Pathological anatomy of chronic bronchitis and bronchiectasis medical

1. Pathological anatomy of chronic
bronchitis, bronchiectasis.

2. • Chronic obstructive pulmonary disease (COPD) is an air flow
restriction caused by an inflammatory response to inhaled
toxins, most often cigarette smoke. Less common causes in
non-smokers are alpha-1-antitrypsin deficiency and various
occupational exposures.
• COPD includes:
• Chronic obstructive bronchitis (clinically established)
• Emphysema (established by histological or X-ray
examination)
• Many patients have symptoms of both diseases.

3. •Chronic obstructive bronchitis is chronic
bronchitis with airway obstruction.
•Emphysema is the destruction of the
pulmonary parenchyma, leading to loss of
elastic strength and damage to the alveolar
septa and radial traction of the airways,
which increases the risk of respiratory
collapse.

4. •Etiology
•There are 2 main causes of COPD:
•Smoking (and other less common
inhalation harmful effects)
•Genetic factors

5. •Complications
•Along with the restriction of air flow and
sometimes respiratory failure, the following
complications occur:
•Pulmonary hypertension
•Respiratory tract infection;
•Weight loss and other pathology

6. • Chronic bronchitis is a disease characterized by
excessive mucus production by the bronchial glands,
leading to the appearance of a productive cough for 3
months. annually for 2 years.
• The morphological substrate of chronic bronchitis is
chronic inflammation of the bronchial wall with
hyperplasia of mucus-producing goblet cells and
mucous glands, which is clinically expressed as a
symptom of sputum secretion.

7. • Etiology. Risk factors.
• Smoking is the most important factor of chronic bronchitis
(tobacco smoke reduces the activity of the movement of the
cilia of the bronchial epithelium, which leads to a violation of
mucociliary clearance, damage to the bronchial
integumentary epithelium with its metaplasia and dysplasia),
tobacco smoking has an inhibitory effect on the activity of
alveolar macrophages, thereby damaging the mechanisms of
local pulmonary protection. Exacerbations of chronic
bronchitis are clearly associated with S02 and N02 emissions
into the atmosphere. High frequency of chronic bronchitis in
workers who have contact with organic, mineral dust and
toxic gases.

8. • Pathogenesis and morphogenesis: based on a
violation of the drainage function of the small bronchi
as a result of prolonged exposure to etiological
factors. At the same time, in the bronchial wall, in
response to damage to the integumentary bronchial
epithelium, the following develop: chronic
inflammation, pathological regeneration (metaplasia),
adaptive hyperproduction of mucus by mucus-
producing goblet cells and mucous glands. Chronic
catarrhal inflammation develops in the bronchi.

9. • Pathological anatomy: the walls of the bronchi become thickened,
surrounded by layers of connective tissue, there is a deformation of
the bronchi. With a prolonged course of chronic bronchitis, baggy and
cylindrical bronchiectasis may occur — the expansion of the bronchial
lumen. Microscopic changes are caused by the development of
chronic mucous or purulent catarrhal inflammation in the bronchi
with metaplasia of the integumentary epithelium and hyperplasia of
the mucous glands and goblet cells. Cellular inflammatory infiltration,
proliferation of granulation tissue are expressed in the bronchial wall,
which can lead to the formation of inflammatory polyps of the
bronchial mucosa, sclerosis and atrophy of the muscular layer.
• Complications of chronic bronchitis are bronchopneumonia, the
formation of foci of atelectasis, obstructive pulmonary emphysema,
pneumofibrosis.

10. • Bronchiectatic disease is a disease characterized by a certain complex of
pulmonary and extrapulmonary changes in the presence of bronchiectasis in the
bronchi (persistent pathological dilation of one or more bronchi containing
cartilaginous plates and mucous glands, with destruction of the elastic and
muscular layers of the bronchial wall).
• Pathogenesis and morphogenesis: there are congenital and acquired
bronchiectasis.
• +Congenital bronchiectasis is formed with various pre- and postnatal defects in
the development of the tracheobronchial tree, which leads to stagnation of
bronchial secretions and infection. The addition of bacterial infection leads to the
destruction of the elastic framework and the muscular membrane of the
bronchial wall, subsequent sclerosis and dilation of their lumen.
• In the development of acquired bronchiectasis, the mechanism of bronchial
obstruction in combination with secondary bacterial infection is of great
importance. Since bronchial obstruction is usually limited to one or more bronchi,
acquired bronchiectasis is local in nature. Bronchiectasis, the pathogenesis of
which is associated with bronchopneumonia preceding them with pronounced
destruction of lung tissue, is observed in complicated measles, diphtheria,
adenovirus infection, influenza. Sometimes bronchiectasis can develop due to the
ingress of a foreign body into the bronchi, caseous masses in tuberculosis,
compression of the bronchi by a tumor.

11. • Causes
(1) Cystic fibrosis (CF)
(2) Infections
(a) TB is the most common cause worldwide.
(b) Mycobacterium avium-intracellulare (typically involves
the right middle lobe and lingula), adenovirus,
Staphylococcus aureus, Haemophilus influenzae
(3) Bronchial obstruction
• Example—proximally located bronchogenic carcinoma
occludes the lumen.
(4) Allergic bronchopulmonary aspergillosis

13. • Pathological anatomy.
• Bronchiectasis has acquired character, is caused by bronchoobstructive
syndrome, preceding bronchopneumonia, ingestion of a foreign body and is local
in nature. The bronchi of the lower lobe of the right lung are most often affected.
• Microscopic examination in the bronchiectasis cavity reveals purulent exudate
containing microbial bodies and exfoliated epithelium. The integumentary
epithelium is represented by bare basal cells, foci of polyposis and squamous
metaplasia. The basement membrane has a corrugated appearance. Dystrophy
and destruction of the cartilaginous plate of the bronchus, atrophy and
destruction of the muscular and elastic layers, sclerosis and diffuse
histiolymphocytic inflammatory infiltration of all layers of the bronchiectasis wall
with an admixture of polymorphonuclear leukocytes are detected. In the
adjacent pulmonary parenchyma, fibrosis fields and foci of obstructive pulmonary
emphysema are observed.
• Complications of bronchiectatic disease are associated with the possibility of
pulmonary bleeding, lung abscesses, pleural empyema, chronic pulmonary heart
failure. Amyloidosis (secondary - AA-amyloid) and brain abscesses. Each of these
complications can cause the death of a patient with bronchiectatic disease.

14. • Bronchiectasis and pneumosclerosis.
Mainly in the subpleural sections of
the lung, the bronchi are cylindrically
expanded, their walls are thickened,
compacted, protrude above the
incision surface or, on the contrary,
thinned, pus (cylindrical
bronchiectasis) is in the lumen. Diffuse
reticular pattern (thin layers of gray
connective tissue) is enhanced in the
surrounding lung tissue, gray
peribronchial connective tissue is
expanded (diffuse reticular and
peribronchial pneumosclerosis).Pleura
is thickened, sclerosed

15. Chronic pulmonary heart:
the heart is enlarged in size
and weight, the wall
thickness of the right
ventricle exceeds 2-3 mm
(hypertrophy mainly of the
walls of the right ventricle),
the myocardium is flabby,
clay-like (fatty degeneration
of cardiomyocytes)

16. Chronic bronchitis.
Pathological changes in the
bronchial mucosa (squamous
metaplasia of the epithelium,
hyperplasia of goblet cells,
hypersecretion of mucus). Pay
attention to the specificity of
the inflammatory infiltrate in
the bronchial wall,
hypertrophy of muscle fibers.

17. Bronchial asthma (from Greek asthma -
suffocation) is a disease in which attacks of
expiratory shortness of breath are observed,
caused by an allergic reaction in the bronchial
tree with impaired bronchial patency.

18. Etiology. The factors causing bronchial asthma are
considered mainly exogenous allergens with the undoubted
role of heredity. Among the reasons that determine
repeated attacks of bronchial asthma, there are infectious
diseases, especially of the upper respiratory tract, allergic
rhinosinusitis, environmental influences, exposure to
substances suspended in the air (room and industrial dust,
smoke, various odors, etc.), meteorological (high humidity
atmospheric air, fogs) and psychogenic (psychogenic
irritations) factors, the use of a number of foods and drugs.

19. The main forms of bronchial asthma are atopic (from
the Latin athopia - hereditary predisposition) and
infectious-allergic.
Atopic bronchial asthma occurs when the body is
exposed to allergens of various origins through the
respiratory tract.
Infectious-allergic bronchial asthma is observed when
exposed to allergens in patients with acute or chronic
bronchopulmonary diseases caused by infectious
agents.

20. Complications of asthma
Acute respiratory failure
Spontaneous pneumothorax
Atelectasis of the lung (blockage of the bronchus by mucous plugs)
Pneumonia
Hyperinflation of the lungs, emphysema of the lungs
A sharp decrease in blood pressure at the time of an asthmatic attack
Sudden cardiac arrest
Myocardial infarction, myocardial dystrophy, pulmonary heart
Metabolic acidosis, acidification of the blood
Hypercapnia (excess concentration of carbon dioxide in the blood)
Respiratory encephalopathy (irreversible brain damage)
Pathologies of the gastrointestinal tract, exacerbation of hernias

21. Bronchial asthma. The change in the shape of the
bronchi, the contents of the lumen, edema, thickening of
the bronchial wall and infiltration of eosinophils and
leukocytes.

22. Bronchial asthma. The change in the shape of the bronchi, the
contents of the lumen, edema, thickening of the bronchial
wall