Pathological anatomy. Cheat sheet: briefly, the most important

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Pathological anatomy. Cheat sheet: briefly, the most important

Lecture notes, cheat sheets

Directory / Lecture notes, cheat sheets

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Table of contents

Introduction to Pathological Anatomy
Dystrophy
Parenchymal and proteinaceous dystrophies
Fatty degeneration
Stromal vascular dystrophy
Mixed dystrophies
Necrosis. apoptosis
Morphogenesis and classification of necrosis
Circulatory disorders
Hyperemia
Thrombosis
Embolism and infarction
Inflammation
Exudative inflammation
Purulent inflammation
Catarrhal, hemorrhagic, putrefactive, mixed and proliferative inflammations
Granulomatous inflammation
Macroscopic classification of foci of tuberculous inflammation; inflammation in syphilis
Immunopathology
Autoimmune diseases. Immunodeficiency syndromes
Regeneration
Types of regenerations. Wound healing
Processes of adjustment Q (adaptation) and compensation
Sclerosis. Kinds
Tumors
Types of tumors
Epithelial tumors
Diseases of the blood. anemia. Classification
Hemoblastosis. Thrombocytopathies
Endocarditis. Myocarditis. Heart disease, cardiosclerosis
Atherosclerosis
Hypertension, ischemic heart disease, cerebrovascular disease, vasculitis
Respiratory diseases
Lung cancer
Diseases of the stomach: gastritis, peptic ulcer
Stomach cancer
Enteritis. Enteropathy
Colitis
Diseases of the biliary system
Hepatitis
Glomerulopathies. Glomerulonephritis
Amyloidosis of the kidneys. Acute renal failure
Interstitial nephritis
Kidney stone disease, polycystic disease, nephrosclerosis, kidney tumors
Diseases of the genital organs and mammary gland
Pituitary and adrenal disorders
Thyroid disease
Diabetes
Diseases of the central nervous system
Classification of infectious diseases
Typhoid fever
Salmonellosis. Dysentery. Cholera
Plague
Anthrax, tuberculosis, sepsis, syphilis
Actinomycosis, candidiasis, aspergillosis
Malaria, amoebiasis

1. Introduction to pathological anatomy

Pathological anatomy studies the structural changes that occur in the patient's body. It is divided into theoretical and practical. Structure of pathological anatomy: general part, particular pathological anatomy and clinical morphology. The general part studies general pathological processes, the patterns of their occurrence in organs and tissues in various diseases.

Pathological processes include: necrosis, circulatory disorders, inflammation, compensatory inflammatory processes, tumors, dystrophies, cell pathology.

Private pathological anatomy studies the material substrate of the disease, i.e., is the subject of nosology.

Tasks of pathological anatomy:

1) study of the etiology of the disease (causes and conditions of the disease);

2) study of the pathogenesis of the disease (development mechanism);

3) the study of the morphology of the disease, i.e. structural changes in the body and tissues;

4) study of the morphogenesis of the disease, i.e. diagnostic structural changes;

5) study of the pathomorphosis of the disease;

6) study of complications of diseases;

7) study of disease outcomes;

8) study of thanatogenesis (mechanism of death);

9) assessment of the functioning and condition of damaged organs.

Tasks of practical pathological anatomy:

1) control of the correctness and timeliness of the clinical diagnosis (autopsy). The timeliness of the diagnosis means that the diagnosis should be made within 3 days, in case of a serious condition of the patient - in the first hours;

2) advanced training of the attending physician (the attending physician is always present at the autopsy). For each case of discrepancy in diagnosis, the clinic conducts a clinical and anatomical conference, where a specific analysis of the disease takes place;

3) direct participation in the formulation of an intravital clinical diagnosis (by biopsy and examination of the surgical material).

Methods for the study of pathological anatomy:

1) autopsy of the bodies of the dead;

2) biopsy (lifetime histological examination, carried out to diagnose and determine the prognosis of the disease).

The research material is called "biopsy". Depending on how it is obtained, biopsies are classified as closed and hidden.

The structure of the biopsy can be liquid, solid or soft. In terms of timing, a biopsy is divided into planned (result on the 6-7th day) and urgent (result within 20 minutes, i.e. at the time of surgery).

Research levels: organismal, organ, systemic, tissue, cellular, subjective and molecular.

2. Dystrophy

Dystrophy is a pathological process that is a consequence of a violation of metabolic processes, with damage to cell structures and the appearance of substances in the cells and tissues of the body that are not normally determined.

Dystrophies are classified:

1) by the scale of the prevalence of the process: local (localized) and general (generalized);

2) due to the occurrence: acquired and congenital. Congenital dystrophies have a genetic condition of the disease.

Hereditary dystrophies develop as a result of a violation of the metabolism of proteins, carbohydrates, fats, in this case, the genetic deficiency of one or another enzyme that is involved in the metabolism of proteins, fats or carbohydrates matters. Later in the tissues there is an accumulation of incompletely converted products of carbohydrate, protein, and fat metabolism. This process can develop in various tissues of the body, but the tissue of the central nervous system is necessarily damaged. Such diseases are called accumulation diseases.

Dystrophies are divided into:

1) according to the type of metabolism that was disturbed: protein, carbohydrate, fat, mineral, water, etc .;

2) according to the point of application (according to the localization of the process): cellular (parenchymal), non-cellular (mesenchymal), which develop in the connective tissue, as well as mixed (observed both in the parenchyma and in the connective tissue). There are four pathogenetic mechanisms.

1. Transformation is the ability of some substances to transform into others having a similar structure and composition. For example, carbohydrates have this ability, transforming into fats.

2. Infiltration is the ability of cells or tissues to fill with an excessive amount of various substances.

3. Decomposition - characterized by the disintegration of intracellular and interstitial structures. There is a breakdown of protein-lipid complexes that are part of the membranes of organelles.

4. Perverted synthesis - the formation of abnormal foreign substances in the cell, which are not formed during the normal functioning of the body. For example, in amyloid degeneration, cells synthesize an abnormal protein, from which amyloid is then formed.

Different types of dystrophies are characterized by their dysfunction of the tissue. With dystrophy, the disorder is twofold: quantitative, with a decrease in function, and qualitative, with a perversion of function, that is, features appear that are not characteristic of a normal cell. An example of such a perverse function is the appearance of protein in the urine in kidney diseases, when there are dystrophic changes in the kidney, or changes in liver tests that appear in liver diseases.

3. Parenchymal and proteinaceous dystrophies

Parenchymal dystrophies are divided into protein, fat and carbohydrate.

Protein dystrophy is a dystrophy in which protein metabolism is disturbed. The process of dystrophy develops inside the cell. Among the protein parenchymal dystrophies, granular, hyaline-drop, hydropic dystrophies are distinguished.

With granular dystrophy, during histological examination, protein grains can be seen in the cytoplasm of cells. Granular dystrophy affects parenchymal organs: kidneys, liver and heart. This dystrophy is called cloudy or dull swelling. This is related to macroscopic features. Organs with this dystrophy become slightly swollen, and the surface on the cut looks dull, cloudy, as if "scalded with boiling water."

Contributes to the development of granular dystrophy for several reasons, which can be divided into 2 groups: infections and intoxications. With this type of dystrophy, the epithelium of the convoluted tubules of the kidney is affected. In normal tubules of the kidneys, even gaps are observed, and with granular dystrophy, the apical cytoplasm is destroyed, and the lumen becomes star-shaped.

Renal granular dystrophy ends in two variants. A favorable outcome is possible when the cause is eliminated, the epithelium of the tubules in this case returns to normal. An unfavorable outcome occurs with continued exposure to a pathological factor - the process becomes irreversible, dystrophy is transformed into necrosis.

The liver with granular dystrophy is also slightly enlarged. When cut, the fabric acquires the color of clay. The histological sign of granular degeneration of the liver is the inconsistent presence of protein grains. It is necessary to pay attention to whether the beam structure is present or destroyed. With this dystrophy, proteins are divided into separately located groups or separately lying hepatocytes, which is called discomplexation of the hepatic beams.

Cardiac granular dystrophy: the heart is also slightly enlarged outwardly, the myocardium becomes flabby, on the cut it resembles boiled meat. Macroscopically, protein grains are not observed.

In histological examination, the criterion for this dystrophy is basophilia. Myocardial fibers differently perceive hematoxylin and eosin. Some areas of the fibers are intensely stained with hematoxylin in lilac, while others are intensely stained with eosin in blue.

Hyaline droplet degeneration develops in the kidneys (the epithelium of the convoluted tubules is affected). It occurs in such kidney diseases as chronic glomerulonephritis, chronic pyelonephritis, and in case of poisoning. Drops of a hyaline-like substance are formed in the cytoplasm of cells. Such dystrophy is characterized by a significant violation of renal filtration.

Hydropic dystrophy can occur in liver cells in viral hepatitis. At the same time, large light drops are formed in hepatocytes, often filling the cell.

4. Fatty degeneration

There are 2 types of fats. The amount of mobile (labile) fats changes throughout a person's life, they are localized in fat depots. Stable (immobile) fats are included in the composition of cell structures, membranes.

Fats perform a wide variety of functions: supporting, protective, etc.

Fat metabolism disorders are three pathologies:

1) proper fatty degeneration (cellular, parenchymal);

2) general obesity or obesity;

3) obesity of the interstitial substance of the walls of blood vessels (aorta and its branches).

Actually fatty degeneration underlies atherosclerosis. The causes of fatty degeneration can be divided into two main groups: infections and intoxications. Nowadays, the main type of chronic intoxication is alcohol intoxication. Often there may be drug intoxication, endocrine intoxication - developing in diabetes.

Fatty degeneration is observed in the same organs as protein - in the liver, kidneys and myocardium.

With fatty degeneration, the liver increases in size, it becomes dense, on the cut it is dull, bright yellow. This type of liver received the figurative name "goose liver".

Microscopic manifestations: fatty drops of small, medium and large sizes appear in the cytoplasm of hepatocytes. As a rule, they are located in the center of the hepatic lobule, but can occupy its entirety.

There is an increase in the heart, the muscle becomes flabby, dull, and if you carefully examine the endocardium, under the endocardium of the papillary muscles one can observe a transverse striation, which is called the "tiger heart".

Microscopic characteristics: fat is present in the cytoplasm of cardiomyocytes. The process has a mosaic character - the pathological lesion extends to cardiomyocytes located along small veins.

In the kidneys, fat is localized in the epithelium of the convoluted tubules. Such dystrophy occurs in chronic kidney diseases (nephritis, amyloidosis), in case of poisoning, general obesity.

Obesity disrupts the metabolism of neutral labile fats, which are formed in excess in fat depots; body weight increases significantly as a result of the accumulation of fat in the subcutaneous fatty tissue, in the omentum, mesentery, in the perirenal, retroperitoneal tissue, in the tissue covering the heart. With obesity, the heart becomes, as it were, clogged with a thick fat mass, and then fat penetrates into the thickness of the myocardium, which causes its fatty degeneration.

In the liver with obesity, fat can be formed inside the cells. The liver takes on the appearance of a "goose liver", as in dystrophy.

It is possible to differentiate the resulting fat in the liver cells using color staining: Nile blue has the ability to stain neutral fat red in obesity, and blue in advanced dystrophy.

5. Stromal vascular degeneration

Stromal-vascular dystrophy is a metabolic disorder in the connective tissue, mainly in its intercellular substance, the accumulation of metabolic products. Depending on the type of impaired metabolism, mesenchymal dystrophies are divided into protein (dysproteinoses), fatty (lipidoses) and carbohydrate. Among dysproteinoses, mucoid swelling, fibrinous swelling, hyalinosis and amyloidosis are distinguished. The first three are associated with a violation of the permeability of the vascular wall.

1. Mucoid swelling is a reversible process. There are superficial shallow changes in the structure of the connective tissue. Due to the action of a pathological factor, decomposition processes occur in the main substance, i.e., the bonds of proteins and aminoglycans break up. Factors that cause mucoid swelling include: hypoxia (hypertension, atherosclerosis), immune disorders (rheumatic disease, endocrine disorders, infectious diseases).

2. Fibrinoid swelling is a deep and irreversible disorganization of the connective tissue, which is based on the destruction of the basic substance of the tissue and fibers, accompanied by a sharp increase in vascular permeability and the formation of fibrinoid. May be due to mucosal swelling. The fibers are destroyed, the process is irreversible.

The outcome of fibrinoid swelling can be necrosis, hyalinosis, sclerosis. Around the zone of fibrinoid swelling, macrophages accumulate, under the influence of which the cells are destroyed and necrosis occurs. Macrophages are able to produce monokines, which promote the reproduction of fibroblasts. Thus, the area of necrosis is replaced by connective tissue - sclerosis occurs.

3. Hyaline degeneration (hyalinosis). This is the outcome of various processes: inflammation, sclerosis, fibrinoid swelling, necrosis, plasma impregnation. Distinguish between hyalinosis of vessels and connective tissue itself. Each can be widespread (systemic) and local.

With local hyalinosis, the outcome is scars, fibrous adhesions of serous cavities, vascular sclerosis, etc. The outcome is unfavorable in most cases, but resorption of hyaline masses is also possible.

4. Amyloidosis - a kind of protein degeneration, which is a complication of various diseases (infectious, inflammatory or tumor nature).

In this case, there is an acquired (secondary) amyloidosis. When amyloidosis results from an unknown etiology, it is primary amyloidosis. A microscopic sign of amyloidosis is the sebaceous sheen of the organ.

There are secondary, or acquired, forms and idiopathic (primary), hereditary (familial, senile, tumor-like). The secondary form is a complication of a wide variety of infections. The causes of primary amyloidosis are unknown.

6. Mixed dystrophies

Mixed dystrophies are spoken of in cases where the morphological manifestations of impaired metabolism accumulate both in the parenchyma and in the stroma, the wall of blood vessels and tissues. They occur when there is a violation of the metabolism of complex proteins - chromoproteins, nucleoproteins and lipoproteins, as well as minerals.

Violation of the exchange of chromoproteins (endogenous pigments). Endogenous pigments in the body perform a specific role:

1) hemoglobin carries out oxygen transfer - respiratory function;

2) melanin protects against UV rays;

3) bilirubin is involved in digestion;

4) lipofuscin provides the cell with energy in hypoxic conditions.

All pigments, depending on the source of formation, are divided into hemoglobinogenic, proteinogenic and lipidogenic. Hemoglobin pigments consist of ferritin, hemosiderin and bilirubin.

Hemosiderin is a pigment that is formed in a small amount under normal conditions during the natural aging of red blood cells and their decay.

There are general and local hemosiderosis. General hemosiderosis occurs with intravascular hemolysis of red blood cells. Causes - various infections (sepsis, malaria, etc.), intoxication (heavy metal salts, fluorine, arsenic) and blood diseases (anemia, leukemia, blood transfusion incompatible with the group or Rh factor). At the same time, the organs are enlarged in volume, compacted, brown or rusty in section.

Local hemosiderosis develops with the breakdown of red blood cells outside the vascular bed, i.e., in the foci of hemorrhages. The most important are 2 localizations of hemosiderosis - in the substance of the brain and lungs.

Hemosiderin appears in the focus of hemorrhage only at the end of the 2nd - beginning of the 3rd day. A hemorrhage in which it is not present is called fresh, and where it is present, it is called old. Hemosiderosis of the lungs or brown induration of the lungs, as hemosiderosis and sclerosis are combined in the lung.

Hematoidin is formed on the 10-12th day in very large and old foci of hemorrhage, which are accompanied by tissue destruction. It is always located in the center of the hearth. Morphological picture: crystals or rhomboid structures of yellow or pink color.

Bilirubin is contained in the form of indirect, i.e. associated with albumin, or unconjugated. Bilirubin is taken up by liver hepatocytes, where it is conjugated with glucuronic acid, and such direct bilirubin enters the intestine. A violation is said to occur with an increase in its amount in the blood serum, followed by staining of the skin and mucous membranes in yellow.

Hemomelanin, or malarial pigment, occurs only in malaria, as it is produced by malarial plasmodium. It is introduced into erythrocytes, and then captured by cells of the reticuloendothelial system.

Melanin is synthesized by melanocytes. Synthesis requires tyrosine and tyrosinase enzymes. Synthesis is regulated by the autonomic, endocrine systems and UV rays themselves.

7. Necrosis. apoptosis

Necrosis is a lifetime necrosis of cells and tissues of the body under the influence of various pathogenic factors. The basis of necrosis is apoptosis.

Apoptosis is the natural and programmed death of a cell as a whole or part of it. It occurs under physiological conditions - this is natural aging (death of erythrocytes, T- and B-lymphocytes), with physiological atrophies (atrophy of the thymus, gonads, skin).

Apoptosis can occur during pathological reactions (during the period of tumor regression), under the action of medicinal and pathogenic factors.

Apoptosis mechanism:

1) condensation of the nucleus;

2) condensation and compaction of internal organelles;

3) cell fragmentation with the formation of apoptotic bodies.

These are small organelles with eosinophilic cytoplasm with remnants of the nucleus. Then they are captured by phagocytes, macrophages, parenchyma and stroma cells. There is no inflammation.

The manifestation of necrosis depends on the strength and nature of the pathogenic factor, the state of the macroorganism itself.

External (macroscopic) signs of necrosis:

1) the tissue structure in the necrosis zone is broken, the tissue is structureless;

2) the consistency of fabrics can be dense when the fabric is dry; this occurs when the tissue is rich in proteins and contains little water and the activity of hydrolytic enzymes is negligible (in the myocardium, liver, spleen and kidneys); the necrosis zone can be soft when the tissue contains a large amount of moisture, there is little protein, hydrolytic enzymes are active (brain, intestines); dry necrosis can turn into wet when infection occurs;

3) the color of the tissue in the area of necrosis may be black or dirty green (with gangrene), which is associated with the formation of pigment under the influence of putrefactive microbes; the appearance of a grayish mass has brain tissue, yellow-gray in tuberculosis and in the intestines, red or red-blue in pulmonary infarction;

4) the smell in the necrosis zone in gangrene is due to the fact that putrefactive microorganisms (Pseudomonas aeruginosa, clostridia) are able to produce hydrogen sulfide, which interacts with iron sulfide.

Microscopic signs of necrosis: changes occur in the parenchyma and stroma. Karyopyknosis (densification of chromatin and reduction of the nucleus), karyorrhexis (disintegration of the nucleus into separate fragments) and karyolysis (the nucleus completely dissolves) occur in the nucleus.

8. Morphogenesis and classification of necrosis

Morphogenesis of necrosis:

1) paranecrosis - dystrophy with a reversible character;

2) necrobiosis - dystrophic processes deepen and become irreversible;

3) cell death - the cell ends its functioning, the morphology is preserved;

4) autolysis or the stage of necrosis itself - all morphological signs are clearly visible.

Autolysis is the process of cell destruction and self-digestion under the action of hydrolytic enzymes of its own structures, as well as under the action of proteolytic enzymes of leukocytes and macrophages.

Necrosis is classified as follows. 1. By etiology:

1) traumatic necrosis is caused by the action of various physical factors (high temperatures, concentrated alkalis and acids);

2) toxic necrosis is caused by bacterial toxins and chemical toxins (so acute renal failure can occur under the influence of salts, mercury, surrogates, medicinal substances);

3) trophoneurotic necrosis occurs with a decrease in vascular and nervous tissue trophism (bedsores);

4) vascular necrosis occurs when blood flow to tissues is stopped, with thromboembolism, thrombosis, with prolonged vasospasm and morphological phenomena of infarction (spleen, myocardium, brain, lungs, intestines, kidneys);

5) allergic necrosis is associated with the action of toxic immune complexes.

2. According to the mechanism of development:

1) direct necrosis - direct effect on the tissue of a pathogenic factor (traumatic, toxic);

2) indirect necrosis - due to the effect on the tissue of not the pathogenic factor itself, but indirectly through the vessels, nerves, etc.

3. According to clinical and morphological forms:

1) coagulative or dry necrosis: cheesy with tuberculosis and syphilis; waxy - in the muscles; fibrinoid in connective tissue disorders and in valves;

2) colliquational necrosis (in the substance of the brain and intestines) - a heart attack;

3) gangrene - tissue necrosis, which communicates with the external environment, is infected with putrefactive microbes with rejection of dead tissue as a result. Localization of gangrene: lower and upper limbs, internal organs that communicate with the external environment (lungs, large intestine, appendix, bladder and uterus). Gangrene can be dry or wet. For dry gangrene, circulatory disorders are necessary, for wet gangrene - venous stasis, edema, lymphostasis.

9. Circulatory disorders

Circulatory disorders are divided into 7 main options:

1) hyperemia, or plethora;

2) bleeding, or hemorrhage;

3) thrombosis;

4) embolism;

5) ischemia, or local anemia;

6) heart attack;

7) stasis.

Venous hyperemia is expressed in increased blood filling of the tissue, the difficulty in outflow of blood matters, while the arterial inflow does not change or is somewhat reduced.

Bleeding is the release of blood from the cavity of the heart and blood vessels into the environment or into the body cavity. Hemorrhage is a type of bleeding, which is characterized by the accumulation of blood in the tissues. Possible internal bleeding into the cavity (hemo-pericarditis, hemarthrosis, hemothorax, etc.). By prescription, hemorrhages are divided into old (in the presence of hemosiderin) and fresh.

According to the type of tissue changes, they differ:

1) hematoma-type hemorrhages - always accompanied by tissue destruction;

2) petechiae, or ecchymosis - small pinpoint hemorrhages that are localized on the skin or mucous membranes;

3) hemorrhagic infiltration, or impregnation; does not cause tissue destruction;

4) bruising.

Mechanisms of hemorrhage: rupture of the wall, separation of the wall and diapedesis of erythrocytes. Outcome: a hematoma in the substance of the brain is converted into a cyst, which contains serous contents. In soft tissues, the hematoma resolves or suppurates.

Thrombosis is the process of intravital blood coagulation in the lumen of a vessel or in the cavities of the heart. This is the irreversible denaturation of proteins and blood cells.

Embolism is the transport of particles by the blood that are not normally observed in it.

There are three central directions of movement of amboluses in the circles of blood circulation:

1) from the left heart to the arterial system;

2) from the veins of the systemic circulation through the right heart into the pulmonary trunk;

3) along the portal vein.

Heart attack - ato necrosis resulting from the cessation of blood supply to the tissue; infarctions are distinguished by color white, red and white with a red rim. According to the shape, which is associated with the type of blood circulation, there are irregular and conical (in the kidneys, lungs). The consistency can be dry and wet.

Stasis - an ato stop of blood flow in the vessels of the micro-circulatory circle, resulting in hemolysis and blood clotting.

10. Hyperemia

Venous hyperemia can be local and general.

With rapidly developing venous congestion, tissue edema occurs, but it does not form in all tissues, but in cavities and those organs where there is space for fluid (in the kidneys and liver).

Transudate (edematous fluid) - occurs during venous stasis, often transparent, and the tissues that it washes are of an unchanged, normal color.

Exudate is a fluid of plasma origin that occurs during inflammation. It is cloudy, grayish-yellow or red. Tissues washed with axsudate acquire a dull tint.

With slowly developing hyperemia, the tissue undergoes brown induration.

Induration is an atom thickening that occurs under conditions of chronic hypoxia. Any tissue of the body that falls into conditions of oxygen starvation begins to actively develop its stroma, and at the expense of connective tissue. An increase in the stroma is an adaptive reaction, since together with the stroma, capillaries grow in the tissue, which contributes to the compensation of hypoxia, in other words, sclerosis occurs.

Microscopic picture: dilated and blood-filled venules.

Local venous stasis: usually associated with blockage or occlusion of a major vein. There are 3 main types of general venous hyperemia: stagnation of the pulmonary circulation, stagnation of the systemic circulation, stagnation of the portal vein. Causes of stagnation in the small circle: left ventricular failure, mitral and aortic defects, compression of the mediastinum of the pulmonary veins by a tumor is the rarest cause. With acute venous stasis of the small circle, which develops from several minutes to several hours, pulmonary edema develops. Cause of death: cardiac and cardiopulmonary failure.

Causes of stagnation of the systemic circulation: venous congestion in the pulmonary circulation, diffuse sclerotic changes in the lungs, right ventricular failure, compression of the trunks of the vena cava by the tumor. With rapidly developing stagnation, edema develops (with hyperemia of the systemic circulation - swelling of the skin and soft tissues), which is called anasarca.

Forms of edema: edema of the abdominal cavity - ascites, edema of the pleural cavity - hydrothorax, edema of the pericardial cavity - hydropericardium, etc. Cyanosis is associated with varicose veins and is more pronounced, the farther the tissue is from the heart.

Stagnation in the portal vein system is usually causally associated with the liver: diffuse sclerotic changes occur - cirrhosis, rarely congestive induction leads to the fact that capillaries in the hepatic lobules are compressed by connective tissue.

Portal hypertension includes a number of clinical manifestations:

1) ascites;

2) varicose dilatation of hepatic portocaval anastomoses (veins of the esophagus and stomach, veins of the rectum, veins of the anterior abdominal wall);

3) congestive enlargement of the spleen (splenomegaly) with further induration.

11. Thrombosis

The reasons:

1) changes in the vascular wall during inflammatory processes, angioedema, atherosclerosis, and hypertension;

2) changes in the speed and direction of blood flow (with heart failure);

3) a number of reasons associated with a change in the chemical composition of the blood: with an increase in coarse proteins, fibrinogen, lipids. Such conditions are observed in malignant tumors, atherosclerosis.

The mechanism of thrombus formation consists of IV stages:

I - phase of platelet agglutination;

II - fibrinogen coagulation, fibrin formation;

III - agglutination of erythrocytes;

IV - precipitation - sedimentation in clots of various plasma proteins.

Depending on the place and conditions under which the formation of a thrombus occurred, there are:

1) white blood clots (platelets, fibrins, leukocytes). These clots form when there is fast blood flow in the arteries;

2) red blood clots (platelets, fibrins, erythrocytes) occur in conditions of slow blood flow, most often in veins;

3) mixed: the place of attachment is called the head, the body is freely located in the lumen of the vessel;

4) hyaline thrombi - a very rare variant (they consist of destroyed erythrocytes, platelets, protein precipitate). It is the protein precipitate that creates a resemblance to cartilage. These thrombi form in arterioles and venules.

In relation to the lumen of the vessel, thrombi are distinguished:

1) clogging (obturating), i.e., the lumen of the vessel is closed by a mass of a blood clot;

2) parietal;

3) in the chambers of the heart and in aneurysms there are spherical thrombi.

Outcomes:

1) the most frequent - organization, i.e., germination of connective tissue occurs;

2) petrification - deposition of lime;

3) secondary softening (colliquation) of a thrombus - develops due to two reasons: microbial enzymatic lysis (when microbes enter the thrombus) and local enzymatic lysis, which develops due to its own enzymes released when damaged.

12. Embolism and infarction

There are 7 types of embolisms.

1. Thromboambolism: the cause of the detachment of a blood clot is its softening, but it can also come off on its own from the place of attachment.

2. Tissue (cellular) ambolism is observed in malignant tumors, when cancer or sarcoma cells grow into the bloodstream, the cells detach from the tumor and circulate with the blood stream; when stuck in the distant branches of the internal organs, they cause tumor ambolism. These distant tumor nodules in relation to the maternal tumor are metastases, and the process itself is called metastasis. In gastric cancer, metastasis occurs through the portal vein to the liver.

3. Microbial ambolism develops with purulent inflammation. With the help of its enzymes, pus melts the surrounding tissues, including blood vessels, microbes get the opportunity to penetrate into the blood through the melted vessel and circulate throughout the body. The larger the abscess, the more likely the introduction of microbes into the blood. The condition that occurs when an atom is observed is called sepsis.

4. Fat ambolism develops with large-scale fractures of tubular bones with crushing. Fat droplets (from the bone marrow) enter the veins and obliterate the capillaries of the lungs.

5. Air ambolism occurs when large veins are injured.

6. Gas ambolism occurs during decompression sickness (for example, divers rise sharply) - the gas composition of the blood changes, nitrogen bubbles begin to spontaneously appear in it (at high pressure - as a rule, during diving - nitrogen is converted in the blood to a greater extent, and when rising, nitrogen does not have time to leave the blood).

7. Embolism by foreign bodies - when bullets and fragments move against the flow of blood under the influence of gravity (retrograde) or along the bloodstream.

Heart attack.

Stages of development of a heart attack.

1. The ischemic stage does not have a macroscopic picture and most often lasts several hours (up to 8-10 hours). Microscopically: disappearance of glycogen and important enzymes in cells.

2. The stage of necrosis - macro- and microscopically, the infarction has a characteristic expression. The duration of the stage is up to a day.

3. Exit stage - often ends with organization. In the brain, a cavity is formed - a cyst, in the heart and other organs there is an organization and formation of a scar. Atom takes a week or more.

13. Inflammation

Inflammation is a complex protective stromal-vascular reaction of the body in response to the action of a pathological factor.

According to the etiology, 2 groups of inflammations are distinguished:

1) banal;

2) specific.

Specific is inflammation, which is caused by certain causes (pathogens). This is inflammation caused by Mycobacterium tuberculosis, inflammation in leprosy (leprosy), syphilis, actinomycosis. Inflammations caused by other biological factors (E. coli, cocci), physical, chemical factors are banal inflammations.

According to the time of the course of inflammation, there are:

1) acute - lasts 7-10 days;

2) chronic - develops from 6 months or more;

3) subacute inflammation - the duration is between acute and chronic.

According to morphology (pathoanatomical classification), exudative and proliferative (productive) inflammation are distinguished. The causes of inflammation can be chemical, physical or biological.

The phases of inflammation are alteration, proliferation and exudation. In the phase of alteration, tissue damage occurs, which pathologically manifests itself in the form of destruction and necrosis. Activation and release of biologically active substances take place, i.e. mediation processes are launched. Mediators of inflammation of cellular origin are mast cells, platelets, basophils, lymphocytes and monocytes; mediators of plasma genesis - collecrein-kinin system, complementary, clotting and anti-clotting systems. The actions of these mediators affect the course of the next phase of inflammation - exudation. Mediators increase the permeability of the vessels of the microvasculature, activate leukocyte chemotaxis, intravascular coagulation, secondary alteration in the very focus of inflammation and the activation of immune mechanisms. During exudation, arterial and venous hyperemia occurs in the focus of inflammation, and the permeability of the vascular wall increases. Proliferation is characterized by the fact that in the focus of inflammation, blood cells accumulate in large numbers, as well as cells of histogenic origin. Neutrophils appear after a few minutes. Leukocytes perform the function of phagocytosis. Neutrophils after 12 hours lose glycogen, fill with fat and turn into purulent bodies. Monocytes that have left the vascular bed are macrophages (simple and complex) that are capable of phagocytosis. There are three types of macrophages. Simple macrophages are transported to epithelioid cells, they are elongated, have a single nucleus and look like an epithelium (in tuberculosis). Giant cells, which are 15-30 times larger than usual, arise by the fusion of several epithelioid cells. They are round in shape, and the nuclei are clearly located on the periphery and are called Pirogov-Langhans cells. The giant cell of foreign bodies can instantly transform into histiocytes. They are round and the nuclei are located in the center.

14. Exudative inflammation

Exudative inflammation is inflammation in which exudative processes predominate. Occurrence conditions:

1) the impact of damaging factors on the vessels of the microvasculature;

2) the presence of special factors of pathogenicity (pyogenic flora, isolation of chemotaxis); distinguish between independent and non-independent types of exudative inflammation. Independent species occur on their own, and non-independent species join them. Independent include serous inflammation, fibrinous and purulent. To dependent - catarrhal, hemorrhagic and putrefactive inflammation. Mixed inflammation is also distinguished - this is a combination of at least 2 types of inflammation.

Serous inflammation is characterized by the accumulation of the liquid part of the exudate containing about 2,5% protein and various cellular forms (platelets, leukocytes, macrophages) and cells of local tissues. Localization everywhere - in the skin, mucous membranes, serous membranes and in the parenchyma of organs. In the serous cavities, fluid accumulations are called exudative pericarditis, pleurisy, and peritonitis. The membranes themselves are edematous, plethoric, and between them there is a liquid. Parenchymal organs become enlarged, flabby, on the cut the tissue is dull, gray, resembling boiled meat. Microscopic views: expanded intercellular spaces, gaps between cells, cells are in a state of dystrophy. The exudate compresses the organs, disrupting their function. But basically the outcome is favorable, sometimes you have to release large amounts of exudate.

The outcome of serous inflammation in parenchymal organs is diffuse small-focal sclerosis and functional disorders.

Fibrinous inflammation: exudate is represented by fibrinogen. Fibrinogen is a blood protein that, going beyond the blood vessels, turns into insoluble fibrin. Intertwining fibrin threads form on the surfaces of the organs of the film - grayish, of various thicknesses. Occurs on the mucous membranes, serous membranes, as well as on the skin. Depending on how the film is connected to the surface, there are croupous (formed on mucous membranes lined with a single-layer epithelium) - if the film is easily separated from the underlying tissue and diphtheria (on stratified epithelium) - if the film is poorly separated. The outcome of fibrinous inflammation depends on the type of inflammation. Croupous films are characterized by easy detachment, while the basement membrane does not suffer, complete epithelialization occurs. On serous membranes - rejection of the film into the cavity, which does not always have time to be resorbed by macrophages, and organization occurs.

As a result, fibrous adhesions are formed between the parietal and visceral sheets of the corresponding serous membrane - adhesions that limit the mobility of organs. Sometimes under the films there is the formation of deep defects - erosion, ulcers.

15. Purulent inflammation

With purulent inflammation, the exudate is represented by polymorphonuclear leukocytes, includes dead leukocytes, destroyed tissues. Color from white to yellow-green. ubiquitous localization. The reasons are varied; First of all - coccal flora. The pyogenic flora includes staphylo-and streptococci, meningococci, gonococci and coli - intestinal, Pseudomonas aeruginosa. One of the factors of the pathogenicity of this flora are the so-called leukocidins, they cause an increase in the chemotaxis of leukocytes towards themselves and their death. In the future, with the death of leukocytes, factors are released that stimulate the chemotaxis of new leukocytes in the focus of inflammation. Proteolytic enzymes, which are released during destruction, are able to destroy both their own tissues and tissues of the body. Therefore, there is a rule: "you see pus - let it out" in order to prevent the destruction of your own tissues.

There are the following types of purulent inflammation.

1. Phlegmon - diffuse, diffuse, without clear boundaries, purulent inflammation. Diffuse infiltration by leukocytes of various tissues occurs (most often - subcutaneous fat, as well as the walls of hollow organs, intestines - phlegmonous appendicitis). Phlegmonous inflammation can occur in the parenchyma of any organs.

2. Abscess - focal, delimited purulent inflammation. Allocate acute and chronic abscess. An acute abscess has an irregular shape, an indistinct, blurred border, and there is no decay in the center. A chronic abscess has a regular shape, with clear boundaries and a decay zone in the center. The clarity of the border is due to the fact that the connective tissue grows along the periphery of the abscess. In the wall of such an abscess, several layers are distinguished - the inner layer is represented by a pyogenic membrane of granulation tissue, and the outer part of the wall is formed by fibrous connective tissue. When an abscess is connected to the external environment with the help of anatomical channels (in the lungs), an air space is formed in the cavity, and the pus is located horizontally (this is noticeable on the x-ray).

3. Empyema - purulent inflammation in the anatomical cavities (empyema of the pleura, maxillary sinuses, gallbladder). The outcome of purulent inflammation depends on the size, shape, localization of foci. Purulent exudate can resolve, sometimes sclerosis develops - scarring of the tissue.

A complication in the form of erosion of surrounding tissues by proteolytic enzymes can lead to the formation of fistulas - channels through which the abscess is emptied outward (self-cleaning) or into the serous membrane (for example, a lung abscess can lead to the development of pleural empyema, liver - to purulent peritonitis, etc. ); bleeding; exhaustion; intoxication, etc.

16. Catarrhal, hemorrhagic, putrefactive, mixed and proliferative inflammations

Catarrhal inflammation - mucus is mixed with the exudate. There is a drain of exudate from the inflamed surface. Typical localization - mucous membranes. The outcome of catarrhal inflammation is the complete restoration of the mucosa.

Hemorrhagic inflammation is characterized by the admixture of red blood cells to the exudate. The exudate becomes red, then, as the pigments are destroyed, it becomes black. It is typical for viral infections, such as influenza, measles, natural (black) smallpox, with endogenous intoxications, for example, intoxication with nitrogenous slags in chronic renal failure.

Putrid (gangrenous) inflammation occurs due to the attachment of putrefactive flora, primarily fusospirochetal, to the foci of inflammation. It is more common in organs that have a connection with the external environment: putrefactive gangrene of the lung, limbs, intestines, etc. Decaying tissues are dull, with a fetid specific odor.

Mixed inflammation. They talk about it when there is a combination of inflammation (serous-purulent, serous-fibrinous, purulent-hemorrhagic or fibrinous-hemorrhagic).

Productive (proliferative inflammation) - the proliferation phase predominates, resulting in the formation of focal or diffuse cellular infiltrates, which can be polymorphic-cellular, lymphocytic-cell, macrophage, plasma-cell, giant-cell and epithelioid-cell. One of the main conditions for the development of proliferative inflammation is the relative stability of damaging factors in the internal environment of the body, the ability to persist in tissues.

Features of proliferative inflammation:

1) chronic undulating course;

2) localization mainly in connective tissues, as well as in tissues whose cells have the ability to proliferate - the epithelium of the skin, intestines.

In morphology, the most characteristic feature is the formation of granulation tissue. Granulation tissue is young, immature, growing connective tissue. Its formation is determined by classical biological properties. The growth and functioning of tissue are antagonistic processes. If the tissue begins to function well, then its growth slows down, and vice versa.

Varieties of productive inflammation:

1) interstitial, or interstitial;

2) granulomatous;

3) productive inflammation around parasitic animals;

4) hypertrophic growths.

Intermediate inflammation usually develops in the structure of parenchymal organs; is diffuse. It can occur in the interstitium of the lungs, myocardium, liver, kidneys.

The outcome of this inflammation is diffuse sclerosis. The function of organs in diffuse sclerosis deteriorates sharply.

17. Granulomatous inflammation

Granular inflammation is a focal productive inflammation in which foci arise in the tissue from cells that have the ability to phagocytosis. These lesions are called granulomas. Granulomatous inflammation occurs in rheumatism, tuberculosis, occupational diseases - when various mineral and other substances settle on the lungs. Macroscopic picture: granular scrap is small, its diameter is 1-2 mm, it is barely visible to the naked eye. The microscopic structure of the granuloma depends on the phase of differentiation of phagocytic cells. The precursor of phagocytes is considered to be a monocyte, which differentiates into a macrophage, then into an epithelioid cell, and then into a giant multinucleated cell. There are two types of multinucleated cells: the foreign body giant cell and the Pirogov-Langhans giant multinuclear cell. Granulomas are divided into specific and nonspecific. A specific variant of productive granulomatous inflammation is called specific, which is caused by specific pathogens and which develops on an immune basis. Specific pathogens are mycobacterium tuberculosis, pale treponema, actinomycete fungi, mycobacterium leprosy, pathogens of rhinoscleroma.

Features of specific inflammation:

1) chronic undulating course without a tendency to self-heal;

2) the ability of pathogens to cause the development of all 3 types of inflammation, depending on the state of the organism's reactivity;

3) a change in inflammatory tissue reactions due to a change in the immunological reactivity of the body;

4) in morphological terms, inflammation is characterized by the formation of specific granules, which have a characteristic structure depending on the pathogen.

Inflammation in tuberculosis: Mycobacterium tuberculosis is capable of causing alterative, exudative, proliferative inflammation. Alternative inflammation develops most often with hypoergy, which is caused by a decrease in the body's defenses. Morphologically it is manifested by caseous necrosis. Exudative inflammation usually occurs in conditions of hyperergy - increased sensitivity to antigens, toxins of mycobacteria. Mycobacterium, when it enters the body, is able to persist there for a long time, in connection with this, sensitization develops.

Morphological picture: foci are localized in various organs and tissues. Initially, serous, fibrinous or mixed exudate accumulates in the foci, later the foci undergo caseous necrosis. If the disease is detected before caseous necrosis, then treatment can lead to resorption of the exudate. Productive inflammation develops under conditions of specific tuberculous non-sterile immunity. The morphological manifestation will be the formation of specific tuberculous granules (in the form of "millet grain"). Most often in the center of the granuloma is a small foci of necrosis.

18. Macroscopic classification of foci of tuberculous inflammation; inflammation in syphilis

The foci are classified into 2 groups: miliary and large. Miliary foci are most often productive, but may be alterative and exudative.

From the large foci, there are:

1) acinous; macroscopically, it resembles a shamrock, as it consists of three stuck together miliary foci; allocate also productive and alternative;

2) caseous focus - in size it is similar to a mulberry or raspberry. Black color. Inflammation is basically always productive, pigments adsorb connective tissue;

3) lobular;

4) segmental;

5) lobar foci.

Lobar foci are exudative foci. Outcomes - scarring, rarely necrosis. In exudative foci - encapsulation, petrification, ossification. For large foci, the formation of a secondary colliquation is characteristic, liquefaction of dense masses occurs. Liquid masses are able to be emptied, cavities remain outside and in place of these foci - cavities.

Inflammation in syphilis. There are primary, secondary, tertiary syphilis. Primary syphilis - inflammation is most often exudative, as it is caused by hyperergic reactions.

Morphological picture: the manifestation of a hard chancre at the site of the introduction of the spirochete - an ulcer with a shiny bottom and dense edges. Usually the chancre is scarred. Secondary syphilis lasts from several months to several years and is accompanied by an unstable state of restructuring of the immune system. There is also a hyperergic reaction at the base, so the inflammation is exudative. Characterized by spirochetemia. Secondary syphilis occurs with relapses, in which rashes are observed - exanthema on the skin and enanthema on the mucous membranes, which disappear without a trace (without scarring).

Inflammation becomes productive in the 3rd phase of the disease - with tertiary syphilis. Formed specific syphilitic granulomas - gummas. Macroscopically, in the center of syphilitic gumma there is a focus of glutinous necrosis, around it is granulation tissue with a large number of vessels and cells. Localization everywhere - intestines, bones, etc. The outcome of the gum is scarring with disfigurement (gross deformation of the organ). The second variant of the course of productive inflammation in tertiary syphilis is interstitial (interstitial) inflammation. The most common localization in the liver and in the aorta is syphilitic aortitis. The outcome is a local expansion (aortic aneurysm), which can rupture, and a blood clot can also form.

Nonspecific granulomas have no characteristic features. They are found in a number of infectious (with rheumatism, typhus, typhoid fever) and non-infectious diseases (with sclerosis, foreign bodies). The outcome is twofold - scarring or necrosis.

19. Immunopathology

Immunopathology studies the processes and diseases resulting from immune conflict and the disturbance of immunological homeostasis. The immune response can be specific and non-specific. The nonspecific immune response consists of mechanical protection, humoral and cellular mechanisms.

Mechanical protection is the first barrier to pathogenesis and is carried out by the epithelial cover due to the movement of cilia (cough, vomiting, sneezing, peristalsis, lacrimal fluid, etc.).

The humoral mechanism is provided by the ability of body fluids to kill the pathogen. So, blood, saliva, lacrimal fluid, intestinal secretion are rich in lysocine, interferon, antibacterial substrates.

Cellular immunity functions through cells such as neutrophils, basophils, macrophages, Kupffer cells, and others that are capable of phagocytosis.

The specific immune response is composed of specificity, immune memory, and recognition.

Specificity is protection only against a specific pathogen.

Memory is the property of the body to maintain immunity throughout subsequent life as a defense against re-infection.

Friend-or-foe recognition is the ability to differentiate one's tissues from those of others and produce antibodies to foreign cells.

Immune reactions are divided into humoral and cellular (central and peripheral). The central ones include the thymus gland, bone marrow, tonsils and a group of lymph nodes of the internal organs. To peripheral - lymph nodes, spleen, blood and reticulo-endothelial system.

Forms of specific reactions that make up immunology: antibody production, immediate-type hypersensitivity, delayed-type hypersensitivity, immunological memory and immunological tolerance. An immediate type hypersensitivity reaction has the morphology of acute immune inflammation. It is characterized by the speed of development, the predominance of alternative and vascular-exudative changes, the slow course of reparative processes.

Alternative changes are characteristic of vessels, ground substance and fibrous structures of the connective tissue. They are represented by plasma impregnation, mucoid and fibrinoid swelling, fibrinoid necrosis. Coarsely dispersed proteins, fibrin, neutrophils, immune complexes and erythrocytes appear in the focus of inflammation. In this regard, the most characteristic (for an immediate hypersensitivity reaction) are fibrinous and fibrinous-hemorrhagic exudates.

Lymphocytic and macrophage infiltration in the focus of immune conflict is an expression of chronic immune inflammation in this reaction.

Autoimmunization (autoallergy, autoaggression) is a condition characterized by the appearance of reactions of the immune system to normal antigens of one's own tissues.

20. Autoimmune diseases. Immunodeficiency syndromes

Autoimmune diseases are diseases based on autoimmunity. There are two groups of autoimmune diseases:

1) organ-specific immune diseases that develop due to damage to the physiological barriers of immunologically isolated organs, which allows the immune system to respond to their unchanged antigens by producing autoantibodies and sensitized lymphocytes. This group includes thyroiditis (Hashimoto's disease), encephalomyelitis, polyneuritis, multiple sclerosis, idiopathic Addison's disease, aspermatogeny, symptomatic ophthalmia;

2) organ-specific autoimmune diseases; leading in these diseases are violations of the control of immunological homeostasis of the lymphoid system. This group of autoimmune diseases includes systemic lupus erythematosus, rheumatoid arthritis, systemic scleroderma, dematomyasitis, secondary thrombotic thrombocytopenic purpura.

Immunodeficiency syndromes are extreme manifestations of the insufficiency of the immune system.

They can be primary, caused by underdevelopment (hypoplasia, aplasia) of the immune system, - hereditary and congenital, or secondary (acquired), arising in connection with the disease or ongoing treatment. Primary immunodeficiency syndromes can be an expression of insufficiency: cellular and humoral immunity.

Combined immunodeficiency states:

1) agammaglobulinemia (hypoplasia of the thymus gland and peripheral lymphoid tissue, lymphopenia, frequent infectious diseases);

2) ataxia, Louis-Barr telangiectasia (hypoplasia of the thymus and peripheral lymphoid tissue, lymphopenia, atrophy of the cerebellar cortex, telangiectasia of the bulbar conjunctiva, mesenchymal malignant tumors, recurrent pneumonia);

3) Nezelof's syndrome (hypoplasia of the thymus gland and peripheral lymphoid tissue, lymphopenia, sepsis).

Cellular immunity deficiency syndrome - Digeorge's syndrome (absence of the thymus and parathyroid glands, absence of T-lymphocytes).

Humoral immunity deficiency syndromes:

1) Bruton's syndrome (the thymus gland is preserved, but there are no B-dependent zones and cells of the plasmocyte series in the lymph nodes and spleen; frequent infectious diseases);

2) West's syndrome (the structure of the lymphoid tissue is preserved, frequent infections of the gastrointestinal tract and respiratory tract in combination with autoimmune diseases, allergies).

Secondary immunodeficiency syndromes include acquired immune deficiency syndrome or AIDS.

Other infections, leukemias, malignant lymphomas, thymoma, and sarcoidosis also lead to the development of secondary immunodeficiency syndromes.

21. Regeneration

Regeneration is the restoration of the structural elements of the tissue to replace the dead. It is a restoration of both structure and function. The factors influencing the course of regeneration include: general (age, intensity of metabolic processes, the state of the hematopoietic and immune systems, etc.) and local (the state of blood vessels, neurotrophic, lymphatic circulation, structural and functional features of organ tissues, the amount of damage).

Regulatory mechanisms of regeneration:

1) humoral factors - substances are released into the blood and inhibit proliferation, increase DNA synthesis and reduce mitotic activity;

2) hormonal factors:

a) pituitary growth hormone stimulates proliferation and active regeneration;

b) mineralocorticoids stimulate, and glucocorticosteroids inhibit the effect on regeneration;

c) thyroid hormones stimulate the regeneration process;

3) immune factors - lymphocytes perform an informational role, T-lymphocytes stimulate the healing effect, and B-lymphocytes inhibit;

4) nervous mechanisms of regulation are primarily associated with the trophic function of the nervous system;

5) functional mechanisms - with a functional supply of an organ and (or) tissue.

Regeneration phases: 1) proliferation phase - there is an increase in the number of cells or ultrastructures; this phase is carried out due to growth factors: platelet, epidermal, fibroblastic, macrophage and lymphocytic;

2) phase of differentiation - young cells mature, their structural and functional specialization occurs.

Regeneration classification:

1) according to the level of regeneration: molecular, cellular, subcellular, tissue, organ, systemic;

2) in form:

a) cellular regeneration occurs in those organs or tissues (in the epidermis, epithelium of the mucous membranes, endothelium and mesothelium of serous membranes, connective and hematopoietic tissues) where there are labile cells that have a limited lifespan; this form of regeneration is carried out by increasing the number of cells (hyperplasia);

b) mixed regeneration occurs in organs and tissues containing stable cells (lungs, liver, kidneys, pancreas, endocrine glands); regeneration is carried out by hyperplasia of the cells themselves;

c) intracellular regeneration occurs exclusively in the ganglion cells of the central nervous system.

22. Types of regenerations. Wound healing

Types of regeneration: physiological, reparative and pathological.

Physiological regeneration is not associated with the action of any damaging factor and is carried out with the help of apoptosis. Apoptosis is a genetically programmed cell death in a living organism. No inflammatory reaction occurs.

Reparative regeneration occurs when various damaging factors (trauma, inflammation) occur. Complete regeneration, or restitution, is a complete structural and functional restoration; incomplete regeneration, or substitution, occurs in organs with an intracellular form of regeneration and in organs with a mixed form of regeneration, but with extensive damage.

Pathological regeneration can be excessive (hyperregeneration), delayed (hyporegeneration), metaplasia and dysplasia. Excessive regeneration occurs with a pronounced activation of the first phase of regeneration. Hyporegeneration occurs when the proliferation phase proceeds sluggishly. This occurs in organs and tissues where there is chronic inflammation and where the processes of vascular and nervous trophism are often disturbed. Metaplasia occurs in organs and tissues with a cellular form of regeneration, and is often preceded by chronic inflammation. With anemia and blood diseases, metaplasia of the yellow bone marrow to red occurs. This is a compensatory mechanism. Dysplasia occurs when proliferation is impaired and during cell differentiation, therefore, atypical cells appear, i.e., having various shapes and sizes, having large hyperchromic nuclei. Such cells appear among ordinary epithelial cells.

There are three degrees of dysplasia: mild, moderate, severe (when almost all cells of the epithelial layer become atypical and are diagnosed as cancer on the spot).

During the regeneration of connective tissue, 3 stages are distinguished.

1. The formation of a young, immature connective - granulation - tissue.

2. Formation of fibrous connective tissue.

3. The formation of scar connective tissue, which contains thick coarse collagen fibers.

Wound healing refers to reparative regeneration. There are four types: direct closure of the defect by the creeping epithelium, healing under the scab, healing by primary and secondary intention. Direct closure of an epithelial cover defect is the simplest healing, which consists in the epithelium crawling onto a surface defect and closing it with an epithelial layer. Healing under the scab refers to small defects, on the surface of which a drying crust (scab) appears from coagulated blood and lymph.

Primary intention is the healing of deep wounds with damage not only to the skin, but also to deep-lying tissues; scar on the 10-15th day. Infected, crushed, contaminated and jagged wounds heal by secondary intention; heal through cleansing with leukocytes and macrophages on the 5-6th day.

23. Processes of adaptation Q (adaptation) and compensation

The ability of an organism to adapt (adapt) to changing environmental conditions has been developed in the process of phylogenesis and ontogenesis.

Adaptation in pathology can reflect various functional states: functional tension, decrease or perversion of tissue (organ) functions, and therefore can manifest itself in various pathological processes: atrophy, hypertrophy (hyperplasia), organization, tissue restructuring, metaplasia and dysplasia.

Atrophy is a life-time decrease in tissue and organ cells in volume, as well as a decrease and even termination of their functions. It occurs both within the normal range and in pathology.

Types of atrophy:

1) physiological - can be during the development of the organism (evolutionary) and during aging (involutional);

2) pathological - is divided into general and local. General atrophy or cachexia can be the result of various reasons - alimentary with a lack of nutrition, impaired absorption in the intestine, etc. Exhaustion - with other diseases (chronic infections such as tuberculosis, brucellosis, chronic dysentery).

Outcome: the process is reversible with timely and comprehensive treatment. An irreversible or pronounced process cannot be treated.

Local atrophy can be neurotic (neurotrophic), dysfunctional, a consequence of circulatory failure, pressure, chemical and physical factors. Neurotic atrophy occurs when the connection between organ tissues and the nervous system is disrupted. Dysfunctional (immobilization) atrophy arises from inactivity during fractures and dislocations.

Under the influence of radiation energy, atrophy is especially pronounced in the bone marrow and genital organs.

Hypertrophy (hyperplasia) is an increase in the volume of a cell or tissue due to the multiplication of cells or an increase in their number and size of intracellular ultrastructures. Two types of hypertrophies are adaptive: neurohumoral and hypertrophic growths.

Organization is the replacement of foci of necrosis of various origins with connective tissue, as well as thrombi, blood clots, fibrinous exudate.

Metaplasia is the transition of one type of tissue to another, related to it. It is more common in the epithelium and connective tissue, less often in other tissues.

Dysplasia is a pronounced violation of the proliferation and differentiation of the epithelium with the development of cellular adaptation and a violation of histoarchitectonics. This is the concept of tissue immunity. There are three stages of dysplasia: mild, moderate and severe.

Compensation is a particular type of adaptation; occurs in conditions of pathology in each damaged organ and when its functional tension takes place in the body. Stages of compensation: formation, consolidation and decompensation.

24. Sclerosis. Kinds

Classification

Sclerosis is a pathological process leading to diffuse or focal compaction of internal organs, vessels, connective tissue structures due to excessive growth of mature dense connective tissue. Moderate sclerosis is called fibrosis. Severe sclerosis is called cirrhosis.

Classification.

1. By etiology and pathogenesis:

1) sclerosis as an outcome of chronic productive inflammation of infectious, infectious-allergic and immunopathological genesis, as well as caused by foreign bodies;

2) sclerosis as an outcome of systemic (rheumatic diseases, systemic congenital dysplasia) and local (Dupuytren's contracture, keloid) disorganization of connective tissue;

3) replacement sclerosis as an outcome of tissue necrosis and atrophy as a result of circulatory and metabolic disorders, exposure to physical and chemical factors;

4) formation of scars as a result of wound healing and ulcerative defects;

5) organization of blood clots, hematomas, fibrin deposits, formation of adhesions, obliteration of serous cavities.

2. By morphogenesis:

1) neoplasm of young connective tissue due to the proliferation of fibroblasts, their enhanced synthesis of collagen, fibrillogenesis and the formation of fibrinous scar tissue;

2) increased collagen synthesis by fibroblasts and fibrillogenesis without pronounced cell hyperplasia, a change in the ratio of cells and fibrous structures in favor of the latter, the transformation of loose connective tissue into fibrous tissue, as well as an increase in mass and a change in the structure of specialized types of connective tissue; 3) sclerosis with stromal collapse as a result of necrosis or atrophy of the parenchyma of internal organs. 3. If the reversibility of sclerotic changes is possible, sclerotic processes can be labile or irreversible, stable or partially reversible, progressive or irreversible.

Regulation of connective tissue growth in sclerosis is carried out by both central (neuroendocrine) and local (regulatory systems) mechanisms.

25. Tumors

A tumor is a pathological process characterized by the uncontrolled reproduction of cells, while the growth and differentiation of cells are disturbed due to changes in their genetic apparatus. Properties of the tumor: autonomous and uncontrolled growth, atypism, anaplasia or new properties that are not inherent in a normal cell and cataplasia.

The structure of the tumor in shape: the shape of the node, mushroom cap, saucer-shaped, in the form of papillae, in the form of cauliflower, etc. Surface: smooth, tuberous, papillary. Localization: in the thickness of the organ, on the surface, in the form of a polyp, diffusely penetrating. On the cut, it can be in the form of a homogeneous white-gray tissue, gray-pink (fish meat), fibrous structure (in the testicles). The size of the tumor depends on the rate and duration of its growth, origin and location. According to the degree of differentiation and growth, the tumor can be:

1) expansive, that is, it grows out of itself, pushing the tissues away. The parenchymal elements surrounding the tumor tissue atrophy, and the tumor is, as it were, surrounded by a capsule. Growth is slower and more often benign. Malignant proceeds in the thyroid gland and kidneys;

2) oppositional growth due to neoplastic transformation of normal cells into tumor cells;

3) infiltrating growth. In this case, the tumor grows into the surrounding tissues and destroys them. Growth occurs in the direction of least resistance (along the interstitial fissures, along the course of nerve fibers, blood and lymphatic vessels).

According to the ratio of tumor growth to the lumen of a hollow organ, there are: endophytic (infiltrating growth deep into the organ wall) and exophytic growth (into the organ cavity).

Homologous tumors - their structure corresponds to the structure of the organ in which they develop (these are mature differentiated tumors). Heterologous tumors: their cellular structure differs from the organ in which they develop (poorly or undifferentiated tumors). Benign tumors are homologous, slow growing, highly differentiated, do not metastasize and do not affect organization. Malignant tumors consist of little or undifferentiated cells, lose their similarity to tissue, have cellular atypism, grow rapidly and metastasize.

Metastases can be hematogenous, lymphogenous, implantation and mixed. In benign tumors, tissue affiliation is easy to determine (unlike malignant ones).

If the histogenesis of a malignant tumor cannot be determined, then such a tumor is called blastoma: large cell, spindle cell, polymorphic cell.

Blastomas are combined groups of tumors, since various malignant tumors can transform into blastoma.

Non-epithelial or mesenchymal tumors develop from connective, adipose, muscle tissue, blood and lymphatic vessels, synovial tissue and bone.

26. Types of tumors

Connective tissue tumors:

1) benign - fibromas - can be found wherever there is connective tissue. The most common localization is the dermis. Fibroma is a well-defined node. There are two types of fibromas: soft fibroma (more tumor cells) and hard (more collagen fibers). Soft fibroma is younger, as it ages, it turns into a hard one;

2) malignant tumors - fibrosarcomas - arise from the elements of the fascia, tendon, from the periosteum. They are localized more often on the limbs, mainly at a young and mature age. Fibrosarcoma is a node without clear boundaries.

Bone tumors are:

1) benign - osteoma. It is observed in small bones of the limbs, bones of the skull. Grows in the form of a node (exostosis);

2) malignant - osteosarcoma. The predominant localization is the ends of long tubular bones and metaepiphyseal joints. It occurs mainly at a young age (up to 30 years). Osteosarcoma, one of the most malignant tumors, metastasizes early.

Cartilage tumors are:

1) benign - chondroma.

Localization in the epiphyses of tubular bones, pelvic bones, femoral head, small bones of the hand; forms:

a) echondroma (location on the surface of the bone);

b) enchondroma (inside the bone).

2) malignant - chondrosarcoma.

Localization is the same as that of the chondroma.

4. Tumors of vascular tissue.

Of the arteries, capillaries - angiomas, lymphatic vessels - lymphangiomas. Angiomas are congenital (purple-bluish spots) and acquired. Malignant vascular tumors are very rare (hemangioendothelioma).

5. Tumors of muscle tissue

Smooth muscles. Benign tumors - leiomyomas. Localization: soft tissues of the lower extremities, internal organs (GIT). Most often in the uterus - fibromyoma is a leiomyoma that has undergone fibrosis. Fibromyoma is not so much a tumor as a dyshormonal proliferative process that occurs in women when the balance of sex hormones is disturbed. Malignant: leiomyosarcomas. They are found in the uterus, soft tissues of the extremities. They are characterized by early metastases.

Striated muscles.

Tumors of the striated muscle:

1) benign - rhabdomyomas;

2) malignant - rhabdomyosarcomas. One of the most malignant tumors. They are extremely rare.

6. Tumors of hematopoietic tissue

Among the tumors of the hematopoietic tissue, there are:

1) leukemia;

2) lymphomas (lymphosarcoma, reticulosarcoma, plasmacytoma or myeloma, lymphogranulomatosis).

27. Epithelial tumors

Epithelial tumors develop from squamous or glandular epithelium that does not perform any specific function. This is the epidermis, epithelium of the oral cavity, esophagus, endometrium, urinary tract, etc.

Benign tumors include papilloma and adenoma. Papilloma is a tumor of squamous or transitional epithelium. It has a spherical shape, dense or soft, with a papillary surface, ranging in size from millet grain to a large pea. It is located above the surface of the skin or mucous membrane on a wide or narrow base. In case of injury, the papilloma is easily destroyed and inflamed, in the bladder it can bleed. After removal of papillomas, in rare cases they recur, sometimes malignant. Adenoma is a tumor of glandular organs and mucous membranes lined with prismatic epithelium. It has the appearance of a well-demarcated node of soft consistency, on the cut the tissue is white-pink, sometimes cysts are found in the tumor. The sizes are different - from a few millimeters to tens of centimeters. Adenomas of the mucous membranes protrude above their surface in the form of a polyp. The adenoma has an organoid structure and consists of cells of prismatic and cubic epithelium. The malignant ones include:

1) cancer in situ is a form of cancer without invasive (infiltrating) growth, but with pronounced atypism and proliferation of epithelial cells with atypical mitoses;

2) squamous cell (epidermal) cancer develops in the skin and mucous membranes covered with flat or transitional epithelium (oral cavity, esophagus, cervix, vagina). The tumor can be keratinizing (cancer pearls are formed) and non-keratinizing;

3) adenocarcinoma (glandular cancer) develops from the prismatic epithelium of the mucous membranes and epithelium of the glands;

4) mucous (colloid) cancer - adenogenic carcinoma, the cells of which have signs of both morphological and functional atypia. Cancer cells produce a huge amount of mucus and die in it;

5) solid cancer is an undifferentiated cancer with severe atypia. Cancer cells are located in the idea of trabeculae, separated by layers of connective tissue;

6) fibrous cancer or skirr is a form of undifferentiated cancer, represented by extremely atypical hyperchromic cells located among the layers and strands of coarse fibrous connective tissue;

7) small cell carcinoma is an undifferentiated cancer consisting of monomorphic lymphocyte-like cells that do not form any structures, the stroma is extremely poor;

8) medullary (adenogenic) cancer. Its main feature is the predominance of the parenchyma over the stroma, which is very small. The tumor is soft, white-pink. It is represented by layers of atypical cells, contains many mitoses, grows rapidly and undergoes necrosis early;

9) mixed forms of cancer (dimorphic cancers) consist of the rudiments of two types of epithelium (squamous and cylindrical).

28. Diseases of the blood. anemia. Classification

Blood diseases develop as a result of dysregulation of hematopoiesis and blood destruction, which is manifested by changes in peripheral blood. Thus, according to the state of peripheral blood indicators, one can say about a malfunction of either the red germ or the white germ. With a change in the red germ, a decrease or increase in the content of hemoglobin and the number of erythrocytes, a violation of the shape of erythrocytes, and a violation of hemoglobin synthesis are observed. Changes in the white germ are manifested by a decrease or increase in the content of leukocytes or platelets. But the analysis of peripheral blood is not always reliable and really reflects the pathological process.

The most complete picture of the state of the hematopoietic system is given by the study of bone marrow punctate (sternum) and trepanobiopsy (iliac crest). All blood diseases are divided into anemia, hemoblastosis, thrombocytopenia and thrombocytopathy.

Anemia is a group of diseases characterized by a decrease in the total amount of hemoglobin. In the peripheral blood, erythrocytes of various sizes (poikilocytosis), shapes (anisocytosis), varying degrees of color (hypochromia, hyperchromia), inclusions (basophilic grains, or Jolly bodies, basophilic rings, or Kabo rings) can appear in the peripheral blood.

And according to bone puncture, the form of anemia is judged by the state of erythropoiesis (hyper- or hyporegeneration) and by the type of erythropoiesis (erythroblastic, normoblastic and megaloblastic).

The reasons for the formation of anemia are different: blood loss, increased blood destruction, insufficient erythropoietic function.

Anemia classification

By etiology: posthemorrhagic, hemolytic and due to impaired blood formation. By the nature of the course: chronic and acute. In accordance with the state of the bone marrow: regenerative, hyporegenerative, hypoplastic, aplastic and dysplastic.

Anemia due to blood loss can be chronic and acute.

Deficiency anemia (due to impaired blood formation), resulting from a lack of iron (iron deficiency), vitamin B12 and folic acid (B12 deficiency anemia), hypo- and aplastic anemia. Iron deficiency anemia hypochromic. B12 deficiency anemia megaloblastic hyperchromic.

Hypo- and aplastic anemias are the result of a profound change in hematopoiesis, especially young elements of hematopoiesis. Oppression occurs up to the suppression of hematopoiesis. Hemolytic anemia occurs as a result of the predominance of blood destruction processes over blood formation. They are classified into anemia with intravascular extravascular hemolysis. Anemias with extravascular hemolysis are divided into erythrocytopathies, erythrocytofermentopathies and hemoglobinopathies.

29. Hemoblastosis. Thrombocytopathies

Hemoblastoses - tumors of the blood system - are divided into two large groups: leukemia (systemic tumor diseases of the hematopoietic tissue) and lymphomas (regional tumor diseases of the hematopoietic or lymphatic tissue).

Classification of tumors of hematopoietic and lymphatic tissue.

1. Leukemias (systemic tumor diseases of the hematopoietic tissue):

1) acute leukemia - undifferentiated, myeloblastic, lymphoblastic, plasmablastic, monoblastic, erythromyeloblastic and megakaryoblastic;

2) chronic leukemia:

a) myelocytic origin - myeloid, erythromyeloid leukemia, erythremia, polycythemia vera;

b) lymphocytic origin - lymphocytic leukemia, skin lymphomatosis, paraproteinemic leukemia, multiple myeloma, primary macroglobulinemia, heavy chain disease;

c) monocytic series - monocytic leukemia and hysteocytosis.

2. Lymphomas (regional tumor diseases of the hematopoietic or lymphatic tissue):

1) lymphosarcoma - lymphocytic, prolymphocytic, lymphoblastic, immunoblastic, lymphoplasmacytic, African;

2) fungal mycosis;

3) Cesari's disease;

4) reticulosarcoma;

5) lymphogranulomatosis (Hodgkin's disease).

Leukemia (leukemia) is a progressive overgrowth of leukemia cells. First, they grow in the hematopoietic organs, and then they are hematogenously thrown into other organs and tissues, causing leukemic infiltrates there.

Leukemia is a polyetiological disease, i.e. a number of factors favor its formation. There are three main ones: viruses, ionizing radiation and chemicals.

Lymphomas are regional neoplastic diseases of the hematopoietic and lymphatic tissue. Lymphosarcoma is a malignant tumor of the cells of the lymphocytic series. Mycosis fungoides is a relatively benign T-cell lymphoma of the skin. In case of Sezari's disease, atypical mononuclear cells with sickle-shaped nuclei - Sezari cells - are found in the tumor infiltrate of the skin, bone marrow and blood. Reticulosarcoma is a malignant tumor of reticular cells and histiocytes.

Lymphogranulomatosis is a primary neoplastic disease of the lymphatic system. The process occurs unicentrically, spread occurs with the help of metastasis.

Thrombocytopathies are a group of diseases and syndromes, which are based on a violation of hemostasis. They are divided into acquired and congenital thrombocytopathies (Chediak-Higashi syndrome, Glanzman's thrombasthenia).

Pathological anatomy: manifested as a hemorrhagic syndrome.

30. Endocarditis. Myocarditis. Heart disease, cardiosclerosis

Among the diseases of the cardiovascular system, the most important are: endocarditis, myocarditis, heart defects, cardiosclerosis, atherosclerosis, hypertension, coronary heart disease, cerebrovascular disease and vasculitis.

Endocarditis is an inflammation of the endocardium (the inner lining of the heart). There are primary (septic, fibroplastic) and secondary (infectious) endocarditis.

Pathological anatomy. The parietal endocardium of the ventricles of the heart becomes sharply thickened due to fibrosis, elastic fibers are replaced by collagen ones, and thrombotic masses appear on the surface of the endocardium.

Thrombosis and thromboembolic complications in the form of heart attacks and hemorrhages are characteristic.

Myocarditis - inflammation of the myocardium, i.e., the muscles of the heart. It can be secondary, due to exposure to viruses, bacteria, rickettsia, etc. As an independent disease, it manifests itself as idiopathic myocarditis, when the inflammatory process occurs only in the myocardium.

Pathological anatomy. The heart is enlarged, flabby, the cavities are distended. The muscles on the cut are motley, the valves are intact. There are 4 morphological forms:

1) dystrophic, or destructive, type;

2) inflammatory-infiltrative type;

3) mixed type;

4) vascular type.

In other organs, there is congestive plethora, degenerative changes in parenchymal elements, vascular thromboembolism, heart attacks and hemorrhages in the lungs, brain, kidneys, intestines, spleen, etc.

3. Heart disease is a persistent, irreversible disorder in the structure of the heart that impairs its function. There are acquired and congenital heart defects, compensated and decompensated. The defect can be isolated and combined.

Pathological anatomy. Mitral valve disease is manifested by insufficiency or stenosis, or a combination of both. With stenosis, vessels appear in the valve cusps, then the connective tissue of the cusps thickens, they turn into scars, sometimes calcify. Sclerosis and petrification of the fibrous ring are noted. With mitral valve insufficiency, compensatory hypertrophy of the left ventricular wall develops.

Aortic valve defect. Fusion of the valve leaflets with each other is noted, lime is deposited in the sclerotic leaflets, which leads to both narrowing and insufficiency. The heart is hypertrophied by the left ventricle. Defects of the tricuspid valve and pulmonary valve have the same pathological anatomical picture.

4. Cardiosclerosis - proliferation of connective tissue in the heart muscle. There are diffuse and focal (scar after myocardial infarction) cardiosclerosis. Pathologically, focal cardiosclerosis is represented by whitish stripes. Diffuse cardiosclerosis or myofibrosis is characterized by diffuse thickening and coarsening of the myocardial stroma due to the neoplasm of connective tissue in it.

31. Atherosclerosis

Atherosclerosis is a chronic disease resulting from a violation of fat and protein metabolism, characterized by damage to the arteries of the elastic and muscular-elastic type in the form of focal deposits in the intima of lipids and proteins and reactive growth of connective tissue.

Etiology. Metabolic (hypercholesterolemia), hormonal (in diabetes mellitus, hypothyroidism), hemodynamic (increased vascular permeability), nervous (stress), vascular (infection, injury) and hereditary factors.

Microscopy. Microscopically, the following types of atherosclerotic changes are distinguished.

1. Fat spots or stripes are areas of yellow or yellow-gray color that tend to merge. They do not rise above the surface of the intima and contain lipids (stained with Sudan).

2. Fibrous plaques are dense, oval or round, white or white-yellow formations containing lipids and rising above the surface of the intima. They merge with each other, have a bumpy appearance and narrow the vessel.

3. A complication of the lesion occurs when the disintegration of fat-protein complexes predominates in the thickness of the plaque and detritus (atheroma) is formed.

4. Calcification or atherocalcinosis is the final stage of atherosclerosis, which is characterized by the deposition of calcium salts into fibrous plaques, i.e., calcification.

Microscopic examination also determines the stages of atherosclerosis morphogenesis.

1. The prelipid stage is characterized by an increase in the permeability of intimal membranes and mucoid swelling; plasma proteins, fibrinogen, and glycosaminoglycans accumulate.

2. The lipoid stage is characterized by focal infiltration of the intima with lipids, lipoproteins, and proteins. All this accumulates in smooth muscle cells and macrophages, which are called foam or xanthoma cells.

3. Liposclerosis is characterized by the growth of young connective elements of the intima, followed by its maturation and the formation of a fibrous plaque, in which thin-walled vessels appear.

4. Atheromatosis is characterized by the breakdown of lipid masses, which look like a fine-grained amorphous mass with crystals of cholesterol and fatty acids. At the same time, existing vessels can also collapse, which leads to hemorrhage into the thickness of the plaque.

5. The stage of ulceration is characterized by the formation of an atheromatous ulcer. Its edges are undermined and uneven, the bottom is formed by the muscular, and sometimes by the outer layer of the vessel wall.

6. Atherocalcinosis is characterized by deposition of lime in atheromatous masses. Dense plates are formed - plaque covers.

Clinically and morphologically, there are: atherosclerosis of the aorta, coronary and cerebral vessels, atherosclerosis of the arteries of the kidneys, intestines and lower extremities. The outcome is ischemia, necrosis and sclerosis. And with atherosclerosis of the vessels of the intestines and lower extremities, gangrene can develop.

32. Hypertension, ischemic heart disease, cerebrovascular disease, vasculitis

Hypertension is a chronic disease, the main clinical sign of which is a persistent increase in blood pressure. Classification. By the nature of the course: malignant and benign hypertension. By etiology: primary and secondary hypertension. Clinical and morphological forms: cardiac, cerebral and renal. A number of factors take part in the development mechanism - nervous, reflex, hormonal, renal and hereditary.

Coronary heart disease (CHD) is a group of diseases caused by absolute or relative insufficiency of coronary blood flow.

The immediate causes are prolonged spasm, thrombosis, atherosclerotic occlusion, as well as psycho-emotional overstrain.

The pathogenetic factors of coronary disease are the same as in atherosclerosis and hypertension.

The course is undulating with short crises, against the background of chronic insufficiency of the coronary circulation.

Myocardial infarction is ischemic necrosis of the heart muscle.

Classification.

By the time of occurrence: acute (first hours), acute (2-3 weeks), subacute (3-8 weeks) and scarring stage.

By localization: in the basin of the anterior interventricular branch of the left coronary artery, in the basin of the circumflex branch of the left coronary artery and the main trunk of the left coronary artery.

According to the localization of the necrosis zone: anteroseptal, anteroapical, anterolateral, high anterior, widespread anterior, posterodiaphragmatic, posterobasal, posterolateral and widespread posterior.

By prevalence: small-focal, large-focal and transmural.

Downstream: necrotic stage and scarring stage. In the necrotic stage (histologically), the infarction is a zone of necrosis, in which islets of preserved myocardium are preserved perivascularly. The zone of necrosis is separated from healthy tissue by a demarcation line (leukocyte infiltration).

Cerebrovascular diseases are diseases that occur as a result of an acute violation of cerebral circulation. Distinguish between transient ischemic attack and stroke. Stroke can be hemorrhagic or ischemic. In transient ischemic attack, the changes are reversible.

Vasculitis is a disease characterized by inflammation and necrosis of the vascular wall. There are local (transition of the inflammatory process to the vascular wall from the surrounding tissues) and systemic vasculitis.

Classification.

According to the type of inflammatory reaction, they are divided into necrotic, destructive-productive and granulomatous. According to the depth of the lesion of the vascular wall, they are divided into endovasculitis, mesovasculitis and perivasculitis, and when combined, into endomesovasculitis and panvasculitis. By etiology: secondary and primary vasculitis.

33. Diseases of the respiratory system

Among respiratory diseases, acute bronchitis, acute inflammatory and destructive lung diseases, chronic nonspecific lung diseases, bronchial and lung cancer, and pleurisy are of the greatest importance.

Acute bronchitis is an acute inflammation of the bronchial tree. Etiology: viruses and bacteria. Predisposing factors are hypothermia, chemical factors and dust, as well as the general state of the immune system.

There are primary and secondary pneumonia (as complications of many diseases). Primary pneumonias are divided into interstitial, parenchymal and bronchopneumonia, secondary pneumonias are divided into aspiration, hypostatic, postoperative, septic and immunodeficiency. According to the prevalence of pneumonia, they are divided into miliary, acinous, lobular, confluent, segmental, polysegmental and lobar. By the nature of the inflammatory process, pneumonia can be serous, serous-leukocytic, serous-desquamative, serous-hemorrhagic, purulent, fibrinous and hemorrhagic.

Acute destructive processes in the lungs.

An abscess is a cavity filled with inflammatory exudate. A lung abscess can be pneumogenic in nature, then necrosis of the lung tissue and its purulent fusion first occur. The molten purulent-necrotic mass is excreted through the bronchi with sputum, a cavity is formed.

Pulmonary gangrene is characterized as a severe outcome of any inflammatory process in the lungs. The lung tissue undergoes wet necrosis, becomes grey-dirty and has a fetid odor.

Chronic nonspecific lung diseases.

The mechanism of their development is different. Bronchogenic - is a violation of the drainage function of the lungs and leads to a group of diseases called chronic obstructive pulmonary disease. The pneumogenic mechanism leads to chronic non-obstructive lung diseases. The pneumonitogenic mechanism leads to chronic interstitial lung disease.

Chronic bronchitis is a prolonged acute bronchitis. The microscopic picture is varied. The phenomena of chronic mucous or purulent catarrh with increasing atrophy of the mucous membrane, cystic transformation of the glands, metaplasia of the integumentary prismatic epithelium into stratified squamous epithelium, and an increase in the number of goblet cells predominate.

Bronchiectasis is an expansion of the bronchi in the form of a cylinder or bag, which can be congenital or acquired, single or multiple. In the wall of bronchiectasis, there are signs of chronic inflammation. Elastic and muscle fibers are replaced by connective tissue. The cavity is filled with pus. The lung tissue that surrounds the bronchiectasis is dramatically altered. Abscesses and fields of fibrosis appear in it. Sclerosis develops in the vessels. Cor pulmonale is formed.

Emphysema is a pathological condition characterized by excessive air content in the lungs and an increase in their size.

Bronchial asthma is a disease characterized by attacks of expiratory dyspnea, which occur as a result of impaired bronchial patency. The causes of this disease are allergens or infectious agents, or a combination of them.

34. Lung cancer

There is the following classification of lung cancer.

1. By localization:

1) radical (central), which comes from the stem, lobar and initial part of the segmental bronchus;

2) peripheral, coming from the peripheral section of the segmental bronchus and its branches, as well as from the alveolar epithelium;

3) mixed.

2. By the nature of growth:

1) exophytic (endobronchial);

2) endophytic (exobronchial and peribronchial).

3. By microscopic form:

1) plaque-like;

2) polyposis;

3) endobronchial diffuse;

4) knotty;

5) branched;

6) knotty-branched.

4. By microscopic appearance:

1) squamous (epidermoid);

2) adenocarcinoma, undifferentiated anaplastic cancer (small cell and large cell);

3) glandular squamous cell carcinoma;

4) carcinoma of the bronchial glands (adenoid-cystic and mucoepidermal).

Radical cancer develops in the mucous membrane of the stem, lobar and initial parts of the bronchial segment. Radical cancer often has a structure of a squamous type than other types. Peripheral cancer often has a glandular appearance and develops from the alveolar epithelium, so it is painless and is detected incidentally during routine examinations or when it moves to the pleura. Highly differentiated squamous cell epidermal carcinoma is characterized by the formation of keratin by many cells and the formation of cancerous pearls. Moderately differentiated cancer is characterized by mitosis and cell polymorphism. Poorly differentiated cancer is manifested by even greater cell polymorphism, a large number of mitoses, keratin is determined only in individual cells. In highly differentiated adenocarcinoma, cells in acinar, tubular, or papillary structures produce mucus. Moderately differentiated adenocarcinoma has a glandular-soloid structure, it contains a large number of mitoses. Poorly differentiated consists of solid structures, and its polygonal cells produce mucus. Undifferentiated anaplastic lung cancer can be small cell or large cell. Small cell carcinoma consists of small lymphoid or oat-shaped cells with a hyperchromic nucleus, the cells grow in sheets or strands. Large cell carcinoma is represented by large polymorphic and multinucleated cells that produce mucus. Glandular squamous cell lung cancer is a mixed cancer, as it is a combination of adenocarcinoma and squamous cell carcinoma.

35. Diseases of the stomach: gastritis, peptic ulcer

The most common are gastritis, peptic ulcer and cancer.

Gastritis is an inflammation of the lining of the stomach. There are acute and chronic gastritis. In acute gastritis, inflammation can cover the entire stomach (diffuse gastritis) or certain parts of it (focal gastritis). The latter is divided into fundic, antral, pyloroanthral and pilo-rhoduodenal gastritis. Depending on the characteristics of morphological changes in the gastric mucosa, the following forms of acute gastritis are distinguished:

1) catarrhal, or simple;

2) fibrinous;

3) purulent (phlegmous);

4) necrotic.

Chronic gastritis can be autoimmune (type A gastritis) or non-immune (type B gastritis). With autoimmune gastritis, the formation of antibodies to parietal cells occurs, so the fundus is more often affected. In connection with the defeat of the parietal cells, the production of hydrochloric acid is reduced. With non-immune gastritis, the antrum is affected and the production of hydrochloric acid is moderately reduced. Topographically, antral, fundal and pangastritis are distinguished. Chronic gastritis is characterized by long-term dystrophic and necrobiotic changes in the epithelium of the mucous membrane, as a result of which there is a violation of its regeneration and structural restructuring of the mucous membrane.

Peptic ulcer is a chronic relapsing disease, morphologically expressed by the formation of gastric or duodenal ulcers. According to localization, ulcers located in the pyloroduodenal zone or the body of the stomach are distinguished, although there are also combined forms.

The reasons for the formation of ulcers are different: the infectious process, allergic, toxic and stress factors, drug and endocrine factors, as well as postoperative complications (peptic ulcers). It is important to note the presence of predisposing factors - this is senile age, male sex, first blood type, etc.

During the formation of an ulcer, an important role is played by erosion, which is a defect in the mucous membrane that does not penetrate beyond the muscle layer. Erosion is formed as a result of necrosis of the mucous membrane area, followed by hemorrhage and rejection of dead tissue.

An acute ulcer has an irregular round or oval shape and resembles a funnel. As the necrotic masses are cleared, the bottom of the acute ulcer, represented by the muscular layer, is revealed. The bottom is painted (due to hematin) in a dirty gray or black color.

There is a period of remission and exacerbation. During the period of remission, there is scar tissue at the edges of the ulcer, the mucous membrane along the edges is thickened and hyperemic. During the period of exacerbation, a wide zone of fibrinoid necrosis appears in the area of the bottom and edges of the ulcer. Fibrinous-purulent or purulent exudate is located on the surface of necrotic masses.

36. Stomach cancer

There is the following classification of stomach cancer.

1. By localization, they distinguish: pyloric, less curvature of the body with a transition to the walls, cardiac, greater curvature, fundic and total.

2. According to the nature of growth, three forms are distinguished:

1) with predominantly exophytic growth (plaque-like, polypous, fungous, or mushroom-like, and ulcerated);

2) with predominantly endophytic infiltrating growth (infiltrative-ulcerative, diffuse);

3) with exoendophytic growth, or mixed.

3. Adenocarcinoma (tubular, papillary, mucinous), undifferentiated (solid, scirrhous, parietal), squamous, glandular-squamous (adenocancroid) and unclassified cancer are isolated microscopically.

Pathological anatomy. Plaque cancer affects the submucosal layer. Polyposis cancer is gray-pink or gray-red in color and rich in blood vessels. These two forms of cancer histologically have the structure of adenocarcinoma or undifferentiated cancer. Fungal cancer is a nodular formation with erosions on the surface, as well as hemorrhages or fibrinous-purulent overlays. The swelling is soft, grey-pink or grey-red, and well circumscribed; Histologically, it appears to be adenocarcinoma. Ulcerated cancer by genesis is a malignant tumor, it is represented by primary ulcerative, saucer-shaped cancer from a chronic ulcer (ulcer-cancer). Primary ulcerative cancer is microscopically represented by undifferentiated cancer. Saucer cancer is a round formation, reaching a large size, with roller-shaped whitish edges and ulceration in the center. The bottom of the ulcer can be represented by other (adjacent) organs. Histologically it is represented by adenocarcinoma. Ulcer-cancer is characterized by the formation of an ulcer at the site and is manifested by the growth of scar tissue, sclerosis and thrombosis of blood vessels, destruction of the muscle layer at the bottom of the ulcer and thickening of the mucous membrane around the ulcer. Histologically, it looks like adenocarcinoma, less often undifferentiated cancer. Infiltrative-ulcerative carcinoma is characterized by severe cancrotic infiltration of the wall and ulceration of the tumor, and histologically it is represented by adenocarcinoma or undifferentiated cancer. Diffuse cancer is manifested by thickening of the stomach wall, the tumor is dense, whitish and immobile.

The mucous membrane has an uneven surface, and folds of uneven thickness with erosions. Defeats can be limited and total. As the tumor grows, the stomach wall shrinks. Histologically, the cancer is an undifferentiated form of carcinoma. Transitional forms have different clinical and morphological forms.

37. Enteritis. Enteropathy

Enteritis, or inflammation of the small intestine: according to localization, inflammation of the duodenum (duodenitis), jejunum (eunit) and ileum (ileitis) are distinguished. Enteritis can be chronic and acute. Acute enteritis histologically can be catarrhal, fibrinous, purulent and necrotic-ulcerative. With catarrhal enteritis, the mucous membrane is plethoric, edematous, covered with serous, serous-mucous or serous-purulent exudate. The inflammatory process also covers the submucosal layer. The epithelium undergoes dystrophy and desquamation, goblet cells are hyperplastic, minor erosions and hemorrhages are noted. With fibrous enteritis, the mucous membrane is necrotic and permeated with fibrinous exudate, gray or gray-brown overlays on the surface.

Depending on the depth of necrosis, inflammation can be croupous and diphtheritic, with rejection of the latter, deep ulcers form. With purulent enteritis, the walls of the intestine are saturated with pus or pustules are formed. With any type of process, hyperplasia and reticulomacrophage transformation of the lymphatic apparatus of the intestine develop. In chronic enteritis, two forms are distinguished - without atrophy of the mucous membrane and atrophic enteritis. For enteritis without atrophy of the mucous membrane, uneven thickness of the villi and the appearance of club-shaped thickenings of their distal parts are characteristic. The cytoplasm of villi enterocytes is vacuolated. Adhesions appear between the enterocytes of the apical parts of the adjacent villi, the stroma of the villi is infiltrated with plasma cells, lymphocytes, and eosinophils. A cellular infiltrate descends from the crypt, which may be cystically dilated. The infiltrate pushes the crypts apart and reaches the muscular layer of the mucous membrane.

Enteropathy is a chronic disease of the small intestine, which is based on hereditary and acquired enzymatic disorders of enterocytes.

Enteropathies include:

1) disaccharidosis deficiency;

2) hypercatabolic hypoproteinemic enteropathy;

3) gluten enteropathy.

Pathological anatomy. There are various degrees of severity of dystrophic and atrophic changes. The villi shorten and thicken, the number of enterocytes decreases, they vacuolize and lose microvilli. The crypts deepen and the membrane thickens, and the mucosa is infiltrated by plasma cells, lymphocytes, and macrophages. In later periods, the villi are absent, and there is a sharp sclerosis of the mucous membrane. With hypercatabolic hypoproteinemic enteropathy (in combination with the above pathological anatomical picture), there is a sharp expansion of the lymphatic capillaries and vessels of the intestinal wall. Histoenzymatic study of biopsy specimens of the intestinal mucosa makes it possible to determine enzymatic disorders for a certain type of enteropathy.

38. Colitis

Colitis is an inflammation of the large intestine. With the defeat of the predominantly blind section, they speak of typhlitis, the transverse colon section - about transverse, the sigmoid - about sigmoiditis and the rectum - about proctitis. Inflammation of the entire colon is called pancolitis. Inflammation can be chronic or acute.

Acute colitis has 7 forms. Catarrhal colitis is manifested by hyperemia and swelling of the mucous membrane, and on its surface there is a serous, mucous or purulent exudate. Fibrinous colitis, depending on the depth of necrosis of the mucous membrane and the penetration of fibrinous exudate, can be croupous and diphtheritic.

Purulent colitis is characterized by phlegmonous inflammation. With hemorrhagic colitis, multiple hemorrhages occur in the intestinal wall, and it is saturated with blood. With necrotizing colitis, not only the mucous layer, but also the submucosal layer undergoes necrosis. Gangrenous colitis is a variant of necrotizing colitis. With ulcerative colitis, ulcers form in the intestinal mucosa, and, as a result, dystrophic or necrotic changes in the intestinal wall occur. Chronic colitis is without atrophy of the mucous membrane and atrophic. In chronic colitis without atrophy of the mucous membrane, the latter is edematous, dull, granular, gray-red or red, with multiple hemorrhages and erosions. The prismatic epithelium undergoes desquamation and thickening. The number of goblet cells in the crypts increases, and the crypts are shortened, with an enlarged lumen.

The mucous membrane is infiltrated with lymphocytes, plasma cells, eosinophils, with the presence of hemorrhages.

The degree of infiltration can be moderate to severe diffuse. In chronic atrophic colitis, the prismatic epithelium thickens, the number of crypts decreases, and smooth muscle elements are hyperplastic. In the mucous membrane, histiolimphocytic infiltration and proliferation of connective tissue predominate.

Nonspecific ulcerative colitis is a chronic relapsing disease that is manifested by inflammation of the colon with suppuration, ulceration, hemorrhages and outcome in sclerotic deformation of the wall. This is an allergic disease characterized by autoimmune aggression. Localized in the rectum, sigmoid or transverse colon. Sometimes the pathological process is localized throughout the colon. Morphologically, acute and chronic forms of nonspecific ulcerative colitis are distinguished. In the acute form, the intestinal wall is edematous, hyperemic, with multiple erosions and irregularly shaped superficial ulcers. Sometimes ulcers can penetrate deep into the muscle layer. In the chronic form, a sharp deformation of the intestine is noted - it becomes shorter, thickens and thickens. The intestinal lumen narrows. Reparative-sclerotic processes prevail. Ulcers granulate and scar, epithelialize incompletely. Pseudopolyps are formed. In the vessels there is a productive endovasculitis, the walls are sclerosed.

Inflammation is productive and manifests itself in the form of infiltration of the intestinal wall with lymphocytes, histiocytes, and plasma cells.

39. Diseases of the biliary system

Hepatosis is a liver disease characterized by dystrophy and necrosis of hepatocytes. May be hereditary or acquired. Toxic liver dystrophy develops as a result of a viral infection, allergies and intoxication. Microscopically, in the first days, fatty degeneration of hepatocytes of the centers of the lobules is noted, which is quickly replaced by their necrosis. As a result, postnecrotic cirrhosis of the liver occurs.

Fatty liver is a chronic disease characterized by increased accumulation of fat in hepatocytes. The reason is metabolic and endocrine disorders. In this case, the liver is large, yellow or red-brown, its surface is smooth. Fat is determined in hepatocytes. In terms of prevalence, disseminated obesity is distinguished (single hepatocytes are affected), zonal (groups of hepatocytes) and diffuse obesity. Obesity of hepatocytes can be dusty, small- and large-drop. There are three stages of fatty hepatosis - simple obesity, obesity in combination with necrobiosis of hepatocytes and mesenchymal cell reaction, and obesity with the beginning restructuring of the lobular structure of the liver.

Cirrhosis of the liver is a chronic disease characterized by structural changes in the liver and scarring. The main pathological processes in cirrhosis are dystrophy and necrosis of hepatocytes, perverted regeneration, diffuse sclerosis, as well as structural restructuring and deformation of the organ. The liver becomes dense, tuberous, as a rule, reduced in size, rarely enlarged. Macroscopically, there are types of cirrhosis: incomplete septal, small-nodular, large-nodular and mixed. Microscopically, monolobular (captures one hepatic lobule), multilobular (captures several hepatic lobules) and monomultilobular cirrhosis are isolated. Hydropic or balloon dystrophy and necrosis occur in hepatocytes. All of the above pathological processes are irreversible, which leads to the constant progression of liver failure and, consequently, to the death of the patient.

The most common disease is cholecystitis, which can be acute or chronic. In acute cholecystitis, catarrhal, fibrinous or purulent inflammation develops. It can be complicated by perforation of the bladder wall and biliary peritonitis.

Gallbladder cancer develops against the background of calculous cholecystitis and is localized in the neck or bottom of the bladder. Cancer usually has the structure of adenocarcinoma.

Diseases of the pancreas are represented by inflammatory and oncological processes.

Pancreatitis is an inflammation of the pancreas. Acute and chronic pancreatitis are distinguished along the course.

Pancreatic cancer can develop in any part of the pancreas, but more often in the head of the pancreas. Cancer develops from the epithelium of the ducts (adenocarcinoma) or from the acini of the parenchyma (acinar or alveolar cancer). The tumor has the appearance of a gray-white node. The death of the patient comes from metastases.

40. Hepatitis

Hepatitis is an inflammation of the liver. According to the etiology, primary and secondary hepatitis are distinguished. Downstream - acute and chronic hepatitis. Primary hepatitis develops as a result of a hepatotropic virus, alcohol or drugs. Secondary hepatitis is the result of another disease, such as infection (yellow fever, typhoid fever, dysentery, malaria, sepsis, tuberculosis), intoxication (thyrotoxicosis, hepatotoxic poisons), lesions of the gastrointestinal tract, systemic connective tissue diseases, etc.

Viral hepatitis occurs as a result of damage to the liver by a virus. There are viruses: A (HAV), B (HBV), C (HCV), D (HDV), E (HEV). Viruses B and C are currently the most common. The following clinical and morphological forms of viral hepatitis are distinguished: acute cyclic (icteric), anicteric, necrotic (fulminant, malignant), cholestatic and chronic. In acute cyclic form, the stage of the peak of the disease and the stage of recovery are distinguished.

In the stage of peak, the beam structure of the liver is disturbed, and a pronounced polymorphism of hepatocytes is observed. Hydropic and balloon dystrophy of hepatocytes predominates, focal and confluent necrosis of hepatocytes are found in various parts of the lobules. In the recovery stage, the liver takes on normal dimensions, hyperemia decreases, the liver capsule is somewhat thickened, dull, and there are small adhesions between the capsule and the peritoneum. Necrotic hepatitis is characterized by progressive necrosis of the liver parenchyma. The liver is reduced in size, becomes wrinkled and turns gray-brown or yellow.

The cholestatic form of hepatitis is based on intrahepatic cholestasis and inflammation of the bile ducts. Microscopically, signs of cholestasis predominate. The bile capillaries and ducts are filled with bile, the bile pigment accumulates in hepatocytes and in stellate reticuloendotheliocytes.

The chronic form of hepatitis is represented by active and persistent hepatitis.

In chronic active hepatitis, dystrophy and necrosis of hepatocytes develop. Cellular infiltration of the portal, periportal and intraportal sclerotic stroma of the liver is characteristic.

Chronic persistent cholangitis is characterized by infiltration of lymphocytes, histiocytes, and plasma cells into sclerotic portal fields. Star-shaped reticuloendotheliocytes are hyperplastic, there are foci of necrosis of the reticular stroma. The structure of the hepatic lobules and the border plate is preserved. Dystrophic processes are minimally expressed. Hepatocyte necrosis is rare. Death in viral hepatitis occurs due to acute or chronic liver failure. Alcoholic hepatitis occurs due to alcohol intoxication. In the acute form of alcoholic hepatitis, the liver is dense and pale, with reddish areas. Hepatocytes are necrotic, infiltrated with neutrophils, and a large amount of alcoholic hyaline (Mallory bodies) appears in them.

41. Glomerulopathies. Glomerulonephritis

Glomerulonephritis is an infectious-allergic or unidentified disease, which is based on bilateral diffuse or focal non-purulent inflammation of the glomerular apparatus of the kidneys with the presence of renal and extrarenal manifestations. Renal symptoms include oliguria, proteinuria, hematuria, cylindruria, and extrarenal symptoms include arterial hypertension, left ventricular and atrial hypertrophy, dysproteinemia, edema, hyperazotemia, and uremia.

Classification.

1. By etiology, glomerulonephritis of established etiology (viruses, bacteria, protozoa) and unknown etiology are distinguished.

2. According to nosology, primary, as an independent disease, and secondary glomerulonephritis (as a manifestation of another disease) are distinguished.

3. According to the pathogenesis, glomerulonephritis can be immunologically conditioned and immunologically unconditioned.

4. Downstream - acute, subacute and chronic.

5. Topographically distinguish intracapillary (pathological process is localized in the vascular glomerulus) and extracapillary (pathological process in the glomerular capsule) glomerulonephritis.

6. By the nature of inflammation - exudative, proliferative and mixed.

7. By prevalence - diffuse and focal glomerulonephritis.

In acute glomerulonephritis, the kidneys are enlarged, swollen, the pyramids are dark red, the bark is grayish-brown in color with small red specks on the surface and incision, or with grayish translucent dots (variegated kidney).

In the chronic course of glomerulonephritis, the kidneys are wrinkled, reduced in size, dense with a fine-grained surface. On the section, the layer of renal tissue is thin, the tissue is dry, anemic, gray in color. There are mesangial and fibroplastic types. Mesangial glomerulonephritis develops as a result of the proliferation of mesangiocytes in response to deposits under the epithelium and in the mesangium of immune complexes. Fibroplastic glomerulonephritis is characterized by sclerosis and hyalinosis of capillary loops and the formation of adhesions in the capsule cavity.

The outcome of chronic glomerulonephritis is unfavorable. The pathological process leads to renal failure, which is manifested by azotemia uremia.

The nephrotic syndrome is characterized by proteinuria, dysproteinemia, hypoproteinemia, hyperlipidemia, and edema. There are primary (idiopathic) nephrotic syndrome and secondary - as a manifestation of renal disease.

Primary nephrotic syndrome can be manifested by three diseases:

1) lipoid nephrosis;

2) membranous nephropathy;

3) focal segmental sclerosis.

42. Kidney amyloidosis. Acute renal failure

Renal amyloidosis, as a rule, is a secondary disease (with rheumatoid arthritis, tuberculosis, bronchiectasis, etc.), and in congenital pathology it is primary.

In the course of amyloidosis, latent, proteinuric, nephrotic and azotemic stages are distinguished.

In the latent stage, the kidneys are not macroscopically changed. The glomerular membrane is thickened and double-circuited, the lumens of the aneurysm are dilated. The cytoplasm of the epithelium of the tubules is impregnated with protein granules. In the intermedial zone and pyramids, the stroma is impregnated with plasma proteins.

In the proteinuric stage, amyloid appears not only in the pyramids, but also in the glomeruli. It is deposited in mesangium and capillary loops, as well as in arterioles. The epithelium of the tubules is subject to hyaline-droplet or hydropic dystrophy, and cylinders are found in their lumen.

In the nephrotic stage, the amount of amyloid increases, localizes in capillary loops, arterioles and arteries, along the tubular membrane. In the pyramids and the intermedial zone sclerosis; amyloidosis increases and is diffuse. The tubules are dilated and clogged with cylinders.

In the azotemic stage, an increase in the growth of amyloid and sclerotic processes is noted, which increases the number of dying nephrons.

Acute renal failure is a syndrome that occurs due to necrosis of the epithelium of the tubules and deep disorders of blood and lymph circulation. In the development of this pathology, two main reasons are distinguished - intoxication and infection. Pathologically, there are 3 stages.

1. The initial shock stage is characterized by venous plethora of the intermedial zone and pyramids with focal ischemia of the cortical layer (collapsed capillaries). The epithelium of the tubules of the main departments is subject to hyaline droplet, hydropic or fatty degeneration. The lumens of the tubules are unevenly dilated, contain cylinders, and sometimes myoglobin crystals.

2. The oligoanuric stage is characterized by pronounced necrotic processes in the tubules of the main departments. The basement membrane of the distal tubules undergoes destruction (tubulorhexis). Edema of the interstitium increases, and leukocyte infiltration and hemorrhage join it. The cylinders overlap the nephron.

3. The stage of recovery of diuresis is characterized by a decrease in edema of infiltration of the kidney, and many glomeruli become full-blooded. Foci of sclerosis are formed.

The macroscopic picture of the kidneys in all stages is the same. The kidneys are enlarged, swollen, edematous, the fibrous capsule is tense and easily removed.

The cortical layer is wide, pale gray in color and sharply demarcated from the dark red pyramids; hemorrhages are noted in the pelvis. The outcome is different: both recovery and death are possible.

43. Interstitial nephritis

There are the following types of interstitial nephritis.

1. Tubulo-interstitial nephritis is a pathological process characterized by immuno-inflammatory lesions of the interstitium and renal tubules. The reasons are varied: intoxication, infection, metabolic disorders, immunological and sensitizing processes, oncology and hereditary pathology. There are primary and secondary tubulo-interstitial nephritis (with Goodpasture's syndrome, kidney rejection reactions).

In acute tubulo-interstitial nephritis, edema and infiltration of the interstitium of the kidneys occur. Depending on the cells that infiltrate, lymphohistiocytic (lymphocytes and macrophages), plasmacytic (plasmocytes and plasmablasts), eosinophilic (eosinophils) and granulomatous (granulomas) variants are isolated. The cellular infiltrate spreads perivascularly, destroying nephrocytes.

In chronic tubulo-interstitial nephritis, lymphohistiocytic infiltration of the stroma is combined with sclerosis, and degeneration of nephrocytes - with their regeneration. Among the cells of the infiltrate, lymphocytes and macrophages predominate, and the basement membrane is thickened. The outcome is nephrosclerosis.

2. Pyelonephritis is an infectious disease characterized by damage to the renal pelvis, calyces and kidney substance, with a predominant lesion of the interstitial tissue. Pyelonephritis can be acute and chronic.

In acute pyelonephritis, the kidney is macroscopically enlarged, the tissue is swollen, full-blooded, the capsule is easily removed. The cavities of the pelvis and calyces are enlarged, filled with cloudy urine or pus, their mucous membrane is dull, with foci of hemorrhages. On the section, the renal tissue is variegated, with the presence of yellow-gray areas surrounded by a zone of plethora and hemorrhage.

Microscopically revealed plethora and leukocyte infiltration of the pelvis and calyx, foci of necrosis of the mucous membrane. The interstitial tissue is edematous and infiltrated with leukocytes. The tubules are prone to dystrophy, and their lumens are clogged with cylinders. The process is either focal or diffuse.

In chronic pyelonephritis, the processes of sclerosis are combined with exudative-necrotic ones: the calyces and pelvis are sclerosed, the mucous membrane is polyposis, the transitional epithelium is replaced by a multilayer one.

In the kidney tissue, chronic intermediate inflammation with proliferation of connective tissue is expressed. The tubules are dystrophic and atrophied, and the remaining tubules are sharply stretched, their epithelium is flattened, the lumen is filled with colloid-like contents.

Arteries and veins are sclerotic. With a long course, a pyelonephritic wrinkled kidney develops.

44. Kidney stone disease, polycystosis, nephrosclerosis, kidney tumors

Kidney stone disease (nephrolithiasis) is a disease characterized by the formation of stones in the renal calyces, pelvis and ureters. The process is chronic.

As a result of violation of the outflow of urine, pyeloectasia and hydronephrosis occur with atrophy of the renal parenchyma. The pelvis and ureter are dilated, inflammation joins, which leads to pyelonephritis up to the melting of the parenchyma. After the inflammatory process, the parenchyma is sclerosed or completely replaced by sclerotic adipose tissue (fat replacement of the kidney). At the site of obturation with a stone, a bedsore with perforation of the ureter can form.

Polycystic kidney disease is an inherited kidney disease with bilateral cystic parenchyma. As a rule, this is a long-term disease that is asymptomatic. Early manifestations of this disease indicate a malignant course.

The kidneys in this disease resemble bunches of grapes, the tissue of which consists of many cysts of various sizes and shapes, filled with serous fluid, colloidal masses or semi-liquid chocolate-colored contents. The cysts are lined with cuboidal epithelium. Sometimes a wrinkled vascular glomerulus is located in the wall of the cyst. The renal tissue between the cysts is atrophied. The outcome is unfavorable - patients die of renal failure.

Nephrosclerosis is a flattening and deformation of the kidneys due to the growth of connective tissue. Macroscopically, the kidneys are dense, the surface is large- and small-hilly. Kidney tissue undergoes structural restructuring due to the growth of connective tissue. The kidney shrinks.

A manifestation of nephrosclerosis is chronic renal failure. A striking clinical sign of chronic renal failure is uremia. In this case, autointoxication occurs, all organs are affected by urea, primarily organs and systems that perform the excretory function of the body (skin, lungs, gastrointestinal tract). At the same time, metabolic damage (myocardial necrosis), productive inflammation (adhesive pericarditis, obliteration of the cavity of the heart shirt), changes in bones (osteoporosis, osteosclerosis, amyloidosis) and the endocrine system (parathyroid hyperplasia) dominate.

Kidney tumors are classified as follows.

1. Epithelial tumors:

1) adenoma (dark cell, clear cell and acidophilic);

2) renal cell carcinoma (clear cell, granular cell, glandular, sarcomatoid, mixed cell);

3) nephroblastoma or Wilms tumor.

2. Mesenchymal tumors are formed from connective and muscle tissue, from blood and lymphatic vessels, they are benign and malignant.

3. Tumors of the renal pelvis:

1) benign (transitional papilloma);

2) cancer of the pelvis (transitional cell, squamous and glandular).

45. Diseases of the genital organs and mammary gland

Diseases of the genital organs and the mammary gland are divided into dyshormonal, inflammatory and tumor.

Dishormonal diseases. These include nodular hyperplasia and prostate adenoma, glandular hyperplasia of the uterine mucosa, endocervicosis, adenomatosis and cervical polyps, benign breast dysplasia.

Nodular hyperplasia and prostate adenoma according to the histological type are divided into 3 forms:

1) glandular hyperplasia;

2) muscular-fibrous (stromal) hyperplasia;

3) mixed form.

Glandular hyperplasia of the uterine mucosa develops as a result of hormonal imbalance and the intake of an excess amount of folliculin or progesterone into the body.

Endocervicosis is an accumulation of glands in the thickness of the vaginal part of the cervix with altered epithelium; distinguish:

1) proliferating endocervicosis;

2) simple endocervicosis;

3) healing endocervicosis.

Adenomatosis of the cervix is a collection of glandular formations under the integumentary epithelium of the vaginal part of the uterus, lined with a single layer of cubic epithelium.

Benign dysplasia of the mammary gland is characterized by impaired differentiation of the epithelium and its atypia and impaired histological structures; differ:

1) non-proliferative form;

2) roliferative form.

Against the background of the above pathological processes, cancer can develop, so they are considered precancerous conditions.

Inflammatory diseases of the genital organs and mammary gland are classified as follows.

1. Endometritis - inflammation of the uterine mucosa.

2. Mastitis - inflammation of the mammary gland.

3. Orchitis - inflammation of the testicle.

4. Prostatitis - inflammation of the prostate gland. Tumors of the genital organs and mammary glands.

Tumors are as follows.

1. Uterine cancer is topographically divided into cancer of the cervix and body of the uterus. Cervical cancer can be non-invasive and invasive. There are cancers in the vaginal part of the cervix (grows exophytically and ulcerates early) and cancer of the cervical canal (has endophytic growth).

2. Testicular cancer is a consequence of malignancy of epithelial serous or mucinous tumors and looks like a tuberous node of various sizes.

3. Breast cancer is microscopically represented by nodular and diffuse forms, as well as cancer of the nipple and nipple field (Paget's cancer).

4. Prostate cancer.

46. Pituitary and adrenal disorders

The human endocrine system consists of two systems - the peripheral endocrine system and the hypothalamic-pituitary system. They are closely related and able to regulate each other. Diseases of the endocrine system can be congenital or acquired.

They manifest as hypofunction, hyperfunction and dysfunction. Structural reorganization manifests itself in the form of dystrophy, atrophy or dysplasia.

Pituitary disorders are as follows.

1. Acromegaly occurs as a result of an excess of growth hormone. It is manifested by stimulation of the growth of connective, cartilaginous and bone tissue, as well as the parenchyma and stroma of internal organs (heart, kidneys, liver). The cause is adenocarcinoma of the anterior pituitary gland.

2. Pituitary dwarfism develops with congenital underdevelopment of the pituitary gland or in violation of its tissue in childhood. It is manifested by general underdevelopment with preserved proportionality. The reproductive organs are underdeveloped.

3. Cerebro-pituitary cachexia manifests itself in increasing cachexia, atrophy of internal organs and a decrease in the function of the genital organs. Microscopically, in the anterior lobe of the pituitary gland, foci of necrosis or scars are localized in their place. In the diencephalon, dystrophic or inflammatory changes are noted. Sometimes brain changes predominate over pituitary ones.

4. Itsenko-Cushing's disease occurs due to hypersecretion of adrenocorticotropic hormone.

There is a bilateral hyperplasia of the adrenal cortex with excessive production of glucocorticosteroids. Clinically manifested by obesity (mainly male type).

Adiposogenital dystrophy is characterized by pathological changes in the pituitary and hypothalamus, which develop as a result of a tumor or neuroinfection. It is manifested by progressive obesity, underdevelopment and a decrease in the function of the genital organs.

Diabetes insipidus occurs when the posterior pituitary gland and diencephalon are affected. The antidiuretic hormone is turned off and, as a result, the concentration furcation of the kidneys is disturbed. It is clinically manifested by thirst (polydipsia) and diabetes (polydipsia).

Adrenal disorders.

Addison's disease or bronze disease. The disease is characterized by damage mainly to the adrenal cortex, while the production of glucocorticosteroids and sex hormones decreases or completely stops. Causes: metastases, autoimmune lesions, amyloidosis, hemorrhages, tuberculosis, disorders of the hypothalamic-pituitary system. There are hyperpigmentation of the skin and mucous membranes, myocardial atrophy, a decrease in the lumen of the aorta and great vessels. Islet cells of the pancreas are hyperplastic, the gastric mucosa is atrophied. Lymphoid tissue and thymus gland are hyperplastic.

47. Diseases of the thyroid gland

Goiter (struma) is an enlargement of the thyroid gland. Morphologically, goiter is divided into:

1) diffuse;

2) nodal;

3) diffuse-nodular. Histologically different:

1) colloid goiter;

2) parenchymal goiter.

Colloidal goiter is histologically represented by follicles of various sizes, which are filled with colloid. The epithelium can grow in the form of papillae.

There is a circulatory disorder in the gland, foci of necrosis and calcification are formed, the connective tissue grows. On cut, the goiter is nodular and dense.

Parenchymal goiter is characterized by proliferation of the epithelium of the follicles. The epithelium grows in the form of solid structures with the formation of small follicle-like formations without colloid or with a small amount of it. The process is diffuse in nature and looks like a homogeneous fleshy tissue of a gray-pink color.

Clinically distinguish:

1) endemic goiter;

2) sporadic goiter;

3) diffuse toxic goiter. Endemic goiter develops as a result of a lack of iodine in the water. In this case, the thyroid gland increases significantly in size, and can be colloidal or parenchymal in structure. The function of the gland is reduced.

Sporadic goiter is histologically and morphologically diverse. The gland increases in size, does not suffer functionally, and can compress organs. In rare cases, moderate papillary proliferation of the epithelium of the follicles and the accumulation of infiltrates in the stroma of the gland are possible.

Diffuse toxic (thyrotoxic) goiter. The reason is the production of autoantibodies to thyrocyte receptors. Morphologically, the degeneration of the prismatic epithelium of the follicles into a cylindrical one is noted, the epithelium undergoes proliferation with the formation of papillae, the stroma is lymphocytally infiltrated, the colloid changes its properties and poorly perceives dyes.

The myocardium is hypertrophied, its interstitial tissue is edematous and lymphoid infiltrated, further developing interstitial sclerosis. In the liver, serous edema occurs with a transition to fibrosis. Nerve cells are dystrophically changed. The adrenal cortex atrophies. Lymphoid tissue is hyperplastic.

Thyroiditis.

Thyroiditis is a true autoimmune disease. Microscopically, diffuse infiltration of the gland tissue by lymphocytes and plasma cells with the formation of lymphoid follicles is noted. The parenchyma of the gland is replaced by connective tissue.

48. Diabetes

Diabetes mellitus is a disease caused by relative or absolute insufficiency of insulin.

Classification:

1) spontaneous diabetes (insulin-dependent type 1 and insulin-independent type 2);

2) gestational diabetes;

3) secondary diabetes;

4) latent diabetes.

Risk factors for etiology and pathogenesis include:

1) genetically determined disorders in the function and number of b-cells (decrease in insulin synthesis, impaired conversion of preinsulin to insulin, abnormal insulin synthesis);

2) environmental factors, violation of the integrity and functioning of b-cells (viruses, autoimmune diseases, obesity, increased activity of the adrenergic nervous system).

Insulin deficiency disrupts glycogen synthesis, increases blood sugar (hyperglycemia), and sugar appears in the urine (glucosuria). Due to neo-glycogenesis, glucose synthesis occurs, which leads to hyperlipidemia, acetonemia and ketonemia. All of these substances lead to acidosis. Vessels are affected and diabetic microangiopathies and macroangiopathies occur.

Pathological anatomy. First of all, the islets of the pancreas are affected, changes occur in the liver, vascular bed and kidneys. The pancreas is reduced in size, its lipomatosis and sclerosis occur. Most islets undergo atrophy and hyalinosis, while other islets hypertrophy compensatory. The liver is enlarged and the liver cells become fatty. Diabetic macroangiopathy is manifested by atherosclerosis of elastic and muscular arteries. In diabetic microangiopathy, the basement membrane of the microcirculatory bed undergoes plasmorrhagic impregnation, and later sclerosis and hyalinosis. In this case, lipogyalin appears. This process is generalized. The kidneys in diabetes are affected in the form of diabetic glomerulonephritis and glomerulosclerosis. There is a proliferation of mesangial cells, in which the formation of a membrane-like substance is enhanced, which leads to hyalinosis of the mesanglion and death of the glomeruli. The process can be diffuse, nodular and mixed. An exudative manifestation of diabetic nephropathy is possible, while fibrin caps are formed on the capillary loops of the glomeruli, the epithelium of the nodal segment of the nephron changes, it becomes high with a light translucent membrane in which glycogen is detected. Death in diabetes occurs as a result of gangrene of the extremities, myocardial infarction, uremia, and rarely from diabetic coma.

49. Diseases of the central nervous system

Diseases of the central nervous system are divided into:

1) dystrophic (degenerative) diseases characterized by a predominance of damage to neurons of various localizations;

2) demyelinating diseases, characterized by a primary lesion of the myelin sheaths (primary demyelination) or axons (secondary demyelination);

3) inflammatory diseases are divided into meningitis, encephalitis and meningoencephalitis.

Alzheimer's disease is clinically manifested by severe intellectual disorders and emotional lability, while focal neurological symptoms are absent. Morphologically characterized by atrophy of the brain, mainly - frontal, temporal and occipital regions. Hydrocephalus may develop.

Amyotrophic lateral sclerosis (Charcot's disease) is a progressive disease of the central nervous system, which is characterized by simultaneous damage to the motor neurons of the anterior and lateral columns of the spinal cord and peripheral nerves. It is clinically manifested by the development of spastic paresis of the muscles of the hands with further attachment of muscle atrophy, increased tendon and periosteal reflexes. The reason is unknown.

Multiple sclerosis (multiple sclerosis) is a chronic progressive disease characterized by the formation of scattered foci of demyelination in the brain and spinal cord, in which glia grows with the formation of foci of sclerosis (plaques). The cause of the disease is unknown, although a viral etiology is suspected. Externally, the superficial sections of the brain and spinal cord are little changed. Sometimes there may be swelling and thickening of the meninges.

Encephalitis is inflammation of the brain associated with infection, intoxication, or trauma. Infectious encephalitis is caused by viruses, bacteria and fungi.

1. Viral encephalitis occurs as a result of a viral infection (arbovirus, herpes virus, enterovirus, cytomegalovirus, rabies virus, etc.). The course of the disease can be acute, sub-acute and chronic. Etiological diagnosis consists in conducting serological tests.

2. Tick-borne encephalitis is an acute viral natural focal disease with transmissible or alimentary transmission. It is caused by tick-borne encephalitis virus, which belongs to arboviruses. The disease is characterized by seasonality. The incubation period is 7-20 days. The disease begins acutely with fever, severe headache, impaired consciousness, epileptic seizures, meningeal symptoms, paresis and paralysis are sometimes possible. Microscopically noted (in the acute form) is the predominance of circulatory disorders and an inflammatory exudative reaction; perivascular infiltrates and neuronophagia often occur. With a protracted course, the proliferative reaction of glia and focal destruction of the nervous system predominate. The chronic course of encephalitis is characterized by fibrillar gliosis, demyelination, and sometimes atrophy of certain parts of the brain.

50. Classification of infectious diseases

Infectious diseases are called diseases caused by infectious agents - viruses, bacteria, fungi. The infectious process depends on the state of the macroorganism, the immune system, on the nature of the interaction between the macro- and microorganism, on the characteristics of the microorganism, etc.

The coexistence of macro- and microorganisms is of three types.

1. Symbiosis - micro and macroorganism coexist in the interests of each.

2. Commensalism - micro- and macroorganism do not influence each other.

3. Parasitism - the life of a microbe at the expense of a macroorganism. The infection can be exogenous, when the pathogen penetrates through the entrance gate, and endogenous (autoinfection), when its own microflora is activated.

Classification.

According to the biological factor:

1) anthroponoses - infectious diseases that occur only in humans;

2) anthropozoonoses - infectious diseases of both humans and animals;

3) biocenoses are a group of anthroponoses and anthropozoonoses transmitted through insect bites.

Etiologically:

1) viral infections;

2) rickettsiosis;

3) bacterial infections;

4) fungal infections;

5) protozoal infections;

6) parasitic infections.

Transfer mechanism:

1) intestinal infections;

2) respiratory infections;

3) transmissible or blood infections;

4) infections of the outer integument;

5) infections with a different mechanism of transmission.

According to the nature of clinical and anatomical manifestations, infections with a primary lesion are distinguished:

1) skin, fiber and muscles;

2) respiratory tract;

3) digestive tract;

4) nervous system;

5) cardiovascular system;

6) circulatory system;

7) urinary tract.

According to the nature of the course, acute, chronic, latent (hidden) and slow infections are distinguished.

There is a change in the lymph nodes in the form of follicular hyperplasia, and then is replaced by depletion of the lymphoid tissue.

Kaposi's sarcoma (multiple idiopathic hemorrhagic sarcoma) is manifested by purple-red spots, plaques and nodes located on the skin of the distal lower extremities with ulceration. Possible involution with the formation of scars and depigmented spots.

51. Typhoid fever

Typhoid fever is an acute infectious disease from the group of anthroponoses. The causative agent is typhoid bacillus. The incubation period is 10-14 days. The coincidence of the clinical cycles of the course of typhoid fever with certain cycles of anatomical changes in the lymphatic formations of the intestine served as the basis for constructing a scheme of morphological changes by stages.

At the first stage of morphological changes, which usually coincides with the 1st week of the disease, in the lymphatic apparatus of the intestines, a picture of the so-called brain-shaped swelling is observed - an inflammatory infiltration of Peyer's plaques and solitary follicles.

In the second stage, corresponding to the 2nd week of the disease, necrosis of the swollen Peyer's patches and solitary follicles occurs (the necrosis stage). Necrosis usually captures only the superficial layers of the lymphatic apparatus of the intestine, but sometimes it can reach the muscular and even the serous membrane.

In the third stage (the period of ulcer formation), approximately corresponding to the 3rd week of the disease, the dead areas of Peyer's patches and solitary follicles are rejected and ulcers form. This period is dangerous with possible severe complications (intestinal bleeding, perforation).

The fourth stage (the period of pure ulcers) corresponds to the end of the 3rd and 4th weeks of the disease; in this period, the bottom of the typhoid ulcer becomes wide, it is cleared and covered with a thin layer of granulation tissue.

The next phase (the period of ulcer healing) is characterized by the process of ulcer healing and corresponds to the 5-6th week of the disease.

Morphological changes can spread to the large intestine, gallbladder, liver. At the same time, ulcers characteristic of typhoid fever are found on the mucous membrane of the gallbladder, and typhoid granulomas are found in the liver; the disease proceeds with symptoms of damage to these organs (jaundice, acholic stools, elevated blood levels of bilirubin, etc.). Damage to the intestines in typhoid and paratyphoid is always combined with damage to the regional lymphatic glands of the mesentery, and often the retroperitoneal glands. Under microscopy, the same macrophage reaction is noted in them, as in the lymphatic apparatus of the intestinal wall. In the enlarged lymph nodes of the mesentery, foci of necrosis are observed, in some cases capturing not only the main mass of the lymph node, but also passing to the anterior sheet of the abdominal integument, which can cause a picture of mesenteric-perforative peritonitis.

52. Salmonellosis. Dysentery. Cholera

Salmonellosis is an intestinal infection caused by salmonella; refers to anthropozoonoses.

With the most common gastrointestinal form of salmonellosis, macroscopically, the presence of edema, hyperemia, small hemorrhages and ulcerations in the mucosa of the gastrointestinal tract is detected. In addition to these changes, in severe and septic forms of the disease, signs of dystrophy and foci of necrosis in the liver, kidneys and other organs are often observed. The reverse development of morphological changes in most patients occurs by the 3rd week of illness.

Dysentery is an acute intestinal infectious disease with a predominant lesion of the large intestine and intoxication phenomena. Macroscopically, the intestinal lumen contains semi-liquid or mushy masses mixed with mucus and sometimes streaked with blood.

Cholera is an acute infectious disease (anthroponosis) with a primary lesion of the stomach and small intestine. The causative agents are Koch's Asian cholera vibrio and El Tor vibrio. The pathological anatomy of cholera consists of local and general changes.

Local transformations are formed (mainly) in the small intestine. The first 3-4 days are designated as the algid (cold) stage of cholera. The mucous membrane of the small intestine is full-blooded, edematous, with small hemorrhages throughout. Many vibrios are found in the intestinal wall. In general, the changes correspond to the picture of the most acute serous or serous-desquamative enteritis. The lymph nodes of the mesentery are somewhat enlarged. The peritoneum is plethoric, dry, with petechial hemorrhages. Dense dark red blood in blood vessels, cavities of the heart, on sections of parenchymal organs. The serous membranes are dry, covered with sticky mucus, stretching in the form of threads. Bile formation is disturbed. The gallbladder is enlarged in size, filled with transparent light bile - "white bile". The kidney acquires a characteristic appearance (the so-called motley kidney) - the cortical layer swells, pale, and the pyramids are filled with blood and acquire a cyanotic hue. The loops of the small intestine are stretched, in its lumen there is a large amount (3-4 l) of a colorless liquid that is odorless, reminiscent of "rice water", without admixture of bile and the smell of feces, sometimes similar to "meat slops". In the liquid there are a large number of cholera vibrios.

In the brain and spinal cord, in the cells of the sympathetic nodes, dystrophic, sometimes inflammatory phenomena occur; there may be hemorrhages in the brain tissue.

53. Plague

Plague is an acute infectious disease caused by the plague bacillus. There are bubonic, skin-bubonic (skin), primary pulmonary and primary septic forms of plague: 1) bubonic plague is characterized by an increase in regional lymph nodes, usually inguinal, less often - axillary and cervical. Such lymph nodes are called primary plague buboes of the 1st order. They are enlarged, soldered, testate, immobile, dark red in color with foci of necrosis. Edema develops around the bubo. Microscopically, a picture of acute serous-hemorrhagic lymphadenitis is observed, a mass of microbes accumulates in the tissue. Proliferation of reticular cells is characteristic. Due to the development of necrosis, purulent inflammation and melting of the lymph node tissue occur, ulcers are formed, which, with a favorable result, are scarred. Hematogenous development of infection leads to the rapid development of plague bacteremia and septicemia, which are manifested by rash, multiple hemorrhages, hematogenous lesions of the lymph nodes, spleen, secondary plague pneumonia, dystrophy and necrosis of parenchymal organs. The rash may take the form of pustules, papules, erythema, with the obligatory formation of hemorrhages, necrosis and ulcers. Multiple hemorrhages are observed in the serous and mucous membranes. The spleen is enlarged 2-4 times, septic, flabby, foci of necrosis are formed, a leukocyte reaction to necrosis is observed. Secondary pneumonia, which occurs as a result of hematogenous infection, has a focal character. A large number of dark red foci with areas of necrosis is a serous-hemorrhagic inflammation, where many pathogens are found. In parenchymal organs, dystrophic and necrotic changes can be observed;

2) the skin-bubonic (skin) form of the plague differs from the bubonic one in that the primary affect occurs at the site of infection. It is represented by a "plague flick tena" (a vesicle with serous-hemorrhagic contents), or a plague hemorrhagic carbuncle. At the site of the carbuncle, edema, thickening of the skin, which becomes dark red, are noted;

3) primary pneumonic plague is extremely contagious. With primary pneumonic plague, lobar pleuropneumonia occurs. Pleurisy is serous-hemorrhagic.

4) primary septic plague is characterized by a picture of sepsis without visible entry gates of infection with a very severe course. Significantly expressed hemorrhagic syndrome (hemorrhage in the skin, mucous membranes, internal organs).

54. Anthrax, tuberculosis, sepsis, syphilis

Anthrax is an acute infectious disease characterized by a severe course in which skin and internal organs are affected; belongs to the group of anthropozoonoses. The causative agent of anthrax is an immobile bacterium Bacterium anthracis, which forms highly resistant spores: they remain in water and soil for decades. There are the following clinical and anatomical forms of anthrax:

1) skin (conjunctival, as a kind of skin);

2) intestinal;

3) primary pulmonary;

4) primary septic.

Tuberculosis is a chronic infectious disease caused by Mycobacterium tuberculosis. Pathologically, there are 3 main types:

1) primary tuberculosis;

2) hematogenous tuberculosis;

3) secondary tuberculosis.

The classical form of the morphological manifestation of primary tuberculosis is the primary tuberculosis complex. In 90% of cases, the foci of the formation of the primary tuberculosis complex are the upper and middle sections of the lungs, but it is also possible in the small intestine, bones, etc.

There are 4 phases of the course of primary pulmonary tuberculosis:

1) pneumonic;

2) resorption phase;

3) sealing phase;

4) formation of the center of Gon. Outcomes of the primary tuberculosis complex:

1) healing with encapsulation, calcification or ossification;

2) progression with the development of various forms of generalization, the addition of nonspecific complications such as atelectasis, pneumosclerosis, etc.

There are 7 forms of secondary tuberculosis: acute focal, fibrinose-focal, infiltrative, acute cavernous, cirrhotic tuberculosis, caseous pneumonia and tuberculoma.

Sepsis is a common infectious disease that occurs due to the existence of a focus of infection in the body. The main morphological features of sepsis are severe dystrophic and necrobiotic changes in the internal organs, inflammatory processes of varying severity in them, as well as a significant restructuring of the immune system. Sepsis has the most typical morphological picture with septicopyemia. The main morphological sign of septicemia is generalized vascular disorders: stasis, leukostasis, microthrombosis, hemorrhage.

Syphilis, or lues, is a chronic infectious sexually transmitted disease caused by Treponema pallidum. Pale treponemas get on the skin or mucous membrane of a healthy person; through the existing microcracks in the stratum corneum, and sometimes through the intercellular gaps of the intact integumentary epithelium, there is a rapid penetration into the tissues.

55. Actinomycosis, candidiasis, aspergillosis

Fungal diseases (mycoses) are a group of diseases caused by fungi. With some mycoses, exogenous infection occurs (trichophenia, scab, actinomycosis, nocardiosis, coccidiomycosis), while with others it is exogenous, that is, autoinfection develops under the influence of adverse factors (candidiasis, aspergillosis, penicillosis, mucormycosis).

There are fungal diseases of the skin (dermatomycoses) and internal organs (visceral mycoses).

1. Dermatomycoses are divided into 3 groups: epidermomycosis, superficial and deep dermatomycosis:

1) epidermycoses are characterized by damage to the epidermis and are caused by epidermophytes of various types (pityriasis versicolor, epidermophytosis);

2) with superficial dermatomycosis, the main changes develop in the epidermis (trichophytosis and scab);

3) deep dermatomycoses are characterized by damage to the dermis itself, but the epidermis also suffers.

2. Visceral mycoses differ according to the etiological factor:

1) diseases caused by radiant fungi (actinomycosis, nocardiosis);

2) diseases caused by yeast-like and yeast fungi (candidiasis, blastomycosis);

3) diseases caused by mold fungi (aspergillosis, penicillosis, mucormycosis);

4) diseases caused by other fungi (coccidioidomycosis, rhinosporidiosis, sporotrichosis, histoplasmosis).

Actinomycosis is a visceral mycosis characterized by a chronic course, the formation of abscesses and granules. Caused by the anaerobic radiant fungus Actinomyces Israeli.

Candidiasis, or thrush, is caused by yeast-like fungi of the genus Candida. This is an autoinfectious disease that occurs when exposed to adverse factors or when taking antibacterial drugs. It can occur locally (skin, mucous membranes, gastrointestinal tract, genitourinary organs, lungs, kidneys) and generalized. With local candidiasis, mucous membranes covered with stratified squamous epithelium are most often affected. The fungus grows superficially, brownish overlays appear, consisting of intertwining threads of pseudomycelium, desquamated epithelial cells and neutrophils. When the fungus penetrates into the thickness of the mucous membrane, foci of its necrosis appear. Necrotic areas are separated from healthy tissue by a demarcation shaft of neutrophils. With a prolonged process, granulation tissue is formed; the process ends with fibrosis. Generalized candidiasis is characterized by the entry of fungi into the bloodstream and the appearance of metastatic foci (candidiasis septicopyemia).

Aspergillosis is caused by several species of the genus Aspergillus. As an autoinfection, it occurs when treated with high doses of antibiotics, steroid hormones and cytostatics.

56. Malaria, amoebiasis

Malaria is an acute or chronic relapsing infectious disease that has different clinical forms depending on the period of maturation of the pathogen, characterized by febrile paroxysms, hypochromic anemia, enlargement of the spleen and liver.

The disease is caused by several species of protozoa of the genus Plasmodium. Once in the bloodstream with a mosquito bite, plasmodia go through a complex development cycle, parasitize in human erythrocytes, reproducing asexually (schizogony). Given the existence of several types of Plasmodium, three-day, four-day and tropical forms of malaria are distinguished.

With three-day malaria, red blood cells are destroyed and anemia occurs. The products released during the breakdown of erythrocytes (hemomelanin) are captured by the cells of the macrophage system, which leads to an increase in the spleen and liver, bone marrow hyperplasia. The organs are filled with pigment and become dark gray, and sometimes black. The spleen is enlarged and plethoric. Subsequently, hyperplasia of cells occurs that phagocytize the pigment. The pulp becomes dark.

In chronic course, the spleen is compacted due to sclerotic processes, on a gray-black incision; its mass can reach 3-5 kg. The liver is enlarged, plethoric, gray-black. The bone marrow of flat and tubular bones has a dark gray color, the cells are hyperplastic with the presence of pigment. Hepatic jaundice develops.

The pathological anatomy of a four-day malaria is similar to a three-day one. Tropical malaria differs from other species in that erythrocytes containing schizonts accumulate in the terminal sections of the bloodstream, where they develop.

The death of such patients is typical for tropical malaria, which is complicated by coma.

Amoebiasis, or amoebic dysentery, is a chronic protozoal disease, which is based on chronic recurrent ulcerative colitis. It is called by protozoa from the class of rhizopods - Entamoeba histolitica. Getting into the wall of the large intestine, the amoeba and its metabolic products cause edema and histolysis, necrosis of the mucous membrane, and the formation of ulcers. Necrotic-ulcerative changes are most often localized in the caecum. Microscopically, areas of mucosal necrosis are swollen and stained dirty gray or greenish. The zone of necrosis penetrates deep into the submucosal and muscular layers. With the formation of an ulcer, its edges become undermined and hang over the bottom. Amoebas are located on the border between necrotic and preserved tissue. A secondary infection can join - then an infiltrate from neutrophils occurs and pus appears. A phlegmonous, or gangrenous, form of colitis is formed. Deep ulcers heal with a scar. Lymph nodes are enlarged, but there are no amoebas in them. Complications can be intestinal and extraintestinal. Of the intestinal, the most dangerous are perforated ulcers, accompanied by bleeding, the formation of stenosing scars after the healing of ulcers, and the development of inflammatory infiltrates around the affected intestine. Of the extraintestinal complications, the most dangerous is a liver abscess.

Author: Kolesnikova M.A.

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