The theme of the
lecture: “Bronchial
asthma. Chronic
obstructive
pulmonary disease.
The syndrome of
bronchial obstruction.
Pulmonary
emphysema"
Ass-prof.N.Bilkevych
Respiratory system anatomy
Syndromes
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Respiratory failure
Bronchial obstruction
Pulmonary emphysema
Lung tissue
consolidation
Mucocilliary
insufficiency
Intoxicaion syndrome
Athelectasis
Cavity in the lungs
Free air in pleural cavity
Liquid in pleural cavity
Mucocilliary insufficiency and respiratory failure
The syndrome of bronchial
obstruction
(lat.) – barrier, obstracle.
 Causes of bronchial obstruction:
 Obstructio




- spasm of bronchial smooth muscles
accumulation of fluid in fine bronchi
- edema of bronchial mucosa
- poor elasticity of lungs
Pulmonary emphysema

Emphysema is a disease caused
by enlargement of the lungs and
an increase in their airiness due to
overstretching of the alveoli or due
to rupture of the alveolar walls.
 The lungs are enlarged.

Exhalation requires greater effort .
 Gas exchange of oxygen and carbon
dioxide in the alveoli due to tissue
damage and blockage is markedly
reduced.
Causes of pulmonary
emphysema
I.


Local
A. Congenital abnormalities of bronchi
B. Compensatory due to lung collapse, scarring or
resection
 C. Partial bronchial obstruction
 Neoplasm
 Foreign body
 D. MacLeod'syndrome
II. Generalized
 A. Idiopathic
 B. Senile
 C. Familial (alpha-1-anti-trypsin deficiency)
 D. Associated with chronic bronchitis, asthma or
pneumoconiosis.
Bronchial asthma
A chronic recurrent
inflammatory disease
of the respiratory
tract, which is
characterized by
reverse bronchial
obstruction and
bronchial
hyperreactivity.
The bronchial obstruction is produced by a
combination of
 mucosal edema,
 constriction of the bronchial musculature,
 excessive secretion of viscid mucus, causing
mucous plugs.
Essentials of Diagnosis:
• Recurrent acute attacks of dyspnea, cough, and
mucoid sputum, usually accompanied by
wheezing.
• Prolonged expiration with generalized wheezing
and musical rales.
• Bronchial obstruction is reversible by drugs
Etiology
40-80% of patients
have a hereditary
predisposition (allergy,
allergic rhinitis and
sinusitis, nasal polyps)
•Acquired etiological
factors
•
Acquired ethiological factors






Domestic allergens
Environmental allergens
Food allergy
drugs
bacterial allergens
Domestic mites, animal
wool, insect allergens,
fungal spores, plant
pollen
Food allergy
 (milk,
wheat flour, fish, food additives,
dyes, conservants)











Acquired ethiological factors
Domestic allergens
( dust, insect allergens, fungi, animal wool,
epidermis)
Environmental allergens
( fungi, insect allergens, pollen etc)
Food allergy
( milk, flour, fish, chemical admixtures to food)
drugs
( antibiotics, enzymes, aspirin)
bacterial allergens
( neisseria, Staphylococcus aureus, Candida
albicans, mycoplasma, helmints)
 drug
allergy
(antibiotics, enzymes, aspirin)
 bacterial
allergens]
(Neisseria, Staphylococcus aureus, fungi
Candida, mycoplasma, roundworms and
other infestations, parainfluenza virus)
Pathogenesis of BA
Immunological mechanisms
Due to:
- Ig E
- basophils
- mast cells
Reaction mediators:
- histamine
- prostaglandins
- leukotrienes
Non-immunological mechanisms
Release
1. Pseudoallergic
 Medications
 food
 plant allergens
of animal origin
biologically
active substances
and activation of
the
complement
system
2. Theory of
β-adrenergic block
In norm
irritant
adren
aline
α-
β-
receptors
receptors
(vascular spasm)
β1-miocardium
(heart rate )
irritant
adrenalinн
ннн
bronchospasm
ATP adenylate cyclase AMP
через
β2-bronchi
(dilatation)
βreceptors
Formation
cyclic
AMP
In bronchial asthma
defect
(congenital)β2-
adenylate cyclase
deficiency
рецепторів
bronchospasm
!!!
cAMP
 3.
Involving neurohumoral and
cellular mechanisms
(influence of parasympathetic
innervation)
 4. Reflectory bronchospasm
а) rhinobronchial reflex
b) cooling of sensitive zones of bronchi
c) gastroesophageal reflux
 5. Psycho-emotional influences
through the autonomic nervous system.
 6. Endocrine mechanisms
 (hormone imbalance).

7. Formation of irreversible bronchial
obstruction under the influence of
recurrent infection.
Сlassification of bronchial asthma
Degree of severity
Course
І
 Intermittent course
ІІ
 Persistent course
ІІІ
 mild
ІV
 moderate
 severe
 Intermittent asthma
Attacks are short and mild
day
<1 time a weak
night
≤2 times a month
Between attacks symptoms are abcent
 Persisting asthma
 mild
Symptoms are permanent but short
day
<1 time a weal but not more than 1 time a
day
night
=1-2 times a month
 moderate
Symptoms are premanent
day
permanently
night
> 1 time a weak
Limitation of physical activity
Night is deranged
 severe
day
Permanent long attacks
night
Limitation of physical activity
Exacerbations may be dangerous for patient’s life
Diagnosis: Intermittent bronchial asthma, m,ild degree of
exacerbation, respiratory insufficiency 0 degree.
Clinical pattern: complaints
Attacks of expiratory dyspnea
Tightness in the chest
Dry cough
General weakness,
dizziness
Clinical pattern
Inspection
 Forsed position of a patient – orthopnoe
 Skin is pale
 Respiration
cyanotic
later
(10-12 per min)
 Wheezes
 Swelling of neck veins
 Mouth is opened
 Viscous white transparent sputum
Inspection of a chest
 Inspiratory position
 Participation of additional respiratory muscles in respiration
 palpation
 Intercostal spaces are wide
 Vocal fremitus is weakened
 The chest is rigid
Percussion
 Bundbox sound
 Upper and lower borders of the lungs are diaplaced upward and
downward
 Respiratory mobility of lungs lower borders is markedly limited
Appearance of a patient during attack of
asthma
Auscultation (before expectoration of sputum)
 Weakened vesicular breathing
 Prolonged expiration
 Dry whistling (high-pitched) rales
Auscultation (during expectoration of sputum)
 Amount of

Amount of
high-pitched rales decreases
low-pitched rales increases
 Appearance of moist rales
Laboratory diagnostics in exacerbation
Blood:
 Moderate lymphocytosis
 eosinophilia
Sputum:

eosinophils
 Charkot-Leyden crystals

Kurshmann’s spirals
Дослідження харкотиння
Instrumental diagnostics
Investigation of external respiratory function
І. Spyrography
 FEV1 < 80%

Tiffneu index (
FEV1 /VLC, %)
ІІ. Pneumotachymetry

Of expiratory force
 In tests with bronchodilators, reverse bronchial
obstruction is determined.
спірограма
Instrumental diagnostics
Investigation of external respiratory function
ІІІ. Peak -fluometry (analysis of peak volumetric velocity
of forced expiration)
Chest X-ray in asthma
X-ray
hypertranslucencv of
lung fields.
Widened intercostal
spaces
Low fiat diaphragm
Increased
retrosternal translucency
Narxow vertical
heart
Large hilar shadows
Diminished
peripheral vascular
pattern
Chest X-ray in bronchial asthma
 increased lung transparency



horizontal placement of ribs
expansion of intercostal spaces
low position if the diafragm
X-ray shows pulmonary emphysema
Endoscopic findings: hyperemia, edema of
bronchial mucosa, hypersecretion
Allergic tests allow to determine
allergens
Positive reaction
Principles of asthma
treatment
I. Etiological
ІІ. Pathogenetic
Etiological
1. Elimination therapy
Pathogenetic
1. Influence on the immunological phase
 specific hyposensitization
 nonspecific hyposensitization
- fasting diet
- treatment with histoglobulin
- treatment with glucocorticoids
- immunomodulatory therapy
2. Influence on the pathochemical
phase
• mast cell stabilizers (ketotifen)
• leuktriene inhibitors (Montelucast)
• protease inhibitors
• antioxidant therapy
Influence on the pathophysiological
phase
bronchodilators
 adrenergic receptor stimulants
 M-cholinoblockers
 phosphodiesterase inhibitors
 Ca ++ antagonists
 Antispasmodics
expectorants
Usage of inhaler
Solotvino (salt caves)
Physiotherapeutic
treatment
• aerosol therapy
• electrophoresis (with bronchodilators)
• ultrasound
• halotherapy
• therapeutic massage
• barotherapy
• breathing exercises
• acupuncture
Resort treatment
Physiotherapy
Climatotherapy
SOFT
WARM
DRY CLIMATE
WITHOUT SHARPY WEATHER CHANGES
MOUNTAIN LOCATION (900 - 1000 m ABOVE
SEA LEVEL)
COASTAL RESORTS WITH LOW HUMIDITY
Chronic obstructive pulmonary
disease

A primary chronic inflammatory
disease with predominant lesions of
the distal airways and lung
parenchyma, formation of
emphysema with development of
incompletely reversible or
irreversible bronchial obstruction
caused by a pathological
inflammatory reaction
Types of bronchitis
 Acute
bronchitis: This is the more common
one. Symptoms last for a few weeks, but it
doesn’t usually cause any problems past
that.
 Chronic bronchitis: exacerbations are
observed for 2 and more years. Total
duration of exacerbation p;eriod is more
than 2 weeks annulary
Chronic obstructive pulmonary
disease (COPD)

The common combination of chronic bronchitis and
emphysema has been termed chronic obstructive airways
disease (COAD) or chronic obstructive pulmonary disease
(COPD).
This is a morbid condition characterized by irreverseble
bronchial obstruction caused by deformation and sclerosis
of bronchial tree due to persistent inflammation.
 Up to 20% of adults worldwide have the disease, and this
proportion is higher in heavily industrialized countries.
Chronic bronchitis occurs in the majority of heavy smokers
(at least 80% of smokers).



It is the third most common cause of death in men over 65
years (60 per 100.000), and is more common in men (8%)
than women (3%).

Risk-factors of COPD
External
 • long-term smoking or passive smoking
 • industrial and domestic harmful substances
 • infections
 • low socio-economic state
 (food restrictions,
 overcoolings, harmful habits)
Internal
 Genetical
predisposition (inherited
deficiency of - α1-antitripsine)
 Bronchial hyperreactivity
 Hypoplasia of the lungs
Pathological mechanisms
 Disorders of functional activity of ciliated epithelium
 Change of sputum viscosity
 Immunodepression (deranged cellular and humoral
defence)
 Air pollutants inactivate α1-antitripsine and inhibitor of
elastase.
Clinical pattern
Complaints
 Cough (usually with mucopurulent sputum)
 Dyspnoe (constant
expiratory)
General inspection
In later stage – diffuse cyanosis, jugular veins swelling
Inspection of a chest
 Emphysematous chest
 Protrusion of supra- and infraclavicular fossa

Participation of additional respiratory muscles
Palpation
 Rigid chest, diffusely weakened vocal
fremitus
Percussion
 • Hyperresonant sound
 • Displacement of the upper border of the lungs up
 • Shifting the lower border of the lungs down
 • Expansion of Kroenig’s area
Auscultation
•Weakened vesicular breathing with prolonged expiratory phase
•Dry rales (wheezes)
Instrumental examination
 External respiratory function
 FEV1 < 80%
 Tiffneu index < 70%
 Spyrometry
(determination of FEV1, VLC, FVLC)
Tests with bronchodilators (Salbutamol test)
shows low reversibility of bronchial obstruction.
Stages of COPD




GOLD 1: Mild
GOLD 2: Moderate
GOLD 3: Severe
GOLD 4: Very severe




Group A: Low risk, less symptoms
Group B: Low risk, more symptoms
Group C: High risk, less symptoms
Group D: High risk, more symptoms
Stages of COPD
1 – chronic bronchitis,
pneumosclerosis (including bronchial
walls)
 Stage 2 – pulmonary emphysema
 Stage 3 – Chronic right-ventricular failure
 Stage
Stage 1 -- Mild -- FEV-1 ≥80%: You may have no
symptoms. You might be short of breath when walking
fast on level ground or climbing a slight hill.
 Stage 2 -- Moderate -- FEV-1 50-79%: If you’re walking
on level ground, you might have to stop every few
minutes to catch your breath.
 Stage 3 -- Severe -- FEV-1 30-49%: You may be too
short of breath to leave the house. You might get
breathless doing something as simple as dressing and
undressing.
 Stage 4 -- Very Severe -- FEV-1 ≤30%: You might have
lung or heart failure. This can make it hard to catch your
breath even when you’re resting. You might hear this
called end-stage COPD.

Treatment








Smoking cessation.
Bronchodilators (Salbutamol)
Corticosteroids, NSAIDs
Combinations of bronchodilators and
corticosteroids (Seretid, Simbicort)
Oxygen
Antibiotics (amoxivullin, cefaosporines)
Expectorants (lasolvan)
Sanation bronchosclpy and surgical removal of
large bullae may be occasionally helpful.
Oxygen therapy
Thank
you for
your attention!
Treatment






The most important step in management is to persuade the patient to
stop smoking.
Bronchodilators may achieve some reversal of airways obstruction
Corticosteroids have a role in some patients.
Surgical removal of large bullae is occasionally helpful.
Oxygen is usually given via nasal cannulae. Occasionally transtracheal
oxygen therapy (TTOT) via a small polyethylene catheter introduced
directly into the trachea. Long-term oxygen therapy from cylinders or an
oxygen concentrator may be of value in patients with chronic stable
respiratory failure. The flow rate and concentration are adjusted to
relieve arterial hypoxaemia while avoiding carbon dioxide narcosis.
Infections are frequent, and it is important to educate patients in the
early recognition of symptoms and signs, for example change of
sputum colour and quality, fever or increasing wheeze. Many patients
should be given a supply of antibiotics to keep at home for selfmedication.
Bronchoscopy is used if it is necessary
ДЯКУЮ ЗА
УВАГУ