Editor

Pulmonologist

Serous-hemorrhagic pneumonia occurs as a complication of certain diseases. Most often it acts as a consequence that appears against the background of a viral infection.

All signs of the disease are clearly expressed, the body is susceptible to severe intoxication. The cough that develops in the first days of pneumonia may be accompanied by bloody sputum. The secreted serous alveolar exudate contains impurities with a considerable composition of erythrocytes.

Etiology and pathogenesis

Serous-hemorrhagic pneumonia develops against the background of a viral or bacterial infection, especially with the following pathologies:

pneumonic plague;
in rare cases, anthrax;
smallpox;
flu;
viral measles;
Leptospira infection.

Pathogenic microorganisms penetrate the lung tissue through airborne droplets or bronchogenic routes, that is, microbes move along the respiratory tract. Less commonly, infection occurs hematogenously, through the blood, or through a diseased nearby organ, such as the liver.

The hemorrhagic type of pneumonia can develop even if it is present.

Damage to lung tissue by serous-hemorrhagic pneumonia

The disease can be complicated by the following factors:

if a person smokes;
during, in particular, a woman is most vulnerable in the 2nd and 3rd trimester;
presence of chronic bronchitis;
chronic pulmonary emphysema;
coronary heart disease and other cardiovascular diseases;
if a person is obese;
reduced immune defense.

The disease occurs against the background of the toxic effects of pathogenic microorganisms on the vascular membrane. As a result:

blood circulation is disrupted;
plethora is formed;
vascular thrombosis.

Due to increased vascular permeability of hematopoiesis, many red blood cells are formed into the alveolar tissue. Therefore, the exudate becomes hemorrhagic.

The source of inflammation has a dense and bright red structure, reminiscent of hemorrhage.

The consequences of the pathology under consideration are gangrene, exudative pleurisy, abscess and purulent-necrotic formations.

In order for inflammation to begin to progress in the lungs, it is not enough to get infected; for this there must be a special soil - weakened immunity, and in particular its following components:

mucociliary transport;
alveolar macrophages;
surfactants (substances that prevent the alveoli from sticking together) of the alveoli;
anti-infective substances of bronchodilator secretions.

Clinical picture

Serous-hemorrhagic pneumonia is always accompanied by manifestations of the initial disease.

After a few days, severe manifestations of pneumonia join them:

cyanosis;
hemoptysis;
severe shortness of breath;
decreased blood pressure;
tachycardia;
the appearance of blood from the nose.

With this disease, body temperature increases to high levels, intoxication develops, doctors assess this condition as severe.

As the pathology develops, the following signs appear:

pulmonary failure;
DIC syndrome;
multiple organ failure.

In advanced cases, if help is not provided in time, other consequences may develop against the background of the underlying pathology:

tracheobronchitis;
pleurisy;
hemorrhagic encephalitis;
abscess of the pulmonary area.

The hemorrhagic type of inflammation is characterized by rapid development and can cause in the patient literally in 3-4 days. If the critical moment was prevented, then long-term treatment should be expected; the person will have general symptoms for a certain time in the form of:

weaknesses;
low-grade fever;
shortness of breath;
sweating;
lingering cough.

Diagnostics

Since the disease develops rapidly, diagnostic measures must be urgent and carried out as soon as possible.

In first place is performing an x-ray of lung tissue. In the image, the specialist should detect subtotal or total darkening and changes in the vessels (plethora).

A blood test is required, which shows the following results:

decrease in leukocytes;
increase in neutrophils;
eosinophilia and lymphocytopenia are present;
the red blood cell count is elevated.

Important! In addition to standard diagnostics, bronchoscopy is used, in which the bronchial lavage fluid is examined. The patient must be consulted by specialists such as a pulmonologist, infectious disease specialist, cardiopulmonologist and others.

The causes of the pathology in question are related to the underlying disease that provoked this complication. Sometimes differential diagnosis with diseases such as:

tuberculous pneumonia;
pulmonary infarction;
bronchiolitis and so on.

Treatment of serous-hemorrhagic disease

Treatment measures should be carried out as early as possible. A sick person must be hospitalized. Otherwise, death is not inevitable; it may occur as early as the third day.

Therapy is carried out comprehensively. Antiviral drugs are prescribed in high dosages. Breathing support measures are carried out. Oxygen therapy is provided. In severe cases, artificial ventilation is performed. Antibiotic therapy is prescribed with broad-spectrum drugs, also parenteral, using increased doses of the drug.

The following medications are also used:

interferons;
glucocorticoids – hormonal drugs;
human immunoglobulin or interferon;
low molecular weight anticoagulants;
infusion therapy:
- the volume of circulating blood channels is restored;
- detoxification.

Some patients receive plasma transfusions and infusion treatment.

With proper therapy, improvement occurs within 2 weeks. If alveolitis is present, the disease will subside in two months.

According to statistics, serous-hemorrhagic pneumonia occupies a leading position in mortality among all pneumonias. An important symptom, which should prompt you to see a doctor immediately, is blood in the sputum.

Prognosis for recovery

The prognosis for recovery will depend on the following factors:

Depending on the causative agent of the disease.
The severity of pneumonia.
From what period was intensive therapy started?
Presence of concomitant diseases.
Age indicators of the patient. The younger the patient, the higher his chances of a speedy recovery.

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Conclusion

All treatment measures for serous-hemorrhagic pneumonia are carried out in the department and intensive care. Even if it seems that the disease has subsided, focal signs of the inflammatory process will remain on the X-ray images for a long time. Complications of the disease are not uncommon; the outcome will depend on the correct and timely organization of treatment.

Hemorrhagic pneumonia. How does hemorrhagic pneumonia manifest?

Hemorrhagic inflammation is characterized by the formation of exudate in tissues, which, in addition to protein-rich fluid, includes a large number of red blood cells and very few leukocytes (hence the name inflammation).

The development of hemorrhagic inflammation is associated with severe damage to the vascular wall: it becomes so porous that red blood cells easily pass through it. With this inflammation, deep inflammatory circulatory disorders (stasis, thrombosis) are noted. All severe forms of infectious diseases (anthrax, swine fever, etc.) occur with phenomena of hemorrhagic inflammation.

The inflammatory process is acute, accompanied by tissue necrosis, for example, necrosis in the lymph nodes in anthrax, skin necrosis in chronic swine erysipelas. Quite often, hemorrhagic inflammation occurs in a mixed form with other inflammations (serous, fibrinous, purulent). For the most part it develops in the gastrointestinal tract, lungs, kidneys, lymph nodes; less often - in other organs.

Rice. 3. Hemorrhagic inflammation of the intestines

The process is usually focal, in the form of hemorrhagic infiltrates of the intestinal wall, mainly the submucosa.

Micro picture.Even with a low magnification of the microscope, one can see that the process has spread to the entire thickness of the mucous and submucous membranes. The mucous membrane is thickened, its structure is disrupted. The glands in it are poorly distinguished, the integumentary epithelium is in a state of necrosis, and is desquamated in areas. The villi are also partially necrotic. The surface of the mucosa, devoid of epithelium, appears in the form of continuous erosion, or ulcer. The connective tissue base of the mucosa is infiltrated with serous-hemorrhagic exudate.

The boundaries of the submucosa are sharply expanded due to the accumulation of exudate in it. Connective tissue bundles have undergone fiber disintegration. The vessels of the mucosa and submucosa (especially capillaries) are heavily injected. Inflammatory hyperemia is especially pronounced in the villi.

At high magnification, details of the lesion can be established. The cells of the integumentary necrotic epithelium are swollen, their cytoplasm is homogeneous, turbid, the nuclei are in a state of lysis or complete disintegration. All interstitial spaces of the mucosa and submucosa are filled with hemorrhagic exudate. The connective tissue fibers are swollen and in a state of lysis.

In a mixed form of hemorrhagic inflammation with fibrinous inflammation, fibrin fibers can be seen in the affected area.

Macro picture:the mucous membrane is thickened, gelatinous in consistency, colored red and dotted with hemorrhages. The submucosa is swollen, thickened, focally or diffusely reddened.

Explanations for the picture

Rice. 4. Hemorrhagic pneumonia

Hemorrhagic pneumonia is an inflammatory process with effusion of serous-hemorrhagic or hemorrhagic exudate into the pulmonary alveoli and interstitial connective tissue. It is observed in the form of diffuse serous-hemorrhagic edema or lobular and lobar inflammatory infarction of the lungs in anthrax and other severe diseases. Hemorrhagic pneumonia often occurs in combination with fibrinous pneumonia and can be complicated by purulent-necrotic processes or gangrene.

Micro picture.At low magnification, one can see greatly dilated vessels filled with red blood cells, especially the alveolar capillaries, which have a tortuous course and protrude nodularly into the lumen of the alveoli. The pulmonary alveoli and alveolar ducts are filled with hemorrhagic exudate, in which an admixture of fibrin, alveolar epithelial cells and single leukocytes are found in areas. The interstitial connective tissue is infiltrated with serous-hemorrhagic exudate, has undergone fiberization, and individual collagen fibers are swollen and thickened.

When combined with fibrinous inflammation, one can observe a staged process (areas of red, gray hepatization), and in case of complications - foci of necrosis and gangrenous decay of the lung tissue.

At high magnification, different areas of the preparation are examined in detail and clarified: changes in the alveolar capillaries, the nature of the exudate in the alveoli and alveolar ducts (serous-hemorrhagic, hemorrhagic, mixed with fibrin), the cellular composition of the exudate (erythrocytes, alveolar epithelium, leukocytes). Then they pay attention to the details of changes in the interstitial connective tissue (nature of infiltration, disintegration and swelling of collagen fibrils).

When the process is mixed with fibrinous inflammation, as well as when complicated by necrosis or gangrene, the corresponding areas of damage to the lung tissue are found and examined.

Macro picture:Depending on the form and nature of the inflammation, the appearance of the organ varies. With diffuse damage, the picture is of serous-hemorrhagic edema. If hemorrhagic pneumonia develops in the lobular or lobar form, the affected areas have sharply defined boundaries and are colored dark or black-red on the surface and on the cut, protrude somewhat under the pleura and above the cut surface, are dense to the touch, sink in water, the surface the cut is smooth, a small amount of bloody fluid drains from it. Expanded, gelatinous, pale yellow or black-red strands of the affected connective tissue clearly protrude on the cut surface.

DRAWINGS

Rice. 1. Serous-catarrhal bronchopneumonia involving interstitial tissue

(according to V.A. Salimov)

1. non-inflamed lung tissue; 2. area of lobar pneumonia; 3. interstitial tissue

Rice. 2. Serous inflammation and pulmonary edema, histostructure, x 100, G-E

Rice. 3. Serous-inflammatory pulmonary edema. Histostructure. Coloring G-E (according to V.A. Salimov)

A (x240). 1. the lumen of the alveoli, filled with exudate with cellular elements; 2. interalveolar septum (hardly noticeable); 3. lymph vessel; 4. valve of the lymph vessel, infiltrated with cells.

B (x480). 1. blood vessel in a state of inflammatory hyperemia; 2. air bubbles; 3. exudate with cellular elements of hematogenous origin and desquamated alveolar epithelium (the last cells are shown by arrows)

Rice. 4. Serous inflammation and pulmonary edema. Histostructure, x400, G-E

Rice. 5. Hemorrhagic inflammation of the intestine, histostructure, x100, type of mucous and submucous membranes, G-E

Rice. 6. Hemorrhagic inflammation of the intestine, histostructure, x400, view of the disintegrated mucous membrane with an emphasis on hemorrhagic exudate and cellular elements in it, G-E

Rice. 7. Hemorrhagic pneumonia due to anthrax in cattle. Histostructure. G-E (according to P.I. Kokurichev)

Explanations for the picture

Rice. 8. Fibrinous pleurisy. Histostructure, x40, G-E

Rice. 9. Fibrinous pleurisy. Histostructure, x150, G-E

Rice. 10. Fibrinous pleurisy. Histostructure, x 400, G-E

Rice. 11. Croupous pneumonia (according to V.A. Salimov)

A – stage of tide: 1. lobar lesion; 2. area of emphysema. B – involving the pericardium: 1. lobar lung damage (beginning of hepatization); 2. fibrinous pericarditis (“villous”, “hairy” heart)

Rice. 12. Lobar pneumonia. Histostructure (stage of tide and red hepatization), x 100. G-E

Rice. 13. Lobar pneumonia. Histostructure (stage of gray hepatization). Coloring G-E, x960 (according to V.A. Salimov)

1. alveoli; 2. weak alveolar septum; 3. hemosiderin deposits

Rice. 14. Lobar pneumonia. Histostructure, x 150. Photograph of a histological specimen at the border of areas of red hepatization (right) and gray hepatization (left), G-E

Rice. 15. Diphtheritic colitis (according to V.A. Salimov)

A – the affected area (circled) is visible through the serous layer; B – follicular ulcers on the mucous membrane (the center of the ulcers is brownish-green, the edges are swollen); B – diphtheritic ulcer: 1. cushion, 2. bottom, 3. mucous membrane in a state of hemorrhagic inflammation

Rice. 16. Diphtheritic colitis. Histostructure. Coloring G-E, x240 (according to V.A. Salimov)

A - review specimen: 1. hyperplasia of lymphoid cells; 2. blood vessel in a state of inflammatory hyperemia; 3. single glands; 4. necrosis of the free edge of the mucous membrane

B – ulcer border: 1. hyperplasia of lymphoid cells; 2. blood vessel; 3. area of hemorrhage

Rice. 17. Diphtheritic inflammation of the large intestine with necrosis of the mucous membrane and part of the submucous membrane. Histostructure, x100. G-E

Rice. 18. Diphtheritic inflammation of the large intestine with necrosis of the mucous membrane and part of the submucosa. Histostructure, x150. G-E

Rice. 19. Diphtheritic inflammation of the large intestine with necrosis of the mucous membrane and part of the submucous membrane. Histostructure, x400. Emphasis on the area of necrosis and perifocal inflammation. G-E

ADDITIONAL DRUGS

Rice. 9. Fibrinous pericarditis

Rice. 20. Fibrinous pericarditis (according to V.A. Salimov)

A – “villous” (“hairy”) heart: 1. heart, 2. lungs in a state of gangrene; B – “shell heart”

Rice. 21. Fibrinous pericarditis. Histostructure. Coloring G-E, (according to V.A. Salimov)

A (x240). 1. dilated blood vessel; 2. area of myocardial fiber disintegration; 3. thickening of the epicardium.

B (x480). 1.dilated blood vessel; 2. scattered and swollen myocardial fibers; 3. fibrinous exudate; 4. the beginning of the growth of connective tissue; 5. fibrin threads.

Rice. 22. Fibrinous pericarditis. Histostructure, x100. Coloring G-E

Rice. 23. Fibrinous pericarditis. Histostructure, x400. Coloring G-E

Explanations for the picture

FIBRINOUS INFLAMMATION

With fibrinous inflammation, exudate comes out of the vessels, containing a high percentage of the fibrinogen protein, which coagulates in the tissues and falls out in the form of a mesh or fibrous mass. In addition to fibrin, the exudate includes erythrocytes and leukocytes. It should be noted that the number of these and other blood cells in the exudate varies depending on the stage of the process. At the beginning of inflammation, the exudate is rich in red blood cells and can even be hemorrhagic in nature (with severe erythrodiapedesis), and there are few leukocytes in it. Subsequently, the red blood cells are gradually hemolyzed, and the exudate is enriched with leukocytes. The latter are especially numerous in the exudate before the stage of resolution of the inflammatory process. This point is important from a pathogenetic point of view, since leukocytes peptonize with their enzymes, dissolve fibrin, which is then absorbed through the lymphatic tract.

Fibrinous inflammation is usually accompanied by total or partial tissue necrosis. The breakdown products of dead tissue cause the coagulation of the exudate, just as in a thrombus the coagulation of blood is associated with the breakdown of platelets.

This type of inflammation is observed in severe infections (cattle plague, swine fever, salmonellosis, etc.), as well as in some poisonings or intoxications (sublimate, urea for uremia, etc.). Fibrinous inflammation manifests itself in two main forms: lobar and diphtheritic.

Croupous inflammation- superficial form of fibrinous inflammation. Developing on the mucous and serous membranes, it is expressed in the formation of filmy overlays (false films) from coagulated exudate on the free surfaces of them, while only the integumentary epithelium becomes necrotic. With this inflammation, the exudate does not saturate the tissue; it sweats and coagulates only on the surface, so its application (film) is easily removed. Inflammation usually develops diffusely and much less often becomes focal.

Diphtheritic inflammation- a deep form of fibrinous inflammation, mainly on the mucous membranes. In contrast to lobar inflammation, in diphtheritic inflammation, the exudate permeates the thickness of the mucous membrane, therefore, it cannot be removed, and if it is removed, then together with the underlying tissue, and a defect remains - a bleeding ulcer. Inflammation often develops focally, in patches, and is accompanied by deep necrosis, spreading not only to the entire thickness of the mucosa, but sometimes to the underlying layers. In the later stages of the process, deep necrosis leads to ulceration of the mucosa (due to decay and rejection of necrotic masses). The ulcers may then fill with granulation tissue and scar.

Rice. 5. Fibrinous pleurisy

Fibrinous pleurisy is a typical example of fibrinous inflammation of the serous membranes. It is characterized by sweating and coagulation of fibrinous exudate on the surface of the pleura, degeneration and necrosis of the integumentary epithelium, as well as serous cell infiltration of the entire thickness of the pleura. In the early stage of the process, inflammatory hyperemia and mild exudation are observed. The exudate, initially serous, begins to coagulate and deposit in small quantities between the cells of the integumentary epithelium. But mainly it falls on the surface of the serous integument, forming a soft fibrous plexus. A few leukocytes are found in the exudate. As exudative-infiltrative processes intensify, necrosis and desquamation of integumentary epithelial cells begin to develop as a consequence. The connective tissue of the pleura is infiltrated with serous cell exudate. If the process does not progress, the exudate is absorbed, followed by regeneration of the epithelium and restoration of the normal structure of the serous cover.

In most cases, there is an organization of exudate, which is expressed as follows. Already at an earlier stage of the process, from the side of the subepithelial connective tissue, young granulation tissue, rich in developing vessels and young forms of cellular elements of tissue and hematogenous origin, begins to grow into the exudate. This tissue gradually replaces the exudate, which is absorbed. Subsequently, young granulation tissue turns into mature fibrous tissue and then into scar tissue.

With simultaneous inflammation of the visceral and parietal layers, they first stick together, and when organization occurs, they grow together with the help of connective tissue adhesions.

Micro picture.During a microscopic examination of the drug, depending on the stage of the process, the picture of changes will be different.

In the early stage, one can see dilated vessels in the subepithelial connective tissue (inflammatory hyperemia), a small amount of fibrin precipitated between the epithelial cells, and its more pronounced accumulations on the surface of the pleura in the form of a soft fibrous mesh, stained with eosin in a pale pink color. A relatively small number of leukocytes with round, bean-shaped and horseshoe-shaped nuclei, stained with hematoxylin in a dark or pale blue color, are found in the exudate. The epithelial cells are swollen, with signs of degeneration; in some places you can see the desquamation of single or small groups of cells. At this stage, the overall epithelial cover is still preserved, so the pleura border is quite well defined. The boundaries of the subepithelial connective tissue are expanded, it is infiltrated with serous-cellular exudate (serous fluid with leukocytes).

At a later stage, when organization comes, the picture changes. On the surface of the pleura you can see abundant deposits of exudate, which looks like a thick, coarse fibrous plexus, and in the deep layers - a homogeneous mass. The exudate is rich in leukocytes, especially in the deep layers. Leukocytes are scattered singly or in groups, the nuclei of many of them are in a state of decay. The richness of leukocytes and homogenization of the exudate indicate the beginning of peptonization (dissolution) of the exudate under the influence of leukocyte enzymes, which is a preparation for its further resorption.

Under the layer of fibrinous exudate lies a paler colored zone (in the form of a wide strip) of overgrown granulation tissue, rich in young vessels (colored red) and cells. The newly formed tissue replaced the fibrinous exudate that was there. At high magnification, you can see that it consists predominantly of fibroblasts with unclear contours of the cytoplasm and a large, round-oval, pale blue nucleus (poor in chromatin). In addition, there are leukocytes, lymphocytes and other forms of cells with more intensely stained nuclei. Between the cells are collagen fibers (pale pink) running in all directions. In some places, the multiplying fibroblasts, together with the vessels, grow into the overlying layer of exudate, which has not yet undergone organization. The described zone is not sharply delimited from the underlying pleura, devoid of epithelial cover, which appears in the form of a thin layer, colored more intensely than the surrounding tissue, in a pinkish-red color.

Macro picture:the appearance of the affected pleura depends on the stage and duration of the process. In the early stages of the process, the pleura is covered with delicate, easily removable fibrinous deposits in the form of network-like plaques of gray-yellowish or pale gray color.

After removing fibrinous deposits, the surface of the pleura is hyperemic, cloudy, rough, and often dotted with small hemorrhages.

At the stage of organization, the pleura is thickened (sometimes very strongly), its surface is uneven, pitted or felt-like, pale gray in color. Fibrinous deposits are not separated. During the process of organization, the serous layers of the pleura can grow together with each other, as well as with the pericardium.

Explanations for the picture

Related information.

Serous inflammation

It is characterized by the abundance and predominance in the exudate of a watery, slightly cloudy liquid, poor in cellular elements and rich in proteins (3-5%). In contrast to the transudate, it is cloudy, slightly opalescent, and the transudate is transparent.

Depending on the location of the exudate, there are 3 forms of serous inflammation:

Serous-inflammatory edema.

Serous-inflammatory dropsy.

Bullous form.

Serous-inflammatory edema is characterized by the accumulation of exudate in the thickness of the organ between the tissue elements. It is more often found in loose tissue: subcutaneous tissue, in the stroma of organs, intermuscular tissue.

Its causes are burns, exposure to acids and alkalis, septic infections, physical factors (penetrating radiation), etc.

Macroscopically, serous-inflammatory edema is manifested by swelling or thickening of the stroma of the affected organ, leading to an increase in the volume of the organ or tissue, pasty consistency, reddened (hyperemia), with hemorrhages of various types. The cut surface also has gelatinous hemorrhages, with copious flow of watery exudate.

Serous-inflammatory edema must be distinguished from ordinary congestive edema, in which there is no macroscopically pronounced hyperemia and hemorrhage.

The outcome of serous-inflammatory edema depends on the nature and duration of the pathogenic factor. When the cause that caused it is eliminated, the serous exudate resolves and the damaged tissue is restored. When it becomes chronic, connective tissue grows in the damaged area.

Fig. 118. Serous inflammation of the subcutaneous tissue in a horse

Fig. 119. Serous inflammation of the stomach wall

Micro picture.

Under a microscope, in organs and tissues between the separated tissue elements (parenchyma cells, connective tissue fibers) a homogeneous, pinkish-colored mass (H-E stain) is visible with a small number of cellular elements (degenerated cells, histiocytes, erythrocytes and leukocytes (hyperemia) ), i.e. this is a serous exudate that permeates the stroma of the organ.

Serous-inflammatory dropsy- accumulation of exudate in closed and natural cavities (pleural, abdominal, in the cavity of the cardiac membrane). The reasons are the same as for serous-inflammatory dropsy, only the exudate accumulates not between the cellular elements, but in the cavities. Typically, the covers of cavities containing serous exudate, in contrast to dropsy, are reddened, swollen, with hemorrhages of various types. The exudate itself is cloudy, slightly opalescent yellowish or reddish in color with thin fibrin threads. With edema, the covers of the cavities are not changed, and the contents of the transudate are transparent. With cadaveric transudation, the serous covers are shiny, smooth, hyperemic without hemorrhages or tarnishing. And in the cavity they find a transparent red liquid. If the cause that caused serous inflammatory dropsy is eliminated, then the exudate resolves and the integument restores its original structure. When the process becomes chronic, the formation of adhesive processes (synechias) or complete fusion (obliteration) of the corresponding cavity is possible. Examples of serous-inflammatory dropsy are peritonitis, pericarditis, serous pleurisy, arthritis.

Bullous form

This is a form in which serous exudate accumulates under any membrane, resulting in the formation of a blister. The causes are burns, frostbite, infections (foot and mouth disease, smallpox), allergic factors (herpes), mechanical (water callus). External blisters vary in size. The smallest blisters with serous fluid are called imperigo, the larger ones are called vesicles, and the larger ones, examples of which are blisters in foot-and-mouth disease, are called aphthae. After the blister ruptures, a crust (crust) forms, which falls off after healing; the process is often complicated by a second infection and undergoes purulent or putrefactive decay. If the bladder does not rupture, the serous fluid resolves, the skin of the bladder shrinks, and the damaged area regenerates.

Target Theme Setting

Morphological features of serous inflammation and qualitative composition of serous exudate. Varieties of forms of serous inflammation (serous inflammatory edema, serous inflammatory edema, bullous form). Etiopathogenesis. Outcomes: In which infectious diseases serous inflammation most often develops.

Etiopathogenesis and morphological characteristics of serous inflammation.
Types of serous inflammation (serous inflammatory edema, serous-inflammatory dropsy, bullous form) and its difference from congestive edema and ascites.
In which infectious diseases is serous inflammation most common?
The outcome of serous inflammation and its significance for the body.

Conversation to familiarize students with their preparedness for classes. The teacher then explains the details.
Study of museum preparations, atlas and slaughterhouse material in order to become familiar with macroscopic (pathoanatomical changes) in serous pneumonia, serous hepatitis, serous inflammation of the skin (bullous form) in foot and mouth disease in cattle. Students, using the description scheme, describe the changes in the form of a brief protocol note and establish a pathological diagnosis. After which these protocols are read out and corrections are made in cases of inaccurate descriptions.
Study of histological preparations under a microscope. The teacher first explains the drugs using slides, then students, under the guidance of the teacher, study changes in serous pneumonia and immediately compare them with pulmonary edema. Find differences. Then drugs for serous inflammation of the skin (bullous form) in foot and mouth disease and serous hepatitis.

Serous inflammation of the lungs of the calf (serous inflammatory edema).
Hyperemia and pulmonary edema.
Serous inflammation of the lymph nodes in porcine pasteurellosis (serous inflammatory edema).
Serous inflammation of the skin in foot and mouth disease in cattle (foot and mouth disease), bullous form.
Serous inflammation of the intestines (serous inflammatory edema).

The study of preparations takes place according to the protocol description of microspecimens.

Remedy: Serous pneumonia

At low magnification of the microscope, it is established that most of the alveoli are filled with a homogeneous pale pink mass, and only a few alveoli do not have exudate, but their lumens are expanded, their diameter is equal to the diameter of 2-3 red blood cells, which is why in these places they are thickened nodularly and protrude into the lumen capillary. In places where the alveoli are overfilled with exudate, red blood cells are squeezed out of the capillaries, and the capillaries are consequently drained of blood. Small arteries and veins are also greatly dilated and filled with blood.

Fig. 120. Serous pneumonia:
1. Dilation of the capillaries of the walls of the alveoli (hyperemia);
2. Expansion of the lumen of the alveoli with accumulated exudate;
3. Hyperemia of a large vessel;
4. Accumulation of lymphoid cells in the bronchus

At high magnification, the serous exudate filling the alveoli appears as a homogeneous or granular mass (depending on the protein content). The same exudate is found in the interstitial peribronchial and perivascular connective tissue. and also in the bronchi. The connective tissue bundles, saturated with exudate, are loosened, their boundaries are expanded, and individual collagen fibers are swollen.

The exudate, mainly in the cavity of the alveoli, contains a small amount of polymorphonuclear leukocytes that have emigrated from the vessels, which can be easily identified by the shape of their nuclei (horseshoe-shaped, bean-shaped, etc.), intensely stained with hematoxylin. The alveolar epithelium is swollen, in many alveoli it is desquamated and necrotic. The rejected epithelial cells can be seen in the lumen of the alveoli along with leukocytes. These cells are quite large, lamellar-shaped, with a large round or oval pale-colored nucleus, poor in chromatin. While in the serous fluid, they swell, acquire a round shape instead of a lamellar one, and subsequently their cytoplasm and nucleus are lysed. Part of the alveoli contains in the exudate individual red blood cells that penetrated here from the respiratory capillaries through diapedesis.

As an expression of proliferative processes, one can note the appearance of histiocytic cells in the adevernitium of blood vessels and young epithelial cells along the alveolar walls. Proliferating cells are small in size, their nuclei are rich in chromatin. Sometimes it is also possible to trace signs of proliferation of the epithelium of the mucous membrane, mainly of the small bronchi.

In general, serous inflammation (or inflammatory edema) of the lungs is characterized by inflammatory hyperemia, accompanied by effusion and accumulation of serous exudate in the cavities of the alveoli, as well as serous edema of the interstitial perivascular and peribronchial connective tissue. Emigration of leukocytes and proliferative processes are weakly expressed. With a strong degree of edema, serous exudate from the alveoli enters the bronchioles, then into the large bronchi, and from here into the trachea.

Serous inflammatory edema, developing lobular or lobar, which is the initial stage of other inflammations of the lung (catarrhal, hemorrhagic, fibrinous) or is observed perifocally, that is, around the foci of lung damage in glanders, tuberculosis and other diseases.

With inflammatory edema, proliferation of adventitial, endothelial and epithelial cells is observed.

Macro picture: the lungs are not asleep, pale gray-red or dark red in color, doughy consistency, float heavily, often drown in water, small hemorrhages are often found under the pleura and in the parenchyma. A cloudy, pinkish, foamy liquid flows from the cut surface. With a strongly pronounced effusion of serous exudate of the same nature, the liquid is located in the large bronchi and the caudal part of the trachea. The cut surface of the organ is juicy, light or dark red in color, against the background of which gelatinous strands of interstitial connective tissue impregnated with serous exudant clearly protrude.

intestines (serous inflammatory edema)

The drug is studied in the following order. First, at low magnification, all layers of the intestinal wall are found and it is determined from which part of the intestine the section was made. Then, focusing on the general picture of the lesion, it is noted that the most demonstrative changes are in the submucosal layer, the boundaries of which are greatly expanded. Instead of loose connective tissue of the usual structure, a widely looped network is found here, formed by thin collagen pieces or fibers, and pale-colored homogeneous or granular masses of exudate are located in bunches. When fixed, it usually curls up and appears in the form of a delicate mesh. In the exudate of the submucosal layer, single cellular elements with a blue nucleus and erythrocytes are found. Clusters of cells are observed mainly along the vessels, dilated and filled with red blood cells. An exudate of this nature, poor in cells, can easily be defined as serous. The noted changes in the vessels characterize pronounced inflammatory hyperemia, accompanied by the emigration of leukocytes and diapedetic hemorrhages, and the accumulation in the submucosal layer of a large amount of serous exudate indicates a pronounced exudative component in the picture of inflammation as a whole.

Fig. 121. Serous inflammation of the intestines:
1. Serous inflammatory edema between the crypts;
2. Desquamated integumentary epithelium of the crypts;
3. Serous edema of the mucous membrane

At high magnification, it can be established that the cellular elements located around the vessels can be classified as polymorphonuclear leukocytes, among which there are multiplying cells of the vascular wall with a round or oval nucleus, pale-stained with hematoxylin. A small number of them indicates a weakly manifested proliferative component.

Moving on to the study of the mucous membrane, pay attention to the integumentary epithelium of the crypts. It underwent degeneration, necrosis (alterative component) and desquamation. Crypts have the appearance of elongated sac-like structureless (or with a poorly distinguishable structure) formations, painted in a gray-bluish color. The recesses (lumens) of the crypts are filled with epithelial decay products. The vessels of the mucous membrane are in a state of inflammatory hyperemia. The thickness of the mucosa is infiltrated in places with serous exudate and leukocytes. In the muscle layer, dystrophy of muscle fibers, partial necrosis and accumulation of a small amount of serous cell exudate between the muscle bundles are noted. The latter also accumulates under the serous membrane, the covering epithelium of which is in a state of dystrophy and is desquamated in areas.

Analyzing the picture of intestinal damage as a whole, we can conclude that it is characterized by the development of acute serous inflammation. The most pronounced serous edema is in the submucosal layer, the structural features of which (loose fiber) contributed to a significant accumulation of exudate in it, which caused fiber disintegration and disruption of the normal structure of the submucosal layer. Inflammatory edema in the remaining layers of the intestinal wall is weakly expressed. In addition to the submucosal membrane, a significant amount of exudate is also distributed into the intestinal lumen.

Macro picture: the intestinal wall is greatly thickened (in horses up to 5-10 cm), the mucous membrane is hyperemic, swollen, dull, sometimes riddled with small hemorrhages. With severe swelling, it is gathered into undulating folds and ridges. On section, the mucosa and especially the submucosa appear in the form of gelatinous infiltrates of a pale yellow color. The intestinal lumen contains a lot of clear or cloudy serous fluid.

Remedy: Serous inflammation
lungs (serous inflammatory edema)

At low magnification of the microscope, it is established that most of the alveoli in the lumens contain a homogeneous pale pink mass and only individual alveoli or groups of them, having expanded lumens, are free from effusion.

The respiratory capillaries are heavily injected with blood, dilated, and in some places nodularly thickened, as a result of which they protrude into the lumen of the alveoli. Hyperemia of the respiratory capillaries is not expressed everywhere; in some places you can see the walls of the alveoli not collapsed, with bloodless capillaries as a result of the pressure on them from the effusion or air accumulated in the alveoli. Small arteries and veins are also greatly dilated and filled with blood.

Fig. 122. Serous inflammatory edema with purulent inflammation:
1. Serous exudate in the lumens of the alveoli;
2. Hyperemia of the capillaries of the alveoli;
3. Vessel hyperemia.

At high magnification, the serous exudate filling the alveoli appears as a homogeneous or granular mass (depending on the protein content). The same exudate is found in the interstitial periobronchial and perivascular connective tissue. and also in the bronchi. Connective tissue bundles, saturated with exudate, are loosened, their boundaries are expanded, and individual collagen fibers are swollen.

The exudate, mainly in the cavity of the alveoli, contains a small amount of polymorphonuclear leukocytes that have emigrated from the vessels, which are easily identified by the shape of their nuclei (horseshoe-shaped, bean-shaped, etc.), intensely stained with hematoxylin. The alveolar epithelium is swollen, in many alveoli it is desquamated and necrotic. rejected epithelial cells can be seen in the lumen of the alveoli along with leukocytes. These cells are quite large, lamellar-shaped, with a large round or oval pale-colored nucleus, poor chromatin. While in the serous fluid, they swell, acquire a round shape instead of a lamellar one, and subsequently their cytoplasm and nucleus are lysed. Part of the alveoli contains in the exudate individual red blood cells that penetrated here from the respiratory capillaries through diapedesis.

As an expression of proliferative processes, one can note the appearance of histiocytic cells in the adventitia of blood vessels and young epithelial cells along the alveolar walls. Proliferating cells are small in size, their nuclei are rich in chromatin. sometimes it is also possible to trace signs of proliferation of the epithelium of the mucous membrane, mainly of the small bronchi.

Serous inflammatory edema, developing lobular or lobar, is often the initial stage of other inflammations of the lung (catarrhal, hamorrhagic, fibrinous) or is observed perifocally, that is, around the foci of lung damage in glanders, tuberculosis and other diseases.

It must be borne in mind that inflammatory pulmonary edema is histologically similar to congestive pulmonary edema. The main distinguishing features that allow for differential diagnosis include the following:

With congestive edema, not only the respiratory capillaries are hyperemic, but also the venous vessels (especially small veins);

In inflammatory edema, proliferation of adventitial, endothelial and epithelial cells is observed.

Macro picture: the lungs are uncollapsed, pale gray-red or dark red in color, dough-like consistency, float heavily or sink in the water, small hemorrhages are often found under the pleura and in the parenchyma. From the surface of the cut and from the lumens of the cut bronchi, a foamy, cloudy liquid, sometimes colored pink, is squeezed out and drains. With severe edema of the same nature, fluid is contained in the large bronchi and the caudal part of the trachea. The cut surface of the organ is smooth, juicy, light or dark red in color, against which expanded gelatinous strands of interstitial connective tissue infiltrated with serous exudate clearly appear.

Drug: Afta for foot and mouth disease in cattle

At low magnification of the microscope, epithelial cells of the spinous layer are visible, which are increased in volume and have a rounded shape. In their cytoplasm, the affected cells are colored paler than unchanged ones; some cells look like vesicles with nuclei in a state of lysis. In other places, in place of the cells, large voids are visible, the size of which is several times larger than the size of the epithelial cells of the spinous layer (these are aphthae formed as a result of the degeneration of the epithelial cells of the spinous layer and the effusion of serous exudate).

Fig. 123. Foot and mouth disease:
voids of varying sizes (vacuoles).

At high magnification, we note in the aphtha zone that the cavity is filled with liquid, in which degenerated cells of the spinous layer of the epidermis are visible. Some are enlarged, pale colored, the nucleus in them is not identified due to its lysis. Other cells contain a nucleus in the form of a vesicle filled with fluid. Neutrophilic leukocytes and single histiocytic cells are visible in the serous fluid. The lid of the vesicle is represented by horn cells. The epithelial cells that make up the wall of the vesicle are represented by degenerated cells of the spinous layer and hyperemia of the capillaries and adjacent vessels. In many epithelial cells, vacuoles containing a clear fluid are visible, the nuclei are in a state of lysis, the cytoplasm is preserved in the form of threads, a serous fluid is visible between the cells, which separates the cells, it contains leukocytes, single histiocytes are visible near the capillaries. Subsequently, dropsy degeneration of the walls of the vesicle occurs, the influx of serous exudate and aphtha increases in size. The lid of the stratum corneum becomes thinner and the aphtha bursts. Exudate pours out.

Fig. 124. Foot and mouth disease:
1. In the cytoplasm of epithelial cells of the spinous layer
voids of varying sizes (vacuoles).

Outcomes. If there is no complication of a second infection, then healing proceeds according to primary healing. If a complication occurs with a purulent or putrefactive infection, then scarring of the aphthae occurs.

Macro picture: aphtha in the form of a bubble of a round, oval or hemispherical shape, filled with a transparent pale yellow liquid. (Bullous form of serous inflammation).

Fig. 125. Foot and mouth aphthae in the rumen.

1.2. Hemorrhagic inflammation

Hemorrhagic inflammation is characterized by a predominance of blood exudate. Typically, this type of inflammation develops with severe septic infections (anthrax, swine erysipelas, pasteurellosis, swine fever, etc.), as well as severe intoxication with potent poisons (arsenic, antimony), and other poisons. In addition, hemorrhagic inflammation can develop during allergic conditions of the body. With all these factors, the porosity of the vessels is sharply disrupted, and a large number of red blood cells exit the vascular wall, as a result of which the exudate takes on a bloody appearance. As a rule, this type of inflammation occurs acutely with the development of necrosis.

Macroscopically, the organ and tissues are saturated with blood, significantly increased in volume and have a blood-red color; bloody exudate flows down the section of the organ. The fabric pattern on the cut is usually erased.

With hemorrhagic inflammation of the gastrointestinal tract, serous membranes of cavities, bloody exudate accumulates in the intestinal lumen and cavities. In the gastrointestinal tract, over time, under the influence of digestive juices, it becomes black.

The outcome of hemorrhagic inflammation depends on the outcome of the underlying disease; in case of recovery, the exudate can be absorbed with the further development of regenerative processes.

Hemorrhagic inflammation must be differentiated: from bruises, in which the boundaries of the bruise are clearly defined, swelling and necrosis are not expressed; hemorrhagic infarctions, in which there is a typical triangle on the cut, and in the intestine they, as a rule, form at the site of volvulus and twisting; from cadaveric transudation, with it the contents are transparent, and the walls of the cavities are smooth and shiny.

Localization of hemorrhagic inflammation is most often observed in the gastrointestinal tract, lungs, kidneys, lymph nodes and less often in other organs.

Theme target setting:

Etiopathogenesis. Morphological characteristics of hemorrhagic inflammation. In which infectious diseases is this type of inflammatory reaction most common? Outcome of hemorrhagic inflammation.

The main focus is on the following issues:

Features in the composition of exudate in hemorrhagic inflammation. Etiopathogenesis of this type of inflammation. Infections in which this type of inflammation most often occurs.
Localization of hemorrhagic inflammation. Morphological characteristics of hemorrhagic inflammation of compact and cavitary organs (peculiarities of coloring of hemorrhagic inflammation in the intestine depending on the duration of the process).
Outcome of hemorrhagic inflammation. Importance for the body.

A conversation to familiarize yourself with the preparedness of students to work on the topic of a laboratory lesson. The teacher then explains the details.
Study of museum preparations and slaughterhouse material in order to become familiar with the macro- and micropicture of hemorrhagic inflammation.
Reading by students of a protocol recording describing the macroscopic picture of hemorrhagic inflammation.

Hemorrhagic pneumonia in cattle pasteurellosis and swine fever.
Hemorrhagic lymphadenitis of the lymph nodes due to swine fever.
Hemorrhagic inflammation of the caeca of chickens with coccidiosis.
Atlas.
Tables.

Microspecimens:

Hemorrhagic pneumonia.
Hemorrhagic inflammation of the intestines.

The teacher on the slides gives a brief description of the micropicture of hemorrhagic pneumonia and hemorrhagic inflammation of the intestines; students independently study these processes under a microscope, schematically sketching the process being studied in notebooks, with an arrow indicating the main microscopic changes in this inflammation.

Drug: Hemorrhagic
pneumonia

Hemorrhagic pneumonia is an inflammatory process with effusion of serous-hemorrhagic or hemorrhagic exudate into the pulmonary alveoli and interstitial connective tissue. It is observed in the form of diffuse serous-hemorrhagic edema or lobular and lobar inflammatory infarction of the lungs in anthrax, equine hemorrhagic disease and other severe diseases. Hemorrhagic pneumonia often occurs in combination with fibrinous pneumonia and can be complicated by purulent-necrotic processes or gangrene.

At low magnification, one can see greatly dilated vessels filled with red blood cells, especially the alveolar capillaries, which have a tortuous course and protrude nodularly into the lumen of the alveoli. The pulmonary alveoli and alveolar ducts are filled with hemorrhagic exudate, in which an admixture of fibrin, alveolar epithelial cells and single leukocytes are found in areas. The interstitial connective tissue is infiltrated with serous-hemorrhagic exudate, has undergone fiberization, and individual collagen fibers are swollen and thickened.

Fig. 126. Hemorrhagic pneumonia:
1. Hemorrhagic exudate in the lumen of the alveoli;
2. Alveolar epithelium, lymphocytes

When combined with fibrinous inflammation, one can observe a staged process (areas of red, gray hepatization), and in case of complications - foci of necrosis and gangrenous decay of the lung tissue.

At high magnification, different areas of the preparation are examined in detail and clarified: changes in the alveolar capillaries, the nature of the exudate in the alveoli and alveolar ducts (serous-hemorrhagic, hemorrhagic, mixed with fibrin), the cellular composition of the exudate (erythrocytes, alveolar epithelium, leukocytes). Then they pay attention to the details of changes in interstitial connective tissue (nature of infiltration, disintegration and swelling of collagen fibrils).

When the process is mixed with fibrinous inflammation, as well as when complicated by necrosis or gangrene, the corresponding areas of damage to the lung tissue are found and examined.

Macro picture: depending on the form and nature of inflammation, the appearance of the organ is not the same. With diffuse damage, the picture is of serous-hemorrhagic edema. If hemorrhagic pneumonia develops in the lobular or lobar form, the affected areas have sharply defined boundaries and are colored dark or black-red on the surface and on the cut, protrude somewhat under the pleura and above the cut surface, are dense to the touch, sink in water, the surface cut, rather dense to the touch, sink in water, the surface of the cut is smooth, a small amount of bloody fluid drains from it. Expanded, gelatinous, pale yellow or black-red strands of the affected connective tissue clearly protrude on the cut surface.

Drug: 2. Hemorrhagic
intestinal inflammation

The process is usually focal, in the form of hemorrhagic infiltrates of the intestinal wall, mainly the submucosa.

Even with a low magnification of the microscope, one can see that the process has spread to the entire thickness of the mucous and submucous membranes. The mucous membrane is thickened, its structure is disrupted. The glands in it are poorly distinguished, the integumentary epithelium is in a state of necrosis, and is desquamated in areas.

The villi are also partially necrotic. The mucosal surface, devoid of epithelium, appears as a continuous erosion or ulcer. The connective tissue base of the mucosa is infiltrated with serous-hemorrhagic exudate. The boundaries of the submucosa are sharply expanded due to the accumulation of exudate in it. Connective tissue bundles have undergone fiber disintegration. The vessels of the mucosa and submucosa (especially capillaries) are heavily injected. Inflammatory hyperemia is especially pronounced in the villi.

In a mixed form of hemorrhagic inflammation with fibrinous inflammation, fibrin fibers can be seen in the affected area.

Macro picture: the mucous membrane is thickened, gelatinous in consistency, colored red and dotted with hemorrhages. The submucosa is swollen, thickened, focally or diffusely reddened.

Fig. 127. Hemorrhagic inflammation of the abomasum of cattle

Fig. 128. Hemorrhagic inflammation of the horse's intestine

Fig. 129. Hemorrhagic inflammation with necrosis of the mucous membrane
small intestine of cattle (intestinal form)
for anthrax

Fig. 130. Hemorrhagic inflammation of the mesenteric lymphatics
cattle knots

1.3. Purulent inflammation

It is characterized by the predominance of neutrophilic leukocytes in the exudate, which, undergoing degeneration (granular, fatty, etc.), turn into purulent bodies. Purulent exudate is a cloudy, thick liquid that is pale yellow, white, or greenish in color. It consists of 2 parts: purulent bodies (degenerated leukocytes), products of the breakdown of tissues and cells and purulent serum, which, during the breakdown of leukocytes, tissues, cells and other elements, is enriched with enzymes, biologically active substances, as a result of which it acquires the properties of dissolving fabrics. Therefore, the cells of organs and tissues, in contact with purulent exudate, undergo melting.

Depending on the ratio of purulent bodies and serum, pus is distinguished between benign and malignant. Benign - its composition is dominated by purulent bodies, its consistency is thick, creamy. Its formation characterizes the body's high reactivity. Malignant pus has the appearance of a turbid, watery liquid; it contains few purulent bodies and is dominated by lymphocytes. Typically, such pus is observed in chronic inflammatory processes (long-term non-healing trophic ulcers, etc.) and indicates low reactivity of the body.

As a result, the following main forms of purulent inflammation are distinguished: purulent catarrh, purulent serositis. With the development of purulent inflammation in tissues or organs, two types are distinguished: phlegmon and abscess.

Purulent catarrh - the mucous membranes are saturated with serous-purulent exudate (mucosal degeneration and necrosis of epithelial cells, hyperemia, swelling of the stroma with infiltration of purulent bodies).

Macro picture. Abundant purulent exudate with an admixture of mucus on the surface of the mucosa. When removing the exudation, erosions are found (areas of the mucosa devoid of integumentary epithelium), the mucosa is swollen, reddened with striped and spotty hemorrhages.

Purulent serositis is a purulent inflammation of the serous covers of natural cavities (pleura, pericardium, peritoneum, etc.). As a result of this process, pus accumulates in the corresponding cavity, which is called empyema. The serous covers are swollen, dull, reddened with erosions and spotty-banded hemorrhages.

Phlegmon is a diffuse purulent inflammation of loose tissue (subcutaneous, intermuscular, retroperitoneal, etc.). The process is characterized initially by the development of serous and serous-fibrinous inflammatory edema of the tissue, followed by rapid necrosis, and then purulent infiltration and melting of the tissue. Cellulitis is more often observed where purulent infiltration occurs easily, for example, along the intermuscular layers, along the tendons, fascia in the subcutaneous tissue, etc. Tissues affected by phlegmonous inflammation are swollen, dense at the beginning of the development of the process and later have a pasty consistency, bluish-red color, and are diffusely saturated with pus on the incision.

The macro picture of phlegmon is characterized by the accumulation of purulent exudate between the separated tissue elements. The vessels are dilated and filled with blood.

An abscess is a focal purulent inflammation, which is characterized by the formation of a delimited focus consisting of a purulent molten mass. Around the formed abscess, a shaft of granulation tissue rich in capillaries is formed, through the walls of which increased emigration of leukocytes occurs.

This shell on the outside consists of layers of connective tissue and is adjacent to unchanged tissue. Inside, it is formed by granulation tissue and a layer of thickened pus, tightly adjacent to the granulations and continuously renewed due to the release of purulent bodies. This pus-producing membrane of the abscess is called the pyogenic membrane. Macroscopically, abscesses can range from barely noticeable to large (15-20 cm or more in diameter). Their shape is round, when palpating superficially located abscesses, fluctuation (ripple) is noted, and in other cases, strong tissue tension.

Fig. 131. Focal purulent inflammation of the liver (abscess)

Fig. 132. Multiple abscesses in the lungs of a sheep

Outcome of purulent inflammation

In cases where the purulent inflammatory process is not delimited by a zone of reactive inflammation, which occurs when the body’s resistance is weakened, generalization of the infection may occur with the development of pyosepsis and the formation of multiple ulcers in organs and tissues. If the reactive forces are sufficient, then the purulent process is delimited by a zone of reactive inflammation and an abscess is formed, then it is opened either spontaneously or surgically. The resulting cavity is filled with granulation tissue, which, when mature, forms a scar. But there may be such an outcome: the pus thickens, turns into necrotic detritus, undergoing petrification. In other cases, an abscess may encyst, when the purulent exudate resolves faster than the connective tissue grows, and a cyst (fluid-filled cavity) forms at the site of the abscess. Phlegmonous inflammation often passes without a trace (exudate resolves), but sometimes abscesses form or diffuse proliferation of connective tissue occurs at the site of phlegmon (elephantiasis of the skin).

Target setting:

Purulent inflammation. Definition of the concept. Characteristics of purulent exudate. Pathological forms of purulent inflammation. Outcomes. Importance for the body.

The main focus is on the following issues:

Purulent inflammation. Definition of the concept. Composition of purulent exudate and its properties.
Morphological characteristics of purulent catarrh, purulent serositis, phlegmon, abscess (macro- and micropicture).
Outcomes of purulent inflammation. Importance for the body.

Conversation with students on a given topic. Clarification of unclear aspects of the process being studied.
Study of the macro- and micropicture of purulent catarrh, purulent serositis, phlegmon, abscess on museum preparations and slaughterhouse material by describing the macropicture and studying the picture of purulent inflammatory processes under a microscope.

List of museum preparations:

Calf purulent bronchopneumonia.
Cattle liver abscess.
Actinomycosis of the scalp of cattle.
Embolic purulent nephritis of the kidney (kidney microabscesses).
Purulent inflammation of the mucous membrane of the trachea of cattle.
Purulent pericarditis in cattle.

List of micropreparations:

Embolic purulent nephritis.
Purulent bronchopneumonia.
Phlegmon of subcutaneous tissue.

Drug: Embolic
purulent nephritis

Embolic purulent nephritis occurs when foreign bacteria are introduced into the kidneys by hematogenous route from primary purulent foci (ulcerative endocarditis, purulent endometritis, bronchopneumonia, etc.). Pyogenic microbes often settle in the arterioles of the glomeruli and here they begin to multiply, causing purulent melting of the glomerular tissue with the subsequent formation of an abscess. Small abscesses, progressing, merge into large ones. In other cases, when foreign microbes clog an arterial branch, a heart attack develops, which undergoes purulent softening. Interstitial connective tissue undergoes purulent infiltration. Dystrophic and necrotic changes are observed in the epithelium of convoluted tubules, this is especially pronounced in the tubules surrounding abscesses.

Under a microscope at low magnification in the initial stage of the development of the process, we find foci of necrosis of the renal tissue (glomeruli or tubules), at the same time we note hyperemia of the capillaries and larger vessels. From the periphery of necrotic areas we note leukocyte infiltration. Leukocytes fill the lumens of the tubules and glomerular capsules. Emboli have the appearance of rough, basophilic-staining formations of various sizes in the form of spots and heaps. At high magnification they appear as a fine-grained mass. In the later stages of the inflammatory process, at low magnification, we note in the parenchyma of the cortical and medulla layers of varying sizes, areas consisting of accumulations of cellular elements, intensely blue (hematoxylin-eosin staining). These are areas of purulent melting of the kidney tissue (abscesses). As a rule, in the cortical layer they are round or oval in shape, in the medulla they are oblong (along the straight tubules). The structure of the renal tissue in abscesses does not differ.

Fig. 133. Embolic purulent nephritis:
1. Serous exudate;
2. Emboli in the form of rough blue formations;
3. Leukocyte infiltration of kidney tissue;
4. Vascular hyperemia

At high magnification, abscesses consist of accumulations of polymorphonuclear leukocytes, their nuclei are changed (deformation, disintegration into lumps, appearance of vacuoles). This indicates their dystrophy. Among the leukocytes we find decaying epithelial cells, fragments of connective tissue fibers, and an admixture of erythrocytes. With special staining, microbes can be detected in abscesses. A fine-grained mesh between the cellular elements is visible in some areas - this is serous exudate. All of the listed components form pus. In the tissues surrounding abscesses, the vessels and capillaries are filled with blood, and hemorrhages occur in places. Epithelial cells in some cases are in a state of granular degeneration, in others - necrosis.

In cases of prolonged purulent inflammation, instead of neutrophils, many lymphocytes appear in the exudate, and along the periphery of the abscess, lymphoid cells, fibroblasts and other cells are visible, which form granulation tissue around it. Over time, it turns into a connective tissue capsule (encapsulation).

Macro picture. The kidneys are enlarged in volume, flabby consistency, hemorrhages and multiple pustules of various sizes are visible from the surface and on the section, from poppy seeds to peas and larger (in the cortical layer they are round, in the medullary layer they are oblong), gray-yellow in color with a red rim along the periphery. The parenchyma is unevenly colored, dark red areas alternate with gray-white ones (hyperemia, hemorrhages, granular degeneration). When the pustules are cut, creamy yellowish-green pus is released from them. In the chronic form of inflammation around the pustules, a pale gray rim of varying width is visible - this is a connective tissue capsule (encapsulation).

Drug: Purulent
bronchopneumonia

With it, the inflammatory process spreads primarily through the bronchi, moving to the alveoli. With extensive lesions, the lung tissue undergoes melting over large areas and is then replaced by connective tissue (carnification and fibrinous hardening of the lung). In other cases of complications, abscess formation of the affected lung occurs or gangrene develops. Purulent bronchopneumonia develops when food is aspirated into the lungs, when pus enters from opened abscesses in the pharynx and larynx, and as a complication of other pneumonia.

At low magnification, we find the affected bronchus (its lumen cannot be determined), filled with purulent exudate, which is intensely colored. Hematoxylin is blue in color due to the large number of leukocytes it contains. Around the bronchus, alveoli are visible, stretched with purulent exudate, which is similar in composition to the contents of the bronchi. The boundaries between the alveoli are poorly distinguished and are determined only by the red network of hyperemic capillaries of the alveoli. (At high magnification, red blood cells are visible in their lumens).

Fig. 134. Purulent bronchopneumonia:
1. The lumen of the bronchus is filled with purulent exudate;
2. Alveoli filled with purulent exudate;
3. Serous exudate in the alveoli

Fig. 135. Purulent pneumonia:
1. Purulent exudate in the alveoli;
2. Hyperemia of the blood vessel;
3. Hyperemia of the capillaries of the alveolar septa of the alveoli;
4. Growth of peribronchial connective tissue;
5. Bronchus.

At high magnification, the exudate in the lumens of the bronchi consists predominantly of polymorphonuclear leukocytes, the nuclei of most of them are in a state of decay. Among the leukocytes are desquamated cells of the bronchial epithelium, single histiocytes and erythrocytes, and serous-mucosal fluid. The mucous membrane is swollen, saturated with polymorphonuclear leukocytes, the integumentary epithelium is desquamated (desquamation). Perebronchial connective tissue is infiltrated with leukocytes. Exudate in the alveoli located around the affected bronchus consists of serous exudate, polymorphonuclear leukocytes, single histiocytes and erythrocytes and desquamated alveolar epithelial cells (pink with a blue nucleus). The alveolar wall is thickened due to the strong expansion of the alveolar capillaries, the diameter of which is equal to the diameter of 2-3 red blood cells. Polymorphonuclear leukocytes are also visible in the lumens of the capillaries. In areas of complete purulent melting of the alveolar walls, they are not distinguished.

Macro picture. The lung is inactive, sharply reddened with multiple hemorrhages; from the surface and on the cut, purulently softened areas of various sizes from a pea to a hazelnut are visible. Purulent masses are gray-yellow or yellow in color. A thick purulent mass is released from the bronchi. Buoyancy test of the affected parts - a piece of the lung sinks in water.

Fig. 136. Ulcers in the lungs of a sheep

Fig. 137. Multiple purulent lesions in the kidney of a foal (septicopyemia)

Remedy: Subcutaneous phlegmon
fiber

Cellulitis in the subcutaneous tissue often develops with severe injuries or deep wounds, followed by the introduction of pyogenic bacteria and subsequent purulent melting of the dead areas.

At low magnification, we note that the most typical changes are noted in the subcutaneous tissue, while the epidermis is little changed (mainly perivascular infiltrates). In the subcutaneous tissue, the connective tissue bundles are infiltrated with leukocytes and serous fluid, as a result of which they appear thickened. In places, continuous accumulations of leukocytes are visible, and the outlines of connective tissue fibers do not differ. Blood clots are visible in some blood vessels. Adipose tissue is also infiltrated with leukocytes. Blood vessels and capillaries are dilated and filled with blood, and cellular accumulations are also visible around the vessels. Lymphatic vessels are also dilated and filled with leukocytes. Some of them contain blood clots. Necrotic connective tissue bundles surrounded by leukocytes are visible.

Fig. 138. Phlegmon of subcutaneous tissue:
1. Necrotic areas of connective tissue bundles;
2. Infiltrate of polymorphonuclear leukocytes

At high magnification, we examine the inflammatory cellular infiltrate; it consists of polymorphonuclear leukocytes, lymphocytes, and serous exudate. In areas of necrosis of connective tissue bundles, a structureless pink mass with blue lumps of nuclear chromatin (disintegrated nuclei) is visible.

Macro picture. The affected area of the skin is swollen, dense at the beginning and a doughy consistency later. Depigmented and hairless skin has patchy or diffuse redness, and thickened cords of lymph vessels are visible. When abscesses develop, fistulous tracts open in the corresponding places, through which pus is released. When cut, areas of necrosis and purulent infiltration of loose tissue are visible.

1.4. Catarrh

Catarrhal inflammation develops on the mucous membranes and the most significant for the composition of catarrhal exudate is the presence of mucus in the composition with other components (products of alteration, exudation, proliferation).

Depending on the predominance of certain components in the exudate, catarrhs are distinguished (serous, mucous, purulent or desquamative, hemorrhagic).

Mucous catarrh - the exudate is dominated by mucus and desquamated degenerated cells of the integumentary epithelium. Essentially this is an alternative type of inflammation. The mucous membrane is usually swollen, reddened with spotty-banded hemorrhages and covered with a large amount of cloudy mucous mass.

Serous cautery - the exudate is dominated by turbid, colorless serous liquid. The mucous membranes are glassy swollen, reddened, and dull.

Purulent catarrh - purulent bodies (degenerated leukocytes) predominate in the exudate. There is a purulent exudate on the surface of the mucosa, upon removal of which erosions (superficial defects of the mucosa) are revealed. The mucous membrane is swollen, reddened with hemorrhages.

Hemorrhagic catarrh is a predominance of erythrocytes in the exudate, which give the exudate a bloody appearance. On the surface of the mucous membranes there is a large amount of mucous, bloody exudate, which, under the influence of hydrochloric acid and enzymes of the gastrointestinal tract, takes on the appearance of a coffee mass or black color. The mucous membrane quickly becomes dirty gray in color.

According to the severity of the course, catarrhs are divided into acute and chronic. In acute catarrhal inflammation, the mucous membrane is swollen, reddened, with spotty and striped hemorrhages, covered with viscous, liquid, cloudy mucus (catarrhal exudate) with an admixture of purulent bodies or red blood cells, depending on the type of catarrh, easily washed off with water.

With chronic catarrhal inflammation, the mucous membrane thickens or unevenly, depending on the focal or diffuse nature of the inflammatory process, and has a lumpy appearance. The color is pale, coarsely folded. Covered with thick, cloudy mucus that is difficult to wash off with water. Folds cannot be straightened by hand.

Target Theme Setting

Morphological features of catarrhal inflammation and its localization. A type of catarrhal inflammation of the mucous membranes based on the nature of the exudate. Morphological manifestations of catarrhal pneumonia. Morphological features of acute and chronic catarrhal inflammation. Outcomes. In which infectious diseases is this type of inflammation most common?

The main focus is on the following issues:

Morphological features of catarrhal exudate in contrast to other types of inflammation (according to the composition of the exudate and the localization of the inflammatory process).
Morphological features of acute and chronic catarrhal inflammation. Exodus.
Etiopathogenesis and pathomorphology of catarrhal bronchopneumonia of its acute and chronic forms and morphological features in contrast to other pneumonias (serous, hemorrhagic, fibrinous, purulent).

A conversation to familiarize students with the preparation for classes, then the teacher explains the details.
Study of museum preparations, atlas and slaughterhouse material in order to become familiar with the macropicture of pathological changes in acute and chronic catarrhal gastroenteritis, catarrhal bronchopneumonia (acute and chronic form). Students, using the description scheme, in the form of a brief protocol note, describe the studied pathological changes in catarrh and, in conclusion, establish a pathological diagnosis. At the end of this work, the protocols are read out and corrections are made to them (in cases of inaccurate descriptions).
Study of pathological processes on histological preparations. The teacher first explains the drugs using slides and drawings on the board, and then students, under the guidance of the teacher, using a teaching aid, study histological changes in acute and chronic enteritis, acute and chronic bronchopneumonia. Students schematically sketch pathological changes during the named processes.

Fig. 139. Catarrhal inflammation of the pig's stomach

Fig. 140. Acute catarrhal inflammation of the intestines

Fig. 141. Catarrhal-purulent bronchopneumonia in a calf

List of wet museum preparations:

Chronic catarrhal inflammation of the stomach.
Acute catarrhal bronchopneumonia.
Chronic catarrhal bronchopneumonia.

List of microslides

Acute catarrhal inflammation of the intestines.
Chronic catarrhal inflammation of the intestines.
Catarrhal bronchopneumonia (acute form).

The study of preparations under a microscope is carried out according to the protocol recording of the description of micropreparations.

Remedy: Acute catarrhal
enteritis

Under a microscope at low magnification we see hyperemia and swelling of the villi; as a result, the villi are thickened, deformed (especially at the ends), there is no epithelial cover at the end of the villi, there are no epithelial cells in the upper parts of many crypts. As a result, the outlines of individual villi are poorly defined; only their ends are distinguishable. In the connective tissue base of the villi, as well as in the thickness of the mucosa, there is an increased content of cells, the vessels are dilated and filled with blood. The boundaries of the follicles are clearly visible. Exudate is visible on the surface of the mucosa.

Fig. 142. Acute catarrhal enteritis:
1. Desquamation of the integumentary epithelium of the villi;
2. Villi are exposed (without integumentary epithelium);
3. Cystically distended glands; 4. Villous atrophy

At high magnification, it is clear that the exudate lying on the surface of the mucous membrane consists of:

From desquamated epithelial cells (these are signs of necrosis), which lie singly in some places, in others in layers in the form of ribbons.
Serous fluid mixed with mucus (which has the appearance of a granular filamentous mass stained bluish (basophilic), darker than serous fluid.
A small number of polymorphonuclear leukocytes, single erythrocytes (blood cells) and histiocytes (tissue cells).

Examining the preserved integumentary epithelium under high magnification, we see that the epithelial cells are in a state of mucous degeneration (an increase in the number of goblet cells). In the depths of the crypts, the epithelium was preserved without major changes. The connective tissue base of the villi and the entire thickness of the mucosa are saturated with serous fluid, polymorphonuclear leukocytes in small quantities and single lymphocytes and histiocytes.

When the submucosal border is swollen, its borders are dilated, the vessels are injected, there are hemorrhages around the vessels, as well as a small accumulation of lymphocytes and histiocytes.

Fig. 143. Acute catarrhal enteritis:
1. Increase in the number of goblet cells in the crypts;
2. Swelling of the connective tissue between the crypts

Macro picture

The mucous membrane is swollen, spotty or streaky reddened (especially at the tops of the folds), sometimes continuous (suffuse) redness is observed. The mucous membrane is covered with viscous, semi-liquid mucus, which is easily washed off with water. With abundant desquamation of the epithelium, the exudate resembles a mealy soup.

Remedy: Chronic catarrh
small intestine

In chronic catarrh, in contrast to acute catarrh, vascular changes are weakly expressed (inflammatory hyperemia, edema due to effusion of serous fluid, emigration of leukocytes), alteration processes are more pronounced (in the form of dystrophic and necrotic changes in the intestinal epithelium and atrophic changes in the villi and glands) and proliferation processes, accompanied by regenerative processes of epithelial cells of the villi and glands and the growth of connective tissue.

At low magnification, we establish that the integumentary epithelium is completely absent, the villi are exposed, and in places reduced (atrophied). The glands are pushed apart and compressed by the growing connective tissue. Many glands are reduced in size (atrophy), in a state of decay and appear as islands among overgrown tissue. The preserved sections of the crypts look like elongated tubes. The lumens of other glands are cyst-like distended. In areas with pronounced atrophic changes, the mucous membrane is thinned. Lymphatic follicles are enlarged, their centers are pale in color. In the submucosa, changes are insignificant; in other cases, growth of connective tissue is noted. The muscle layer is thickened.

Fig. 144. Chronic catarrh of the small intestine:
1. Exposed villi without integumentary epithelium;
2. Cystically distended glands;
3. Atrophy of the glands;
4. Thickening of the muscle layer

At high magnification, in areas where the epithelium is preserved, its mucous degeneration and the disintegration of its cells are visible. From the surviving epithelial cells of the deep parts of the crypts, epithelial regeneration occurs. The resulting young cells are intensively stained with hematoxylin, and their nuclei are usually located in the center. In atrophying glands, the cells are wrinkled, reduced in volume, their nuclei are pyknotic, and the lumens of the glands are collapsed. In areas of growing interstitial connective tissue, fibroblasts, histiocytes, plasma cells with an admixture of lymphocytes and polymorphonuclear leukocytes are found in large numbers. Blood vessels without hyperemia. In lymphatic follicles, there is a proliferation of reticular cells in their germinal centers. In the muscle layer you can see hypertrophy of muscle fibers. sometimes an overgrowth of connective tissue. There are no changes in the serous membrane.

In the hypertrophic version of chronic catarrh, regeneration of epithelial cells of the mucous membrane occurs with simultaneous growth of connective tissue. As a result of this process, the mucous membrane thickens, the folds become rough, do not melt when smoothed by hand, sometimes the growths resemble polypous formations, protruding into the intestinal lumen. the growing epithelium of the glands is located in several layers, the excretory ducts of the hyperplastic glands are laced. The cells retain the ability to secrete secretions, but due to the closure of the lumen, the secretion is not released, but accumulates in the lumen, forming cystic cavities overflowing with secretions. Over time, connective tissue elements turn into scar tissue, the glands atrophy and atrophic chronic catarrh develops, characterized by thinning of the mucosa, its dryness, due to atrophy of the glands.

Macro picture

The mucous membrane is colored pale gray or grayish-white, sometimes with a brown or ashy tint, at first it is thickened evenly or unevenly, depending on the focal or diffuse nature of the inflammatory process, it is roughly folded, the folds do not straighten out, and later, with the aging of the connective tissue, atrophic processes develop , the mucous membrane thins in areas and becomes dense.

With hypertrophic chronic catarrh, the mucous membrane sharply thickens, folded or lumpy, sometimes covered with villous polypous growths, when cut into which cystic cavities are often discovered.

Drug: Catarrhal
bronchopneumonia

Catarrhal bronchopneumonia is characterized by:

Catarrhal exudate.
The process spreads endobronchially.
Bronchopneumonia begins in small patches, affecting individual lobules mainly of the apical lobes, and only in later stages can it take on a lobar character.

Fig. 145. Catarrhal bronchopneumonia:
1. Thickening of the interalveolar septa;
2. Accumulation of catarrhal exudate in the bronchi;
3. Growth of connective tissue around the bronchi;
4. Accumulation of catarrhal exudate in the alveoli

The micropicture of catarrhal bronchopneumonia is characterized by hyperemia of the capillaries of the alveoli and peribronchial blood vessels, accumulation of catarrhal exudate in the small bronchi, serous cell effusion in the alveoli, degeneration and desquamation of the alveolar epithelium.

With the endobronchial spread of the process, at low magnification the affected bronchus is found, the lumen of which is filled with cellular exudate. At high magnification, we see that the exudate consists of mucus, leukocytes, desquamated ciliated epithelial cells, and sometimes single erythrocytes and histiocytes are visible. The entire thickness of the mucosa is saturated with serous cell exudate, swollen, the number of goblet cells is increased, which indicates their mucous degeneration. The remaining layers of the bronchial wall are not changed, there is no swelling and cellular infiltration of the tissue surrounding the bronchus, as happens with the peribronchial spread of the process, which is observed much less frequently. Then we examine the alveoli surrounding the affected bronchus. The walls of some alveoli, in which there is little exudate, are represented by a red mesh (this is capillary hyperemia). In other alveoli, overcrowded with cellular exudate, hyperemia is not visible (the exudate has squeezed out red blood cells from the capillaries of the alveoli). The exudate consists of a homogeneous pink mass containing leukocytes, desquamated cells of the alveolar epithelium, erythrocytes, and single histiocytes. In the affected alveoli, located closer to the affected bronchus, leukocytes predominate in the exudate, and in the peripheral parts there is serous fluid and desquamated cells. The alveoli surrounding the inflamed foci are dilated and have the shape of irregular cavities containing air (vicarious emphysema).

With the development of inflammation, serous edema and lympholeukocyte infiltration develops in the interstitial connective tissue and interalveolar septa. Fibroblast proliferation occurs. Hyperemia begins to subside, and cellular proliferation increases. The interalveolar septa become indistinguishable, the alveoli undergo necrosis and in their place, as well as in the interstitium of the lungs and interalveolar septa, cellular proliferation increases, further leading to the growth of connective tissue and induration (compaction) of the lung.

Macro picture

The affected lobules are enlarged, but not as much as in lobar pneumonia, they are colored blue-red or gray-blue-reddish (splenization of the organ), i.e. the tissue becomes spleen-like. The cut surface of the affected parts is moist, when pressed, cloudy, sometimes bloody fluid is released, and cloudy, viscous mucus is released from the cut bronchi. With an increase in cell proliferative processes, i.e. transition of the inflammatory process into a chronic form in the corresponding areas, gray-red spots and dots appear on a general blue-red background. dilated pale gray strands of edematous connective tissue are clearly visible. In chronic cases, the inflamed areas of the lung are pale gray in color and have a dense consistency, resembling the pancreas.

Fig. 146. Acute catarrhal bronchopneumomia in a lamb

Fig. 147. Inflammation of the right lung of a lamb: catarrhal – anterior and middle lobes

1.5. Fibrinous inflammation

Fibrinous inflammation is characterized by the formation of a dense effusion - fibrin, which is mixed with the exudate. When sweating, fresh films of fibrin look like elastic translucent yellow-gray masses that permeate the tissue (deep diphtheritic inflammation), or are located in the form of films on the inflamed surface of the cavity (superficial fibrinous inflammation). After sweating, the fibrinous mass thickens, loses transparency and turns into a crumbly gray-white substance. Under a microscope, fibrin has a fibrous structure. The etiology of fibrinous inflammation is associated with the influence of virulent pathogens (widespread pneumonia, rinderpest, swine fever, swine paratyphoid fever, etc.), which with their toxins cause increased permeability of the vascular wall, as a result of which large protein molecules of fibrinogen begin to pass through it. Croupous inflammation (superficial) is characterized by the deposition of fibrin on the surface of natural cavities. Its localization is on the serous, mucous, and articular integuments. A film of fibrin forms on their surface, which is easily removed, revealing the swollen, reddened, dull shell of the organ. As a rule, the process is diffuse in nature.

In the intestine, fibrin accumulates and forms rubber-like casts that close the intestinal lumen. On serous integuments, these films, thickening, undergo organization (fibrinous pleurisy, fibrinous pericarditis). An example of this organization is the "hairy heart". In the lungs, fibrin fills the cavity of the alveoli, giving the organ the consistency of liver (hepatization), the cut surface is dry. Fibrin in the lungs can be absorbed or grow into connective tissue (carnification).

Fig. 148. Fibrinous inflammation of the pulmonary pleura

Fig. 149. Fibrinous warty endocarditis in chronic swine erysipelas

Fig. 150. Diphtheritic necrotic lesions on the calf tongue due to necrobacteriosis

Fig. 151. Fibrinous pneumonia of the horse due to necrobacteriosis

Fig. 152. Focal diphtheric colitis in a piglet with paratyphoid fever

Fig. 153. Diphtheric flaking colitis in a piglet with chronic paratyphoid fever

Fig. 154. Fibrinous pleurisy in cattle with peripneumonia

Fig. 155. Fibrinous pericarditis

Diphtheritic (deep) inflammation is characterized by the deposition of fibrin deep in the organ between tissue and cellular elements. As a rule, the process is focal in nature, and the area of the affected mucous membrane has the appearance of a dense, dry film that is difficult to remove from the surface. When films and bran-like deposits are removed, a defect is formed (notch, ulcer), which then undergoes organization (overgrowth with connective tissue). Despite the severe nature of the inflammatory process, diphtheritic inflammation proceeds more favorably than lobar (superficial) inflammation, since it is focal in nature, while lobar inflammation is diffuse.

Target Theme Setting

Morphological features of fibrinous inflammation and its localization. Types of fibrinous inflammation (deep, superficial) according to the depth of the inflammatory process, their distinctive features. Morphological features of lobar pneumonia (stages of the inflammatory process). Outcomes of fibrinous inflammation on mucous membranes, serous membranes, articular surfaces. outcome of fibrinous pneumonia. In which infectious diseases is this type of inflammation most common? What infectious diseases are accompanied by fibrinous pneumonia?

The main focus is on the following issues:

Morphological features of the composition of fibrinous exudate (micro-macro picture).
Localization of fibrinous inflammation. features of the morphological manifestation of fibrinous and diphtheritic inflammation. Exodus.
Morphological features of fibrinous pneumonia. acute and chronic form of the course. Exodus. In what infectious diseases does this type of inflammation occur? Distinctive features of fibrinous pneumonia from other pneumonias (serous, hemorrhagic, purulent, catarrhal).

A conversation to familiarize students with the preparation of the topic of the lesson, then the teacher explains the details.
Study of macroscopic changes in fibrinous inflammation of the mucous membranes, serous integuments, articular surfaces, lungs on slaughterhouse confiscates, wet and dry preparations, atlas. Students, using the scheme of macroscopic description of organs, describe the studied macroscopic changes in fibrinous inflammation in the form of a short protocol note. Then read out indicating the pathological diagnosis. Adjustments are being made.
Studying the micropicture of fibrinous pneumonia under a microscope. Students, using the protocol description of the drugs and the teacher’s explanations, study the various stages of development of fibrinous pneumonia and sketch them out schematically in notebooks, indicated by an arrow.

List of wet museum preparations

Fibrinous pericarditis.
Fibrinous inflammation of the intestines (porcine paratyphoid fever).
Diphtheritic inflammation of the intestines (paratyphoid).
Fibrinous pleurisy (pasteurellosis).
Fibrinous pneumonia (stage of gray, red and yellow hepatization).

List of microslides

Fibrinous pneumonia (stage of flushing and red hepatization).
Fibrinous pneumonia (stage of gray and yellow hepatization).

Fibrinous (lobar) pneumonia

Features of fibrinous pneumonia:

Fibrinous exudate.
The lobar nature of fibrinous inflammation from the very beginning of the development of the inflammatory process.
The lymphogenous pathway of spread, and therefore the interlobular tissue, is affected, and as it continues, as a rule, fibrinous inflammation spreads to the pleura and pericardium. In this regard, fibrinous pneumonia is complicated by fibrinous pleurisy and pericarditis.

Features of fibrinous pneumonia: fibrinous exudate; the lobar nature of fibrinous inflammation from the very beginning of the development of the inflammatory process; the lymphogenous route of spread, and therefore the interlobular tissue, is affected, and as it continues, as a rule, fibrinous inflammation spreads to the pleura and pericardium. In this regard, fibrinous pneumonia is complicated by fibrinous pleurisy and pericarditis.

There are 4 stages in the development of fibrinous pneumonia:

Stage 1 – hyperemia (flush of blood).

Stage 2 – red hepatization (red hepatization).

Stage 3 - gray hepatization (gray hepatization).

Stage 4 - yellow hepatization (resolution of the process).

pneumonia (red hepatization stage)

At low magnification we see that the capillaries of the alveoli and the blood vessels of the pulmonary septa are greatly dilated and filled with blood. As a result of this, the capillaries of the alveoli protrude kidney-shaped into the cavity of the alveoli, which makes it seem that the wall of the alveoli is built of a red looped mesh. In the lumens of some alveoli and small bronchi there are red blood cells and exudate.

Fig. 156. Fibrinous pneumonia in cattle
(areas of red hepatization):
1. Hyperemia of the capillaries of the alveoli;
2. Serous exudate in the perifocal zone of fibrinous inflammation

At high magnification, the exudate is visible in the form of a felt-like, mesh or filamentous mass (fibrin), colored pink. The exudate contains a lot of red blood cells, an admixture of polymorphonuclear leukocytes and desquamated (pink with a pale vesicular nucleus) cells of the alveolar epithelium, and single histiocytes. In some alveoli there is a lot of fibrin, and it forms a continuous mesh. In others there are only individual intertwining threads. In those alveoli that are filled with red blood cells, fibrin is not detected. There are alveoli in which serous exudate is visible. In the lumens of the alveolar ducts and small bronchi, fibrinous exudate is in the same form as in the alveoli.

Swelling of collagen fibers is observed in the interstitial connective tissue. They are thickened, some bundles of fibers have undergone fiberization and are infiltrated with serous-fibrinous-cellular exudate.

At high magnification, sharply dilated lymphatic vessels embedded in the interstitial, perivascular and peribronchial connective tissue are visible. They are filled with fibrinous exudate (felt-like, filamentous masses). Vascular thrombosis is observed. Areas of necrosis (structureless pink mass) are also visible in the interstitium, around which demarcation inflammation has formed (infiltration of leukocytes (blue cells) at the border of necrotic tissue).

Macro picture.

In this stage, a large number of lobules are affected (lobar in nature) from the very beginning. The affected lobes, light red and dark red in color, are enlarged, compacted, the changes in the section are similar, reminiscent of liver tissue (red hepatization). Pieces cut from the affected areas drown in the form.

Drug: Fibrinous (lobar)
pneumonia (gray hepatization stage)

At low magnification we see that the lumens of the alveoli are stretched by the exudate rich in leukocytes that has accumulated in them. As a result, the alveolar septa are thinned, and their capillaries are empty, due to their compression by exudate. In areas where the alveoli are overcrowded with leukocytes, the septa are not detected (due to their melting by purulent exudate).

Fig. 157. Fibrinous pneumonia in cattle
(areas of gray hepatization):
1. Thinning of the partitions, desolation of capillaries;
2. Fibrin fibers, leukocytes in the lumen of the alveoli;
3. Fine-grained exudate and a large number of leukocytes

At high magnification, fibrin fibers filling the lumens of the alveoli stretch from one alveoli to another. (This is clearly visible when stained for fibrin). There are many leukocytes in the exudate, but no red blood cells are visible (hemolysis). In other alveoli, the exudate contains many leukocytes and fine-grained, homogeneous exudate (peptonization, i.e., the breakdown of exudate under the influence of leukocyte enzymes). The picture of changes in the bronchi, as well as interstitial connective tissue, is similar to that described in the stage of red hepatization, but more pronounced.

In particular, lymphatic and blood vessels (thrombosis) and interstitial connective tissue (necrosis) are more severely affected. Macroscopically, the affected lobules are gray and yellow in color. The gray areas are dense in consistency, reminiscent of the liver, the yellow areas are softened (resolution stage). Interlobular connective tissue – its borders are thickened. The affected lymphatic and blood vessels, their thrombosis and embolism and grayish, dense foci of necrosis are visible in the form of nostril-dilated holes.

Outcome: The exudate can be completely absorbed (peptonization). After which there is a complete restoration of the alveolar and bronchial epithelium (complete resolution of the inflammatory process). But the interalveolar septa and interlobular connective tissue always remain thickened after the end of the inflammatory process. If the exudate does not completely resolve, then the dead areas grow with connective tissue (lung carnification), i.e. the inflammatory process ends with incomplete resolution.

Macro picture of fibrinous pneumonia

Lobarity of lung damage from the beginning of its development. Marbling of the pattern of the affected areas from the surface and in the section. Some lobules are red, others are gray, others are yellowish (this gives the organ a marbling pattern). The strands of interlobular connective tissue are sharply expanded. Lymphatic vessels in the form of a rosary. Their thrombosis is noted. Fibrin plugs can be removed from the bronchi and alveoli. Often the process spreads to the pleura and pericardium with the subsequent development of fibrinous pleurisy and pericarditis.

Fig. 158. Fibrinous inflammation of the lungs of cattle (areas of red and gray hepatization)

Fig. 159. Fibrinous pleurisy in a sheep

Fig. 160. Fibrinous inflammation of the lungs of cattle. Most lobules are in the stage of gray hepatization

Fig. 161. Fibrinous pneumonia with necrosis of lung tissue in cattle

Control questions:

The essence of serous inflammation. Morphological picture.
Morphological picture of pathological forms of serous inflammation (serous inflammatory edema, serous-inflammatory dropsy, bullous form).
In what infectious diseases are these forms of inflammation most common?
Outcome of serous inflammation. Examples. Importance for the organism.
How does hemorrhagic inflammation differ from other types of exudative inflammation?
How is hemorrhagic inflammation manifested morphologically in compact organs and cavities?
What infectious diseases are most often accompanied by hemorrhagic inflammation?
Outcome of hemorrhagic inflammation. Examples. Importance for the body.
Composition of purulent exudate and its properties. Examples.
Pathoanatomical forms of manifestation of purulent inflammation depending on the localization of the inflammatory process (purulent catarrh, purulent serositis (empyema), abscess, phlegmon). Examples.
Macro picture of purulent embolic nephritis, purulent bronchopneumonia, phlegmon.
Outcomes of purulent inflammation (purulent catarrh, purulent serositis, abscess, phlegmon). Examples.
The essence of catarrhal inflammation. Features of localization and composition of exudate.
Morphological signs of acute and chronic catarrhal inflammation of the mucous membranes.
Morphological characteristics of acute and chronic catarrhal bronchopneumonia.
In what infectious diseases is catarrhal inflammation most common? Examples.
outcome of catarrhal inflammation. Examples. Importance for the body.
features and morphological composition of fibrinous exudate. Localization of fibrinous inflammation.
Morphological signs of fibrinous (superficial) and diphtheritic (deep) fibrinous inflammation of the mucous membranes. Exodus. Fibrinous inflammation of the serous covers and articular surfaces. Exodus.
Morphological features of fibrinous pneumonia (stages of development of the process). Exodus. Importance for the body.
In what infectious diseases is this type of inflammation observed? Examples. Importance for the body.

is an inflammation of the lungs caused by a viral infection. Symptoms of the disease are similar to the common cold; patients complain of fever, cough, rhinitis, general weakness and malaise.

The clinical picture depends on the type of pathogen and the state of the patient’s immunity. Pneumonia due to influenza can be complicated by secondary bacterial inflammation of the respiratory tract, pleurisy, and respiratory distress syndrome.

Causes of the disease

The influenza virus is transmitted by airborne droplets, through close contact with an infected person, through household items, and personal hygiene items. It penetrates the mouth or nose, then affects the cells of the mucous membranes of the tracheobronchial tree and the alveoli of the lungs.

The most common causative agents of influenza pneumonia are immunocompetent influenza viruses type A, B, parainfluenza, respiratory syncytial (RSV), and adenovirus. The incubation period of the disease lasts 3–5 days; a few days after infection, the bacterial flora joins the viral flora.

Pneumonia due to influenza most often affects young children, the elderly, people with weakened immune defenses of the body, those suffering from chronic heart diseases, upper respiratory tract diseases, bronchial asthma, arterial hypertension, and coronary artery disease. Those at risk include smokers, HIV-infected people, patients with cancer pathologies who have undergone chemotherapy.

Characteristic symptoms of pneumonia

Viral pneumonia in most cases occurs in an acute form, the high temperature lasts up to 2 weeks, and daily fluctuations in the thermometer are observed. The pathology is characterized by seasonal epidemic outbreaks of influenza occurring in the autumn-spring period, cold, damp weather.

Specific manifestations of pneumonia:

Viral pneumonia

general weakness, malaise, fatigue;
hyperthermia up to 38.5–39°;
chills;
rhinitis, nasal congestion;
dry or wet cough;
increased sweating;
lack of appetite;
dyspnea;
cyanosis of the nasolabial triangle;
aches, pain in muscles, joints.

Parainfluenza pneumonia affects newborn infants and preschool children. In children, signs of intoxication of the body are clearly expressed in the form of nausea, vomiting, headache, and dyspeptic disorders. Hyperthermia usually does not exceed subfebrile levels, respiratory symptoms are moderate (cough, rhinitis).

Adenoviruses cause uncomplicated pneumonia with severe lymphadenopathy and tonsillitis. In severe cases of viral pneumonia in children and people with immunodeficiency, a high temperature rises to 40°, tonic convulsions, hemorrhagic syndrome, respiratory failure, severe vomiting, and diarrhea occur.

The most severe complications include empyema, lung abscess, collapse, influenza encephalitis, hypoxemic coma, and death is possible within the first week from the onset of the disease.

Primary viral pneumonia

This form of pneumonia develops a few days after infection with the influenza virus. In the first 2–3 days, patients are bothered by the usual symptoms of a cold, which quickly increase and progress. Fever, shortness of breath, cyanosis of the skin, and difficulty breathing are observed. The cough is wet with the release of a small amount of sputum, sometimes blood appears in the liquid.

Primary influenza pneumonia most often occurs in people suffering from diseases of the heart, kidneys, and respiratory system. Pathogens are found in bronchial secretions and lung parenchyma. The disease is classified:

acute interstitial pneumonia;
hemorrhagic pneumonia.

In the first case, damage to the interstitial tissue of the lung occurs with impaired respiratory function. The disease is severe, causes fibrotic, sclerotic changes in the pulmonary parenchyma and often has an unfavorable outcome.

Primary hemorrhagic pneumonia after influenza causes the accumulation of large numbers of red blood cells in the bronchial exudate and interstitial tissue of the lungs. The pathology is most severe in smoking patients, pregnant women, people with chronic diseases of the cardiovascular, endocrine, respiratory systems, and severe immunodeficiency states.

Hemorrhagic pneumonia is accompanied by hemoptysis, shortness of breath, cyanosis of the skin, nosebleeds, decreased blood pressure, and tachycardia. Against the background of high body temperature and severe intoxication of the body, DIC syndrome and respiratory failure quickly develop.

Post-influenza pneumonia joins flu symptoms after 5–6 days. The effect of the virus greatly reduces the body's immune defense and creates favorable conditions for the proliferation of pathogenic microflora in the respiratory tract. The causative agents of the pathology can be Staphylococcus aureus, Haemophilus influenzae, and pneumococci.

The development of secondary bacterial pneumonia is facilitated by weakened immunity and the following factors:

taking cytostatics, corticosteroids, antibiotics;
blood diseases: leukemia, anemia, lymphoma;
HIV infection, AIDS;
diabetes;
oncological diseases;
chemotherapy performed;
addiction;
prolonged hypothermia.

In patients, after the fever subsides, the body temperature rises again, purulent, viscous sputum mixed with blood is coughed up. Viral agents and pathogenic bacteria are detected in bronchial secretions.

Diagnostic methods

When examining patients with primary pneumonia against the background of influenza, the percussion sound does not change; its dullness is noted during the addition of a secondary bacterial infection and the formation of infiltration foci in the lungs. Breathing, auscultation, wheezing, crepitus.

Pulmonary atelectasis - its types

With viral pneumonia, wet wheezing alternates with dry wheezing, changes occur within 1–2 days. The pathological process is explained by the progression of atelectasis, the accumulation of exudate that closes the lumen of the bronchi.

X-ray examination reveals an increase in the vascular pattern, foci of parenchymal infiltration (usually in the lower segments); in rare cases, the inflammatory process spreads to the entire lobe of the respiratory organ. Based on the results of a blood test, leukopenia and lymphocytopenia, an increased titer of antibodies to the viral agent, and an increase in ESR are diagnosed. To confirm the etiology of pneumonia, bronchial lavages are performed.

Differential diagnosis is carried out with cancer, pulmonary infarction, atypical, aspiration inflammation, bronchiolitis obliterans. When making a diagnosis, the epidemiological situation, the presence of specific antibodies in the patient’s blood, respiratory symptoms and confirmation of viral etiology based on the results of sputum culture are taken into account.

Drug treatment of pneumonia

Patients are advised to stay in bed, drink more fluids (at least 2.5 liters per day), take vitamins and high-calorie foods. Etiotropic therapy for pneumonia due to influenza is carried out with antiviral drugs:

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Antibiotics are prescribed for a mixed form of microflora in the respiratory tract in the event of a bacterial infection.

Patients with pneumonia are prescribed a wide range of medications (,) in order to relieve the acute inflammatory process, reduce swelling of the lung tissue, and prevent severe complications. If a viral infection is combined with chlamydia, additional antibacterial agents are prescribed:

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Symptomatic treatment of pneumonia is carried out with antipyretic and mucolytic drugs (Ambroxol, Lazolvan, Nise), which expand the lumen of the bronchi and facilitate the discharge of viscous sputum. Nonsteroidal anti-inflammatory drugs (Diclofenac, Ibuprofen) help relieve pleural pain, lower temperature, and reduce body and joint aches. For symptoms of respiratory failure, oxygen inhalations are given.

Medicines for pneumonia must be taken for 10–14 days. To strengthen the immune system, it is recommended to use vitamin complexes (Aevit, Complivit) and immunomodulators (Echinacea, Immunal). During treatment of influenza and pneumonia, patients should eat boiled meat, rich broths, dairy and fermented milk products, and fresh vegetables.

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Prevention of viral pneumonia

The main preventive measures include vaccination of the population during seasonal outbreaks of influenza. Hardening, vitamin therapy, a balanced diet, and giving up bad habits help strengthen the immune system. During the cold season, it is allowed to take immunomodulators: Aflubin, Anaferon. It is important to promptly treat concomitant diseases of internal organs.

It is necessary to avoid contact with infected patients, wash your hands with soap after visiting crowded places or riding public transport. People working in large teams during an epidemic must wear protective gauze bandages, which must be changed every 2 hours. It is recommended to regularly ventilate the apartment, monitor the temperature and humidity. If the air is too dry, you need to use humidifiers.

A person who falls ill with pneumonia after the flu is placed in a separate room and given personal hygiene items, dishes, and bed linen. The room must be wet cleaned daily with the addition of antiseptic preparations to the water and dust wiped off.

Measures to prevent secondary pneumonia include observation by a pulmonologist after treatment of the acute stage of the disease. After 1, 3 and 6 months, it is recommended to take a blood test, urine test, and conduct a biochemical study - rheumatic tests.

Consequences of viral pneumonia after influenza

If there are chronic pathologies of internal organs, it is necessary to carry out timely supportive treatment. Mandatory sanitation of the oral cavity, respiratory tract, and treatment of carious teeth are also indicated. After prolonged inflammation, a vacation by the sea or in a specialized sanatorium will speed up recovery.

Viral pneumonia develops when a person is infected with influenza viruses. The disease is characterized by a rapid course with high fever and severe signs of general malaise. If treatment is not started in a timely manner, the pathology quickly progresses and can lead to the development of severe complications, including death.

^ TOPIC XVIII

INTRODUCTION TO INFECTIONS.

BRONCHITIS AND PNEUMONIA, ACUTE AND CHRONIC. FLU. LUNG CANCER.

Infectious - are diseases caused by infectious agents: viruses, bacteria, fungi.

Invasive is a disease caused by the introduction of protozoa and helminths into the body.

Bronchitis - inflammation of the bronchi, complicated by impaired ventilation, cleansing, warming, and humidification of air penetrating into the respiratory tract.

^ Complications of bronchitis : pneumonia, bronchiectasis, atelectasis, emphysema, pneumosclerosis, hypertension of the pulmonary circulation (precapillary), right ventricular hypertrophy, the so-called “cor pulmonale”.

Pulmonary precapillary hypertension pulmonary circulation - characterized by increased pressure in the trunk and large branches of the pulmonary artery, sclerosis, as well as spasm and hypertrophy of small branches of the pulmonary artery, hypertrophy of the right ventricle of the heart.

Precapillary pulmonary hypertension - characterized by an increase in the ventricular index above 0.4 - 0.5.

^ Ventricular index - the ratio of the mass of the right ventricle of the heart to the mass of the left ventricle.

Bronchiectasis - uneven expansion of the lumen of the bronchi. They are classified according to their shape: fusiform, cylindrical, saccular bronchiectasis.

According to pathogenesis, they are distinguished: retention and destructive.

^ Destructive bronchiectasis - occur when there is purulent melting of the bronchial wall and have perifocal inflammation.

Retention bronchiectasis- arise due to impaired evacuation of contents during wall atony; There is no perifocal inflammation.

Pneumosclerosis associated with the proliferation of connective tissue in the lungs. Pneumosclerosis can be: reticular, small- and large-focal.

Causes of pneumosclerosis:

carnification,
development of granulation tissue,
lymphostasis in the fibrous layers of the lung.

Carnification – organization of fibrinous exudate in the alveoli.

Atelectasis - collapse of the alveoli.

By volume they are distinguished:

acinous,
lobular,
subsegmental,
segmental,
equity,
linear atelectasis.

According to pathogenesis there are:

contractile,
obstructive,
surfactant-dependent atelectasis.

Lung collapse - compression of the lung from the outside.

Emphysema - increase in lung volume due to increased airiness of the pulmonary parenchyma distal to the terminal bronchiole.

Focal and diffuse emphysema. According to pathogenesis, they are distinguished: obstructive, compensatory, due to loss of elastomeric tone.

Flu - respiratory infection - caused by virus A, B, C. The virus, settling in the epithelium of the bronchi, alveoli, capillary endothelium, penetrating into the blood, causes viremia, characterized by a vasoparalytic effect. From here, hemorrhages in the brain (hemorrhagic encephalitis), hemorrhagic pulmonary edema are possible. Locally, in the upper parts of the respiratory tract, catarrhal-hemorrhagic inflammation, hemorrhagic tracheitis, and bronchitis are possible.

Pneumonia -inflammation of the respiratory part of the lungs.

Based on the nature of the exudate, pneumonia is distinguished:

purulent,
fibrinous,
serous,
hemorrhagic.

Based on the size of the foci, types of exudative pneumonia are distinguished:

acinous,
lobular,
subsegmental,
segmental.

Interstitial pemmonia - an inflammatory process that unfolds not in the parenchyma, but in the interstitial tissue of the lung.

Lobar pneumonia - lobar, fibrinous, pleuropneumonia.

Stages of lobar pneumonia:

tide,
red liver,
gray liver,
permissions.

There are atypical forms:

Central - lesion deep in the lung without involvement of the pleura
Massive - exudate fills the lumen of large bronchi, so bronchial breathing is not heard
Total - all lobes are affected at the same stage of the process
Migratory - different lobes are affected by a process at different stages
Kpypsielous - the exudate has a mucus-like appearance and the smell of burnt meat.

Intrapulmonary complications of lobar pneumonia:

carnification (organization of fibrin inside the alveoli),
suppuration-abscesses,
gangrene.

Extrapulmonary complications of lobar pneumonia:

meningitis,
pericarditis,
brain abscess.

Pneumonia due to influenza– “large mottled influenza lung”: foci of serous-hemorrhagic and fibrinous inflammation, atelectasis, emphysema, foci of purulent bronchopneumonia.

Lung cancer most often develops from the bronchial epithelium (bronchogenic cancer) and only in 1% of cases from the alveolar epithelium (pneumoniogenic cancer).

^ By localization There are basal (central cancer), peripheral and mixed (massive) cancer.

According to histological structure– adenocarcinoma, squamous cell, undifferentiated cancer.

Metastasizes Lung cancer lymphogenously in the hilar, bifurcation lymph nodes, lymph nodes of the neck, etc. and hematogenously.

^ STUDY MACRO-PREPARATIONS:

13. Croupous pneumonia in the red hepatic stage.

The lobe of the lung on the section is dense, red in color

161. Croupous pneumonia in the stage of gray hepatization.

The lower lobe of the lung is dense, airless, pale gray in color. The cut surface is fine-grained.

^ 162. Croupous pneumonia with abscess formation.

The lobe of the lung is dense, airless throughout, with an erased structure on the section; in the upper part of the lung there is a focus of tissue melting with the formation of a cavity (abscess).

^ 160. Croupous pneumonia leading to gangrene.

The lobe of the lung is dense, gray. In the lower part of the specimen, the apex of the lung is necrotic, black,

520, 309. Purulent meningitis.

The pia mater is thickened, the convolutions are flattened, there is creamy gray-yellow pus in the furrows, the vessels are full of blood.

321, 327. Brain abscesses.

A section of the brain reveals cavities with grayish, loose walls.

439. Fibrinous pericarditis (“hairy” heart).

The epicardium is covered with fibrinous deposits that look like intertwined grayish hairs

525. Chronic pneumonia with abscesses.

The lobe of the lung is compacted with connective tissue cords, cavities (abscesses) with a thick capsule are visible in the depths, and there is a zone of sclerosis around it. The pleura is thickened.

^ 568. Chronic pneumonia in the acute stage.

On the section, the lung tissue is stringy, the walls of the bronchi are thickened, the lumens are expanded (bronchiectasis). In the lower part, the lung tissue is dense, light yellow in color (fibrinous-purulent pneumonia).

302. Congenital bronchiectasis.

A cross-section of the lung shows dilated bronchi. There is no carbon pigment in the lung tissue.

^ 23. Acquired bronchiectasis.

The walls of the bronchi on a section of the lung are thickened, white-gray in color, their lumens are expanded; black charcoal pigment is visible in the lung tissue

111. Reticular pneumosclerosis (post-tuberculosis).

The lung is enlarged in size, swollen, pale gray in color when cut through. A fine mesh of connective tissue is clearly visible

457. Pulmonary heart.

The wall of the right ventricle is hypertrophied and thickened in the section. The heart valves are not changed.

^ 89. Lung cancer with metastases to regional lymph nodes.

A section of the lung shows foci of tumor tissue, dense consistency, whitish in color. Similar tissue is found in the hilar lymph nodes.

328. Hemorrhagic tracheobronchitis with influenza.

The mucous membrane of the trachea and bronchi is full-blooded, swollen

^ 197. Hemorrhagic pneumonia with influenza.

In the lung tissue there are dense, airless dark red foci of hemorrhagic inflammation, merging with each other in places. In addition, foci of necrosis are visible

^ STUDY MICROPREPARATIONS:

81. Croupous pneumonia, stage of gray hepatization.

(Pneumococcal lobar pleuropneumonia).

The alveoli are filled with exudate containing fibrin in the form of pink threads, a large number of leukocytes and some red blood cells. In some places, accumulations of microbes are visible in the form of dark purple spots.

55. Fibrinous-purulent pneumonia with necrosis.

In the area of inflammation, the alveoli are filled with fibrin and leukocytes. In areas of necrosis, the interalveolar septa are not visible.

^ 142. Chronic pneumonia with carnification and pneumosclerosis.

In the carnification zone, the alveoli are filled with fibrin, into which fibroblasts grow (fibrin organization). The zone of pneumosclerosis is represented by mature connective tissue, in which collagen fibers and large vessels predominate.

94. Small cell lung cancer (undifferentiated).

The tumor consists of monomorphic, elongated, hyperchromic cells. The stroma is poorly developed, there are many foci of necrosis.

123. Squamous cell keratinizing lung cancer.

“Cancer pearls” are visible among the layers of atypical epithelium.

A t l a s (drawings):

104	– lobar pneumonia

TESTS: choose the correct answers.

472. Synonyms for lobar pneumonia, reflecting the features of this disease, are:

1-lobar pneumonia

2- fibrinous pneumonia

3- pleuropneumonia

473. According to classical concepts, the stages of lobar pneumonia are:

1st stage of tide

2- red liver

3- gray liver

4-permissions

474. The components of exudate in the alveoli in lobar pneumonia are:

1- neutrophil leukocytes

2- red blood cells

475. Complications of lobar pneumonia caused by hematogenous generalization of infection include:

1- brain abscess

2- purulent mediastinitis

3- purulent meningitis

4- acute ulcerative or polypous-ulcerative endocarditis

476. Typical complications of pneumonia caused by Klebsiella include:

1- necrosis of lung tissue, in place of which abscesses form

2- bronchopleural fistulas

3- carnification

477. Features of staphylococcal pneumonia include:

1- tendency to abscess formation

2- hemorrhagic exudate

3- formation of cavities in the lung tissue (pneumatocele)

4- possible development of pneumothorax

478. Pyeumocystis pneumonia can develop in patients:

1- for AIDS

2- with cytostatic chemotherapy, especially for leukemia and lymphomas

3- during corticosteroid therapy

4- in weakened children in the first months of life

479. Characteristic morphological signs of Pneumocystis pneumonia are:

1- interstitial inflammation

2- many plasma cells in the infiltrate (synonym - plasma cell pneumonia).

3- foamy exudate in the alveoli

480. The forms of bronchiectasis are:

1- cylindrical

2-bag

3- fusiform

481. During life, it was found that the patient had shortness of breath, the epigastric angle was obtuse, the apexes of the lungs were located above the collarbones, and a box sound was detected on percussion. Make a diagnosis:

1- emphysema

2- atelectasis of the lung

482. The main disease in the diagnosis of an adult may include:

1- focal pneumonia

2- lobar pneumonia

483. Pulmonary atelectasis can be caused by:

1- pneumonia

2- compression of the lung from the outside

3- bronchial obstruction

484. Bronchopneumonia can be the underlying disease:

1- in early childhood

2- in adulthood

3- in old age

485. The causative agent of acute pneumonia can be:

1- streptococcus

2- viruses

3- Vibrio cholerae

486. The etiology of lobar pneumonia may be associated with:

1- with pneumococcus

2- with Friedlander stick

3- with legionella

487. The etiology of lobar pneumonia may be associated with:

1- with staphylococcus

2- with pneumococcus

3- with E. coli

488. Friedlander's pneumonia is caused by:

1- Neisseria

2- klepsiella

3- pneumococcus

489. Exudate from lobar pneumonia is:

1- serous character

2-fibrinous-hemorrhagic nature

3-fibrinous-purulent character

490. Exudate from focal pneumococcal pneumonia has:

1-purulent character

2- serous character

3- serous-desquamative character

4- fibrinous character

491. Carnification of the lung in lobar pneumonia is:

1- outcome

2- complication

3- manifestation

492. Extrapulmonary complications of lobar pneumonia include:

1- aspergillosis

2- mitral valve endocarditis

3- brain abscess

493. Pulmonary complications of lobar pneumonia include:

1- lung abscess

2- pleural empyema

3- lung cancer

494. With all focal pneumonia the following is observed:

1- emphysema

2- carnification

3- acute bronchitis

4- pneumosclerosis

5- alveolitis

495. Chronic obstructive pulmonary diseases include:

1- bronchiectasis

2- chronic bronchitis

3- gangrene of the lung

4- emphysema

496. As a result of all diseases of the group of chronic obstructive pulmonary diseases, the following develops in the tissues of the latter:

1- cavern

2- emphysema

3- pneumosclerosis

497. The main causes of death in patients with chronic obstructive pulmonary diseases are:

1-pulmonary heart failure

2- anemia

3- renal failure (renal amyloidosis)

498. The leading factors in the development of pulmonary heart failure in chronic obstructive pulmonary diseases are:

1- precapillary hypertension

2- post-capillary hypertension

3- increased vascular permeability

4- decreased vascular permeability

5- violation of the air-blood barrier

499. In bronchiectasis, macroscopic manifestations are:

1- deformation and expansion of the lumen of the bronchi

2- deformation and narrowing of the lumen of the bronchi

3- limited pathological process

4- purulent contents in the lumen of the bronchi

500. The detection of Charcot-Leyden crystals in the patient’s sputum most likely indicates the presence of:

1- bronchial asthma

2- lung carcinoma

3- lung abscess

4- silicosis

5- tuberculosis

501. Influenza viruses settle inside the following cells:

1- alveolar macrophages

2- epithelium of bronchioles

3- alveolar epithelium

4- capillary endothelium

502. Characteristic changes in the lungs during influenza with pulmonary complications are:

1- destructive panbronchitis

2- foci of atelectasis and acute emphysema

3- bronchopneumonia with a tendency to abscess formation and hemorrhage

4- none of the above

TOPIC XIX

^ DIPHTHERIA. SCARLET FEVER. MEASLES

Diphtheria - an acute infectious disease, characterized by toxic damage mainly to the cardiovascular and nervous systems and a local inflammatory process with the formation of fibrinous films in the pharynx. Refers to airborne anthroponoses.

In areas covered with multilayered epithelium (throat, pharynx), diphtheritic inflammation in which the fibrinous film is tightly bound to the underlying tissue. On mucous membranes covered with single-layer columnar epithelium (larynx, trachea, bronchi), it develops lobar inflammation in which the film is easily separated from the underlying tissue.

Local lesions in diphtheria - characterized by the development of the primary infectious complex, which consists of:

primary affect (fibrinous inflammation of the mucous membrane in the area of the entrance gate),
lymphangitis,
regional lymphadenitis.

Forms of diphtheria by localization:

diphtheria of the throat,
respiratory tract diphtheria,
diphtheria of the nose, less often of the eyes, skin, wounds.

Diphtheria intoxication affects:

Nervous system
The cardiovascular system
Adrenal glands

Damage to the nervous system due to diphtheria - characterized by damage to the sympathetic nodes and peripheral nerves. Damage to the glossopharyngeal nerve leads to paralysis of the soft palate, impaired swallowing, and nasal voice.

Parenchymal myocarditis - myocardial damage in diphtheria, because Cardiomyocytes are primarily affected by diphtheria exotoxin.

Damage to the adrenal glands in diphtheria may lead to collapse.

True croup - suffocation due to fibrinous inflammation of the larynx caused by Lefler's wand.

Early cardiac paralysis due to diphtheria - caused by toxic parenchymal myocarditis.

Late cardiac paralysis - associated with parenchymal neuritis.

Death from diphtheria is caused by acute insufficiency of the pituitary-adrenal system, toxic myocarditis or true croup.

Scarlet fever - acute streptococcal disease; characterized by fever, general intoxication, sore throat, punctate exanthema, tachycardia. Refers to airborne anthroponoses. It often begins with catarrhal stomatitis: the oral mucosa is dry, hyperemic, desquamation of the epithelium, the so-called. “raspberry tongue”, dry and cracked lips.

Primary infectious complex in scarlet fever:

1. catarrhal or necrotizing tonsillitis (affect),

2. lymphadenitis of the cervical lymph nodes.

Forms of scarlet fever- according to the severity of the current they are distinguished:

light,
moderate,
severe, which can be septic or toxicoseptic.

There are two periods of scarlet fever - the first with symptoms of intoxication - degeneration of parenchymal organs and hyperplasia of immune organs, in particular, with severe hyperplasia of the spleen, and locally - with necrotizing tonsillitis and exanthema. The second period begins at 3-4 weeks.

Complications of the first period of scarlet fever - are purulent-necrotic in nature:

purulent otitis media,
mastoiditis,
sinusitis,
brain abscess,
meningitis,
septicopyemia,
phlegmon of the maxillofacial region and neck (hard and soft phlegmon).

Hard cellulitis – severe swelling, necrosis of soft tissues, fiber, tendency to chronicity.

Soft cellulitis – acute course, first serous exudate, then purulent, necrosis, abscess formation.

Features of the topography of the soft tissues of the face and cheeks contribute to rapid spread to the mediastinum, subclavian and axillary fossae, and into the cranial cavity (abscesses, meningitis). Maybe arrosive bleeding from large vessels. Necrotizing otitis media. In case of immunodeficiency it is possible putrefactive inflammation(symbiosis of anaerobes, staphylococci, streptococci, E. coli) and sepsis.

Complications of the second period of scarlet fever - are allergic in nature:

glomerulonephritis,
myocarditis,
vasculitis,
synovitis,
arthritis.

Exanthema with scarlet fever - looks like petechiae on red skin; pallor of the nasolabial triangle is characteristic.

Measles. The causative agent, an RNA-containing myxovirus, penetrates through the conjunctiva, respiratory tract, penetrates the lymph nodes of the neck, and causes viremia.

Develops on the mucous membranes of the oral cavity enanthoma, on the skin - exanthema– large spotted papular rash.

In children in the prodromal period, “red spots” with a diameter of 1.5-2.0 mm appear on the mucous membrane of the soft and hard palate. On the mucous membrane of the cheeks in the area of the molars - the so-called Koplik-Filatov spots– whitish nodules with a diameter of up to 2.0 mm, surrounded by a rim of hyperemia. They are formed due to coagulation of the surface layer of squamous epithelium with a slight inflammatory infiltration. If you are immunocompromised, measles may become more complicated but my(necrosis of the oral mucosa and soft tissues of the cheeks), necrotizing bronchitis, chronic bronchiolitis, metaplasia of the bronchial epithelium from glandular to stratified squamous, pneumonia with giant cell reactions.

^ STUDY MACRO-PREPARATIONS:

98. Measles pneumonia.

A section of the lung shows whitish foci of necrosis around the bronchi.

Dummy 3. Measles rash.

A papular rash is visible on the pale background of the arm.

Dummy 25. Measles necrosis of the labia mucosa.

Dummy 7. Cheek noma.

308. Fibrinous inflammation of the pharynx and larynx in diphtheria (true croup).

The mucous membrane of the trachea is covered with a grayish film, which is tightly connected to the underlying tissues, peeling off in places

562. Infectious heart.

The cavity of the left ventricle is increased in diameter (dilatation), the apex is rounded

428. Apoplexy of the adrenal gland.

There is extensive hemorrhage (hematoma) in the adrenal medulla.

151. Acute glomerulonephritis.

The kidney is slightly enlarged, swollen, with small red speckles on the surface

520, 309. Purulent meningitis.

The pia mater is thickened due to infiltration of leukocytes

Dummy 6. Scarlet fever rash on the face.

On the hyperemic background of the skin of the child’s face, a petechial rash and a rash-free white nasolabial triangle are visible

^ STUDY MICROPREPARATIONS:

46. Diphtheritic inflammation of the pharynx in diphtheria (demonstration).

The mucous membrane of the pharynx is necrotic. impregnated with fibrinous exudate, forming a thick film tightly fused to the underlying tissues. The submucous membrane is congested, edematous, infiltrated with leukocytes

158. Croupous tracheitis (demonstration).

The mucous membrane of the trachea, normally covered with columnar epithelium, is necrotic, saturated with fibrinous exudate, forming a thin, easily removable film

^ 162. Necrotizing tonsillitis with scarlet fever (Fig. 354).

In the mucous membrane and tissue of the tonsils, against the background of congestion of the vessels, foci of necrosis and leukocyte infiltration are visible.

18. Exudative (serous) extracapillary glomerulonephritis.

In the expanded cavity of the glomerular capsule there is an accumulation of serous exudate. The glomeruli are reduced in volume. There are dystrophic changes in the epithelium of convoluted tubules.

28. Fatty degeneration of the myocardium – “tiger heart”.

A t l a s (drawings):

Tests: choose the correct answers.

503. Early cardiac paralysis due to diphtheria can be caused by:

1- fatty degeneration of the myocardium

2- parenchymal myocarditis

3- interstitial myocarditis

504. Intoxication with diphtheria is more pronounced when inflammation is localized:

2- larynx

505. Possible causes of death from diphtheria are:

1- early cardiac paralysis

2- late cardiac paralysis

3- collapse

506. The components of the fibrinous film in diphtheria include:

1- necrotic epithelium of the mucous membrane

2- red blood cells

4- leukocytes

507. Morphological manifestations of myocarditis in diphtheria at the microscopic level are:

1- fatty degeneration of cardiomyocytes

2- small foci of necrosis (myolysis) of the heart muscle

3- edema and cellular infiltration of the interstitium

508. The most common causes of death due to diphtheria are:

1- asphyxia

2- heart failure

3- pneumonia

509. In the entrance gates of diphtheria, inflammation has the character of:

1- productive

2- fibrinous

3-purulent

4- hemorrhagic

5-putrefactive

510. Changes that occur in the heart during diphtheria include:

1- fibrinous pericarditis

2- purulent myocarditis

3- toxic myocarditis

4- heart defect

5- recurrent verrucous endocarditis

511. Characteristic changes in the pharynx during scarlet fever include:

1- tonsil necrosis

2- necrosis of underlying tissues

3- colonies of microbes in the necrosis zone

4- pallid pharynx

5- bright red throat

512. The complication period of the second period of scarlet fever is:

1- first week

2- 3-4 week

513. The inflammatory process from the pharynx spreads through the esophagus

1- for measles

2- for scarlet fever

3- for diphtheria

514. Changes in regional lymph nodes during scarlet fever are of the following nature:

1- necrosis

2- anemia

3- hypoplasia

4- sclerosis

5- atrophy

515. General changes in scarlet fever include:

1- skin rash

2- dystrophic changes in parenchymal organs

3-necrotizing tonsillitis

4- hyperplasia of lymph nodes and spleen

516. The child’s temperature has risen to 40°C, the pharynx and tonsils are bright red. On the 2nd day, a pinpoint rash appeared on the entire body, except for the nasolabial triangle. Cervical lymph nodes are enlarged and soft. This picture is typical for:

2- diphtheria

3- scarlet fever

517. A child with scarlet fever developed hematuria and proteinuria after 3 weeks. Scarlet fever became more complicated:

1- glomerulonephritis

2- nephrosclerosis

3- amyloid lipoid nephrosis

518. Catarrhal inflammation in measles develops on the mucous membranes:

2- trachea

3- intestines

4- bronchi

5- conjunctiva

519. The main characteristics of measles include:

1-acute highly cantagious infectious disease

2-causative agent - RNA virus

3- catarrhal inflammation of the mucous membranes of the upper respiratory tract, conjunctiva with signs of necrosis

4- maculopapular rash

5- true croup

520. Characteristics of croup in measles:

1- true

2- false

3- occurs with symptoms of edema and necrosis of the mucous membrane of the larynx with the development of reflex muscle spasm

521. With measles the following develops:

1- bronchopneumonia

2- fibrinous pneumonia

3- interstitial pneumonia

522. Complications of measles are:

1- bronchitis, including necrotic or purulent-necrotic panbronchitis

2- peribronchial pneumonia

3- pneumosclerosis

523. The causative agents of measles and influenza are:

1- bacteria

524. Bilshovsky-Filatov-Koplik spots are detected:

1- on the palms and soles

2- on the extensor surface of the forearm

3- on the tongue

4- on the inner surface of the cheeks

5- on the head

525. The most common complication of measles pneumonia is:

1- sclerosis of lung tissue

2- bronchiectasis

3- chronic pneumonia

526. The nature of exanthema in measles is:

1- the background of the rash is pale

2- the background of the rash is red

3- rash papular

4- roseola rash

527. Koplik-Filatov spots in measles are localized on:

1- gums

2- buccal mucosa against incisors

3- buccal mucosa against second molars

528. Changes in the pharynx during measles are characterized by:

1- fibrinous films on the tonsils

2- red throat

3- pale throat with red spots

Hemorrhagic pneumonia. How does hemorrhagic pneumonia manifest?

Remedy: Serous pneumonia

intestines (serous inflammatory edema)

Remedy: Serous inflammation lungs (serous inflammatory edema)

Drug: Afta for foot and mouth disease in cattle

1.2. Hemorrhagic inflammation

Drug: Hemorrhagic pneumonia

Drug: 2. Hemorrhagic intestinal inflammation

1.3. Purulent inflammation

Drug: Embolic purulent nephritis

Drug: Purulent bronchopneumonia

Remedy: Subcutaneous phlegmon fiber

1.4. Catarrh

Remedy: Acute catarrhal enteritis

Remedy: Chronic catarrh small intestine

Drug: Catarrhal bronchopneumonia

1.5. Fibrinous inflammation

pneumonia (red hepatization stage)

Drug: Fibrinous (lobar) pneumonia (gray hepatization stage)

Control questions:

Causes of the disease

Characteristic symptoms of pneumonia

Primary viral pneumonia

Diagnostic methods

Drug treatment of pneumonia

Prevention of viral pneumonia

Consequences of viral pneumonia after influenza

Etiology and pathogenesis

Clinical picture

Diagnostics

Treatment of serous-hemorrhagic disease

Prognosis for recovery

Reference materials (download)

Conclusion

Remedy: Serous inflammation
lungs (serous inflammatory edema)

Drug: Hemorrhagic
pneumonia

Drug: 2. Hemorrhagic
intestinal inflammation

Drug: Embolic
purulent nephritis

Drug: Purulent
bronchopneumonia

Remedy: Subcutaneous phlegmon
fiber

Remedy: Acute catarrhal
enteritis

Remedy: Chronic catarrh
small intestine

Drug: Catarrhal
bronchopneumonia

Drug: Fibrinous (lobar)
pneumonia (gray hepatization stage)