Editor

Pulmonologist

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

All signs of the disease are pronounced, the body is subject to severe intoxication. Cough that develops in the early 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 lesion, especially with the following pathologies:

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

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

The hemorrhagic type of pneumonia can also develop if present.

The defeat of the lung tissue serous-hemorrhagic pneumonia

The disease can be complicated by the following factors:

if the person smokes;
during, especially the most vulnerable woman in the 2nd and 3rd trimester;
the presence of chronic bronchitis;
emphysema of the lungs of a chronic course;
ischemic 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 disturbed;
plethora is formed;
vascular thrombosis.

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

The focus of inflammation is distinguished by a dense and bright red structure, resembling a 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, there is not enough infection, for this there must be a special soil - weakened immunity, and in particular the following components:

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

Clinical picture

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

After a few days, they are joined by severe manifestations of pneumonia:

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

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

As the pathology develops, the following signs join:

pulmonary insufficiency;
DIC;
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;
encephalitis of hemorrhagic type;
abscess of the lung region.

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

weaknesses;
subfebrile temperature;
shortness of breath;
sweating;
lingering cough.

Diagnostics

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

In the first place is performance of radiographs of the lung tissue. In the picture, the specialist should detect blackouts of a subtotal or total nature and changes in the vessels (plethora).

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

decrease in leukocytes;
an increase in neutrophils;
eosinophilia and lymphocytopenia are present;
elevated erythrocyte count.

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

The causes of the pathology under consideration are related to the underlying disease that provoked this complication. Sometimes differential diagnosis may be required with diseases such as:

tuberculosis pneumonia;
lung infarction;
bronchiolitis and so on.

Treatment of the serous-hemorrhagic type of the disease

Therapeutic measures should be carried out as early as possible. Without fail, a sick person is hospitalized. Otherwise, a lethal outcome is not inevitable, it can occur as early as on the third day.

Therapy is carried out in a complex manner. Antiviral drugs are prescribed in high dosage. Respiratory support measures are being taken. Oxygen therapy is provided. In severe cases, artificial ventilation of the lungs is performed. Antibiotic therapy is prescribed with broad-spectrum drugs, also parenteral with the use of high doses of the drug.

The following medicines are also used:

interferons;
glucocorticoids - hormonal drugs;
human type 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. In the presence of alveolitis, the disease will subside in two months.

Serous hemorrhagic pneumonia, according to statistics, occupies a leading position in terms of death among all pneumonias. An important symptom that should prompt immediate medical attention is blood in the sputum.

Recovery prognosis

The prognosis for recovery will depend on the following factors:

Depending on the causative agent of the disease.
The severity of the pneumonia.
From what period was intensive therapy started?
Presence of comorbidities.
Patient's age. The younger the patient, the higher his chances of a speedy recovery.

Reference materials (download)

Click on the selected document to download:

Conclusion

All therapeutic measures for serous hemorrhagic pneumonia are carried out in the department and intensive care. Even if it seems that the disease has receded, focal signs of the inflammatory process will remain on the radiographs 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 the tissues, which, in addition to a protein-rich fluid, includes a large number of red blood cells and very few white blood cells (hence the name of inflammation).

The development of hemorrhagic inflammation is associated with a sharp lesion of the vascular wall: it becomes so porous that erythrocytes 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 symptoms of hemorrhagic inflammation.

The inflammatory process is acute, accompanied by tissue necrosis, for example, necrosis in the lymph nodes with anthrax, skin necrosis with chronic 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 intestine

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

Micropicture.Already at a low magnification of the microscope, one can see that the process has spread to the entire thickness of the mucous and submucosal membranes. The mucosa is thickened, its structure is broken. The glands are poorly distinguished in it, the integumentary epithelium is in a state of necrosis, desquamated in areas. The villi are also partially necrotic. The surface of the mucosa, 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 defibration. Mucosal and submucosal vessels (especially capillaries) are heavily injected. Inflammatory hyperemia is especially pronounced in the villi.

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

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

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

Explanations for the figure

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 pulmonary infarction in anthrax and other serious diseases. Hemorrhagic pneumonia often occurs in combination with fibrinous pneumonia and may be complicated by purulent-necrotic processes or gangrene.

Micropicture.At low magnification, one can see strongly dilated and filled with erythrocytes vessels, especially alveolar capillaries, which have a tortuous course and nodular protrude into the lumen of the alveoli. The pulmonary alveoli and alveolar passages are filled with hemorrhagic exudate, in which fibrin admixture, alveolar epithelial cells and single leukocytes are found in areas. Interstitial connective tissue is infiltrated with serous-hemorrhagic exudate, has undergone defibration, individual collagen fibers are swollen, thickened.

When combined with fibrinous inflammation, one can observe the staging of the 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 parts 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 attention is paid to the details of changes in the interstitial connective tissue (the nature of infiltration, defibration and swelling of collagen fibrils).

In a mixed process with fibrinous inflammation, as well as in case of complications with necrosis or gangrene, the corresponding areas of lung tissue damage are found and examined.

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

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. lumen of the alveoli filled with exudate with cellular elements; 2. interalveolar septum (inconspicuous); 3. lymphatic vessel; 4. lymphatic valve infiltrated with cells.

B (x480). 1. a 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, histological structure, x100, view of the mucosa and submucosa, G-E

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

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

Explanations for the figure

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 the tide: 1. lobar lesion; 2. area of emphysema. B - with involvement of the pericardium: 1. lobar lesion of the lungs (beginning of hepatization); 2. fibrinous pericarditis ("villous", "hairy" heart)

Rice. 12. Croupous pneumonia. Histostructure (stage of hot flash and red hepatization), x 100. G-E

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

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

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

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

A - the site of the lesion (circled) is visible through the serous cover; B - follicular ulcers on the mucous membrane (the center of the ulcers is brownish-green, the edges are swollen); B - diphtheritic ulcer: 1. roller, 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 preparation: 1. hyperplasia of lymphoid cells; 2. a blood vessel in a state of inflammatory hyperemia; 3. solitary glands; 4. necrosis of the free edge of the mucous membrane

B - the border of the ulcer: 1. hyperplasia of lymphoid cells; 2. blood vessel; 3. site of hemorrhage

Rice. 17. Diphtheritic inflammation of the large intestine with necrosis of the mucosa and part of the submucosa. Histostructure, x100. G-E

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

Rice. 19. Diphtheritic inflammation of the large intestine with necrosis of the mucosa and part of the submucosa. 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 defibration; 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. G-E coloring

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

Explanations for the figure

fibrinous inflammation

With fibrinous inflammation, exudate comes out of the vessels, containing a high percentage of fibrinogen protein, which coagulates in the tissues and falls out in the form of a mesh or fibrous mass. In addition to fibrin, the composition of the exudate includes erythrocytes and leukocytes. It should be noted that the number of those 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 erythrocytes and can even be hemorrhagic in nature (with severe erythrodiapedesis), and there are few leukocytes in it. In the future, erythrocytes 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 in pathogenetic terms, 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 decay products of dead tissue and cause the coagulation of the exudate, just as in a blood clot, blood coagulation is associated with the breakdown of platelets.

This type of inflammation is observed in severe infections (rinderpest, swine fever, salmonellosis, etc.), as well as in some poisonings or intoxications (mercuric chloride, urea in uremia, etc.). Fibrinous inflammation appears in two main forms: croupous and diphtheritic.

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

Diphtheritic inflammation- a deep form of fibrinous inflammation, mainly on the mucous membranes. Unlike croupous inflammation in diphtheritic inflammation, the exudate permeates the thickness of the mucosa, therefore, it cannot be removed, and if it is removed, then together with the underlying tissue, and a defect remains - a bleeding ulcer. Inflammation develops more often focally, in patches and is accompanied by deep necrosis, extending not only to the entire thickness of the mucosa, but sometimes also to the underlying layers. In the later stages of the process, deep necrosis leads to ulceration of the mucosa (due to the decay and rejection of necrotic masses). 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 integuments. It is characterized by sweating and clotting 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 amounts between the cells of the integumentary epithelium. But mainly it falls on the surface of the serous cover, forming a soft fibrous plexus. There are few leukocytes in the exudate. As the exudative-infiltrative processes intensify, as a result of them, necrosis and desquamation of the cells of the integumentary epithelium begin to develop. The connective tissue of the pleura is infiltrated with serous cell exudate. If the process does not progress, the exudate resolves with subsequent 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 begins to grow into the exudate, rich in emerging vessels and young forms of cellular elements of tissue and hematogenous origin. This tissue gradually replaces the exudate, which is then absorbed. In the future, young granulation tissue turns into mature fibrous, and then into scar tissue.

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

Micropicture.Microscopic examination of the drug, depending on the stage of the process, the picture of changes will be different.

At an early stage, one can see dilated vessels in the subepithelial connective tissue (inflammatory hyperemia), a small amount of fibrin that has fallen out 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. In the exudate, a relatively small number of leukocytes with round, bean-shaped and horseshoe-shaped nuclei, stained with hematoxylin in dark or pale blue, are found. The epithelial cells are swollen, with symptoms of dystrophy, in places one can see the desquamation of single or small groups of cells. At this stage, the epithelial cover as a whole is still preserved, so the border of the pleura is quite well defined. The boundaries of the subepithelial connective tissue are expanded, it is infiltrated with serous cell exudate (serous fluid with leukocytes).

At a later stage, when organization sets in, the picture changes. On the surface of the pleura, one can see abundant overlays of exudate, which has the form of a dense 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 in leukocytes and the 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 more pale 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 here. At high magnification, it can be seen that it consists mainly of fibroblasts with unclear contours of the cytoplasm and a large, round-oval, pale blue nucleus (poor chromatin). In addition, there are leukocytes, lymphocytes and other forms of cells with more intensely stained nuclei. Collagen fibers extending in all directions (pale pink) are located between the cells. In some places, 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 pleura below it, devoid of an epithelial cover, which appears as 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 overlays in the form of reticulate deposits of a gray-yellowish or pale gray color.

After removal of fibrinous overlays, the surface of the pleura is hyperemic, cloudy, rough, 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, of a pale gray color. Fibrinous overlays are not separated. In the process of organization, the serous pleura can grow together with each other, as well as with the pericardium.

Explanations for the figure

Similar information.

Serous inflammation

It is characterized by an abundance and predominance in the exudate of a watery, slightly cloudy liquid, poor in cellular elements and rich in proteins (3-5%). Unlike 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 common 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, doughy consistency, reddened (hyperemia), with hemorrhages of a different nature. The cut surface is also with gelatinous hemorrhages, with a copious flow of watery exudate.

Serous-inflammatory edema must be distinguished from the usual 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. During the transition to a chronic form, 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

Micropicture.

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

Serous-inflammatory dropsy- accumulation of exudate in closed and natural cavities (pleural, abdominal, in the cavity of the heart shirt). The reasons are the same as for serous-inflammatory dropsy, only the exudate accumulates not between the cellular elements, but in the cavities. Usually, the integuments of cavities containing serous exudate, in contrast to dropsy, are reddened, swollen, with hemorrhages of a different nature. The exudate itself is cloudy, slightly opalescent yellowish or reddish in color with thin fibrin filaments. With edema, the covers of the cavities are not so changed, and the contents of the transudate are transparent. With cadaveric extravasation, the serous integuments are shiny, smooth, hyperemic without hemorrhages and tarnishing. And in the cavity at the same time they find a transparent red liquid. If the cause that caused the serous inflammatory dropsy is eliminated, then the exudate resolves and the integument restores its original structure. With the transition of the process into a chronic one, the formation of adhesive processes (synechia) 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 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 bubbles with serous fluid are called imperigo, larger ones are called vesicles, and extensive ones, examples of which are blisters in foot-and-mouth disease, are called aphthae. After the rupture of the bladder, a crust (crust) is formed, which disappears after healing, the process is often complicated by a secondary infection and undergoes purulent or putrefactive decay. If the bladder does not burst, the serous fluid resolves, the skin of the bladder shrinks, and the damaged area regenerates.

Theme Target

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

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

A conversation with the aim of familiarizing students with the preparedness for classes. Then the teacher explains the details.
The study of museum preparations, atlas and slaughter material in order to familiarize 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 record and establish a pathoanatomical diagnosis. After that, these protocols are read out and adjustments are made in cases of inaccurate description.
The study of histological preparations under a microscope. The teacher first explains the preparations with the help of slides, then the students, under the guidance of the teacher, study the changes in serous inflammation of the lungs and immediately compare them with pulmonary edema. Find differences. Then drugs serous inflammation of the skin (bullous form) with 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 with foot and mouth disease in cattle (foot and mouth aphtha), bullous form.
Serous inflammation of the intestine (serous inflammatory edema).

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

Drug: Serous pneumonia

With a small magnification of the microscope, it establishes that most of the alveoli are filled with a homogeneous pale pink mass, and only single alveoli do not have exudate, but their lumens are expanded, their diameter is equal to the diameter of 2-3 erythrocytes, which is why in these places they are nodular thickened and protrude into the lumen capillary. In places where the alveoli are filled with exudate, erythrocytes are squeezed out of the capillaries, and as a result, the capillaries are bled. Small arteries and veins are also strongly dilated and filled with blood.

Fig.120. Serous inflammation of the lungs:
1. Expansion 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 looks like a homogeneous or granular mass (depending on the protein content). The same exudate is found in the interstitial peribronchial and perivascular connective tissue. as well as in the bronchi. Connective tissue bundles impregnated with exudate are loosened, their boundaries are expanded, 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 rather large, lamellar in shape, with a large round or oval pale-colored nucleus, poor in chromatin. Being in the serous fluid, they swell, acquire a round shape instead of a lamellar one, and later their cytoplasm and nucleus are lysed. Part of the alveoli contains individual erythrocytes in the exudate, which have penetrated here from the respiratory capillaries by means of diapedesis.

As an expression of proliferative processes, one can note the appearance of histiocytic cells in the adventitia of 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 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 alveolar cavities, as well as serous edema of the interstitial perivascular and peribronchial connective tissue. Emigration of leukocytes and proliferative processes are poorly expressed. With a strong degree of edema, serous exudate from the alveoli enters the bronchioles, then into the large bronchi, and from there into the trachea.

Serous inflammatory edema, developing lobularly or lobarno, 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 lesions with glandular tuberculosis and other diseases.

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

Macropicture: lungs that have not fallen asleep, pale gray-red or dark red in color, test-like consistency, swim heavily, often drown in water, small hemorrhages are often found under the pleura and in the parenchyma. A cloudy, pinkish, frothy liquid flows from the cut surface. With a pronounced effusion of serous exudate of the same nature, the fluid is 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 section of the intestine the cut is made. Then, focusing on the overall 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 bundles of pale-colored homogeneous or granular masses of exudate. When fixed, it usually rolls 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. Accumulations of cells are observed mainly along the vessels, dilated and filled with erythrocytes. of this nature, the exudate, poor in cells, can be easily identified as serous. The noted changes in the vessels characterize a pronounced inflammatory hyperemia, accompanied by the emigration of leukocytes and diapedetic hemorrhages, and the accumulation of a large amount of serous exudate in the submucosal layer indicates a pronounced exudative component in the picture of inflammation as a whole.

Fig.121. Serous inflammation of the intestine:
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 attributed to polymorphonuclear leukocytes, among which there are proliferating cells of the vascular wall with a round or oval nucleus, pale-stained with hematoxylin. A small number of them indicates a weak proliferative component.

Turning to the study of the mucous membrane, pay attention to the integumentary epithelium of the crypts. He underwent dystrophy, necrosis (alternative 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 (clearances) of the crypts are filled with the decay products of the epithelium. Mucosal vessels in a state of inflammatory hyperemia. The thickness of the mucosa is locally infiltrated with serous exudate and leukocytes. In the muscle layer, muscle fiber dystrophy is noted, partially their necrosis and the accumulation of a small amount of serous cell exudate between the muscle bundles. The latter also accumulates under the serous membrane, the integumentary 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. Serous edema is most pronounced in the submucosal layer, the structural features of which (loose fiber) contributed to a significant accumulation of exudate in it, which caused defibration 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 submucosa, the exudate in a significant amount is also divided into the intestinal lumen.

Macropicture: the intestinal wall is strongly thickened (up to 5-10 cm in horses), the mucosa is hyperemic, swollen, dull, sometimes riddled with small hemorrhages. With a sharp edema, it is collected in unsteady folds and rollers. On section, the mucosa and especially the submucosa appear as pale yellow gelatinous infiltrates. The intestinal lumen contains a lot of clear or cloudy serous fluid.

Drug: Serous inflammation
lungs (serous inflammatory edema)

With a small 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 enlarged lumens, are free from effusion.

Respiratory capillaries are heavily injected with blood, dilated, nodular thickened in places, as a result of which they protrude into the lumen of the alveoli. The hyperemia of the respiratory capillaries is not everywhere expressed, in some places you can see the walls of the alveoli not collapsed, with bloodless capillaries as a result of pressure on them from 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 lumen of the alveoli;
2. Hyperemia of alveolar capillaries;
3. Hyperemia of the vessel.

At high magnification, the serous exudate filling the alveoli looks like a homogeneous or granular mass (depending on the protein content). The same exudate is found in the interstitial periobronchial and perivascular connective tissue. as well as in the bronchi. Connective tissue bundles impregnated 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 easy to determine 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 rather large, lamellar in shape, with a large round or oval pale-colored nucleus, poor chromatin. Being in the serous fluid, they swell, acquire a round shape instead of a lamellar one, and later their cytoplasm and nucleus are lysed. Part of the alveoli contains individual erythrocytes in the exudate, which have penetrated here from the respiratory capillaries by means of diapedesis.

As an expression of proliferative processes, one can note the appearance of histiocytic cells in the adventitia of 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 small bronchi.

Serous inflammatory edema, developing lobularly or lobarno, is often the initial stage of other inflammations of the lung (catarrhal, hemorrhagic, fibrinous) or is observed perifocally, that is, around the foci of lung lesions in glanders, tuberculosis and other diseases.

It must be borne in mind that inflammatory pulmonary edema in the histological picture is similar to congestive pulmonary edema. As the main distinguishing features that allow differential diagnosis, the following can be indicated:

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.

Macropicture: lungs that have not fallen asleep, pale gray-red or dark red in color, test-like consistency, swim heavily or sink in water, small hemorrhages are often found under the pleura and in the parenchyma. From the surface of the incision and from the gaps of the cut bronchi, a foamy, cloudy liquid is squeezed out and flows down, sometimes colored pink. With severe edema of the same nature, the 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 the expanded gelatinous strands of interstitial connective tissue infiltrated with serous exudate clearly protrude.

Preparation: Afta with foot and mouth disease in cattle

With a small magnification of the microscope, epithelial cells of the spiny layer are visible, which are enlarged in volume, rounded in shape. In their cytoplasm, affected cells are paler in color than unaltered 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 greater 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:
various sizes of emptiness (vacuoles).

At high magnification, we note in the aphtha zone - the cavity is filled with liquid, in which degenerate cells of the spiny layer of the epidermis are visible. Some are enlarged, pale colored, the nucleus is not defined in them, due to its lysis. Other cells contain a nucleus in the form of a bubble filled with liquid. In the serous fluid, neutrophilic leukocytes, single histiocytic cells are visible. The lid of the vesicle is represented by horny cells. The epithelial cells that make up the wall of the vesicle are represented by degenerate cells of the spinous layer and hyperemia of the capillaries and adjacent vessels. In many epithelial cells, vacuoles are visible containing a clear liquid, 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 is poured out.

Fig.124. Foot-and-mouth disease:
1. In the cytoplasm of the epithelial cells of the spiny layer
various sizes of emptiness (vacuoles).

Outcomes. If there is no complication of secondary infection, then the primary healing proceeds. If there is a complication of a purulent or putrefactive infection, then scarring of the aphtha occurs.

Macro picture: aphthae 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 scar.

1.2. Hemorrhagic inflammation

Hemorrhagic inflammation is characterized by a predominance of blood in the exudate. Usually 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 in allergic conditions of the body. With all these factors, the porosity of the vessels is sharply disturbed, and a large number of red blood cells go beyond the vascular wall, as a result of which the exudate takes on a bloody appearance. As a rule, this type of inflammation proceeds acutely with the development of necrosis.

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

With hemorrhagic inflammation of the gastrointestinal tract, serous membranes of the cavities in the intestinal lumen and cavities, bloody exudate accumulates. 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 development of regenerative processes in the future.

Hemorrhagic inflammation must be differentiated: from bruises, with them the boundaries of the bruise are sharply expressed, swelling and necrosis are not expressed; hemorrhagic infarctions, with them on the cut a typical triangle, and in the intestine they, as a rule, are formed at the site of inversions and twisting of it; from cadaveric extravasation, with it the contents are transparent, and the walls of the cavities are smooth, 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 what infectious diseases is this type of inflammatory reaction most common? Outcome of hemorrhagic inflammation.

The 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 is most common.
Localization of hemorrhagic inflammation. Morphological characteristics of hemorrhagic inflammation of compact and cavitary organs (color features of hemorrhagic inflammation in the intestine depending on the duration of the process).
Outcome of hemorrhagic inflammation. Significance for the body.

A conversation to get acquainted with the readiness of students to work on the topic of a laboratory lesson. Then the teacher explains the details.
The study of museum preparations and slaughter material in order to familiarize with the macro- and micropicture in hemorrhagic inflammation.
Reading by students of a protocol record of a description of the macroscopic picture in hemorrhagic inflammation.

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

Micropreparations:

Hemorrhagic pneumonia.
Hemorrhagic inflammation of the intestine.

The teacher on slides gives a brief description of the micropicture of hemorrhagic pneumonia and hemorrhagic inflammation of the intestine, students independently study these processes under a microscope, schematically sketching the process under study in notebooks, with the 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 pulmonary infarction in anthrax, bloodstained disease of horses and other serious diseases. Hemorrhagic pneumonia often occurs in combination with fibrinous pneumonia and may be complicated by purulent-necrotic processes or gangrene.

At low magnification, one can see strongly dilated and filled with erythrocytes vessels, especially alveolar capillaries, which have a tortuous course and nodular protrude into the lumen of the alveoli. The pulmonary alveoli and alveolar passages are filled with hemorrhagic exudate, in which fibrin admixture, alveolar epithelial cells and single leukocytes are found in areas. Interstitial connective tissue is infiltrated with serous-hemorrhagic exudate, has undergone defibration, individual collagen fibers are swollen, thickened.

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

At high magnification, various parts of the preparation are examined in detail and clarified: changes in the alveolar capillaries, the nature of the exudate in the alveoli and alveolar passages (serous-hemorrhagic, hemorrhagic, mixed - with fibrin), the cellular composition of the exudate (erythrocytes, alveolar epithelium, leukocytes). Then, attention is paid to the details of changes in the interstitial connective tissue (the nature of infiltration, defibration and swelling of collagen fibrils).

In a mixed process with fibrinous inflammation, as well as in case of complications with necrosis or gangrene, the corresponding areas of lung tissue damage are found and examined.

Macropicture: depending on the form and nature of inflammation, the appearance of the organ is not the same. With diffuse lesions - a picture of serous-hemorrhagic edema. If hemorrhagic pneumonia develops in a lobular or lobar form, the affected areas have sharply defined borders and are colored dark or black-red from 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, dense to the touch, drown in water, the surface of the cut is smooth, a small amount of bloody fluid flows from it. Expanded gelatinous pale yellow or black-red strands of the affected connective tissue clearly protrude on the surface of the incision.

Preparation: 2. Hemorrhagic
intestinal inflammation

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

Already at a low magnification of the microscope, one can see that the process has spread to the entire thickness of the mucous and submucosal membranes. The mucosa is thickened, its structure is broken. The glands are poorly distinguished in it, the integumentary epithelium is in a state of necrosis, desquamated in areas.

The villi are also partially necrotic. The surface of the mucosa, 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 defibration. Mucosal and submucosal vessels (especially capillaries) are heavily injected. Inflammatory hyperemia is especially pronounced in the villi.

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

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

Fig.127. Hemorrhagic inflammation of the abomasum of cattle

Fig.128. Hemorrhagic inflammation of the horse intestine

Fig.129. Hemorrhagic inflammation with mucosal necrosis
bovine small intestine (intestinal form)
with 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 has a pale yellow, white, greenish color. It consists of 2 parts: purulent bodies (degenerate leukocytes), decay products of tissues and cells and purulent serum, which, during the decay 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 - purulent bodies predominate in its composition, its consistency is thick creamy. Its formation characterizes the high reactivity of the body. Malignant pus has the appearance of a cloudy 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 a 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 of them are distinguished: phlegmon and abscess.

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

Macro picture. Abundant purulent exudate with an admixture of mucus on the surface of the mucosa. When the exudate is removed, erosions are found (areas of the mucosa devoid of integumentary epithelium), the mucosa is swollen, reddened with hemorrhages of a striated and spotted nature.

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

Phlegmon - diffuse purulent inflammation of loose tissue (subcutaneous, intermuscular, retroperitoneal, etc.). The process is characterized at first by the development of serous and serous-fibrinous inflammatory edema of the cellular tissue, followed by its rapid necrosis, and then by purulent infiltration and tissue melting. Phlegmon 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, swollen, dense at the beginning of the development of the process and later of a pasty consistency, bluish-red in color, are diffusely saturated with pus on the cut.

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

Abscess - 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 is formed, rich in capillaries, through the walls of which there is an increased emigration of leukocytes.

This shell on the outside consists of layers of connective tissue and is adjacent to the 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 subtle to large (15–20 cm or more in diameter). Their shape is rounded, when feeling superficially located abscesses, fluctuation (swelling) 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 there is no delimitation of a purulent inflammatory process, a zone of reactive inflammation, which occurs with a weakened resistance of the body, generalization of infection can occur with the development of pyosepsis and the formation of multiple abscesses in organs and tissues. If the reactive forces are sufficient, then the purulent process is delimited by the 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 ripe, forms a scar. But there may be such an outcome: the pus thickens, turns into necrotic detritus, which undergoes petrification. In other cases, encystation of an abscess is possible, 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 (the exudate resolves), but sometimes abscesses form or diffuse proliferation of connective tissue occurs at the site of phlegmon (elephantiasis).

Target setting:

Purulent inflammation. Concept definition. Characteristics of purulent exudate. Pathological forms of purulent inflammation. Outcomes. Significance for the body.

The focus is on the following issues:

Purulent inflammation. Concept definition. Composition of purulent exudate and its properties.
Morphological characteristics of purulent catarrh, purulent serositis, phlegmon, abscess (macro and micro picture).
Outcomes of purulent inflammation. Significance for the body.

Conversation with students on a given topic. Clarification of unclear aspects of the process under study.
The study of macro- and micro-pictures of purulent catarrh, purulent serositis, phlegmon, abscess on museum preparations and slaughterhouse material by describing the macro-picture and studying the picture of purulent inflammatory processes under a microscope.

List of museum preparations:

Purulent bronchopneumonia of the calf.
Liver abscess in cattle.
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 the subcutaneous tissue.

Drug: Embolic
purulent nephritis

Embolic purulent nephritis occurs when foreign bacteria enter the kidneys by the hematogenous route from primary purulent foci (ulcerative endocarditis, purulent endometritis, bronchopneumonia, etc.). Pyogenic microbes often settle in the arterioles of the glomeruli and begin to multiply here, causing purulent fusion of the glomerular tissue, followed by the 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. Purulent infiltration is exposed to interstitial connective tissue. In the epithelium of the convoluted tubules, dystrophic and necrotic changes are observed, 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 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, heaps. At high magnification, they are a fine-grained mass. In the later stages of the inflammatory process, at low magnification, we note areas in the parenchyma of the cortical and medulla of various sizes, consisting of clusters of cellular elements, of an intense blue color (stained with Hematoxylin-Eosin). These are areas of purulent fusion of the renal tissue (abscesses). As a rule, in the cortical layer they are round or oval in shape, in the medulla they are oblong in shape (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 formations of blue color;
3. Leukocyte infiltration of the kidney tissue;
4. Vascular hyperemia

At high magnification, abscesses consist of an accumulation of polymorphonuclear leukocytes, their nuclei are changed (deformation, disintegration into lumps, the appearance of vacuoles). This indicates their dystrophy. Among the leukocytes we find decaying epithelial cells, fragments of connective tissue fibers, 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 a serous exudate. All of these components and form pus. In the tissues surrounding the abscesses, the vessels and capillaries are overflowing with blood, and in places there are hemorrhages. Epithelial cells in some cases in a state of granular dystrophy, in others necrosis.

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

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

Preparation: Purulent
bronchopneumonia

With it, the inflammatory process spreads primarily through the bronchi, passing to the alveoli. With extensive lesions, the lung tissue undergoes fusion over large areas, and then is replaced by connective tissue (carnification and fibrinous hardening of the lung). In other cases of complications, abscess formation of the affected lung occurs or its 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 pneumonias.

With a small increase, we find the affected bronchus (its lumen is not determined), filled with purulent exudate, which is intensely colored. Hematoxylin in blue, due to the content of a large number of leukocytes in it. 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 mesh of hyperemic alveolar capillaries. (At high magnification, erythrocytes 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 a 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 lumen of the bronchi consists mainly of polymorphonuclear leukocytes, most of their nuclei are in a state of decay. Among the leukocytes are desquamated cells of the bronchial epithelium, single histiocytes and erythrocytes, serous-mucous fluid. The mucosa is edematous, impregnated with polymorphonuclear leukocytes, the integumentary epithelium is desquamated (desquamation). Perebronchial connective tissue is infiltrated with leukocytes. The exudate in the alveoli located around the affected bronchus consists of serous exudate, polymorphonuclear leukocytes, single histiocytes and erythrocytes, and desquamated cells of the alveolar epithelium (pink with a blue nucleus). The wall of the alveolus is thickened due to the strong expansion of the alveolar capillaries, the diameter of which is equal to the diameter of 2-3 erythrocytes. In the lumen of the capillaries, polymorphonuclear leukocytes are also visible. In areas of complete purulent fusion, the alveolar walls are not distinguished.

Macro picture. The lung was not sleeping, 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 of gray-yellow or yellow color. A thick purulent mass is released from the bronchi. A test for buoyancy of the affected parts - a piece of the lung sinks in water.

Fig.136. Pustules in the lungs of a sheep

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

Preparation: Phlegmon subcutaneous
fiber

Phlegmon in the subcutaneous tissue often develops with severe injuries or deep wounds, followed by the introduction of pyogenic bacteria and subsequent purulent fusion of 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 it). 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 are not distinguished. Thrombi are visible in some blood vessels. Adipose tissue is also infiltrated with leukocytes. The blood vessels and capillaries are dilated and overflowing with blood, cell clusters are also visible around the vessels. Lymphatic vessels are also dilated and filled with leukocytes. In some of them, blood clots are found. Visible necrotic connective tissue bundles surrounded by leukocytes.

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

At high magnification, we consider an inflammatory cell infiltrate, it consists of polymorphonuclear leukocytes, lymphocytes, and serous exudate. In areas of necrosis of the connective tissue bundles, a structureless pink mass with blue clumps of nuclear chromatin (decayed nuclei) is visible.

Macro picture. The affected area of the skin is edematous, dense at the beginning and doughy in the future. Depigmented skin and devoid of hair has a patchy or diffuse redness, thickened cords of lymphatic vessels are visible. With the development of abscesses, fistulous passages open in the appropriate places, through which pus is released. When cut, areas of necrosis and purulent infiltration of loose fiber are visible.

1.4. Catarrh

Catarrh 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 (alteration products, exudation, proliferation).

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

Mucous catarrh - mucus and desquamated degenerated cells of the integumentary epithelium predominate in the exudate. Essentially, this is an alternative type of inflammation. The mucosa is usually swollen, reddened with patchy-striated hemorrhages and covered with a large amount of cloudy mucous mass.

Serous caterpillar - cloudy, colorless serous fluid predominates in the exudate. The mucous membranes are vitreous swollen, reddened, dull.

Purulent catarrh - purulent bodies (degenerate leukocytes) predominate in the exudate. On the surface of the mucosa there is a purulent exudate, upon removal of which erosions (surface defects of the mucosa) are found. The mucosa is swollen, reddened with hemorrhages.

Hemorrhagic catarrh - the 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, enzymes of the gastrointestinal tract, takes the form of coffee mass or black color. The mucous membrane quickly becomes a dirty gray color.

According to the severity of the course of catarrh, acute and chronic are distinguished. In acute catarrhal inflammation, the mucosa is swollen, reddened, with spotty and striped hemorrhages, covered with viscous, liquid, cloudy mucus (catarrhal exudate) with an admixture of purulent bodies or erythrocytes, depending on the type of catarrh, easily washed off with water.

In chronic catarrhal inflammation, the mucosa thickens or unevenly, depending on the focal or diffuse nature of the inflammatory process, and has a bumpy appearance. The coloration is pale, coarsely folded. Covered with thick, cloudy mucus, difficult to wash off with water. The folds are not straightened by hand.

Theme Target

Morphological features of catarrhal inflammation and its localization. A kind of catarrhal inflammation of the mucous membranes according to the nature of the exudate. Morphological manifestations of catarrhal inflammation of the lungs. Morphological features of acute and chronic catarrhal inflammation. Outcomes. In what infectious diseases is this type of inflammation most common?

The focus is on the following issues:

Morphological features of catarrhal exudate, in contrast to another type 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, unlike other pneumonias (serous, hemorrhagic, fibrinous, purulent).

A conversation to familiarize students with the preparation for classes, then the teacher explains the details.
The study of museum preparations, atlas and slaughterhouse material in order to familiarize with the macro picture 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 record describe the studied pathoanatomical changes in catarrhs and, in conclusion, establish a pathoanatomical diagnosis. Upon completion of this work, the protocols are read out and corrections are made to them (in cases of inaccurate description).
The study of pathoanatomical processes on histological preparations. The teacher first explains the preparations with the help of slides and drawings on the board, and then the students, under the guidance of the teacher, use the methodological manual to study histological changes in acute and chronic enteritis, acute and chronic bronchopneumonia. Students schematically sketch pathological changes in these processes.

Fig.139. Catarrh of the stomach of a pig

Fig.140. Acute catarrhal inflammation of the intestine

Fig.141. Catarrhal-purulent bronchopneumonia in a calf

List of wet museum preparations:

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

List of micropreparations

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

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

Drug: 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 and in the upper sections of many crypts. As a result, the outlines of individual villi are poorly expressed, 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. The villi are exposed (without integumentary epithelium);
3. Cystic distended glands; 4. Villous atrophy

At high magnification, it can be seen that the exudate lying on the surface of the mucous membrane consists of:

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

Examining the preserved integumentary epithelium with a strong increase, 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 strong changes. The connective tissue base of the villi and the entire thickness of the mucosa are saturated with serous fluid, polymorphonuclear leukocytes in a small amount, and single lymphocytes and histiocytes.

With edema of the submucosal border, it is dilated, the vessels are injected, there are hemorrhages in the circumference of 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 crypts;
2. Edema of the connective tissue between the crypts

macro picture

The mucosa is swollen, patchy or striped, reddened (especially along the tops of the folds), sometimes there are continuous (suffuse) redness. The mucosa is covered with viscous, semi-liquid mucus, well washed off with water. With abundant desquamation of the epithelium, the exudate resembles mealy soup.

Remedy: Chronic catarrh
small intestine

In chronic catarrh, in contrast to acute catarrh, vascular changes are poorly expressed (inflammatory hyperemia, edema due to serous fluid effusion, leukocyte emigration), 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 villi and glands and growth of connective tissue.

At low magnification, we establish that the integumentary epithelium is completely absent, the villi are exposed, in some places they are reduced (atrophied). The glands are moved apart and squeezed by the growing connective tissue. Many glands are reduced in size (atrophy), in a state of decay, and present as islands among overgrown tissue. The surviving sections of the crypts look like elongated tubes. The lumens of other glands are cyst-like stretched. In areas with pronounced atrophic changes, the mucosa is thinned. Lymphatic follicles are enlarged, their centers are painted in a pale color. In the submucosa, the changes are insignificant, in other cases there is an increase in the connective tissue. The muscle layer is thickened.

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

With a large increase in areas where the epithelium is preserved, its mucous dystrophy and the decay of its cells are visible. On the part of the preserved epithelial cells of the deep parts of the crypts, the epithelium is being regenerated. The resulting young cells are intensely stained with hematoxylin, and the nuclei in them are usually located in the center. In the atrophying glands, the cells are wrinkled, reduced in volume, the nuclei in them are pycnotic, 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 the phenomenon of hyperemia. In the lymphatic follicles, there is a proliferation of reticular cells in their germinal centers. In the muscle layer, hypertrophy of the muscle fibers can be seen. sometimes overgrowth of connective tissue. There are no changes in the serous membrane.

In the hypertrophic variant 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 mucosa thickens, the folds become rough, do not melt when smoothed by hand, sometimes the growths resemble polyposis 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. Cells retain the ability to secrete a secret, but due to the infection of the lumen, the secret is not released, but accumulates in the lumen, forming cystic cavities overflowing with secret. Over time, the 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 mucosa is colored pale gray or grayish-white, sometimes with a brown or ashy tint, initially thickened evenly or unevenly, depending on the focal or diffuse nature of the inflammatory process, coarsely folded, the folds do not straighten out, later atrophic processes develop with the aging of the connective tissue , the mucosa becomes thinner in patches, becomes dense.

In hypertrophic chronic catarrh, the mucosa becomes sharply thickened, folded or bumpy, sometimes covered with villous polypous growths, which, when cut, often reveal cystic cavities.

Preparation: catarrhal
bronchopneumonia

Catarrhal bronchopneumonia is characterized by:

Catarrhal exudate.
The spread of the process is endobronchial.
Bronchopneumonia begins with small foci, affecting individual lobules, mainly of the apical lobes, and only at 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, the accumulation of catarrhal exudate in the small bronchi, serous cell effusion in the alveoli, degeneration and desquamation of the alveolar epithelium.

With endobronchial spread of the process, at low magnification, it finds the affected bronchus, the lumen of which is filled with cellular exudate. At high magnification, we see that the exudate consists of mucus, leukocytes, desquamated cells of the ciliated epithelium, 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 bronchus wall are not changed, there is no edema and cellular infiltration of the tissue surrounding the bronchus, as is the case with the peribronchial spread of the process, which is observed much less frequently. Then we consider 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, overflowing with cellular exudate, hyperemia is not visible (the exudate has squeezed out the erythrocytes from the alveolar capillaries). The exudate consists of a homogeneous pink mass containing leukocytes, desquamated cells of the alveolar epithelium, erythrocytes, single histiocytes. In the affected alveoli, located closer to the affected bronchus, leukocytes predominate in the composition of the exudate, and serous fluid and desquamated cells predominate in the peripheral parts. The alveoli surrounding the inflamed foci are expanded, have the form of irregular cavities containing air (vicar emphysema).

With the development of inflammation, serous edema and lymphocytic infiltration develops in the interstitial connective tissue and interalveolar septa. Fibroblast proliferation occurs. Hyperemia begins to subside, and cell proliferation increases. The interalveolar septa become indistinguishable, the alveoli undergo necrosis and in their place, as well as in the interstitium of the lungs, interalveolar septa, cell 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 croupous pneumonia, they are colored blue-red or gray-blue-reddish (splenization of the organ), i.e. tissue becomes similar to the spleen. The surface of the cut of the affected parts is wet, when pressed, a muddy, sometimes bloody, discharge is separated, and cloudy, viscous mucus is released from the cut bronchi. With the intensification of cell proliferative processes, i.e. the transition of the inflammatory process into a chronic form in the corresponding areas against a general blue-red background, gray-red spots and dots appear. expanded pale gray strands of edematous connective tissue stand out well. In chronic cases, the inflamed areas of the lung are pale gray in color and firm in texture, resembling the pancreas.

Fig.146. Acute catarrhal bronchopneumonia in a lamb

Fig.147. Inflammation of the right lung of the 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. Fresh fibrin films, when sweated out, look like elastic translucent yellow-gray masses that impregnate 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 its transparency and turns into a crumbly gray-white substance. Under the microscope, fibrin has a fibrous structure. The etiology of fibrinous inflammation is associated with the impact of virulent pathogens (epidemic pneumonia, rinderpest, swine fever, swine paratyphoid fever, etc.), which, with their toxins, cause increased permeability of the vascular wall, as a result, large protein molecules of fibrinogen begin to pass through it. Croupous inflammation (superficial) - characterized by the deposition of fibrin on the surface of natural cavities. Its localization is on serous, mucous, articular integuments. A film of fibrin is formed on their surface, which is easily removed, exposing the swollen, reddened, dull shell of the organ. As a rule, the process is diffuse.

In the intestine, fibrin accumulates and forms rubber-like casts that close the intestinal lumen. On the serous integument, these films, condensing, 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 the liver (hepatization), the cut surface is dryish. Fibrin in the lungs can be absorbed or grow into connective tissue (carnification).

Fig.148. Fibrinous inflammation of the pulmonary pleura

Fig.149. Fibrinous verrucous endocarditis in chronic swine erysipelas

Fig.150. Diphtheritic necrotic foci on the tongue of a calf with necrobacteriosis

Fig.151. Fibrinous pneumonia of the horse with necrobacteriosis

Fig.152. Focal diphtheria colitis in a pig with paratyphoid

Fig.153. Diphtheric acute colitis in a pig with chronic paratyphoid

Fig.154. Fibrinous pleurisy of cattle with peripneumonia

Fig.155. Fibrinous pericarditis

Diphtheritic (deep) inflammation is characterized by the deposition of fibrin in the depths of the organ between tissue and cellular elements. As a rule, the process is focal in nature, and the area of the affected mucosa looks like a dense, dryish film that is difficult to remove from the surface. When removing films and bran-like overlays, a defect (notch, ulcer) is formed, which then undergoes organization (infection with connective tissue). Despite the severe nature of the inflammatory process, diphtheritic inflammation proceeds more favorably than croupous (superficial), as it is focal in nature, and croupous is diffuse.

Theme Target

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

The 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.
The study of macroscopic changes in fibrinous inflammation of the mucous membranes, serous integuments, articular surfaces, lungs on slaughterhouse confiscated products, wet and dry preparations, atlas. Students, using the scheme of macroscopic description of organs, in the form of a brief record describe the studied macroscopic changes in fibrinous inflammation. Then read out with an indication of the pathoanatomical diagnosis. Adjustments are being made.
The study of the micropicture of fibrinous pneumonia under a microscope. Students, using the protocol description of the preparations and the teacher's explanations, study the various stages of the development of fibrinous pneumonia and sketch them schematically in notebooks marked with an arrow.

List of wet museum preparations

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

List of micropreparations

Fibrinous pneumonia (stage of a rush of blood and red hepatization).
Fibrinous pneumonia (stage of gray and yellow hepatization).

Fibrinous (croupous) pneumonia

Features of fibrinous pneumonia:

fibrinous exudate.
Lobar nature of fibrinous inflammation from the very beginning of the development of the inflammatory process.
The lymphogenous pathway of distribution, and consequently, the interlobular tissue is affected, and as a rule, fibrinous inflammation proceeds 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 pathway of spread, and consequently, the interlobular tissue is affected, and as a rule, fibrinous inflammation proceeds to the pleura and pericardium. In this regard, fibrinous pneumonia is complicated by fibrinous pleurisy and pericarditis.

In the development of fibrinous pneumonia, 4 stages are distinguished:

Stage 1 - hyperemia (blood rush).

2nd stage - red hepatization (red hepatization).

3rd stage - gray hepatization (gray hepatization).

4th stage - yellow hepatization (permission process).

pneumonia (stage of red hepatization)

At low magnification, we see that the capillaries of the alveoli, the blood vessels of the pulmonary septa, are greatly expanded 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 from a red looped mesh. In the lumen of some alveoli, small bronchi, erythrocytes and exudate.

Fig.156. Fibrinous inflammation of the lungs of cattle
(sites of red hepatization):
1. Hyperemia of alveolar capillaries;
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. There are many erythrocytes in the exudate, an admixture of polymorphonuclear leukocytes and desquamated (pink with a pale-colored vesicular nucleus) cells of the alveolar epithelium, single histiocytes. There is a lot of fibrin in some alveoli, and it forms a continuous mesh. In others, there are only separate 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 lumen of the alveolar ducts and small bronchi, the exudate is fibrinous 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 defibration 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. Interstitium areas of necrosis (unstructured pink mass) are also visible, around which demarcation inflammation has formed (leukocyte infiltration (blue cells) at the border of necrotic tissue).

Macro picture.

In this stage, a large number of lobules (lobar character) are affected from the very beginning. The affected lobes of light red and dark red are enlarged, thickened, similar changes on the cut, reminiscent of liver tissue (red hepatization). Pieces cut out from the affected areas sink in the form.

Preparation: Fibrinous (croupous)
pneumonia (stage of gray hepatization)

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

Fig.157. Fibrinous inflammation of the lungs of cattle
(areas of gray hepatization):
1. Thinning of 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, the fibrin fibers that fill the gaps of the alveoli stretch from one alveolus to another. (This is clearly seen when stained for fibrin). There are many leukocytes in the exudate, erythrocytes are not 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, the lymphatic and blood vessels (their thrombosis) and interstitial connective tissue (its necrosis) are more affected. Macroscopically affected lobules are gray and yellow. 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 dilated holes.

Outcome: The exudate can be completely absorbed (peptonization of it). Then 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 is not completely absorbed, then the dead areas grow into connective tissue (lung carnification), i.e. the inflammatory process ends with incomplete resolution.

Macropicture of fibrinous pneumonia

Lobarity of the lung lesion 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 dilated. 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 passes to the pleura and pericardium, followed by the 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 of the lobules are in the stage of gray hepatization

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

Test 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. Significance 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. Significance for the body.
Composition of purulent exudate and its properties. Examples.
Pathological anatomical manifestations of purulent inflammation depending on the localization of the inflammatory process (purulent catarrh, purulent serositis (empyema), abscess, phlegmon). Examples.
Macropicture of purulent embolic nephritis, purulent bronchopneumonia, phlegmon.
Outcomes of purulent inflammation (purulent catarrh, purulent serositis, abscess, phlegmon). Examples.
Essence of catarrh. 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 catarrh. Examples. Significance for the body.
feature and morphological composition of fibrinous exudate. Localization of fibrinous inflammation.
Morphological signs of fibrinous (superficial) and diphtherigic (deep) fibrinous inflammation of the mucous membranes. Exodus. Fibrinous inflammation of the serous integument and articular surfaces. Exodus.
Morphological features of fibrinous pneumonia (stage development of the process). Exodus. Significance for the body.
In what infectious diseases is this type of inflammation observed? Examples. Significance 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 with influenza can be complicated by secondary bacterial inflammation of the respiratory tract, pleurisy, 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, personal hygiene items. Penetrates into 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), adenovirus. The incubation period of the disease lasts 3-5 days, a few days after infection, the bacterial flora joins the viral one.

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

Typical symptoms of pneumonia

Viral pneumonia in most cases proceeds in an acute form, the high temperature lasts up to 2 weeks, 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 babies and preschool children. In babies, signs of intoxication of the body in the form of nausea, vomiting, headache, and dyspeptic disorders are pronounced. Hyperthermia usually does not exceed subfebrile marks, 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, the 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 after 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 concerned about the usual symptoms of a cold, which quickly increase and progress. There is fever, shortness of breath, cyanosis of the skin, shortness of breath. The cough is wet with the release of a small amount of sputum, sometimes blood impurities appear in the composition of the liquid.

Primary influenza pneumonia is most often found in people suffering from diseases of the heart, kidneys, and respiratory system. Activators are found in a bronchial secret, a parenchyma of lungs. The disease is classified:

acute interstitial pneumonia;
hemorrhagic inflammation of the lungs.

In the first case, the interstitial tissue of the lung is damaged with a violation of the respiratory function. The disease proceeds in a severe form, causes fibrous, sclerotic changes in the lung parenchyma and often has an unfavorable outcome.

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

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

Post-influenza inflammation of the lungs joins the symptoms of influenza after 5-6 days. The action of the virus greatly reduces the immune defense of the body, creates favorable conditions for the reproduction of pathogenic microflora in the respiratory tract. The causative agents of pathology can serve as Staphylococcus aureus, Haemophilus influenzae, pneumococcus.

The development of secondary bacterial pneumonia contributes to the weakening of the immune system and the following factors:

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

In patients, after the fever subsides, the body temperature rises again, purulent, viscous sputum with blood impurities is coughed up. In the bronchial secret, viral agents and pathogenic bacteria are detected.

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, the formation of infiltration foci in the lungs. Breathing, auscultated, wheezing, crepitus.

Atelectasis of the lungs - its types

With viral pneumonia, wet rales alternate with dry ones, changes occur within 1-2 days. The pathological process is explained by the progression of atelectasis, the accumulation of exudate, which closes the lumen of the bronchi.

An x-ray examination reveals an increase in the vascular pattern, foci of infiltration of the parenchyma (more often in the lower segments), in rare cases, the inflammatory process extends to the entire lobe of the respiratory organ. According to the results of a blood test, leukopenia and lymphocytopenia, an increased titer of antibodies to a viral agent, and an increase in ESR are diagnosed. To confirm the etiology of pneumonia, bronchial washings are carried out.

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.

Medical treatment of pneumonia

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

A drug	A photo	Price
		from 910 rub.
		from 64 rubles
		from 704 rubles

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

Patients with pneumonia are prescribed broad-spectrum drugs (,) in order to relieve an acute inflammatory process, reduce swelling of the lung tissue, and prevent serious complications. If a viral infection is combined with or chlamydia, antibacterial agents are additionally prescribed:

A drug	A photo	Price
		from 28 rub.
		from 694 rubles
		from 216 rubles
		from 222 rub.
		from 265 rubles

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

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

A drug	A photo	Price
		from 27 rub.
		from 164 rubles
		from 197 rub.
		from 99 rub.
		from 158 rubles

Prevention of viral pneumonia

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

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

A person who has pneumonia after the flu is placed in a separate room, individual hygiene items, dishes, and bed linen are isolated. Indoors, it is necessary to carry out daily wet cleaning with the addition of antiseptic preparations to the water, and wipe the dust.

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 the internal organs, it is necessary to perform supportive treatment in a timely manner. It also shows the mandatory sanitation of the oral cavity, respiratory tract, treatment of carious teeth. After prolonged inflammation, rest 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 pronounced signs of general malaise. With untimely treatment, the pathology progresses rapidly and can lead to the development of severe complications up to death.

^ THEME XVIII

INTRODUCTION TO INFECTION.

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

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

Invasive - called diseases when protozoa and helminths are introduced into the body.

Bronchitis - inflammation of the bronchi, complicated by a violation of ventilation, purification, warming, humidification of the air penetrating into the respiratory section.

^ 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. The shape is distinguished: spindle-shaped, cylindrical, saccular bronchiectasis.

By pathogenesis, they are distinguished: retention and destructive.

^ Destructive bronchiectasis - occur with purulent fusion of the bronchial wall, have perifocal inflammation.

Retention bronchiectasis- arise as a result of a violation of the evacuation of the contents during atony of the wall; no perifocal inflammation.

pneumosclerosis associated with proliferation of connective tissue in the lungs. Pneumosclerosis happens: mesh, 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.

Distinguished by volume:

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

According to pathogenesis, they are distinguished:

contractile,
obstructive,
surfactant-dependent atelectasis.

collapsed lung - compression of the lung from the outside.

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

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

Flu - respiratory infection - caused by a 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, bronchitis are possible.

Pneumonia -inflammation of the respiratory tract of the lungs.

According to the nature of the exudate, pneumonia is distinguished:

purulent,
fibrinous,
serous,
hemorrhagic.

According to the size of the foci, the types of exudative pneumonia are distinguished:

acinous,
lobular,
subsegmental,
segmental.

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

Croupous pneumonia - lobar, fibrinosis, pleuropneumonia.

Stages of croupous pneumonia:

high tide,
red hepatization,
gray hepatization,
permissions.

There are atypical forms:

Central - a lesion in the depth of the lung without involvement of the pleura
Massive - exudate fills the lumen of large bronchi, so bronchial breathing is not audible
Total - all shares are affected in the same stage of the process
Migrating - different lobes are affected by a process that is at a different stage
Kpipsieleznaya - exudate has a mucus-like appearance and the smell of burnt meat.

Intrapulmonary complications of croupous pneumonia:

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

Extrapulmonary complications of croupous pneumonia:

meningitis,
pericarditis,
brain abscess.

Pneumonia with influenza- "large motley influenzal lung": foci of serous-hemorrhagic and fibrinous inflammation, atelectasis, emphysema, foci of purulent bronchopneumonia.

Lung cancer often develops from the epithelium of the bronchi (bronchogenic cancer) and only in 1% of cases from the alveolar epithelium (pneumonogenic cancer).

^ By localization Distinguish radical (central cancer), peripheral and mixed (massive) cancer.

By histological structure- adenocarcinoma, squamous cell, undifferentiated cancer.

Metastasizes lung cancer lymphogenously to the hilar, bifurcation lymph nodes, neck lymph nodes, etc. and hematogenously.

^ EXPLORE MACRO PREPARATIONS:

13. Croupous pneumonia in the stage of red hepatization.

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

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 cut, in the upper part of the lung, the focus of tissue melting with the formation of a cavity (abscess).

^ 160. Croupous pneumonia with outcome in gangrene.

The lobe of the lung is dense, gray In the lower part of the preparation, the tip 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 plethoric.

321, 327. Abscesses of the brain.

On the section of the brain, cavities with grayish, loose walls are visible.

439. Fibrinous pericarditis (“hairy” heart).

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

525. Chronic pneumonia with abscesses.

The lobe of the lung is sealed with connective tissue strands, cavities (abscesses) with a thick capsule are visible in depth, around the sclerosis zone. The pleura is thickened.

^ 568. Chronic pneumonia in the acute stage.

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

302. Congenital bronchiectasis.

On section of the lung, dilated bronchi are visible. There is no carbon pigment in the lung tissue.

^ 23. Acquired bronchiectasis.

The walls of the bronchi on the section of the lung are thickened, white-gray, their gaps are expanded in the lung tissue, a black carbon pigment is visible

111. Mesh pneumosclerosis (posttuberculous).

The lung is enlarged, swollen, on a pale gray section A fine network of connective tissue is clearly visible

457. Pulmonary heart.

The wall of the right ventricle is hypertrophied, thickened on the cut. Heart valves are not changed.

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

On the section of the lung, foci of tumor tissue, dense consistency, whitish color are visible. Similar tissue in the hilar lymph nodes.

328. Hemorrhagic tracheobronchitis with influenza.

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

^ 197. Hemorrhagic pneumonia in influenza.

In the lung tissue, dense, airless, dark red foci of hemorrhagic inflammation merge in places. In addition, foci of necrosis are visible.

^ EXPLORE MICROSPREGATIONS:

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 a few erythrocytes. In places, accumulations of microbes in the form of dark purple spots are visible.

55. Fibrinous-purulent pneumonia with necrosis.

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

^ 142. Chronic pneumonia with carnification and pneumosclerosis.

In the zone of carnification, the alveoli are filled with fibrin, into which fibroblasts grow (organization of fibrin). 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.

Among the layers of atypical epithelium, “cancer pearls” are visible.

A t l a s (drawings):

104	- lobar pneumonia

Tests: choose the correct answers.

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

1- lobar pneumonia

2- fibrinous pneumonia

3- pleuropneumonia

473. Stages of croupous pneumonia according to classical concepts are:

1-stage tide

2- red hepatization

3- gray hepatization

4- permissions

474. Components of exudate in alveoli in lobar pneumonia are:

1- neutrophilic leukocytes

2- erythrocytes

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

1- brain abscess

2- purulent mediastinitis

3- purulent meningitis

4- acute ulcerative or polyposis-ulcerative endocarditis

476. Typical complications of pneumonia caused by Klebsiella include:

1- necrosis of the 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. Pieumocystis pneumonia can develop in patients:

1- with AIDS

2- with cytostatic chemotherapy, especially for leukemias and lymphomas

3- in corticosteroid therapy

4- in weakened children of the first months of life

479. Characteristic morphological features of pneumocystis pneumonia are:

1- interstitial inflammation

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

3- foamy exudate in the alveoli

480. Forms of bronchiectaea are:

1- cylindrical

2- baggy

3- fusiform

481. During life, it was found that the patient has shortness of breath, the epigastric angle is obtuse, the tops of the lungs are determined above the collarbones, and a box sound is determined during percussion. Make a diagnosis:

1- emphysema

2- lung atelectasis

482. As the main disease in the diagnosis of an adult, the following may appear:

1- focal pneumonia

2- croupous pneumonia

483. Lung atelectasis can be caused by:

1- pneumonia

2- compression of the lung from the outside

3- bronchial obturation

484. Bronchopneumonia can be the main 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- cholera vibrio

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

1- with pneumococcus

2- with Friedlander stick

3- with legionella

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

1- with staphylococcus

2- with pneumococcus

3- with Escherichia coli

488. Friedlander's pneumonia is caused by:

1- Neisseria

2- clepsiella

3- pneumococcus

489. Exudate in croupous pneumonia is:

1- serous character

2- fibrinous-hemorrhagic character

3- fibrinous-purulent character

490. Exudate in focal pneumococcal pneumonia has:

1- purulent character

2- serous character

3- serous-desquamative character

4- fibrinous character

491. Lung carnification in croupous 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 croupous pneumonia include:

1- lung abscess

2- pleural empyema

3- lung cancer

494. With all focal pneumonia observed:

1- emphysema

2- carnification

3- acute bronchitis

4- pneumosclerosis

5- alveolitis

495. Chronic obstructive pulmonary diseases include:

1- bronchiectasis

2- chronic bronchitis

3- lung gangrene

4- emphysema

496. In the outcome of all diseases of the group of chronic obstructive pulmonary diseases in the tissues of the latter develops:

1- cavity

2- emphysema

3- pneumosclerosis

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

1- pulmonary heart failure

2- anemia

3- renal failure (amyloidosis of the kidneys)

498. In the development of pulmonary heart failure in chronic obstructive pulmonary diseases, the leading is:

1- precapillary hypertension

2- postcapillary hypertension

3- increase in vascular permeability

4- decrease in vascular permeability

5- violation of the air-blood barrier

499. Macroscopic manifestations of bronchiectasis 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. Detection of Charcot-Leiden crystals in the patient's sputum most likely indicates the presence of:

1- bronchial asthma

2- lung carcinomas

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 in influenza with pulmonary complications are:

1- destructive panbronchitis

2- focuses 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 stratified epithelium (pharynx, pharynx), diphtheritic inflammation in which the fibrinous film is tightly bound to the underlying tissue. On the mucous membranes covered with a single-layer cylindrical epithelium (larynx, trachea, bronchi), develops croupous inflammation, in which the film is easily separated from the underlying tissue.

Local lesion in diphtheria - characterized by the development of a 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 pharynx,
respiratory diphtheria,
diphtheria of the nose, less often - eyes, skin, wounds.

With diphtheria intoxication, the following are affected:

Nervous system
The cardiovascular system
Adrenals

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

Parenchymal myocarditis - myocardial damage in diphtheria, tk. Diphtheria exotoxin primarily affects cardiomyocytes.

Adrenal damage in diphtheria may lead to collapse.

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

Early cardiac paralysis in diphtheria - due to toxic parenchymal myocarditis.

Late heart palsy associated with parenchymal neuritis.

Death in diphtheria is due to acute insufficiency of the pituitary-adrenal system, toxic myocarditis or true croup.

Scarlet fever - acute streptococcal disease; characterized by fever, general intoxication, tonsillitis, punctate exanthema, tachycardia. Refers to airborne anthroponoses. 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 necrotic angina (affect),

2. lymphadenitis of the cervical lymph nodes.

Forms of scarlet fever- according to the severity of the flow, they distinguish:

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

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

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

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

Solid phlegmon - severe edema, necrosis of soft tissues, cellulose, a tendency to a chronic course.

Soft phlegmon - 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 the rapid spread to the mediastinum, subclavian and axillary fossa, into the cranial cavity (abscesses, meningitis). maybe arrosive bleeding from large vessels. Necrotizing otitis media. Possibly with immunodeficiency putrefactive inflammation(symbiosis of anaerobes, staphylococci, streptococci, Escherichia coli) and sepsis.

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

glomerulonephritis,
myocarditis,
vasculitis,
synovitis,
arthritis.

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

Measles. The causative agent of the RNA-containing myxovirus is introduced through the conjunctiva, the respiratory tract, penetrates into the lymph nodes of the neck, causing viremia.

On the mucous membranes of the oral cavity develops 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 buccal mucosa in the region of the molars - the so-called Koplik-Filatov spots- whitish nodules up to 2.0 mm in diameter, surrounded by a rim of hyperemia. They are formed due to coagulation of the surface layer of the squamous epithelium with a small inflammatory infiltration. Immunodeficiency can make measles worse 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.

^ EXPLORE MACRO PREPARATIONS:

98. Measles pneumonia.

On a section of the lung, whitish foci of necrosis around the bronchi are visible.

Fake 3. Measles rash.

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

Model 25. Measles necrosis of the mucous membrane of the labia.

Fake 7. Cheek nome.

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 with the underlying tissues, exfoliates in places

562. Infectious heart

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

428. Adrenal apoplexy.

In the adrenal medulla, extensive hemorrhage (hematoma).

151. Acute glomerulonephritis.

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

520, 309. Purulent meningitis.

The pia mater is thickened due to leukocyte infiltration

Fake 6. Scarlet rash on the face.

On the hyperemic background of the skin of the child's face, a petechial rash is visible, a white nasolabial triangle free from the rash

^ EXPLORE MICROSPREGATIONS:

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 soldered to the underlying tissues. The submucosa is plethoric, edematous, infiltrated with leukocytes

158. Croupous tracheitis (demonstration).

The mucous membrane of the trachea, normally covered with a cylindrical epithelium, is necrotic, impregnated with fibrinous exudate, forming a thin, easily detachable film

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

In the mucous membrane and tissue of the tonsils, against the background of plethora of 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. In the epithelium of the convoluted tubules dystrophic changes.

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

A t l a s (drawings):

Tests: choose the correct answers.

503. Early paralysis of the heart in diphtheria can be caused by:

1- fatty degeneration of the myocardium

2- parenchymal myocarditis

3- interstitial myocarditis

504. Intoxication in diphtheria is more pronounced with the localization of inflammation:

2- larynx

505. Possible causes of death from diphtheria are:

1- early paralysis of the heart

2- late heart paralysis

3- collapse

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

1- necrotic mucosal epithelium

2- erythrocytes

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 in diphtheria are:

1- asphyxia

2- heart failure

3- pneumonia

509. At the entrance gate in diphtheria, inflammation has the following character:

1- productive

2- fibrinous

3- purulent

4- hemorrhagic

5- putrid

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

1- fibrinous pericarditis

2- purulent myocarditis

3- toxic myocarditis

4- heart disease

5- recurrent warty endocarditis

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

1- tonsil necrosis

2- necrosis of underlying tissues

3- colonies of microbes in the area of necrosis

4- pale pharynx

5- bright red pharynx

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

1- first week

2-3-4 weeks

513. Inflammatory process from the pharynx spreads through the esophagus

1- for measles

2- with scarlet fever

3- with diphtheria

514. Changes in regional lymph nodes in scarlet fever are characterized by:

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- necrotic angina

4- hyperplasia of the lymph nodes and spleen

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

2- diphtheria

3- scarlet fever

517. A child with scarlet fever has hematuria and proteinuria after 3 weeks. Scarlet fever worsened

1- glomerulonephritis

2- nephrosclerosis

3- amyloid-lipoid nephrosis

518. Catarrhal inflammation in measles develops on mucous membranes:

2- trachea

3- intestines

4- bronchi

5- conjunctiva

519. The main characteristics of measles include:

1-acute highly contagious infectious disease

2- causative agent - RNA virus

3- catarrhal inflammation of the mucous membranes of the upper respiratory tract, conjunctiva with 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. Measles 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 found:

1- on the palms and feet

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- papular rash

4- roseolous rash

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

1- gums

2- buccal mucosa against incisors

3- buccal mucosa against second molars

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

1- fibrinous films on the tonsils

2- red pharynx

3- pale throat with red spots

Hemorrhagic pneumonia. How does hemorrhagic pneumonia manifest?

Drug: Serous pneumonia

intestines (serous inflammatory edema)

Drug: Serous inflammation lungs (serous inflammatory edema)

Preparation: Afta with foot and mouth disease in cattle

1.2. Hemorrhagic inflammation

Drug: Hemorrhagic pneumonia

Preparation: 2. Hemorrhagic intestinal inflammation

1.3. Purulent inflammation

Drug: Embolic purulent nephritis

Preparation: Purulent bronchopneumonia

Preparation: Phlegmon subcutaneous fiber

1.4. Catarrh

Drug: Acute catarrhal enteritis

Remedy: Chronic catarrh small intestine

Preparation: catarrhal bronchopneumonia

1.5. fibrinous inflammation

pneumonia (stage of red hepatization)

Preparation: Fibrinous (croupous) pneumonia (stage of gray hepatization)

Test questions:

Causes of the disease

Typical symptoms of pneumonia

Primary viral pneumonia

Diagnostic methods

Medical treatment of pneumonia

Prevention of viral pneumonia

Consequences of viral pneumonia after influenza

Etiology and pathogenesis

Clinical picture

Diagnostics

Treatment of the serous-hemorrhagic type of the disease

Recovery prognosis

Reference materials (download)

Conclusion

Drug: Serous inflammation
lungs (serous inflammatory edema)

Drug: Hemorrhagic
pneumonia

Preparation: 2. Hemorrhagic
intestinal inflammation

Drug: Embolic
purulent nephritis

Preparation: Purulent
bronchopneumonia

Preparation: Phlegmon subcutaneous
fiber

Drug: Acute catarrhal
enteritis

Remedy: Chronic catarrh
small intestine

Preparation: catarrhal
bronchopneumonia

Preparation: Fibrinous (croupous)
pneumonia (stage of gray hepatization)