Pathological processes and regressive tissue changes in livestock animals

Regressive processes: how atrophy, cachexia, and necrosis destroy an animal's organism

Growth, development, and tissue death in livestock animals are a continuous biological process. However, under the influence of diseases and adverse housing conditions, it can shift into a pathological form. Regressive (hypobiotic) processes lead to a weakening of organ functions, a decline in metabolism, and a loss of herd productivity.

One such manifestation is atrophy — a reduction in the volume and mass of organs accompanied by a weakening of their functions. Under normal conditions, it can be physiological, for example, during the drying-off of a mammary gland or after giving birth. Pathological atrophy, however, always signals serious disorders and requires the attention of a veterinary specialist.

Pathological atrophy develops under the influence of the following factors:

• mechanical pressure (compression by harness, tumor, bandage, or hydatid cyst);
• circulatory impairment (circulatory atrophy due to insufficient blood flow);
• nervous system damage (paresis and paralysis of central or peripheral origin);
• insufficient functional load on an organ;
• hormonal imbalances (thyroid or pituitary gland dysfunction);
• prolonged starvation.

The extreme stage of body depletion is cachexia, which is accompanied by a sharp drop in body weight. In this state, all physiological functions of the animal are reduced: muscles lose strength, bones become brittle, and optic nerve atrophy leads to blindness. It is virtually impossible to restore the productivity of livestock in such a state.

In an unfavorable outcome, the pathological process ends in necrosis — tissue death. In practice, one encounters dry necrosis (protein coagulation in tuberculosis), wet necrosis (tissue liquefaction during lung necrosis), and gangrene. Gangrene can be dry, wet, or gaseous and develops under the influence of pathogenic microorganisms.

Dystrophy, excessive growth, and tumor processes in tissues

Dystrophy is characterized by changes in the physicochemical properties of cells and a decrease in their performance. Either ballast begins to accumulate excessively in the tissues, or the content of essential elements is critically reduced. Depending on the type of metabolic disorder, dystrophy can be protein, fatty, carbohydrate, or mineral.

Fatty dystrophy occurs when lipid metabolism is impaired, and fat accumulates in organs not intended for it — the liver, kidneys, and muscles. Extracellular disorders manifest as obesity due to overfeeding or emaciation due to underfeeding. Mineral dystrophy is expressed by the loss of calcium salts (osteodystrophy) or tissue calcification.

The opposite of decline are hyperbiotic processes, which lead to an increase in the mass and volume of organs. The organism initiates them to compensate for lost functions or in response to increased load. In veterinary practice, one most often encounters the following forms of growth:

• hypertrophy (true — due to specific elements, or false — due to the proliferation of connective tissue);
• work hypertrophy (e.g., enlargement of the left ventricle of the heart due to aortic stenosis);
• compensatory hypertrophy (upon the loss of function of one of the paired organs);
• regeneration (complete tissue restoration or incomplete — with the formation of a scar or bone callus).

A special group of pathologies is tumor growth — the uncontrolled division of altered cells by the organism. Benign neoplasms grow slowly and do not invade surrounding tissues, whereas malignant ones destroy organs, metastasize, and lead to death. Injuries, radiation, exposure to petroleum products, alkaloids, or viruses lead to the development of tumors.

Local circulatory disorders should be understood as a change in the normal blood circulation of a specific area of an organ or tissue; while the total amount of blood in the organism remains unchanged. Local circulatory disorder is expressed either as an overflow of blood — hyperemia, or a decrease in blood supply — anemia.

Arterial hyperemia is an increase in the blood filling of a given area of an organ or tissue due to an increased inflow of blood to it via the supplying arteries, while the outflow of blood generally remains normal. External signs:

5) a certain increase in the volume of the hyperemic area.

Tissue swelling arises because, due to an increase in blood pressure in the vessels, the vascular wall expands, becomes more permeable, and fluid begins to exude intensively into the tissue. The consequences of hyperemia depend on localization, duration, state of the vessels, and degree of hyperemia. Hyperemia in the central nervous system and heart is the most dangerous, as vessel damage (rupture and hemorrhage) is possible. Sometimes it is used for therapeutic purposes, as it enhances blood supply.

Venous hyperemia is an increase in blood volume within a specific organ or tissue due to impaired blood outflow. Causes include factors that interfere with normal blood outflow:

1) blockage of veins by a blood clot — a thrombus or embolus,

2) compression of veins by bandages, harness, or tumors,

This creates an obstacle to blood flow in large veins, resulting in blood stasis in the lower parts of the body.

1) a bluish discoloration of the hyperemic area caused by the presence of reduced (venous) hemoglobin,

2) a decrease in temperature associated with increased heat dissipation (vessels are dilated) and reduced heat production,

3) an increase in the volume of the hyperemic area caused by vessel dilation and transudate effusion.

Venous hyperemia causes impaired tissue nutrition, the consequences of which depend on its severity and duration.

Figure 2 – Venous hyperemia (tongue of a frog-

In case of venous stasis, the following disturbances are observed:

1) transudation - extravasation of fluid from blood vessels into surrounding tissues, subsequently leading to edema or dropsy (in cavities),

2) diapedesis - passage of erythrocytes through vessel walls - a type of hemorrhage caused by high pressure in the vessels.

3) stasis - complete cessation of blood circulation, accompanied by dilation of small vessels and their engorgement with blood.

The cessation of blood circulation leads to impaired tissue nutrition, intoxication of the body by toxic products, and necrobiotic processes in tissues.

4) circulatory disorder leads to tissue atrophy or the proliferation of connective tissue and organ induration

Local anemia (ischemia, from Greek "to hold back") is a reduction or cessation of arterial blood supply to an organ or tissue. Ischemia is characterized by the following signs: pallor, decreased temperature, sensory distortion ("numbness", tingling), pain, and impaired or loss of function. Depending on the causes leading to the development of ischemia, it is classified into several types:

a) compression ischemia develops due to the compression of an arterial vessel by a growing tumor, scar tissue, foreign body, etc.

b) hematogenous (angiospastic) ischemia - the result of narrowing or blockage of a vessel by a thrombus, embolus, or intimal proliferation due to inflammation.

c) endogenous ischemia - appears upon the narrowing of an arterial vessel by arteriosclerotic thickenings.

d) reflex ischemia - occurs due to the irritation of skin, mucous membrane, or tissue receptors by mechanical, physical, or chemical factors. For example, pain caused by the compression and irritation of sensory nerves leads to the reflex spasm of small arteries and veins. In humans, reflex ischemia of facial vessels is observed during fear or anger.

e) paralytic ischemia occurs during organ paralysis, where blood flow to the organ decreases sharply. Collateral anemia develops as a result of blood flow away from a given organ and its increased influx to another part of the body. For example, engorgement of abdominal organs with blood (rumen puncture) can cause collateral anemia of the brain.

Clinical ischemia manifests as pallor, decreased temperature, decreased volume, and reduced metabolism in the ischemic area of tissue or organ.

The outcome of local anemia depends on the size of the compressed vessel, the duration of the blockage, the physiological importance of the vessel, and the presence of collateral circulation. An important feature of an ischemic area is that it is always characterized by tissue oxygen starvation, the cessation of nutrient access, and the retention of metabolic end-products within the tissues. The most severe consequences of ischemia are noticeable in vital organs (brain, heart, kidneys, etc.).

Stasis (from Greek "stoppage, immobility") - complete cessation of blood flow, accompanied by vessel dilation and their engorgement with blood cells. Stasis can be ischemic - when blood flow into the capillary network ceases, or venous - when blood flow from capillaries into the venous network stops. The main cause of stasis development is increased resistance to blood flow in the microcirculatory network, which is more commonly observed in inflammatory processes. Prolonged stasis in vital organs (heart, brain) can cause death, while in other organs it causes necrotic changes, such as gangrene of frostbitten tissues.

Infarct (Latin "stuffed, crowded") - a focus of necrosis in tissues due to the cessation of blood circulation in them. Causes of an infarct can be various types of blockages or vessel spasms, and it is most commonly found in organs with poorly developed anastomoses between arterial vessels (kidneys, spleen, heart muscle).

Because arteries have a tree-like structure, infarcts are characterized by a cone-like shape, with the apex of the cone facing inward into the organ and the base facing its surface. The leading phenomenon in the mechanism of an infarct is ischemia and hypoxia, leading to tissue necrosis. Depending on the degree of blood circulation and blood filling, infarcts are divided into white (ischemic) and red (hemorrhagic).

White infarcts have a pale color because they develop due to the complete cessation of tissue blood supply and the lack of blood inflow to the necrotic area from neighboring vessels and capillaries.

Red infarcts develop when a supplying vessel is incompletely occluded. Insufficient blood supply to a tissue area leads to its necrosis and simultaneous blood infiltration. Blood is retained in the vessels and tissues, literally stuffing them. Hence the origin of the term "infarct" (Latin: to stuff, to pack). Additionally, there is a mixed infarct, in which, due to circulatory disturbance, its central part corresponds to a white infarct, while the periphery is flooded with blood (red infarct).

Over time, inflammation develops around the infarct, and the necrotic area may be resorbed, encapsulated, or replaced by connective tissue, leaving behind a whitish wedge-shaped scar.

1) on the size of the occluded or narrowed vessel: the larger it is, the more dangerous the consequences,

2) on the speed of lumen narrowing: with slow occlusion, blood circulation via anastomoses has time to be restored,

4) on the sensitivity of the tissue to a disruption in blood supply.

Such a disturbance is especially dangerous in vital organs (heart, nervous tissue). Prolonged anemia can lead to the death of the tissue or organ.

Collateral circulation. When even a large artery lumen is blocked, blood circulation may be restored via lateral branches - collaterals. If the sum of the collaterals' lumens is equal in diameter to the occluded artery, blood supply is restored quite quickly. Venous outflow can also be restored via collaterals. However, in some organs, collaterals are absent: the brain, heart, kidneys, spleen, lungs, and retina of the eye; therefore, necrosis frequently occurs in these organs when blood circulation is disturbed.

Hemorrhage is a pathological process in which blood escapes from a vessel into the external environment. External and internal hemorrhages are distinguished. Causes: mechanical vessel damage, sclerosis, ulcers, pathological processes. The loss of 50 percent of blood causes death.

Thrombosis is the ante-mortem formation of solid masses (thrombi) within the lumen of blood vessels, precipitated from the blood, usually adhered to the vessel wall and obstructing normal blood flow. A thrombus consists of elements: erythrocytes, coagulated fibrin, blood platelets, and leukocytes. Types of thrombi: red and white.

Conditions for thrombus formation: slowing of blood flow, damage to the vessel wall, and changes in blood quality.

1) agglutination (clumping together) of platelets and leukocytes,

Outcomes of thrombi: organization, canalization, petrification, resorption. The consequences depend on the size of the vessel, the size of the thrombus, and the importance of the organ.

Embolism is the obstruction of blood and lymphatic vessels by particles not normally found in the blood – emboli. Endogenous emboli are particles of detached tissues, fat, or thrombi. Exogenous emboli include air, bacterial, parasitic, and foreign body embolisms.

Figure 5 – Embolism (A); occlusion of a blood vessel by an embolus (B)