Respiratory diseases with bronchial obstruction

Содержание

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Definition of BO BO - condition develops due to the presence

Definition of BO

BO - condition develops due to the presence of

obstacles to the outgoing air flow in the respiratory tract.
BO syndrome is a complex of symptoms of obstructive respiratory failure.
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Types of BO By prevalence: 1. Local: tumor foreign body diseases

Types of BO

By prevalence:
1. Local:
tumor
foreign body
diseases with intrathoracic LAP
2. Diffuse:
Chronic obstructive

bronchitis
Emphysema of the lungs
Bronchial asthma
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Types of BO By duration: 1.Reversible (BA); 2. Irreversible (COB, EL). life time

Types of BO

By duration:
1.Reversible (BA);
2. Irreversible (COB, EL).
life time

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Mechanisms 1. Reversible: spasm of SMC wall edema impaired mucus secretion

Mechanisms

1. Reversible:
spasm of SMC
wall edema
impaired mucus secretion

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2. Irreversible: fibrosis of the wall pathological expiratory collapse of bronchioles

2. Irreversible:
fibrosis of the wall
pathological expiratory collapse of bronchioles (due to

the lost of alveolar support and destruction)
hyperplasia of the epithelium of the bronchial mucosa
hypertrophy of bronchial submucosal glands
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BA is a disease characterized by chronic inflammation of the airways

BA is a disease characterized by chronic inflammation of the airways

and recurrent bronchospasm, which leads to respiratory symptoms (wheezing, shortness of breath, chest congestion, and cough)
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Pathomorphology mast cell

Pathomorphology

mast cell

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Inflammation in BA (AD) The development of AD is based on

Inflammation in BA (AD)

The development of AD is based on chronic

inflammation in the airways.
Mast cells
Eosinophils
T-lymphocytes
Neutrophils
Macrophages
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Bronchial hyperreactivity BHR - the possibility of developing bronchospasm under the

Bronchial hyperreactivity

BHR - the possibility of developing bronchospasm under the action

of a stimulus that does not cause bronchospasm in a healthy person
Inflammation in the airways in AD leads to BHR
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Provoking factors of the bronchospasm Allergen triggers (have a protein structure)

Provoking factors of the bronchospasm

Allergen triggers (have a protein structure) -

cause sensitization (the appearance of specific IgE) and provoke bronchospasm through an IgE-dependent allergic reaction
Aeroallergens:
household (house dust mite, cockroaches)
pollen (ragweed ...)
epidermal (animal allergens)
fungal allergens (mold)
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IgE-depended allergic reaction

IgE-depended allergic reaction

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Provoking factors of the bronchospasm Nonspecific triggers (non-allergenic) - provoke bronchospasm

Provoking factors of the bronchospasm

Nonspecific triggers (non-allergenic) - provoke bronchospasm in

the presence of bronchial hyperreactivity
Exercise stress
Cold air
Tobacco smoke
Laughter, emotions
Smells (perfumes, household chemicals, exhaust gases, gasoline, varnish-and-paint products ...)
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Symptoms Wheezing rales Feeling of chest congestion Dyspnea Unproductive cough (may

Symptoms

Wheezing rales
Feeling of chest congestion
Dyspnea
Unproductive cough (may be the dominant symptom

!)
Choking… is a symptom of severe asthma exacerbation
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Choking appears with non-stopping severe attack of asthma, which is regarded

Choking
appears with non-stopping severe attack of asthma, which is regarded as

a severe exacerbation of asthma and requires urgent hospitalization and emergency care
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About asthma symptoms (it may help in diagnosis) Provocation (exercise, exposure

About asthma symptoms (it may help in diagnosis)

Provocation (exercise, exposure to

an allergen, cold air, laughter, irritants)
Paroxysmal
Reversibility (spontaneous or after inhalation of a bronchodilator)
Variability
Symptoms often worsen at night or early in the morning
Viral respiratory infections often cause exacerbations of asthma
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Patient examination Important ! signs of bronchial obstruction appear only at

Patient examination

Important !
signs of bronchial obstruction appear only at the time

of an attack of bronchospasm:
- inability to speak in sentences with a severe attack
- orthopnoe, sitting position with an inclination forward with an emphasis on the hands
- wheezing, breathing with difficulty prolonged exhalation
- participation in the respiration of additional muscles
with a severe attack - diffuse cyanosis
- achypnoe
- on auscultation - wheezes
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History of life Childhood (early beginning) Occupational hazards (risk of occupational

History of life

Childhood (early beginning)
Occupational hazards (risk of occupational BA)
Living conditions

(mold, house dust mites, pets ...)
Smoking
Heredity (many patients have familial AD cases, but not all)
Allergic history
Other diseases associated with AD - allergic rhinitis, atopic dermatitis (not in all patients)
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Tests Confirmation of variability of bronchial obstruction Peak expiratory flow (PEF)

Tests

Confirmation of variability of bronchial obstruction
Peak expiratory flow (PEF) monitoring -

peak flowmetry
Spirometry + test with bronchodilator
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Peakflowmeter

Peakflowmeter

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Criteria of bronchial obstruction variability Positive test with bronchodilator (assessed 15

Criteria of bronchial obstruction variability

Positive test with bronchodilator (assessed 15 min

after 400 mcg salbutamol)
FEV1 increase> 12% or 200 ml from the initial
Increased PEF variability measured twice a day
mean PEF variability> 10%
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Положительный тест с бронхолитиком

Положительный тест с бронхолитиком

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Can a patient with asthma have normal spirometry and peak flow results?

Can a patient with asthma have normal spirometry and peak flow

results?
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Allergic tests Skin scarification tests (prick tests) with allergen panel Blood level of specific IgE

Allergic tests

Skin scarification tests (prick tests) with allergen panel
Blood level of

specific IgE
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Others Eosinophilia is detected in a small number of patients with

Others

Eosinophilia is detected in a small number of patients with AD
In

the analysis of sputum, eosinophils can be detected in some patients
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Treatment Long-term (in many patients lifelong) basic anti-inflammatory therapy with inhaled

Treatment

Long-term (in many patients lifelong) basic anti-inflammatory therapy with inhaled glucocorticoids

(ICS)
Use of short-acting bronchodilators (SAB) (salbutamol) as needed
With proper treatment with ICS, asthma symptoms stop, the need for SAB is minimal, there are no restrictions on physical activity and there are no exacerbations of asthma (controlled asthma)
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Chronic bronchitis CB - “smoker's cough” when other causes of cough

Chronic bronchitis

CB - “smoker's cough” when other causes of cough are

excluded (such as asthma, bronchiectasis, tuberculosis, cancer, pulmonary fibrosis, sarcoidosis, ACE inhibitors)
The pathological basis of CB is the hyperproduction of sputum in the bronchi in response to prolonged irritation by inhaled particles and gases (more often tobacco smoke)
The only symptom of CB is a chronic cough with little sputum.
Long-term exposure to tobacco smoking or occupational exposure to inorganic dust will be mandatory for the development of CB.
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Smokers usually do not seek medical help at the stage of

Smokers usually do not seek medical help at the stage of

CB, since the cough in this case is not severe and painful.
Smokers should be actively asked about coughing
The only treatment is to quit smoking
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CB = Chronic productive cough + Long-term exposure to tobacco smoking

CB =

Chronic productive cough
+
Long-term exposure to tobacco smoking
+
Other causes

of chronic cough have been ruled out
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Smoking CB Inflamation and fibrosis Destruction of alveolar wall in distal bronchi Irreversible BO COPD 50%

Smoking
CB
Inflamation and fibrosis Destruction of alveolar wall
in distal bronchi
Irreversible

BO
COPD

50%

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Emphysema Pathomorphological concept Destruction of the lung parenchyma with destruction of

Emphysema

Pathomorphological concept
Destruction of the lung parenchyma with destruction of alveolar septa

due to exposure to tobacco smoke
Now pulmonary emphysema is a component of the diagnosis of COPD.
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EL pathogenesis Smoking Activation of alveolar macrophages Proteases> Antiproteases (α1-antitrypsin) Destruction

EL pathogenesis

Smoking
Activation of alveolar macrophages
Proteases> Antiproteases (α1-antitrypsin)
Destruction of the alveolar walls
Decreased

elastic traction of the lungs
Decreased alveolar support of bronchioles
Early expiratory collapse of bronchioles
(irreversible bronchial obstruction)
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COPD Chronic obstructive pulmonary disease is a disease with progressive irreversible

COPD

Chronic obstructive pulmonary disease is a disease with progressive irreversible bronchial

obstruction that develops due to chronic inflammation caused by the prolonged action of inhaled pathogenic particles
Symptoms include breathing difficulty, cough, mucus (sputum) production and wheezing.
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C(O)B EL COPD / ХОБЛ

C(O)B
EL

COPD / ХОБЛ

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Pathogenesis - Long-term smoking (smoking experience 20 packs / years or

Pathogenesis

- Long-term smoking (smoking experience 20 packs / years or

more, women may have less smoking experience)
- Occupational exposure to inorganic dust (miners)
- Genetic predisposition that determines an excessive inflammatory response to inhaled particles
COPD develops in 20-30% of smokers
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With the development of bronchial obstruction (narrowing of the distal AW),

With the development of bronchial obstruction (narrowing of the distal AW),

the volumetric velocity of the expiratory air flow is limited, which is the main feature of COPD.
A patient with COPD cannot quickly exhale large volumes of air due to an increase in the resistance of the AW, at first this feature manifests during physical activity
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Air traps (dynamic hyperinflation) With bronchial obstruction, it is impossible to

Air traps (dynamic hyperinflation)

With bronchial obstruction, it is impossible to quickly

breathe out a required volume of air
During physical exertion, with increased breathing, the expiration time decreases, which does not allow to fully exhale the required volume of air (air trap), and the next inhalation begins after the incomplete removal of air from the alveoli
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"Air traps" lead to an increase in the residual volume and

"Air traps" lead to an increase in the residual volume and

a decrease in VC, disrupt the mechanics of the respiratory muscles
Hyperinflation develops already in the early stages of the disease and serves as the main mechanism for the onset of shortness of breath during exertion in COPD
When the load stops and the respiratory rate decreases, hyperinflation (air traps) are resolved

Air traps (dynamic hyperinflation)

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COPD hystory

COPD hystory

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Symptoms: complaints Shortness of breath on exertion, in the terminal stage

Symptoms: complaints

Shortness of breath on exertion,
in the terminal stage

- at minimal exertion and at rest
Patients can avoid shortness of breath for a long time by limiting physical activity (slow pace of walking, avoid climbing stairs)
Often, patients first visit a doctor because of shortness of breath, which limits their daily activities (at stages III-IV of COPD)
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Cough Most patients with COPD have a productive cough with little

Cough
Most patients with COPD have a productive cough with little sputum.
During

periods of exacerbation, the cough increases, the sputum becomes purulent
COPD cough is rarely a reason to see a doctor
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Examination Central cyanosis in severe COPD due to arterial hypoxemia. Flushing

Examination

Central cyanosis in severe COPD due to arterial hypoxemia.
Flushing of the

neck and upper chest is common
In some COPD patients, exhalation through the pursed lips, which increases the pressure in the airway during exhalation and decreases respiratory collapse of the bronchioles.
Some patients have a symptom of finger clubbing ("drumsticks“)
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Chest examination Barrel chest in emphysematous COPD In severe patients with

Chest examination

Barrel chest in emphysematous COPD
In severe patients with COPD, the

involvement of additional respiratory muscles is observed. The inclusion of the scalenae and sternocleidomastoideus muscles in the act of respiration is an indicator of further deterioration of respiratory mechanic disorders .
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Palpation and percussion With emphysema and pulmonary hyperinflation, a boxed (hyperresonant)

Palpation and percussion
With emphysema and pulmonary hyperinflation, a boxed (hyperresonant) percussion

sound is determined.
Auscultation
Emphysema silence the main breathing sound and even heart sounds
Adventitious breathing sounds:
Monophonic (rhonchi) and polyphonic high pitched wheezes may be heard
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Spirometry

Spirometry

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Chest X-ray Signs of hyperinflation (flattened diaphragm, increased transparency of the

Chest X-ray

Signs of hyperinflation (flattened diaphragm, increased transparency of the lungs,

disappearance of the vascular pattern)
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COPD diagnosis = Long-term exposure to smoking + Detection of irreversible

COPD diagnosis =

Long-term exposure to smoking
+
Detection of irreversible BO on

spirometry (Tiffno index <0.7)
+
Other causes of irreversible BO are excluded
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Treatment principles QUITING SMOKING is the only treatment that can slow

Treatment principles

QUITING SMOKING is the only treatment that can slow

the progression of COPD
Bronchodilators on demand (for shortness of breath, before exercise) and on an ongoing basis
With the development of severe RF, long-term home oxygen therapy
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