct projection:
Emphysematous form of the chest.
Increased transparency of lung tissue
Spirometry: lung volumes
Maximum
forced inspiration
Full breath

Respiratory General
volume FVC
capacity
lungs

Full exhalation
Residual volume
Maximum
forced exhalation
Normal expiratory volume loop
Speed ( l / s ) For bronchial asthma:
FVC, MVL, FEV1 and
Tiffno index, PSVP were
sharply reduced with a
slightly reduced VC.
PSV
MOS 75

MOS 50

MOS 25

FVC volume ( l )
 Instrumental diagnosis of bronchial
asthma (continued)
 Skin tests to determine
sensitization to allergens (pollen,
household, epidermal)
 Determination of total IgE in the
blood (normally from 0-100 IU) by
enzyme-linked immunosorbent
assay
 Determination of specific IgE in
blood by enzyme-linked
immunosorbent assay
Main groups of drugs:
ANTI-INFLAMMATORY DRUGS
Inhaled glucocorticosteroids (Pulmicort, Becotide, Flexotide)
Combined glucocorticosteroids
 Seretide Multidisc (Flexotide + salmoterol)
 Symbicort Turbuhaler (Budesonide + formoterol)
 Foster (Beclomethasone + formoterol)
 Foradil Combi (budesonide + formoterol)

Mast cell membrane stabilizers /Cromones/

(sodium cromoglycate, nedocromil sodium)
 Preparations: Intal, Tailed, Kropoz
Combination drugs
 Preparations: Intal + (Intal + salbutamol), Ditek
BRONHOLYTICS
Short-acting β2-agonists (adrenergic agonists)
 Medicines: Salbutamol, Berotec, Berotec N, Asthmopen,
Terbutaline.
Long-acting β2 agonists
 Drugs: Formoterol (Foradil)
 Salmoterol (Serevent)
Methylxanthines (theophylline)

Anticholinergic drugs (Atrovent)

Antileukotriene drugs (montelukast (Singulair), zafirlukast)

Systemic glucocorticosteroids (prednisolone,
dexamethasone)
 GINA, 200 7
Stages of BA therapy
Stage 1 Stage 2 Stage 3 Stage 4 Level 5
Patient education
Environmental control
β2 - agonist, β2 - agonist, rapid acting on demand
rapid acting on
demand

Disease Control Choose one Choose one Add one or more Add one or both
Drug Options

Low dose ICS Low dose ICS + Medium or high Minimum possible
long-acting β2 - doses of ICS + dose of oral
agonist long-acting β2 - corticosteroids
agonist

Anti-leukotriene drug * Medium or high Antileukotriene Antibodies to IgE

doses of ICS drug

Low doses of ICS + Theophylline

antileukotriene sustained release
drug

Low dose ICS +

sustained release
theophylline
Methods of drug delivery for the treatment of
bronchial asthma
 Nebulizer - This device converts the liquid dosage
form of a drug into an aerosol form . Medicines
reach the bronchial mucosa bypassing the
gastrointestinal tract.
The dispersion of aerosols produced by most
nebulizers ranges from 0.5 to 10 microns
 Spacer - reduces the side effects of inhaled
corticosteroids, because delivers drugs to the
bronchi.
 Airolazer, turbohaler, multidisc, etc.
 spacer
nebulizer

Metered-
dose
aerosol
inhaler

Dosed
powder
inhaler
Peak flowmetry
 Using a peak flow meter at home to monitor bronchial
asthma by determining peak expiratory flow (PEF).
 Peak expiratory flow (PEF, l/min) is the maximum volumetric
expiratory flow rate measured during a forced expiratory
maneuver using a peak flow meter.

 Peak flowmetry is a reliable and objective method for:

- clarification of the diagnosis of bronchial asthma in laboratory
conditions
- assessing the effectiveness of treatment
- identifying early signs of an incipient exacerbation
Peak flow monitoring

Peak expiratory flow

(PEF) l/min.

Purposes of peak
flowmetry:
- clarification of the diagnosis of
bronchial asthma in laboratory
conditions
- assessing the effectiveness of
treatment
- identifying early signs of an
incipient exacerbation
 COPD is a disease characterized by
airflow limitation that is not
completely reversible.

 Airflow limitation is progressive and is

associated with an abnormal inflammatory
response of the lungs to inhaled pathogenic
particles or gases.
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 According to WHO, the prevalence of COPD among
men is 9.34:1000,
among women – 7.33:1000. people over 40
predominate .

There is a trend towards an increase in the incidence

of COPD in people over 40 years of age: only for
the period from 1990 to 1999. this figure increased
by 25% in men and 69% in women.
A further increase in incidence is predicted in the
coming years.

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 Inflammation

Small bronchus disease Destruction of parenchyma

(bronchiolitis) (emphysema)

Airflow limitation
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 COPD BEB
BA Cystic fibrosis
(2000)

COPD: obstructive bronchitis,

BA, Pulmonary emphysema, PEB, cystic fibrosis
(mid 90s)

Chronic obstructive bronchitis

Asthmatic bronchitis
Chronic pneumonia
(1975-1976)

Progressive airflow limitation

A.A. Vizel, I.Yu. Wiesel, 2007

 WWW.GOLD.COM

COPD
Bronchial asthma

Sensitizing agent Pathogenic agent

Inflammation,
characteristic of COPD
Inflammation. characteristic of asthma CD8+ T lymphocytes
CD 4+ T lymphocytes Macrophages, neutrophils
eosinophils
+ imbalance of proteinases-deproteinases

+ oxidase stress

Fully reversible Completely irreversible

Airflow limitation Airflow limitation
 Stage division is based on the degree of airflow
limitation determined by spirometry.

Increased risk of COPD ( O) normal spirometry, chronic

symptoms (cough, sputum production)

I /Mild/: FEV1/FVC <70%, FEV1≥80% predicted, chronic

cough and sputum production usually but not always

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II /middle/:
FEV1/FVC<70%, 50%≤FEV1<80% of predicted,
Chronic cough and sputum production usually, but not always
III /Severe/: FEV1/FVC<70%, 30%≤FEV1<50% of normal
values, chronic cough, shortness of breath and sputum
production usually, but not always.
IV /Extremely severe/ : FEV1/FVC<70%, FEV1<30% of normal
values, FEV1<50% of normal values in combination with
CDF or right ventricular failure.

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Main risk factors for COPD
External factors Internal factors
 smoking (both active and  Genetic predisposition ( α 1-
passive), antitrypsin deficiency ).
 long-term exposure to
occupational irritants (dust,  Airway hyperresponsiveness
chemical pollutants, fumes of
acids and alkalis)
 atmospheric and home air
 Lung growth during fetal
pollution ripening
 Infections
 Socioeconomic status

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Pathophysiology of COPD

Inflammation
(leukotrienes, proteinases, neuropeptides)

Mucus hypersecretion and cilia dysfunction

Airflow limitation
and pulmonary hyperinflation

Hypoxemia (Pa O 2 < 60 mm Hg) and hypercapnia

Pulmonary hypertension, cor pulmonale

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COPD complaints

CHRONIC DISCHARGE
COUGH Sputum

EXPIRATORY DYSPNEA

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Anamnesis.
1) Smoking index (pack/years) = (number of cigarettes
smoked per day * smoking experience (years))/20
ICC >10 pack/year is a risk factor for the development
of COPD
2) the presence of factors provoking exacerbation
3) presence of concomitant diseases
4) the effectiveness of previous treatment
Physical examination

Bronchial obstruction is indicated by

wheezing exhalation and prolongation
of expiratory time >5 seconds.
 Diagnostics
UAC: with exacerbation of COPD, neutrophilic leukocytosis with band shift,
accelerated ESR
Polycythemia (increased red blood cell count, high hemoglobin, low ESR,
increased hematocrit )
Microscopic examination of sputum: with exacerbation, the sputum
becomes more viscous and acquires a purulent character. Examined for
atypical cells.
A.G. Chuchalin, 2004
Arterial blood gas study :
This test is performed when FEV1 < 40% or there are signs of respiratory
failure or right heart failure.
Determination of α 1-antitrypsin
Assessed in patients diagnosed with COPD at a young age ( < 45 years).
If the serum concentration of α 1-antitrypsin is less than 15-20% of the normal
level, then there is a high probability that the patient suffers from a
homozygous type of deficiency α 1-antitrypsin.
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Chest X-ray:
1. Signs of hyperinflation:
Flattened diaphragm in lateral projection
Increased retrosternal space
2. Increased lung transparency
3.Rapid disappearance of the vascular pattern

Bronchoscopic examination
The same study (obtaining a secretion and bacteriological analysis of it)
should be resorted to in cases of frequently recurring exacerbations and
ineffectiveness of antibacterial therapy .

ECG - signs of overload of the right heart

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 COPD TREATMENT

Non-drug Medication

Treatment of COPD Treatment of COPD

STABLE FLOW PERIOD OF EXACTION

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Principles of treatment of stable COPD:

1.Stepwise intensification of therapy depending on the severity of

the disease

2. Regular treatment should be carried out for a long time at the

same level , if there are no pronounced side effects and the
course of the disease does not worsen

3. The response of an individual patient to therapy varies , so

regular monitoring of the patient and modification of therapy if
necessary is necessary.
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Bronchodilators are the basis of symptomatic
treatment of COPD (A)

Fenoterol

Short acting Salbutamol

β2 -agonists

Long-acting Formoterol

Salmeterol

short-acting Ipratropium bromide

Anticholinergics

Long-acting Tiotropium bromide

Aminophylline
Methylxanthines WWW.GOLD.COM
Theophylline
Treatment of COPD at every stage

IV stage –
Stage II- III –
Stage I - extremely heavy
medium-heavy heavy
light
Actively reducing exposure to risk factors ; flu vaccination
Add a short-acting bronchodilator as needed
Add a long-acting drug to your routine treatment
bronchodilator, add rehabilitation
Add iGCS when
repeated exacerbations
Add long
oxygen therapy for
HDN ; consider
expediency
surgical treatment
 Combination of asthma and
COPD

COPD
BA BA+COPD
 criteria COPD BA

The appearance of clinical Typically in people over 40 Most often children and
manifestations of diseases years of age young people

smoking typical Not typical

Extrapulmonary Not typical characteristic

manifestations of allergies
Clinical manifestations Constant, slowly Appear in fits and starts
(cough, shortness of breath) progressing

BA in relatives Not typical typical

Bronchial obstruction Little reversible or Reversible

irreversible, Bronchidilation test is
bronchodilation test - positive
negative
Daily dynamics of PSV <15% >15%

Pulmonary heart Typically in severe cases Not typical

Type of inflammation Nonfiction predominates E/f prevail

Efficiency of GCS low high

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