Общая патологическая анатомия животных = Introduction to the pathological anatomy of animals. Учебно-методическое пособие

3.Changing the consistency of the organ-it becomes dense, cut with difficulty as a result of the growth of CT.

4.Changing the surface of the body – the surface can remain smooth, but most often it is fine-carbon (shagreen) due to the growth of CT, or coarse-carbon with regeneration nodes (with liver cirrhosis). On the surface and in the section clearly reveal scars.

5.In the cavernous bodies can be observed:

A.Proportional reduction of the cavity and thinning of the organ wall. It's concentric atrophy. Like in the heart.

B.Thinning of the wall and enlargement of the cavity – eccentric atrophy – for example, in the intestine.

The outcomes of alteration (necrosis, atrophy, dystrophy)

Outcomes depend on:

1.Type of alterative process

2.Body resistance

3.Time and strength of pathogenic factors

The following outcomes are most typical of necrosis and severe dystrophy.

Outcomes:

1.With reduced resistance, the focus of alteration, such as necrosis, dystrophy, gradually turns into unchanged tissue without visible boundaries.

2.With increased resistance on the border between dead or drastically changed dystrophic tissue develops an edge area of inflammation (demarcative, reactive). There is an intense cell infiltration, consisting of micro-and macrophages, epithelioid and lymphoid cells, connective tissue cells (fibroblasts, fibroblasts, histiocytes). It also noted a powerful injectivity of blood vessels, as they are in a state of inflammatory hyperemia. Then the cell elements give way to the growth of CT.

3.As a result of the reproduction of cellular CT elements observed replacement of the dead substrate on CT, that is, the organization.

4.Sclerosis – the growth of CT.

5.Encapsulation – the formation of a CT capsule around the necrosis site, in which the dead substrate is locked. Special cases of encapsulation:

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A.Sequestration is the purulent melting of a dead substrate along the periphery of the border with the capsule. Example: a tubercular cavity.

B.Carnification is the germination of the dead substrate of CT.

B. Dystrophic calcification-petrification-is the loss of calcium salts in CT, as well as into the dead substrate.

D. Sewerage-is the formation of a channel through a section of dead tissue with lining its endothelium and the resumption of blood flow.

Violation of local blood and lymph circulation

These disorders include: hyperemia, ischemia (anemia), hemorrhage, thrombosis, embolism, heart attacks, violations of tissue fluid (edema).

Hyperemia

It is an increase in blood filling of the organ or tissue. Hyperemia (full blood) may be:

1.general or local

2.arterial or venous

3.acute or chronic

4.according to the left ventricular variant, right ventricular variant, mixed.

Arterial hyperemia is an increase in blood filling of the organ due to the increased blood flow through the arterial bed.

According to the mechanism of development it can be identified as;

1.Vasomotor hyperemia - as a result of irritation or paralysis of vasodilators or vasoconstrictors. This includes the action of extreme temperatures, chemicals. It appears as swelling, tumefaction and erythema in the skin and mucous membranes.

2.Collateral arterial hyperemia – occurs around the area of the organ or tissue that is deprived of normal blood supply due to thrombosis, embolism, narrowing or spasm of the artery. At the same time, the pressure below the obstacle increases and collaterals – shunts are opened, which, being in a state of arterial hyperemia, lead to the normalization of blood supply.

3.Vacant arterial hyperemia – is associated with a sharp decrease in atmospheric pressure, and consequently, with a sharp decrease in the

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partial pressure of oxygen in the air. It can be a mountain, altitude sickness.

4.Inflammatory arterial hyperemia is a constant companion of inflammation, one of the signs of an inflammatory reaction.

5.Postanemic arterial hyperemia – occurs after a short anemia. Morphological characteristics: the organs increased in volume,

bright red or scarlet color, clearly noticeable fine mesh of blood vessels, from the surface of a cut a red or red blood flows down.

Venous hyperemia (venous stasis)

Increased blood filling of the organ due to a violation or difficulty in the outflow of blood through the veins. Most often observed in the limbs, parenchymal organs, gastrointestinal tract.

With acute general venous hyperemia, oxygen starvation of tissues is observed, as a result of which the permeability of blood vessels increases sharply, plasma impregnation of tissues and the formation of edema occurs. Afterwards, diapedesis of red blood cells and small-point hemorrhages can be observed. All these factors in the tissue cause dystrophy and necrosis.

In acute general venous hyperemia, the organs are enlarged in volume, have a cyanotic shade, dark cherry, edematous. This is most clearly noted in the lungs, gastrointestinal tract and skin.

Chronic general venous hyperemia – occurs much more often than acute venous hyperemia and leads to irreversible changes in the tissues.

Pathogenesis: in the chronization of the process, there is an aggravation of oxygen starvation of tissues, plasma and hemorrhage, this gives a push for the growth of CT, that is, sclerosis.

With venous hyperemia on the left ventricular variant, there is a stagnation in the small circle of blood circulation. In the acute process, there is hyperemia of the lungs, interstitial and alveolar pulmonary edema, as well as a powerful desquamation of the alveolar epithelium. The lungs are enlarged in volume, dark cherry with a bluish tint of color, from the cut surface an abundance of dark blood flows. In the chronic process, irreversible phenomena develop. The stroma grows in CT, which leads to fibrosis or induration of the lungs. The continuing venous stagnation leads to a sharp vascular porosity and the release of red blood cells. They are destroyed, and leaving them hemoglobin is

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absorbed by the alveolar macrophages, in which hemosiderin is formed. These cells are called siderocytes or "cells of cardiac defect".

As a result, the lungs become brown due to the accumulation of hemosiderin. Lungs in chronic venous stasis are called "brown induration of the lungs."

Venous hyperemia in the right ventricular option

It is characterized by stagnation in a large circle of blood circulation with venous hyperemia in the liver, kidneys and other organs. The most striking changes are observed in the liver, kidneys and skin. The liver is enlarged in volume, the edges are rounded, the capsule is tense. On the cut the liver has nutmeg pattern (“nutmeg liver").

In the chronic process in the center of the hepatic lobules hepatocytes atrophy, CT takes their place and cirrhosis develops ("Muscat cirrhosis").

Kidneys increase in volume, dense, the capsule is tense and difficult to remove, the cut pattern of the organ is smoothed, the border between the cortical and brain substance is determined with difficulty. Dark thick blood flows from the cut surface.

Clinical significance depends on the degree of hypoxia. In severe hypoxia in vital organs develop conditions that are not compatible with life. In other organs multiple sclerosis develops.

Ischemia

Reduction of blood filling of the organ as a result of insufficient blood flow to the organ. At the same time there is insufficient blood supply. The change in tissue that occurs in ischemia is due to the developing hypoxia and the degree of sensitivity of the tissue to it. In acute ischemia, necrotic processes develop in the tissue, in chronic – atrophic processes, which leads to sclerosis of the stroma.

Depending on the causes and conditions of ischemia there are the following types:

1.Angiospasculatory – as a result of spasm of arteries.

2.Obturatory – in consequence of closing the lumen of the arteries by a thrombus or an embolus.

3.Compressive – as a result of compression of the artery tumor, exudate, tourniquet, ligature.

4.Redistributive ischemia – observed as a result of the redistribution of blood from one vessel to another.

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The clinical significance of ischemia is determined by the degree of hypoxia.

Arterial hyperemia, venous hyperemia and ischemia are disorders of blood filling.

Vascular permeability disorders

Hemorrhages

This is the output of blood from the lumen of the blood vessel or the heart cavity into the environment (external bleeding) or in the body cavity (internal bleeding).

A common case of bleeding is hemorrhage – it is the expiration of blood from the vessel, when blood accumulates in the tissues.

There are the following types of hemorrhages:

1.Hematoma (blood tumor) – a cluster of clotted blood in the tissues with a violation of its integrity and the formation of the cavity.

2.Hemorrhagic impregnation is a hemorrhage while preserving tissue elements.

3.Bruising is a planar hemorrhage, located under the epidermis, mucosa.

4.Petechiae and ecchymoses are point and striped hemorrhages. Causes of bleeding:

1.Rupture of the vessel wall – haemorrhagia per rexi – in

inflammation, necrosis, aneurysm of the vessel wall.

2.Corrosion of the vessel wall – haemorrhagia per diabrosi – in inflammation, necrosis, malignant tumor

3.As a result of increased permeability of the vascular wall – haemorrhagia per diapedesis – develops as a result of a sharp increase in the permeability of the vascular wall in hypoxia, venous stasis, etc.

Clinical significance is determined by: the species and age of the animal, the volume of lost blood, the location of hemorrhage. Hemorrhages in vital organs can lead to the death of the animal. Loss of up to 20% of blood volume does not cause visible changes. Loss of up to 30-40% of blood leads to severe metabolic and circulatory changes up to collapse and shock. Loss of more than 55% of blood is usually fatal.

Macropicture: hemorrhages appear as dot and stripe accumulations of blood often dark red.

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Microscopically, they are determined in the form of clusters of blood in the form of puddles or blots, which are widely removed from each other by parenchymal elements. Hemorrhage leads to a violation histoarchitectonic tissue and therefore may cause atrophy and necrosis of parenchymatous elements.

Disturbance of blood flow and condition

Stasis

This is a sharp slowdown and stop of blood flow in the microcirculatory canal.

Etiology: general disorders of blood circulation, the action of physical factors (extreme temperatures), the action of chemical factors (poisons), the action of infectious, infectiousallergic and autoimmune factors.

Under the influence of these factors sludge of formed elements of blood appear, i.e. the adhesion to each other of erythrocytes, leukocytes, platelets with the increase of the viscosity of the plasma. This leads to a change in capillaries, slowing, and then stopping of the bleeding.

According to the mechanism of development can be determined

1.Stagnant capillary stasis – develops with difficulty in blood flow (with paralysis of vasomotors, blockage of arteries).

2.True capillary stasis – develops with intravascular aggregation of red blood cells, that is, with the sludge syndrome.

Macroscopically, stasis is not different from acute venous hyperemia. There is blood filling of vessels, cyanosis and compaction of organs.

Clinical significance: this is a reversible phenomenon. Long-term stasis leads to irreversible hypoxic phenomena-necrobiosis and necrosis.

Thrombosis

Thrombosis is the blood clotting in vivo with the formation of clots from the components of the blood with the possible subsequent blockage of blood vessels. Conditions of thrombosis:

A. Local conditions of thrombosis:

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1.changes in the vessel wall (vessel intima alteration – erosion, ulcers, retraction, protrusion, inflammation).

2.slowing and disruption of blood flow with the development of turbulent movement.

B. General conditions of thrombosis:

1.violation of regulation of blood coagulation and anticoagulation systems

2.changes in blood composition and its rheological properties. Mechanism of thrombosis:

Coagulation (plasma coagulation) is a complex biochemical process that leads to the formation of fibrin, an insoluble protein in the blood stream. The process of fibrin formation is as follows: fibrinogen of blood plasma is a jelly - like transparent mass. Under the action of biologically active substances fibrinogen loses its transparency, condenses, and becomes a gray color, the globules of protein align together and form a fiber – fibrin. The fibers in the form of a gentle mesh fall out on the site of the vessel's intima alteration. The next stage of thrombosis is bonding-conglutination. In this stage the platelets under the action of Hageman factor in the result of physical and chemical changes the vitreous stick together and form plaques, which together with the threads of fibrin become warty nodules, firmly attached to the intima of the vessel. Then there is the agglutination of red blood cells. It occurs under the influence of toxic products and other reasons. As a result, red blood cells are stuck in the fibrin threads and a blood clot is formed.

Morphological characteristics of blood clots

Clots are: hyaline, white, red and mixed (layered).

Hyaline thrombus is observed in small arteries and veins, is a white mass of fibrin, platelets and is formed in burns, frostbites and infections with septic course.

White blood clots - gray-white-yellow dense crumbling mass, consisting of platelets, leukocytes, fibrin fibers. Such clots have a mesh structure and are formed slowly with rapid blood flow, that is, in the arteries.

Red blood clots – consist of fibrin, red blood cells, mixed with white blood cells and platelets. Such clots are dryish, brittle, dark red. They are formed quickly, with a slow current in the blood veins.

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Mixed blood clots are the alternation of red and white blood clots. In a blood clot, especially in mixed, the head, body and tail distinguished. The clot is always attached to the head of the intima of the vessel. In relation to the lumen of the vessel thrombus can be clogged (completely closes the lumen of the vessel), parietal (fills only

part of the vessel).

Outcomes of thrombosis: the favorable outcomes are: autolysis of the thrombus, the thrombus formation (sprouting CT), the thrombus calcification (petrification – this occurs most often in the veins that causes the development of stones phleboliths), sewerage – development in bridging the clot canal with its lining by endothelium and resumption of blood flow.

Adverse conditions include: separation of the thrombus with the development of thromboembolism, septic destruction of the thrombus, an increase in the volume of the thrombus.

Difference between a thrombus and postmortem blood clots

Blood clots are always firmly connected to the intima of the vessel, dense to the touch, rough, dryish on the surface and the cut. Postmortem clots of blood are wet, shiny, gelatinous, structure and form they repeat of the cast of the vessel, are easily removed from the vessel.

Clinical significance is determined by the speed of thrombosis, localization and prevalence. Occlusive thrombus is very dangerous, in the arteries, they lead to the development of necrosis and heart attacks.

Embolism

This circulation in the vascular bed of the particles, normally not occurring here, followed by possible blockage of the vessels. These particles are called emboli. Embolism is classified according to:

1.the nature of the emboli (embolism exogenous, endogenous embolism)

2.embolism of a large or small circle of blood circulation

Exogenous embolism – develops when emboli enters the vascular bed from the outside. This includes:

1. air embolism (develops as a result of incorrect administration of drugs or when injuring large veins, while air is sucked into the veins).

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There is an accumulation of air in the right part of the heart, which leads to blood foaming and paralysis, seizures, severe agony.

2.gas embolism – the animals are almost nowhere to be found. Decompression sickness. It is associated with the rapid transition of nitrogen from dissolved to gaseous state with the rupture of the vessel.

3.microbial embolism – circulation of microbial colonies (especially dangerous pyogenic microorganisms). They stop in the MCR, which leads to the development of metastatic purulent inflammation.

4.embolism by foreign bodies – lime, cholesterol, etc.

Endogenous embolism – circulation in the vascular bed of emboli formed in the body.

1.Pulmonary embolism is circulation in the bloodstream of the thrombus or its part to the occlusion of the vessel. Most often observed in the lungs, kidneys, spleen, intestines, brain. In this case, a heart attack develops as a result of vasospasm. In the kidney, spleen, intestines and lungs, heart attacks are hemorrhagic.

2.Fat embolism – blood or lymph transfer of fat droplets, which is observed in injuries, bone thawing with bone marrow injury. Is determined microscopically by the coloration of the tissues with Sudan III.

Clinical significance of embolism: determined by the type of embolus. The most important is thromboembolism, fat embolism. Thromboembolism often leads to heart attacks, and with thrombosis of the vessels of the limbs, gangrene develops.

Cell and tissue embolism – circulation in the blood of cells and tissues, which is observed when the body's own tissues are crushed, as well as metastasis of malignant tumors.

Inflammation (inflammatio)

Inflammation is the most ancient and complex vascularmesenchymal reaction to damage, aimed not only at the elimination of the damaging agent, but also to the restoration of damaged tissue. In general, inflammation is a complex protective-adaptive reaction developed in the process of evolution, aimed at the destruction or elimination of the phlogogenic agent and combining three components:

1. damage – alteration

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2.vascular reaction, exudation and emigration

3.proliferation

Etiology:

Any factor that causes inflammation is called a phologogenic factor or phologogenic agent. The causes of inflammation are divided into:

1.physical – radiation energy, injuries, dust, extreme temperatures,

etc.

2.chemical factors – toxins, poisons, some medicines, etc.

3.biological factors – viruses, bacteria, fungi, animals-parasites, immune complexes, etc.

Pathogenesis of inflammation:

The development of inflammation begins with an alteration. Alterative manifestations are dystrophic, necrotic and / or atrophic changes in the inflamed focus. We distinguish:

A. Primary alteration. It occurs under the direct influence of the phlogogenic factor and is manifested most often locally.

B. Secondary alteration. It occurs when the products formed in the focus of inflammation influence the tissue during the primary alterations. In this case, dystrophic, atrophic and necrotic processes occur as a result of innervation disorders, blood circulation and other causes.

Feature: the predominance of dystrophic and necrotic processes in the focus of inflammation indicates acute inflammation.

The presence of atrophy indicates chronic inflammation. Necrotic changes occur in the inflammation as a result of exposure to the tissue or organ gross factors – that are trauma, burns, thrombosis, stasis, etc. Focus of necrosis in this case may be from several mm to several cm or more.

Dystrophy in the focus of inflammation occurs under the action of less intense phlogogenic factors – these are toxic substances (most often of microbial origin). In inflammation there are granular, vacuolar, mucoid, fatty dystrophies.

Atrophy in the focus of inflammation indicates a chronicity of the process, when the phlogogenic agent affects the tissue weakly, but chronically. In this case, the number of parenchymal elements in the inflamed tissue is sharply reduced, but connective tissue (CT) multiplies.

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