Macro preparation nutmeg description. Violations of the exchange of nucleic acids. Mineral metabolism disorders. Pathological calcification. Formation of stones. Hemorrhagic infarcts of the brain

The kidney is enlarged, dense (the edge is pointed on the cut), dark red with a bluish tinge.

Cyanotic induration of the spleen.

The spleen is enlarged, dense, dark red with a bluish tint.

Muscat liver.

The liver on the section of a variegated type.

Hemorrhage in the brain (hematoma) with a breakthrough in the lateral ventricles of the brain.

In the region of the subcortical nodes of the brain, a cavity filled with red blood clots is visible.

Hemorrhage into the ventricle of the brain (hemocephaly), along the periphery - petechiae and hemorrhagic infiltration.

The walls of the lateral ventricle of the brain are saturated with dark red blood. On the periphery there are small dotted foci of dark red color (petechiae), in the upper part above the lateral ventricle there is uniform impregnation of the brain tissue with blood (hemorrhagic infiltration).

Varicose veins of the rectum (hemorrhoids).

The rectum in its lower part - plexuses of hemorrhoidal veins are varicose, dark purple in color. In the lumen of some vessels obturating thrombi.

Hemorrhages on the mucous membrane of the pelvis in the kidney.

Kidney in section. On the mucous membrane of the pelvis, multiple foci of dark red color are visible, of different sizes - from dotted to 3 mm.

Hemorrhages on the skin (hemorrhagic infiltration and petechiae).

There is a brown spot on the skin and small exact hemorrhages of a dark red color.

Bleeding into the intestinal lumen (melena).

Large intestine in section. The mucous membrane of the large intestine is saturated with black blood.

Juxtamedullary shunt.

On the section of the kidney, the bark is pale gray, and the medulla is full-blooded, dark red.

5. Model. On the skin of the body, multiple petechial hemorrhages (petechiae) and a rounded focus with clear borders of a cyanotic appearance (vacant hyperemia) are visible.

EXPLORE MICROSPREGATIONS:

Brown induration of the lungs.

In the lumen of the alveoli and in the interalveolar septa, macrophages containing hemosiderin in the cytoplasm - the so-called "cells of heart disease" and free hemosiderin (from dead cells). The vessels of the lung are dilated and full-blooded. The interalveolar septa are thickened due to the growth of connective tissue in them (induration) and overflow of capillaries with blood.

1a. Brown induration of the lungs. (Pearls stain for iron). Demonstration.

In lung tissue, hemosiderin grains stained blue-green according to Perls due to the fact that hemosiderin contains iron.

Muscat liver.

Plethora of central veins and capillaries of the inner third of the lobules. Hepatocytes in the centers of the lobules are atrophied, but preserved on the periphery.

4. Stases in the vessels of the brain.

The capillaries are dilated and filled with adherent erythrocytes.

Hemorrhage in the brain.

The focus of hemorrhage with the formation of a cavity due to the expansion of the brain tissue by the outflow of blood - hematoma . Around him, soaking the brain tissue with blood - hemorrhagic infiltration and petechial hemorrhages petechiae .

A t l a s (drawings):

67 - nutmeg liver

68.69 - brown induration of the lungs

77.78 - stasis in the capillaries of the brain

Tests: choose the correct answers.

105. The main reasons for the development of stasis are:

1- infections.

2- intoxication.

3- venous congestion.

106. The main ways of collateral circulation in liver cirrhosis are:

1- porto-abdominal

2- porto-esophageal

3- porto-lumbar

107. Consequences of venous hyperemia are:

1- induration

2- thrombosis

3- lymphostasis

4- bleeding

108. Hemorrhage includes:

2-purpura

3- ecchymosis

4- melanosis

5- hematocele

109. To stop bleeding leads to:

1- migration of leukocytes

2- erythrocyte diapedesis

3- blood clotting

4 cell infiltration

110. Staz is:

1- slowing down the blood flow

2- decrease in blood outflow

3- stop blood flow

4- blood clotting

5- hemolysis of erythrocytes

111. In case of chronic venous plethora, the organs:

1- reduced in size

2- have a flabby texture

3- have a dense texture

4- clayey type

5- slimed

112. Chronic venous plethora in the lungs occurs:

1- cloudy swelling

1- lipofuscinosis

2- brown induration

3- mucoid swelling

4- fibrinoid swelling

113. General venous plethora develops:

1- with compression of the superior vena cava

2- with heart disease

3- with compression of the tumor of the renal vein

4- with thrombosis of the portal vein

114. Nutmeg hyperemia of the liver can be caused by:

1- tricuspid valve insufficiency

2- mitral stenosis

3- portal stasis

4- hypertension of the pulmonary circulation

5- acute coronary insufficiency

115. With "nutmeg" hyperemia in the liver develop:

1- hyperemia of the central veins

2- hyperemia of the portal vein branches

3- hepatic cell atrophy

116. Figurative name of the type of liver in chronic venous plethora:

1- greasy

2- sago

4- nutmeg

5-glazed

117. The main cause of venous plethora is:

1- decreased blood flow

2- obstruction of outflow of blood

3- increased blood flow

4- increase in blood flask

5- stop blood flow

118. Venous plethora can be:

1- collateral

2- inflammatory

119. Decompensation of the "right heart" occurs:

1- brown induration of the lungs

2- nutmeg liver

3- cyanotic induration of the kidneys

120. Signs of chronic cardiovascular insufficiency are:

1- common edema

2- myxedema

3- ischemic infarcts of the kidneys

4- vasculitis

5- lymphadenopathy

121. The development of stasis is characterized by:

1- loss of fibrin

2- damage to the vessel

3- erythrocyte agglutination

4- leukodiapedesis

122. Signs of shock may include:

1- formation of microthrombi in parenchymal organs

2- desolation of large vessels

3- plethora of large vessels

123. The concept of disseminated intravascular coagulation is equivalent to:

1- consumption coagulopathy

2- thrombohemorrhagic syndrome

3- hyperhypocoagulation syndrome

THROMBOSIS. EMBOLISM

Thrombosis- intravital blood coagulation with the formation of a blood clot in the lumen of a vessel or cavity of the heart, called a thrombus.

A thrombus differs from a post-mortem blood clot: dryness, brittleness; the thrombus crumbles in the hands, is attached to the wall of the vessel. The post-mortem clot lies freely in the lumen of the vessel, without expanding the lumen, and has an elastic consistency.

The formation of blood clots is carried out as a result of the action of the following factors:

1- components of the vessel wall,

2- platelet apparatus,

3- plasma coagulation factors.

A thrombus can be: parietal, when most of the lumen of the vessel is free or obstructive.

If the thrombus grows rapidly along the blood flow, it is called progressive.

Freely lying thrombus in the atrial cavity is called spherical.

Depending on the method of occurrence and structure, 4 main types of blood clots are distinguished: white, red, mixed and hyaline.

White blood clot- macroscopically has a white color, soldered to the wall of the vessel, its surface is corrugated, dull, it crumbles, layering is revealed on the cut. It is formed slowly with a fast flow of blood in the arteries. A white thrombus is usually parietal.

Red blood clot formed during rapid clotting and slow blood flow. Macroscopically, the thrombus is red and loose, easily separated from the vessel wall, more often clogging and occurs in the veins.

Mixed thrombus consists of elements of both white and red blood clots, found in veins, arteries, aneurysms of arteries and the heart. On the section in the aneurysms of blood vessels, the thrombus has a layered structure.

Hyaline thrombi multiple and occur in the vessels of the microvasculature. They occur in shock, extensive tissue trauma, burns. The basis of hyaline thrombi is necrotic erythrocytes.

Pathology of hemostasis: disseminated intravascular coagulation syndrome (DIC) (synonym: thrombo-hemorrhagic syndrome) and thromboembolic syndrome.

Thrombo-hemorrhagic syndrome (DIC) is characterized by the formation of disseminated blood clots in the microvasculature and is often combined with simultaneous blood incoagulability leading to massive hemorrhages.

They speak of thromboembolic syndrome in cases where there is a repeated detachment of blood clots or their parts, which turn into thromboemboli and circulate in the blood, causing the formation of heart attacks.

thrombosis outcomes. Favorable for the body - aseptic autolysis, organization, sewerage, vascularization, petrification.

Unfavorable outcomes of thrombosis are transformation into thromboembolus, septic fusion of blood clots.

Embolism- circulation in the blood or lymph of particles that do not occur under normal conditions and blockage of blood vessels by them.

Embolism happens:

1 - direct (by blood flow)

2- paradoxical

3- retrograde (against blood flow)

Depending on the type of bodies circulating in the blood and lymph, embolisms are divided into:

1- thromboembolism

2- fatty

3- air

4- gas

5- tissue

6- microbial

7- embolism by foreign bodies.

EXPLORE MACRO PREPARATIONS:

Similar information.

MICRO PREPARATIONS. To study, draw and designate the listed morphological features.

1. Acute venous plethora (edema) of the lungs A) dilated, full-blooded blood vessels of the interalveolar septa, b) in the lumen of the alveoli, eosinophilic content (protein transudate) with an admixture of macrophages and desquamated epithelium.

2. Hemorrhage in the brain. Stained with hematoxylin and eosin. A) accumulation of hemolyzed and preserved erythrocytes in the brain tissue, b) there is no brain substance in the center of the hemorrhage (stratification of brain tissue with blood), V) pericellular and perivascular edema.

3. Brown induration of the lungs. Perls reaction. In the lung tissue on the background A) plethora and edema, b) deposits of hemosiderin, which gives a positive reaction to iron and its grains turn bluish-green, there are growths of connective tissue in the alveolar septa, around the bronchi and blood vessels.

4. Chronic venous plethora of the liver (“nutmeg liver”). Stained with hematoxylin and eosin. In the center of the lobules are found A) expansion and plethora of veins and sinusoids, discomplexation of hepatic beams, b) necrosis and atrophy of hepatocytes. On the periphery of the lobules, the blood filling of the sinusoids is normal, the structure of the hepatic beams is preserved, the hepatocytes are in a state of V) fatty degeneration.

MACRO PREPARATIONS.

1. Acute plethora of meninges in influenza. In the preparation of the brain. The pia maters are edematous, gelatinous with dilated full-blooded blood vessels, the convolutions are smoothed.

Causes: flu.

Complications: cerebral edema on the background of serous meningitis. Outcomes: usually full recovery.

2. Nutmeg liver. In the preparation, the liver is enlarged in size, dense in consistency, with a smooth surface and a rounded front edge. The cut surface of the organ is variegated, gray-yellow (fatty degeneration of hepatocytes along the periphery of the lobules) with dark red specks (central stagnant parts of the lobules) and resembles nutmeg.

Causes: chronic heart failure with the development of venous stasis in the systemic circulation: cardiosclerosis of various origins, malformation of the tricuspid valve. Hypertension in the pulmonary circulation, chronic lung diseases resulting in pneumosclerosis.

Complications And outcomes: transition to congestive fibrosis (cirrhosis) of the liver, development of portal hypertension syndrome, ascites, splenomegaly, varicose expansion of porto-caval anastomoses, bleeding, anemia.

3. Brown induration of the lungs. The drug is light, enlarged, brown ("rusty") color, dense consistency. Layers of white dense tissue (pneumosclerosis) are visible around the bronchi, vessels and diffusely in the lung tissue. Changes are more pronounced in the lower and posterior sections of the lung.

Causes: chronic heart failure.

Complications And outcomes: respiratory failure exacerbates chronic heart failure - pulmonary heart failure progresses.

All circulatory disorders are divided into general and local, but such a division is conditional, since a general circulatory disorder affects blood circulation in individual organs and vice versa, a circulatory disorder in any organ affects blood circulation throughout the body.

The practical course includes only local disorders, which are discussed below.

Types of local circulation: hyperemia, hemorrhage, thrombosis and embolism, heart attacks.

Disorders of the lymphatic circulation are caused by changes in the patency or integrity of the lymphatic vessels, lesions of the lymph nodes, circulatory disorders and inflammatory changes in the organs. Distinguish the following types of disorders of lymphatic circulation: lymphostasis, lymphorrhagia, thrombosis and embolism of the lymphatic vessels. Moreover, all these processes are usually accompanied by changes in the composition and amount of lymph.

LOCAL CIRCULATION DISORDERS

Hyperemia;

hemorrhages;

thrombosis and embolism;

Heart attack.

Theme target setting:

Definition of the concept of hyperemia (acute and chronic congestive), hemorrhage (morphological manifestations of hemorrhage), thrombosis and embolism, infarction. Morphological characteristics and etiopathogenesis of hyperemia, hemorrhage, thrombosis and embolism, infarction.

outcomes of these processes. Infectious septic diseases in which local circulatory disorders are observed.

their clinical significance. Disorders of lymphatic circulation (lymphostasis, lymphorrhagia, thrombosis and embolism of lymphatic vessels). Outcomes. clinical significance.

1. Etiopathogenesis and morphological characteristics of acute and chronic congestive hyperemia. Distinctive features from hypostasis. Outcomes. clinical significance.
2. Etiopathogenesis and morphological characteristics of thrombosis and embolism. Distinctive features of intravital thrombus from postmortem. Outcomes. clinical significance.
3. Etiopathogenesis and morphological characteristics of infarction (white, red, mixed). Features of the pathomorphological manifestation of infarcts depending on the architectonics of the arterial system of organs (kidneys, lungs, spleen, heart, brain). Outcomes. clinical significance.
4. Etiopathogenesis and morphological characteristics of various types of lymph circulation disorders. Lymphostasis. Thrombosis and embolism of the lymphatic vessels. clinical significance.
5. Etiopathogenesis and morphological characteristics of various types of hemorrhages (petechial, ecchymosis, vibex, suffusion). Outcomes. clinical significance.

1. A conversation to get acquainted with the readiness of students to conduct a laboratory lesson on the topic. Then the teacher explains the details.
2. The study of museum preparations in order to familiarize themselves with macroscopic changes in acute and chronic congestive hyperemia, thrombosis and embolism, hemorrhages, heart attacks. Students orally, and then in writing, using the scheme, learn to describe pathological processes related to local circulatory disorders.
3. Examination of histological preparations under a microscope. Under the guidance of a teacher, students find hemorrhages, hyperemia, thrombosis and embolism of blood and lymphatic vessels, heart attacks. Draw schematically in notebooks marked with arrows.

List of important museum preparations

Atherosclerosis of the aorta with parietal thrombus;

aortic aneurysm;

Myocardial scars (after a heart attack);

Rupture of the heart with tamponade;

Fibrous pericarditis;

Pasteurellosis. fibrinous pneumonia;

Hemorrhage in the brain;

Hemorrhagic infarction of the lung.

1. HYPEREMIA

Hyperemia is an excess of blood in an organ or tissue. It can be arterial or venous. Venous passive, congestive occurs much more often than arterial. It often spreads to the entire organ, and sometimes captures entire areas of the body. In the vast majority of cases, congestive hyperemia is the result of a cardiac disorder or lung disease. The most characteristic sign of venous hyperemia is the expansion of small and large veins and capillaries.

Normally, under a microscope, the diameter of a capillary is equal to the diameter of one erythrocyte. In a large blood vessel, the erythrocyte column occupies a central place, and on the periphery of the vessel there is a light plasma layer. With hyperemia, the capillaries expand, and their diameter becomes equal to 2-3 or more erythrocytes. In large vessels, hyperemia is manifested by the expansion of the erythrocyte column and the narrowing of the plasmotic column. The adhesion of red blood cells to the intima of a vessel is called stasis. (The blood vessel is as if stuffed with red blood cells). With prolonged stasis, acute congestive hyperemia becomes chronic, manifested by the effusion of the liquid part of the blood, and then the formed elements outside the vascular wall. The tissues surrounding the vessel are in a state of edema, if these phenomena occur in the liver, then ascites develops. If the cause that caused hyperemia and edema are eliminated, then the liquid is resorbed and the organ or tissue returns to its original state. If the cause is not eliminated, then degeneration and necrosis of cells and tissues occurs in the edema zone, and later connective tissue grows, leading to organ compaction.

Macropicture of acute congestive hyperemia: the compact organ is somewhat swollen, flabby with venous, dense with arterial hyperemia, painted in a dark cherry color, blood flows on the cut. Mucous and serous integuments: the pattern of the vessels is pronounced, previously invisible vessels are visible, the integuments are somewhat swollen, the blood vessels are overflowing with blood.

Macropicture of chronic congestive hyperemia. The organ is edematous in the initial phases of development, reddened, with the development of the process, the organ increases in volume evenly or unevenly (depending on the growth of the connective tissue), dense consistency, alternation of dark red and light gray areas is noted, brownish spots of hemosiderin are visible.

Fig.71. Inflammatory hyperemia of the skin in swine erysipelas

Micropicture of acute and chronic hyperemia. Normally, in a blood vessel, the erythrocyte column is located centrally, plasmatic along the periphery. The capillary diameter is equal to the diameter of one erythrocyte. In acute congestive hyperemia, the erythrocyte column expands and the plasma column narrows, the adhesion of erythrocytes to the intima of the vessels indicates stasis. The diameter of the capillaries increases to a diameter of 2-3 or more erythrocytes - they seem to be stuffed with erythrocytes.

With the development of chronic hyperemia, first the liquid part of the blood, and then the formed elements, go beyond the vascular walls. The metabolism in the tissues is disturbed, dystrophic, necrotic and inflammatory processes develop, which leads to the growth of connective tissue elements that replace the dead parenchyma of the organ, blood vessels thicken. Brown-brown lumps of hemosiderin are visible.

Theme target setting:

Etiopathogenesis. Morphological characteristics of hyperemia (micro- and macro picture). Exodus. Significance for the body.

The focus is on the following issues:

Definition of the concept of hyperemia. Etiopathogenesis of hyperemias and their classification. Morphological characteristics of acute and chronic hyperemia and their fundamental difference. Exodus. Significance for the body.

1. Exchange of information on key issues related to congestion.
2. The study of museum preparations in order to understand the macropicture of acute and chronic hyperemia, and then the micropicture.

Students respond in writing and then verbally, describe the processes seen according to the scheme. Examine preparations under a microscope.

Acute congestive hyperemia of the liver.

Cirrhosis of the liver.

Acute congestive hyperemia of the mesentery.

Drawings of the pathoanatomical atlas.

List of histopreparations

Acute congestive hyperemia and pulmonary edema.

Acute congestive hyperemia of the liver.

Chronic congestive hyperemia of the liver.

Chronic congestive hyperemia of the lungs.

Drug: Acute congestive hyperemia of the liver

Venous hyperemia of the liver is quite common and is more pronounced than venous hyperemia of other abdominal organs.

Fig.72. Acute congestive hyperemia of the liver:
1. Intralobular capillaries are filled with blood;
2. Atrophy of the hepatic beams.

This happens because any obstruction of blood flow in the posterior vena cava is primarily reflected in the hepatic veins.

When examining the preparation with a low magnification of the microscope, it is necessary first of all to pay attention to the central parts of the lobules. Due to the peculiarities of blood circulation in the liver, the first changes occur, as a rule, in the region of the central veins. The latter, as well as the intralobular capillaries flowing into them, are greatly expanded and filled with blood.

On the periphery of the lobules, closer to the interlobular connective tissue, hyperemia is mild or absent. The beams in the center of the lobules are more or less separated from each other, and in some cases, as it were, have broken up into groups of cells. It seems that these groups of cells or even individual liver cells are freely located among the clusters of erythrocytes. This impression is reinforced by the fact that with the usual hematoxylin-eosin staining, the walls of highly dilated capillaries remain invisible.

Fig. 73. Acute congestive liver hyperemia (diffuse form):
1. Central vein;
2. Hyperemia of intra-bar capillaries;
3. Atrophy of the hepatic beams.

Then they proceed to study the details of the preparation at high magnification of the microscope, paying attention to the central and peripheral parts of the lobules.

The hepatic beams of the centers of the lobules are thin, broken in places. The boundaries of the liver cells are indistinct, and their nuclei in the bulk are reduced, darkly colored, and some of them have uneven, jagged contours - a state of pycnosis.

In the liver cells, yellow-brown or brown granules of the lipofuscin pigment can sometimes be found, which is explained by a long-term metabolic disorder in them.

The cytoplasm of the liver cells of the middle and peripheral parts of the lobules often contains unstained cells. The latter corresponds to drops of fat, which, when treated with alcohol, turned out to be dissolved. Among obese cells, cricoid forms are often found, similar to cells of adipose tissue. The entire body of such cells is occupied by one fat drop, and the nucleus is pushed aside to its periphery.

Fig. 74. Acute congestive liver hyperemia (diffuse form):
1. Central vein (blood stasis in it);
2. Hyperemia of capillaries between the hepatic beams;
3. Atrophy of the hepatic beams.

Macroscopically, the liver from the surface and on the cut is variegated, has a nutmeg pattern (nutmeg liver). This is due to the fact that the centers of the lobules, due to the accumulation of blood there, turn red, brownish-red or blue-red, the periphery - in a pale gray or gray-yellow (from fat) color. The volume of the liver is somewhat enlarged, the capsule is tense, a lot of dark venous blood flows from the cut surface.

Drug: Chronic congestive hyperemia of the liver

Studying the preparation at low magnification, it is noted that there is almost no blood in the center of the lobules. On the contrary, the periphery of the lobules is full-blooded, and here one can see the remains of preserved hepatic beams. Next, thickening of the walls of the central and sublobular veins and the growth of fibrous connective tissue around them are established.

Fig. 75. Chronic congestive hyperemia of the liver:
1. In the triads of the liver, the growth of fibrous connective tissue;
2. Remains of preserved hepatic beams

Fig. 76. Chronic congestive hyperemia:
1. Growth of interlobular connective tissue.

Fig. 77. Chronic hyperemia of the liver:
1. Thickening of the wall of the central vein;
2. Hyperemia of capillaries near the central vein

The lumens of these veins are somewhat collapsed. Some of them still contain some blood, while others are empty. There is also an increased amount of fibrous connective tissue between the lobules around the triads. At high magnification, they begin to study the preparation from the center of the lobules, where they establish the absence of hepatic beams and their replacement with newly formed fibrous tissue while thickening the walls of the central veins. Collagen fibers gradually tighten the intralobular capillaries and central veins, leading them to desolation, which is why hyperemia is noticeable mainly only on the periphery of the lobules. The liver cells and vascular endothelium preserved on the periphery of the lobules contain dust-like brown grains of the hemosiderin pigment, the formation of which was the result of the breakdown of erythrocytes. The proliferation of connective tissue is also noted around the lobules, mainly along the sub- and intralobular veins, the walls of which are thickened due to this.

Macroscopically, the liver at this stage retains a nutmeg pattern to some extent, at the same time it takes on a denser texture and can be somewhat reduced in volume - congestive cirrhosis of the liver. Thickening of the liver is due to the growth of connective tissue in it. The degree of compaction is an indicator of the age of the process.

Preparation: Acute congestive hyperemia and pulmonary edema

With congestive hyperemia of the lungs, the capillaries of the septa and veins of the interlobular connective tissue expand and overflow with blood. Examining the histological preparation, already at a low magnification of the microscope, one can see that the structure of the lung is greatly changed. The lumens of the alveoli and bronchioles are partially or completely filled with a pinkish or grayish-pinkish film, and the blood vessels (veins and respiratory capillaries) are heavily engorged with blood. For a more detailed study, it is necessary to find such a section of the preparation where the alveolar structure of the lung tissue is most clearly visible. At high magnification, unevenly dilated capillaries are visible here, which in places clearly protrude into the lumen of the alveoli and give the alveolar septa a thickened appearance. If in the liver, due to the compactness of the organ, there is no accumulation of edematous fluid (trasudate), then in the lung this fluid is found in large quantities in cavities - alveoli. Trasudate, or rather transudate protein, remaining after dehydration of the preparation with alcohol, is noticeable in the alveoli or in the form of the smallest granularity that fills the gaps of the alveoli in whole or in part. In the latter case, the transudate film contains air in the form of uncolored cells of various sizes. Some alveoli are almost completely filled with air, in the transudate only a narrow strip is located near the alveolar septa, there are few cellular elements in the transudate.

Usually it contains a few erythrocytes, single lymphocytes, neutrophilic leukocytes and desquamated cells of the alveolar epithelium. Separate cells should be differentiated mainly by nuclei, since the protoplasm is stained in the same color as the transudate and does not have sharp boundaries with it. The nuclei of desquamated epithelial cells are large, pale in color and round-oval or vesicular in shape.

Fig. 78. Edema and hyperemia of the lungs:
1. Expansion and overflow of blood in the capillaries of the alveoli and alveolar septa;
2. The lumens of the alveoli are filled with a gray-pink film (edema of the pulmonary alveoli).

These cells are much larger than blood cells.

At the same time, the connective tissue around the blood vessels, bronchi and between the lobules can be subjected to edema, which causes swelling and thickening of the collagen fibers there.

Drug: Chronic congestive hyperemia
or brown induration of the lungs

Chronic congestive hyperemia of the lungs differs from acute proliferation of connective tissue and the deposition of a large amount of hemosiderin pigment in the lung tissue.

With a low magnification, first of all, areas of the lung tissue are found in which the alveolar structure is almost completely absent, and especially in places where there is a strong growth of fibrous connective tissue. The alveoli here are with slit-like cavities, but at the same time there are alveoli with enlarged lumens and strongly thickened walls. In some alveoli, an accumulation of dark brown hemosiderin pigment is noticeable.

Fig. 79. Brown induration of the lungs:
1. Growth of fibrous connective tissue between the alveoli;
2. Accumulation of hemosiderin pigment

By examining a section of the organ there with a high magnification of the microscope, a fibrous connective tissue rich in cells is found. According to the preserved slit-like lumens of the alveoli and the accumulation of pigment in them, it can be concluded that the development of the connective tissue proceeded along the partitions and led to alveolar atelectasis and complete obliteration of their cavities.

Studying the accumulation of hemosiderin, they are convinced that the bulk of the latter is located in rounded cells (alveolar macrophages) that fill the gaps of the alveoli. There is so much pigment in these cells that it obscures the nuclei of alveolar macrophages. Hemosiderin, as in the liver, is formed from red blood cells. The latter, by diapedesis, exit the dilated capillaries, admixture with the transudate, and then are phagocytosed by the cells. The causes of chronic stagnation of blood in the lungs are usually various heart defects, such as valve insufficiency, so the pigment cells located in the alveoli are called heart disease cells.

The capillary network in the thickened partitions becomes invisible. This is explained by the fact that the latter become empty due to compression by their growing connective tissue, as well as as a result of the proliferation of the endothelium, which closes the lumen of the capillaries.

At autopsy, such lungs are found in a state of atelectasis, a dense consistency and painted in a gray-brown or rusty-brown color - hemosiderosis. The compaction of the lungs caused by the proliferation of connective tissue is called induration, thus, in general, there is a picture of brown induration of the lungs.

2. BLEEDING

With hemorrhages, erythrocytes or all components of the blood exit the blood vessel and accumulate in tissues or in any natural cavities of the body. The outpouring of blood is called hemorrhage. It is customary to distinguish three types of hemorrhages:

1. Hemorrhage after rupture of the wall of a blood vessel (cuts, bruises, injections, gunshot wounds, etc.).
2. Hemorrhages without noticeable gross violations of the integrity of the vascular wall (poisoning, infectious diseases, inflammatory reaction, and other causes). Diapedetic hemorrhages.
3. Hemorrhage due to erosion of the vessel wall (ulcerative or inflammatory process, tumor, tuberculosis, glandular and other processes).

Macro picture of hemorrhages. Hemorrhages look like dots (petechial hemorrhages), spots of various shapes and sizes (ecchymosis), in the form of stripes, which is mainly observed on the tops of the folds of the mucous membranes and diffuse, i.e. solid, which often develop under the shell of the organ (into the submucosa, under the soft or hard shell, etc.). Dots, spots, stripes, solid hemorrhages of a dark red color, in old cases, if the body has remained alive, hemosiderin clumps are visible in these places, which dissolve over time.

Micropicture. Under the microscope, free-lying red blood cells, fresh or hemolyzed, that have gone beyond the blood vessels and capillaries, are visible.

Exodus. Erythrocytes are hemolyzed, disintegrate, and in their place, if the death of the organism has not occurred, local reticular cells produce hemosiderin in the form of rusty-brown clumps, which resolves over time.

Target setting of the theme.

Etiopathogenesis. Morphological characteristics of various types of hemorrhages (macro and micro). Outcomes. Significance for the body.

The focus is on the following issues:

Definition of the concept of hemorrhage.

Types of hemorrhages and their classification according to the etiological principle.

Types of hemorrhages and their classification according to the morphological principle.

Outcomes and significance for the organism.

Fig.80. Hemorrhages in the mucous membrane of the bladder

Fig.81. Multiple petechial hemorrhage in the pleura of a calf.

Fig.82. Spotted hemorrhages under the serous cover of the colon of the horse

Fig.83. Spotted hemorrhages in the skin of a pig with plague

Fig.84. Pinpoint hemorrhages on the costal pleura of a pig with swine fever

Fig. 85. Suffuse hemorrhages under the epicardium and endocardium in swine fever

Fig.86. Multiple small-spotted hemorrhages under the serous cover of the intestine

Fig.87. Hemorrhages under the epicardium of a foal

Fig.88. Multiple hemorrhages under the epicardium

1. Mutual information about the pathological process "Hemorrhage".
2. The study of museum preparations by describing in notebooks macroscopic changes according to the description scheme, and then microscopic ones.

List of museum preparations

Point (petechial hemorrhages on the epicardium).

Spotted and punctate hemorrhages on the skin and in the kidneys with swine fever.

Hemorrhages in the serous covers of the intestine.

Hemorrhages under the costal pleura.

Suffusion under the dura mater.

List of micropreparations.

Diapedetic hemorrhages in the kidney and in the heart muscle.

The teacher explains the pathological changes on histological preparations, and then the students independently sketch in their notebooks schematically in the form of a diagram with the pathological changes indicated by an arrow.

Preparation: Diapedetic hemorrhage in the kidney

Studying the drug at low magnification, it is noted that the blood vessels of the glomeruli and intertubular connective tissue are heavily engorged with blood. Around them, in places, there is a noticeable accumulation of a large number of red blood cells, like a blood puddle.

Erythrocytes are located either in the intertubular connective tissue or in the lumen of the glomerular capsules. One of the areas with hemorrhage is studied at high magnification. The convoluted tubules, which are in the focus of the hemorrhage, are strongly compressed and far removed from each other by continuous accumulations of blood. Their epithelium is in a state of granular dystrophy, often necrobiosis, because of which such tubules do not have gaps, there are no boundaries between individual epithelial cells, and the nuclei are in a state of lysis and pycnosis. Such changes are even more pronounced in those tubules, the lumen of which contains erythrocytes that have penetrated here from the glomerular capsules or from the interstitial tissue. If hemorrhages occurred relatively long before the death of the animal, the erythrocytes located outside the blood vessel are painted pale, and their contours are shaded.

Fig.89. Diapedetic hemorrhage in the kidney:
1. The blood vessels of the glomeruli are filled with blood;
2. Capillaries of the intertubular connective tissue are filled with blood;
3. The border between the cells of the convoluted tubules is not visible, there is no lumen;
4. Lysis of the nuclei of the epithelium of the convoluted tubules

The fate of such hemorrhages depends on the degree of tissue damage (necrobiosis). With dystrophy of one epithelium, a complete recovery is observed. If, at the same time, the connective tissue is also necrotic - the stroma of the organ, incomplete healing occurs in the form of the organization of a dead area with the formation of a scarred connective tissue of a brownish or rusty-brown hue (pigmentation with hemosiderin).

At autopsy, diapedetic hemorrhages in the kidneys are common in all domestic animals with intoxication and various infectious diseases. They are localized in the cortical and medulla, most often in the cortical. If such hemorrhages are located on the periphery of the cortical layer, then after removing the serous capsule from the kidneys, they appear on the surface in the form of dark red dots and small spots.

Preparation: Bleeding into skeletal muscle in Zenker's necrosis

With a slight magnification of the microscope, against the background of accumulation of blood, homogeneous pink or pink-purple clumps of disintegrated muscle fibers are found randomly scattered and far from each other. Large accumulations of blood are also noted in the intermuscular connective tissue or fatty tissue that separates the muscle bundles. In some muscular connective tissue layers (free of blood), cellular infiltrates are visible in the form of an accumulation of nuclei, painted in blue.

Fig.90. Bleeding into the muscle:
1. Accumulation of blood between clumps of muscle fibers;
2. Homogeneous lumps of disintegrated muscle fibers

Turning to the examination of the parts of the preparation that are free from blood, it is noted that, according to the nature of the changes in the striated muscles, namely, the uneven thickening of the muscle fibers, the loss of transverse striation, the breakdown of the contractile substance into large clumps, sometimes even with a rupture of the sarcolemma and the absence of a large number muscle nuclei, we have a waxy or Zenker necrosis.

Studying under high magnification the area with hemorrhage, it is established that along with a large accumulation of erythrocytes there are leukocytes, lymphocytes, as well as strands of precipitated fibrin. The presence in the area of ​​hemorrhage of all the components of the blood, as well as the rupture of muscle fibers into separate clumps and their separation by blood accumulations at a long distance from each other, confirms the fact of a hemorrhage that occurred due to rupture of the vessel. The rupture of muscle fibers into such homogeneous lumps indicates that the hemorrhage is secondary, and the waxy necrosis of the muscles is primary. When studying blood pools, attention is paid to the relatively pale color of erythrocytes and the absence of clear contours in most of them (hemolysis), as well as to the detection of hemosiderin pigment at the site of hemorrhage. The appearance of a cellular infiltrate in the intermuscular connective tissue layers bordering the hemorrhage zone should be considered as the formation of a reactive zone (accumulation of lymphoid and epithelioid cells, histiocytes, and other forms), due to which the resorption and organization of the dead area subsequently occurs, and then the formation of a scar connective fabrics.

Macro picture: the muscles are somewhat swollen, flabby in texture, their pattern is smoothed, pale pinkish-gray, yellowish-gray or clayey in color. Hemorrhages against this background appear in the form of narrow or wide stripes or dark or brownish-red spots of various sizes.

3. THROMBOSIS AND EMBOLISM

Thrombosis is the process of intravital blood coagulation in the cavities of the heart and blood vessels and their attachment to the wall. The resulting bundle is called a thrombus. In relation to the lumen of the blood vessel, thrombi are divided into parietal, extended and clogging, according to their structure and composition - into hyaline, white, red and mixed, the latter also include layered ones.

Thrombosis conditions:

1. Damage to the vascular wall.
2. Slow down blood flow.
3. Changes in the physico-chemical composition of the blood (violation of its coagulation system).

White blood clots are formed with a fairly fast blood flow in large arterial vessels and, as a rule, parietal. Red with slow blood flow in the veins and, as a rule, clog. Embolism - mechanical blockage of blood vessels by any particles carried by the blood stream. The particle that causes the blockage is called an embolus. Emboli can be tumor cells, detached blood clots, fatty particles, etc.

In appearance, blood clots can be red (their main component consists of erythrocytes), white (consists of platelets, clotted fibrin and leukocytes). These thrombi in their pure form are almost rare. Often you have to deal with mixed blood clots. The head of this thrombus is usually attached to the vascular wall and has a layered structure. Alternation of red and white areas is noted, blood clots are dryish, brittle. Often can serve as a source for embolism. Unlike them, post-mortem thrombi are moist-shiny red or lemon-yellow, elastic, easily removed from the cavity in which it lies and repeats its shape.

Fig.91. Thrombosis of blood vessels in the horse's liver.

Fig.92. White blood clot in a large vessel of the lungs of a horse

thrombosis outcome:

1. Embolism followed by infarction.
2. Organization of a thrombus (germination from the side of the muscular wall of the vessel of connective tissue into a thrombus).
3. Obliteration (infection of the lumen of the vessel).

Target setting

Etiopathogenesis of thrombosis and embolism. Morphological characteristics of thrombosis and embolism. Outcomes. Significance for the body.

The main focus is on:

1. Definition of the concept of thrombosis and embolism.
2. Causes and factors contributing to the formation of blood clots and emboli.
3. Classification of thrombi in relation to the vascular wall. Morphological characteristics (micro - and macro picture).
4. Classification of blood clots according to structure and composition. Morphological characteristics (micro - and macro picture).
5. Distinguishing features of a post-mortem convolution from an intravital thrombus.
6. Types of embolisms.
7. Outcomes of thrombosis and embolism.

1. Mutual information about thrombosis and embolism. Clarification and clarification of unclear aspects of the processes under study.
2. The study of museum preparations in order to familiarize with macroscopic changes in thrombosis and embolism by describing macroscopic changes, and then micropreparations by examining micropreparations under a microscope.

List of museum preparations:

Parietal thrombus in aortic arteriosclerosis.

A post-mortem blood clot in the heart of a cadaver of a chicken or calf.

Thromboembolism in the human lung.

Then proceed to the study of micropreparations.

List of micropreparations

Thrombosis of the pulmonary artery (red thrombus).

Mixed thrombus.

Thrombus organization.

Preparation: Mixed thrombus

Red and white blood clots in their pure form are practically relatively rare. More often you have to deal with mixed blood clots, which are very similar in structure to red ones, especially in areas rich in red blood cells. A distinctive feature of a mixed thrombus is that it contains many leukocytes. Leukocytes, like erythrocytes, are unevenly distributed in a thrombus. Most of the leukocytes are found on the periphery of the thrombus, closer to the wall of the blood vessel; in the center of the thrombus, where there are clusters of erythrocytes, they are found in fewer numbers. Leukocytes, like erythrocytes, lie between the fibers of coagulated fibrin singly or in groups.

Fig.93. Mixed thrombus:
1. Layered-mixed thrombus

Some features have stratified-mixed thrombi. Such thrombi can be of two kinds. The first of them on the cross section have the form of alternating concentrically arranged layers, of which some consist of thick or thin layers of tightly coagulated fibrin, and others of randomly scattered needle-shaped hemosiderin crystals. Among the crystals in some places there are blue lumps of wrinkled or decayed (rexis) nuclei of leukocytes. Erythrocytes in such thrombi look like shadows or are not detected at all.

The second ones (the tail part of an extended thrombus is taken for study) consist of separate compact, alternating layers, differing from each other only in color intensity. Some of them are stained with hematoxylin-eosin in bluish-gray, others in pinkish-gray, and others in blue and even dark blue (deposition of lime salts). All layers consist of a lumpy-granular mass.

Drug: Organization of a blood clot

The organization of a thrombus is called the replacement of its connective tissue. The starting material for the growth and formation of granulation tissue are the connective tissue cells of a thrombosed vessel. The most successful is the organization of a clogging thrombus.

At the beginning of the process, with a low magnification of the microscope, an increased reproduction of the endothelium is detected, which is introduced into the already somewhat loosened thrombus mass in separate wedges in places more diffusely. At this time, the individual membranes of the vascular wall are still clearly visible.

At high magnification, it can be seen that the cells of the proliferating endothelium are of various shapes. Most often they are elongated and look like young fibroblasts, but rounded and oval shapes are also found. In the future, simultaneously with the organization of thrombotic masses, the entire intima is infiltrated by lymphoid and epithelioid cells, as a result of which its boundaries are smoothed out. Further, the reproduction of connective tissue cells is also enhanced in the muscular membrane of the vessel wall. Its individual muscle fibers move away from each other, and between them accumulate more and more epithelioid and lymphoid cells. Muscle fibers gradually atrophy, and the boundaries of the muscular membrane disappear. By this time, the thrombotic masses have resolved, and the entire lumen of the blood vessel is filled with young connective tissue, which then turns into mature connective tissue. At the end of the process, scar connective tissue remains in place of the blood vessel. There is a complete obliteration of the blood vessel.

Fig.94. Thrombus organization:
1. Enhanced reproduction of the endothelium;
2. Young fibroblasts

The organization of a parietal thrombus proceeds with the same regularity, but on a limited scale and in a limited area. Endothelial cells and cells originating from the intima also grow into the thrombus, but the muscular membrane is little affected in this process. After the complete organization of the thrombus, scar connective tissue remains in this area, which forms thickenings of various sizes on the inner membrane of the blood vessel.

4. HEART HEART

A heart attack is the intravital necrosis of an organ or tissue site as a result of a rapid blockage or spasm of the artery that feeds this area. Its causes are: thrombosis, embolism, vasospasm and congestive hyperemia. Heart attacks are more common in those organs whose arteries have weak anastomoses or have lost elasticity (arteriosclerosis, plasmorrhagia, etc.).

According to the macroscopic appearance, heart attacks are divided into: anemic, hemorrhagic and mixed. On the cut, they have a characteristic wedge-shaped or triangular shape with the base facing the surface, and the apex - deep into the organ. (Repeats the structure of a branched arterial vessel). The color of dead tissue will be different. An anemic infarction occurs when the inflow of arterial blood is completely stopped and squeezed out as a result of reflex vasospasm. Congestive heart attacks are only hemorrhagic. Hemorrhagic on the background of congestive hyperemia. In the intestine, brain, heart, infarctions on the cut do not have a triangular shape (since the structure of the vessels is different than in the spleen and kidneys).

The outcome of a heart attack: if the death of the body does not occur in the infarct zone, reactive inflammation develops and connective tissue grows, with superficial heart attacks, the capsule sinks during organization, and the organ takes on a bumpy appearance. If the heart attack has developed in the depth of the organ, then macroscopically, a gray-white or yellowish-white connective tissue scar is visible at the end of the process.

Fig.95. Hemorrhagic infarcts of the spleen in swine fever.

Fig.96. Anemic white infarct in horse spleen

Fig.97. Anemic white infarction in horse kidney

Fig.98. White heart attack with a red rim in the kidney with swine fever

Fig.99. Kidney infarctions in swine fever

The outcome of myocardial infarction has a peculiar character. The infarcted area softens, and if the area penetrates a significant thickness of the heart wall, an aneurysm of the heart wall may develop in these places.

Theme target setting:

Etiopathogenesis. Morphological characteristics (micro - and macro picture). Outcomes. Significance for the body of a heart attack.

The focus is on the following issues:

1. Definition of a heart attack.
2. Factors and conditions contributing to the occurrence of a heart attack.
3. Classification and morphological characteristics of heart attacks.
4. Outcomes of heart attacks. Significance for the body.

1. Mutual information on the pathological process "Infarcts".
2. The study of museum preparations in order to familiarize with the macroscopic manifestations of heart attacks. Students describe in writing the macropicture of various infarctions, and then the micropicture of the processes and sketch them.

List of museum preparations

Hemorrhagic infarction in the lung.

Anemic infarction of the spleen.

Displaced infarction in the spleen in swine fever.

List of micropreparations

Anemic renal infarction.

Hemorrhagic infarction of the kidney.

Drug: Anemic (embolic) kidney infarction

Examining the histological preparation with the naked eye, it is noted that the anemic infarction of the kidney, if it fits in the cut, has a wedge-shaped or triangular shape, with the apex facing the medulla. With hematoxylin-eosin, this triangle is stained pink, and the border areas are pink-blue or blue-violet.

Fig.100. Anemic (embolic) renal infarction:
1. Structureless pale colored convoluted tubules with lysed
nuclei of epithelial cells. The boundaries between cells are erased;
2. Hyperemia (acute) of vessels.

With a low magnification of the microscope, the necrotic area is first examined, and then the living tissue and, especially, its border with the infarction part. The blood vessels in the dead area are empty and only sometimes at the border with living tissue can they be filled with red blood cells (especially the vessels of the glomeruli). The outlines of the tubules and glomeruli are preserved (if the infarction is of recent origin), but the boundaries of the cells in many tubules are invisible, in others they are swollen, pale colored and structureless, and appear as tiny blue dots between the tubules and in the glomeruli. The lumens of some tubules are revealed from swelling of the cells, and in some of them a granular substance is formed. On the border with a heart attack - in the living part, the blood vessels are dilated and filled with red blood cells. Sometimes there are diapedetic hemorrhages. If some time has passed since the onset of a heart attack, an accumulation of cells is noticeable between the tubules and in the lumen of some tubules. Somewhat retreating, mainly in the tubules of the medulla, deposits of calcium salts can be observed, which is established by diffuse or spotty staining of the tubules in blue.

At high magnification in the infarction zone, all tissues are in a state of coagulation necrosis and decay. The nuclei of the epithelium of the tubules are completely or partially lysed, and the nuclei in the glomeruli and between the tubules are in a state of pycnosis and rexis. In the borderline, with a heart attack, living tissue in most cells, the structure is preserved and only in some tubules of the nucleus, swollen and pale colored (a state of lysis). Examining the blood vessels, it is confirmed that some of the erythrocytes are outside the vessels. In the lumens of some tubules and between them, an accumulation of polymorphonuclear leukocytes is found, and epithelioid, lymphoid cells and histiocytes are found between the tubules. Infiltration with leukocytes and histiocytic cells indicates the beginning of the organization of an anemic infarction. At a later stage, fibrous connective tissue develops in the border zone and grows into the dead tissue. In the future, the processes of disintegration and resorption of necrotic tissues intensify, tissue cells gradually fill the entire area of ​​the infarction, at the end of the process, a mature connective tissue is formed here, which fuses with the capsule of the area and draws it deep into the organ.

Macropicture: from the outer surface of the kidneys, anemic infarcts look like gray-white spots of different sizes and shapes.

In pale color, they differ sharply from the surrounding tissue, especially when the heart attacks are bordered by a dark red rim (border zone of hyperemia). Their cut surface is cloudy, dryish, the pattern of the renal tissue is smoothed, and the wedge-shaped shape is distinct. After the organization of a heart attack, a depression or depression is noticeable on the surface of the kidney. The capsule in this area is not removed, and a gray-brown scarred connective tissue, sometimes wedge-shaped, is visible on the cut. With multiple infarctions, the organization leads to the fact that the kidney takes on a bumpy, unevenly pitted appearance and becomes very dense in consistency.

Drug: Hemorrhagic infarction of the kidney

In the kidneys, hemorrhagic infarction, as well as anemic infarction, is usually of thrombo-embolic origin, therefore it has a wedge-shaped shape, but unlike anemic it is colored dark red.

At a low magnification, attention is fixed, first of all, on the border zone with a heart attack. Her blood vessels are dilated and filled with blood. The dead area itself looks like a massive hemorrhage. The bulk of the blood is located between the tubules and, to a lesser extent, in the lumen of the tubules and glomerular capsules. As a result, the intertubular layers are greatly expanded. The tubules have lost their shape and structure, are squeezed and devoid of lumen, the epithelial lining is absent, in general they have the appearance of a different outline of the fields, painted in pink-gray or pinkish-violet tones. In some tubules, preserved nuclei are still visible in some places, but they are absent in most tubules (lysis). For a more detailed study, set a large increase. Even a cursory examination of the infarction confirms that necrosis has occurred here. If the glomeruli are clearly visible, then only traces remain of the tubules. The glomeruli located in the infarction zone are somewhat enlarged, most of them closely adjoin the capsules, and their vessels are very filled with blood. Between individual glomerular capsules and glomeruli there are narrow gaps filled with erythrocytes or a homogeneous pinkish substance.

Most of the nuclei of the endo - and perithelium of the glomeruli are in a state of pycnosis, and the nucleus of the cells lining the capsule is in a state of lysis. In place of the lining epithelium of the tubules, a homogeneous or granular border is visible. The epithelial nuclei are either absent (lysis) or have the appearance of shadows, and only single nuclei are found wrinkled (pycnosis). The nuclei preserved in separate tubules are located incorrectly. The epithelium of those tubules, the lumens of which contain erythrocytes, has turned into a homogeneous non-nuclear narrow border. Erythrocytes in such tubules most often do not have boundaries between themselves, stick together with each other and form a homogeneous mass. The intertubular connective tissue is very wide, pushes the tubules far from each other, compresses them.

Fig.101. Hemorrhagic infarction of the kidney:
1. Hemorrhages in the intertubular zone;
2. Necrosis of the convoluted tubules

In these layers there are a lot of red blood cells located in the lumen of the vessels and outside them. The latter lie rather closely to each other, but still retain their outlines (if the heart attack is of recent origin).

Among the erythrocytes, dark blue pyknotic nuclei of cells of the connective tissue, vascular endothelium and lymphocytic leukocytes are sometimes found here. The connective tissue scar, which is a consequence of the organization of hemorrhagic infarction of the kidneys, is usually painted in a rusty-brown color, due to the presence of hemosiderin pigment in it. The kidney capsule above this scar is pulled deep into the cortical layer. Hemorrhagic infarcts in the kidneys are often multiple, formed in animals with certain diseases in the last days of life, which is why they are usually found in the initial stages of the process.

Drug: Anemic infarction of the spleen

With a slight increase, a pale pink area is found, against the background of which blue dots stand out separately or in groups.

This area is surrounded by a wide, sometimes narrow stripe, reddish or orange. Outside of the strip is the tissue of the spleen with a pattern specific to it. Next, they proceed to the study of all three zones at high magnification of the microscope. The first - the central - or oxyphilic zone consists of a structureless and lumpy-granular mass containing a small amount of dark blue clumps of nuclear chromatin (karyopyknosis, karyorrhexis). A heap-like accumulation of pycnotic nuclei, as shown by a large increase, is observed at the site of dead lymph follicles. In general, the appearance of this zone corresponds to that of coagulation necrosis. The second - a reddish or orange zone is represented by accumulations of red blood cells (hemorrhagic belt).

The latter are located partly in dead, partly in living tissue. When studying the third zone, it can be established that the tissue in it is alive, retaining a specific structure. Changes in trabeculae are very demonstrative. For study, you can take one trabecula, part of which is immersed in the infarct zone, and part is in living tissue. The area of ​​the trabecula, located in the dead tissue, has a uniform homogeneous appearance, is painted in pink (eosin) color and does not contain nuclei (lysis). The site located in living tissue has a structure common to trabeculae. When erythrocytes stuff not only the border zone, but the entire dead area, they speak of a hemorrhagic infarction of the spleen. Later, at the site of the infarction, due to organization, a wedge-shaped scar is formed, which, growing together with the capsule of the spleen, draws it deep into the organ.

When organizing a hemorrhagic infarction, the connective tissue, due to the presence of hemosiderin in it, turns brownish-rusty.

Fig.102. Anemic infarction of the spleen:
1. Necrosis of the red pulp of the spleen;
2. Necrosis of the follicle of the spleen.

Fig.103. Anemic infarction of the spleen:
1. Organization of anemic infarction
(growth of fibroblastic elements in the area of ​​necrosis).

Macroscopically anemic infarcts of the spleen are dense in consistency and appear through the capsule in the form of gray-white irregularly shaped spots. Their cut surface is also white-gray in color, has a wedge-shaped shape with the apex facing deep into the organ.

The drawing of the spleen in the infarction area is completely (smoothed) along the periphery, the area is surrounded by a dark red rim - a zone of hyperemia.

"Amyloidosis of the spleen"(sago spleen). The spleen is enlarged, dense to the touch, its surface is smooth, the capsule is tense. On the section, the surface is changed - against the background of a dark cherry pulp, enlarged follicles are determined, having the appearance of translucent red grains resembling sago grains.

"Arteriolosclerotic nephrosclerosis"(primary wrinkled kidney). The kidneys are significantly reduced in size, their surface is evenly granular: the sunken areas correspond to the foci of replacement scarring at the site of the dead glomeruli, which act as grains - to hypertrophied glomeruli. On the section, there is a sharp thinning of the cortical and medulla layers and the growth of fatty tissue around the pelvis. Primary wrinkled kidneys are the main manifestation of the renal form of hypertension.

"Atherosclerosis of the aorta". The intima of the aorta is variegated. Areas of yellow and gray-yellow color (fat spots) are visible, which merge in some places (fat strips), but do not rise above the surface of the intima. Large areas are occupied by rounded white or white-yellow formations that rise above the surface (fibrous plaques). In some places they merge with each other, giving the intima a bumpy appearance, in some places they ulcerate. In places of manifestations, grayish-red thrombotic overlays are visible, sometimes with the formation of microaneurysms.

"Biliary cirrhosis of the liver". The liver is reduced in size, greenish-brown in color, has a fine-grained surface. The fixing fluid is colored brownish-green.

"Saucer-shaped stomach cancer". In the preparation from the mucosal side, a rounded tumor-like formation, 4-5 cm in diameter, with raised whitish edges in a roller-like manner, is determined. Ulceration is defined in the center. Education without clear boundaries.

"Bronchiectasis on the background of chronic pneumonia". Many bronchi with sharply dilated lumens look like saccular and cylindrical cavities filled with pus. The walls of the bronchi are sharply thickened, dense, whitish, protrude above the surface of the lung. The lung tissue around bronchiectasis is compacted, low-air, whitish-gray.

"Brown lung induration"(hemosiderosis of the lungs). The lungs are enlarged in size, of a dense consistency, red-brown in color, on the cut with many brownish inclusions and whitish layers.

"Recurrent warty endocarditis". The heart is enlarged in size and mass. The leaflets of the mitral valve are thickened, sclerosed, represented by dense opaque hyalinized tissue, fused together. The chords are shortened and thickened. The left atrioventricular orifice is narrowed, stenosis predominates. Along the edge of the sclerosed valve, on the surface facing the atrium, small fresh thrombotic overlays - warts are visible.

"Secondary-shrunken kidney"(chronic glomerulonephritis with an outcome in wrinkling). The kidney is reduced in size, dense consistency, the surface is finely bumpy (alternating areas of atrophy and sclerosis with areas of hypertrophied nephrons). On the section, the layer of renal tissue is thin, the cortical substance is especially thinned. The tissue of the kidney is grayish. The cut surface is granular, the layers are not differentiated from each other.

"Gangrene of the gut". The preparation shows that the intestinal loops are edematous, thickened, flabby, black-red in color. The serous membrane is dull, covered with fibrin. This is wet gangrene, which develops with the participation of putrefactive microorganisms.

"Gangrene of the foot". In the preparation, foot tissues are visible, reduced in volume, dry, black. This is dry gangrene. The black color of necrotic tissues is due to iron sulfide formed from blood pigments under the action of air. Areas of dry gangrene may be sloughed off (mutilation).

"Hemangioma of the liver". In the liver tissue, a blue-purple nodule is determined, on a section of a spongy structure with a finely tuberous surface.

"Hepatocellular cancer". In the liver tissue, a round-shaped tumor-like formation is determined, growing into the liver tissue, on a brownish-gray incision with areas of necrosis and hemorrhage.

"Hyalinosis of the capsule of the spleen". The spleen is enlarged, its capsule is thickened, whitish, translucent.

"Hydronephrosis". The kidney is sharply enlarged in size, its cortical and medulla layers are thinned; poorly distinguishable pelvis and calyx stretched. Stones are visible in the cavity of the pelvis.

"Hypernephroid Cancer of the Kidney". In the kidney, a tumor node is determined, on a cut that has a motley appearance against a bright yellow background, areas of hemorrhage and foci of tissue destruction are determined.

"Myocardial hypertrophy". The mass and size of the heart are increased. Significantly thickened wall of the left ventricle, increased volume of trabecular and papillary muscles of the left ventricle. The cavities of the heart are narrowed (concentric hypertrophy).

"Purulent leptomeningitis". The pia maters are thickened, dull, saturated with greenish-yellow purulent exudate. These changes are especially pronounced on the basal surface of the brain and the outer surface of the anterior parts of the hemispheres in the form of a "bonnet" or "cap".

"Purulent embolic nephritis". The kidney is slightly enlarged. From the surface and on the cut in the cortex and medulla, multiple gray-yellow foci (0.1-0.3 cm) containing pus are visible.

"Gummas in the liver." A section of the liver tissue is visible in the macropreparation. On the incision, grayish foci are determined, represented by foci of necrosis. Along the periphery of the foci, there is an overgrowth of coarse fibrous connective tissue.

"Caseous pneumonia". The entire upper lobe of the lung is dense to the touch, on the pleura - massive fibrinous overlays; on the section, the lung tissue is represented by yellowish-gray dryish masses of a cheesy appearance.

"Stones in the kidneys". In the renal pelvis, gray calculi with uneven edges are visible. The cavities of the pelvis, calyces are sharply expanded, the kidney tissue is thinned, atrophic (hydronephrosis).

"Gall Bladder Stones". The cavity of the gallbladder is filled with many yellow-brown stones of medium size. The wall of the bladder is thickened whitish in color: soldered to the lower surface of the liver due to inflammatory changes (concomitant cholecystitis).

"Hemorrhage in the brain." In the brain tissue, accumulations of coagulated blood of a brownish-red color are visible; in the area of ​​hemorrhage, the substance of the brain is destroyed (hematoma).

"Croupous pneumonia (stage of red hepatization)". The whole lobe of the lung is affected, which is enlarged, loose, airless tissue, on the cut with a smeared pattern, red-purple. Pleura with yellowish-gray overlays of fibrin, with hemorrhages.

"Croupous pneumonia (stage of gray hepatization)". The lobe of the lung is affected, which is enlarged, dense, airless tissue, fine-grained (fibrin plugs), gray in the cut. The pleura in the area of ​​the affected lobe is dull, covered with a gray-yellow fibrinous coating.

"Large-focal post-infarction cardiosclerosis". An extensive whitish scar (the site of a former infarction) is visible in the posterior wall of the left ventricle of the heart. In the myocardium there are small whitish layers.

"Small nodular cirrhosis of the liver". The liver is reduced in size, dense, uneven nodes are visible from the surface and in the section, more than 1 cm in diameter, separated by wide fields of connective tissue.

"Lung with flu." The mucous membrane of the trachea and main bronchi is plethoric, there are hemorrhages; it is dull, covered with a gray-yellow film, with areas of necrosis. The lungs are enlarged in size, on the cut they have a variegated appearance - "a large variegated influenzal lung": red foci (hemorrhages) are combined with foci of blue (atelectasis), grayish-yellow (fibrinous-purulent pneumonia) and pinkish (emphysema areas) colors.

"Lipoma". The drug is represented by a tumor-like formation, densely elastic consistency, having clear boundaries and surrounded by a capsule. On section, the tissue of the tumor is yellowish in color.

"Lipofuscinosis of the heart"(brown myocardial atrophy). The heart is reduced in size. There is no fatty tissue under the epicardium, the course of the vessels is tortuous. The heart muscle is brown.

"Metastasis of squamous cell carcinoma in the heart". In the myocardial tissue, a grayish formation is determined, which does not have clear boundaries.

"Melanoma metastases in the liver". In the liver tissue, multiple formations of a rounded shape of dark brown and black color with clear contours are visible.

"Micronodular cirrhosis of the liver". The liver is reduced in size, dense consistency, with a uniform fine-grained surface, the nodes are less than 1 cm in diameter, separated by layers of connective tissue.

"Miliary tuberculosis of the lung". Light swollen, increased airiness. Numerous small (about 0.1-0.2 cm in diameter) millet-like tubercles of yellowish-gray color, dense to the touch, are visible from the surface (on the pleura) and on the cut.

"Mitral stenosis". The heart is enlarged in volume and mass. The wall of the left ventricle is thickened up to 2 cm. The leaflets of the mitral valve are sharply thickened, deformed, represented by a dense opaque tissue; the chords are considerably shortened and thickened. In places, calcification is noted in the valves, the valves are fused, which significantly narrows the lumen of the left atrioventricular opening, it becomes slit-like. Significantly expanded cavity of the left atrium.

"Muscovy Liver". The organ is enlarged in size, of a dense consistency, the surface is smooth, with sharp edges. On the section - a variegated appearance: reddish-brown areas alternate with yellow, which resembles nutmeg. Changes in the color of the liver are due to venous congestion and the peculiarities of its angioarchitectonics.

"Impaired tubal pregnancy". The fallopian tube is sharply enlarged, edematous, there are focal hemorrhages. In the central part, a perforated hole of irregular shape, with uneven edges, is determined. Red-brown masses are determined in the cavity of the pipe.

"Necrotic nephrosis". The kidney is enlarged, swollen, edematous fibrous capsule is tense, easily removed. The broad, pale gray cortical layer is sharply demarcated from the dark red pyramids. Hemorrhages are seen in the intermediary zone of the kidney and pelvis.

"Obturating aortic thrombus". In the area of ​​bifurcation of the abdominal aorta, grayish-red masses are determined, completely filling the lumen of the vessel (obturating thrombus).

"Acute verrucous endocarditis". Normal sized heart. The leaflets of the mitral valve are dull, the chords are thin. On the free edge of the valves on the surface facing the atrium, small, gray-pink loose overlays - warts are visible.

"Acute myocardial infarction". In the posterior wall of the left ventricle, a yellow-white irregularly shaped necrosis focus with a hemorrhagic corolla is visible.

"Acute endometritis with thrombophlebitis of the pelvic veins". The uterus is enlarged, flabby in consistency, the mucous membrane is necrotic, riddled with pus, brownish-black. Myometrial veins gape, their lumens are obturated with thrombotic masses.

"Local pneumonia". On the section, the lung is of a mottled appearance with yellow-gray foci of dense consistency, protruding above the cut surface. The walls of the bronchi are thickened, in the lumen - mucopurulent contents.

"Liver with obstructive jaundice". The liver is enlarged in size, its surface is small-hilly. On section, the liver tissue is greenish in color. Sharply dilated bile ducts filled with dark green bile are visible. The fixing fluid is colored brown.

"Squamous cell carcinoma of the epiglottis". In the area of ​​the epiglottis, a formation up to 2 cm with fuzzy contours is determined. On section, the tumor tissue is grayish in color, enlarged.

"Polycystic Liver". The liver is enlarged in size; on the incision in the liver tissue, multiple thin-walled cysts of various sizes are determined, filled with yellowish transparent contents.

"Polyposis of the stomach". On the mucous membrane of the pyloric part of the stomach, multiple formations on legs are visible, rising above the surface and occupying the entire surface. The folds of the gastric mucosa are rough and deformed.

"Kidney in multiple myeloma". The kidney is reduced in size, the surface is bumpy, in the section, the tissue of the kidney with multiple foci of brownish color, the layers are thinned, poorly differentiated from each other.

"Bubble drift". The tumor consists of many vesicles of various sizes (from millet grain to cherry in size) containing a colorless transparent liquid.

"Rhabdomyosarcoma of the hip". The drug is represented by a section of the femur with surrounding tissues, in which a grayish tumor tissue is determined (reminiscent of "fish meat"), which does not have clear boundaries. Grayish-yellow areas of necrosis and hemorrhage are visible in the tumor tissue. The tumor grows into the muscles, subcutaneous fat and skin, where the site of ulceration is determined.

"Cancer of the body of the uterus". The uterus is enlarged in size, the incision reveals a tumor-like formation growing from the mucous membrane of the papillary type, without clear boundaries, brownish in color, with ulcerations and hemorrhages, growing into the cervical canal.

"Spleen in leukemia". The spleen is sharply enlarged in size, the capsule is tense, dark red with a brownish tint on the cut.

"Septic endometritis". The uterus is enlarged, flabby in consistency, the mucous membrane is necrotic, riddled with pus, black. Myometrial veins gape, their lumens are obturated with thrombotic masses.

"Serous ovarian cystadenoma". The drug is represented by a single-chamber cystic formation of a rounded shape, with thin walls and transparent yellowish contents. The inner surface of the cyst is smooth.

"Staphylococcal pneumonia with abscess formation". The lungs are enlarged in size, dense consistency. On the section, there are yellow-purple areas of different sizes, in some places there are whitish foci of a stranded appearance. In the lower sections there are cavities, covered from the inside with purulent gray-whitish masses. The lung tissue is plethoric, areas of emphysematous expansions are visible along the anterior surface.

"Tuberculosis of the adrenal glands". The adrenal glands are enlarged. On the section, grayish foci are determined, filled with curdled masses, irregularly shaped, without clear boundaries.

"Tuberculosis of the kidney" The kidney is slightly enlarged. In the cortical substance, in the area of ​​the pyramids and in the area of ​​the pelvis, there are multiple foci of irregular shape, up to 2 cm in size, containing grayish cheesy necrotic masses.

"Tuberculosis meningitis". The pia mater in the region of the base of the brain, swollen, dull, with many loose adhesions, is saturated with a gelatinous type of exudate containing fibrin and necrotic masses.

Troubleaking endocarditis. The heart is enlarged. Its cameras are stretched. The wall of the left ventricle is thickened. The valve leaflets are thickened, sclerosed, hyalinized, fused together and sharply deformed. Ulcerations are visible along their outer edge. On the surface of the valves there are massive thrombotic deposits in the form of polyps, which easily crumble.

"Nodular colloid goiter". The enlarged size of the gland is visible, its consistency is dense, the surface is knotty. In the section, the nodes are represented by cells of different sizes, filled with brown-yellow colloidal content.

"Fibroxanthoma of the heart". In the region of the left ventricle, a tumor-like formation is determined, having the form of a node up to 6 cm in diameter, of a soft consistency. On the section, the tumor has a mottled appearance with the presence of brown, gray areas, foci of hemorrhages and necrosis.

"Fibromyoma of the uterus". In the body of the uterus, multiple nodes of various sizes are determined. On the section, the nodes are whitish in color, dense in consistency, have a fibrous structure. The nodes have clear boundaries, surrounded by a capsule.

"Chronic aneurysm of the heart". The heart is enlarged. The wall of the left ventricle in the area of ​​the apex is thinned, whitish (represented by scar connective tissue) and swells. The myocardium around the bulge is hypertrophied. In the resulting aneurysm, grayish-red thrombotic masses are visible, which can be a source of thromboembolic complications.

"Chronic placental insufficiency". The placenta is reduced in size, there is a decrease in weight. On the maternal surface, brownish-red areas of hemorrhages and grayish-yellow areas of infarcts are determined. The placental lobes are flattened.

"Chronic gastric ulcer". On the lesser curvature, a deep defect in the wall of the stomach is visible, capturing the mucous and muscular membranes, oval-round in shape with very dense, callused, ridge-like raised edges. The edge facing the esophagus is undermined; the edge facing the pylorus is gently sloping and looks like a terrace formed by the mucous membrane, submucosa and muscular membrane of the stomach wall. The bottom of the ulcer is represented by a dense whitish tissue.

"Central lung cancer". In the region of the root of the lung, a tumor-like formation of a grayish color with areas of hemorrhage is determined, which does not have clear contours, a dense consistency, narrowing the lumen of the bronchi.

"Cysticercosis of the brain". The preparation shows a section of brain tissue. The section reveals numerous rounded cavities up to 0.5 cm in diameter, clearly demarcated from the surrounding brain tissue.

"Shock Kidney". The kidney is enlarged, swollen, edematous. The fibrous capsule is tense and can be easily removed. The broad, pale gray cortical layer is sharply demarcated from the dark red pyramids. In the intermedial zone of the kidney and the pelvis, hemorrhages are noted.

"Echinococcosis of the liver". The liver is enlarged. Echinococcus occupies almost the entire lobe of the liver and is represented by numerous cellular structures (multi-chamber echinococcal cavities), clearly delimited by a connective tissue capsule from the unchanged liver tissue.

Tablet number 1.

1. N/11 Caseous necrosis in the lung

1. The focus of necrosis is represented by a structureless mass, stained pink by eosinophils.

2. Around the focus area of ​​demarcation inflammation with the growth of SD.

3. Detritus (karyolysis), karyorrhexis, pycnosis are reliable morphological signs of necrosis.

4. Possible outcomes of caseous necrosis: scarring, encapsulation.

2. N/13 Lung infarction

1. The site of necrosis is saturated with blood (erythrocytes are hemolyated).

2. Around the necrosis of SDT with plethoric vessels.

3. In the zone of necrosis, the vessels are filled with blood clots.

4. In the zone of necrosis, foci of purulent fusion of necrotic tissue.

5. Morphogenesis of red lung infarction: occlusion, pulmonary embolism (mixed type of blood supply).

3. O/121 Pulmonary edema

1. In the lumen of the alveoli, eosinophilic contents, desquamated cells of the alveolar epithelium.

2. Plethora of capillaries of interalveolar septa, arteries and veins.

3. Fluid in the lumen of the alveoli - transudate.

4. Types of pulmonary edema according to the mechanism of development: cardiac, allergic, toxic.

5. Macroscopic view of the lungs with edema: - enlarged, heavy, dough-like consistency, a large amount of foamy liquid (with air) flows from the cut surface.

6. Complications of pulmonary edema: hypostatic pneumonia. Death.

4. O/7 Nutmeg liver

1. Hemorrhages in the center of the lobules.

2. Necrosis of hepatocytes in the center of the lobules.

3. On the periphery of the lobules, the structure of the hepatic beams is preserved.

4. Hepatocytes in a state of fatty degeneration.

5. Sinusoids on the periphery of the lobules are empty.

6. The mechanism of uneven blood filling of the liver: The distribution of venous blood from the central part is hindered by higher pressure in the hepatic artery system at the periphery of the lobule. Chronic hypoxia leads to the proliferation of connective tissue along the sinusoids (capillaryization of the sinusoids), which is a reflection of the development of the capillary-parenchymal block. In the end, nutmeg fibrosis is formed, and then nutmeg (cardiac) small-nodular cirrhosis of the liver.

5. G/29 Hemosiderosis of the lung.

1. The interalveolar septa are dilated due to pronounced plethora of capillaries.

2. Plethora of veins.

3. In the lumen of the alveoli, erythrocytes, alveolar macrophages and cells loaded with brown pigment (siderophages).

4. Processes that form hemosiderosis of the lung: diapedesis of erythrocytes from hyperemic venous vessels, diffuse growth of connective tissue in the interalveolar septa around the bronchi and vessels, which gives the organs a brownish color and a dense texture - brown induration of the lungs.

5. Outcomes of hemosiderosis of the lung: brown induration of the lungs, pneumosclerosis.

6. O/19 Venous thrombosis.

1. Red blood clot in a vein, consisting of red blood cells

2. In one area, the vein wall is thinned, infiltrated with leukocytes, focal perivenular hemorrhage.

3. In the second vein "organizing thrombus":

A) a thrombus obturates the lumen of the vein

B) red thrombus

C) one part of the thrombus consists of erythrocytes with signs of agglutination

D) The other part of the thrombus consists of hemolyzed erythrocytes with an admixture of leukocytes and fibrin threads

E) part of the thrombotic masses is replaced by SDT, which grows along with the capillaries from the side of the intima; gaps lined with endotheliocytes or without it (sewerage) are visible.

E) Changes in the surrounding tissue that contribute to thrombosis: violation of the integrity of the vascular wall, slowing down and disruption of blood flow, infiltration by leukocytes.

7. O/49 - septic thromboembolism of the kidney

1. The focus of necrosis, close to the shape of a triangle (heart attack)

2. In the area of ​​the apex of the infarction, a vessel with a thromboembolism.

3. As part of a thromboembolus, fibrin, leukocytes and colonies of microbes are visible.

4. Microbial emboli in small vessels in the focus of infarction.

5. Around the infarction there is a wide zone of leukocyte infiltration and plethora of vessels of the medulla.

6. Main complications of microbial embolism: septic organ fusion.

8. O/5 Liver steatosis, stained with sudanIII

1. small and large drops of yellow fat in the cytoplasm of hepatocytes

2. Drops of fat are localized diffusely throughout the entire lobule of the liver.

3. Morphogenesis of fatty degeneration of the liver: small-drop (in the center of the lobules) or large-drop obesity (along the periphery).

4. Outcomes of liver steatosis: recovery or necrosis of obese hepatocytes.

9. O/3 Cholesterosis of the gallbladder

1. Folds of the mucous membrane of the gallbladder of different thickness and height, covered with prismatic epithelium.

2. In the apical parts of the stroma of the villi, there are accumulations of xanthoma cells.

3. The structure of xanthoma cells: cells contain cholesterol, "foamy", transparent, light when stained with hematoxylineosin.

4. Macroscopic view of the gallbladder mucosa in cholesterosis: due to the alternation of yellow stripes and small spots.

5. Cholesterosis of the gallbladder is most often combined with fatty degeneration of the liver.

10. O / 25 - hydropic dystrophy of the epithelium of the tubules of the kidney

1. The cytoplasm of the epithelium of the convoluted tubules, swollen with vacuoles of various sizes.

2. Balloon dystrophy of epitheliocytes with colliquacylon necrosis is visible in some tubules.

3. Nuclei of dystrophic nephrocytes are pale and pyknotic in dead epithelial cells.

4. Morphogenesis of hydropic dystrophy. Hydropic degeneration occurs either due to damage to the membrane-enzyme systems (in the kidneys), disruption of the Na-K pumps.

5. Develops with nephrotic syndrome.

11. O/57 - gouty tophus

1. Zones of necrosis of the periarticular tissue.

2. Amorphous masses of sodium urate.

3. Inflammatory infiltrate consisting of macrophages and giant multinucleated cells of foreign bodies.

4. Growth of connective tissue.

5. The development of gout is associated with a violation of the metabolism of nucleoproteins (excessive formation of uric acid).

12. G/143 Pigmentary cirrhosis of the liver with hemochromatosis

1. The liver is divided into lobules by wide layers of connective tissue

2. Accumulations of macrophages loaded with hemosiderin in the connective tissue.

3. Small grains of hemosiderin are visible in hepatocytes.

4. , 5 Pigmentary cirrhosis develops with primary hemochromatosis. Primary hemochromatosis due to a genetic defect associated with increased absorption of iron from food, its manifestations are pigmentary cirrhosis of the liver, diabetes mellitus, bronze coloration of the skin and cardiomegaly.

13. O/78 - skin neurofibroma

1. tumor nodule in the dermis

2. the border of the tumor with the dermis is clear, but without a capsule

3. the color of the tumor is bluish

4. the tumor consists of tightly lying fibers and spindle-shaped cells

5. the tumor grows, braiding the sebaceous and sweat glands

6. histogenetic