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

Pathomorphology of renal amyloidosis

Macro: kidney is dramatically increased in volume, capsule is tense, kidneys are of unusual light pink color, the boundary of cortex and medulla on the cut is smooth.

Micro: at the beginning of the process amyloid is deposited in the vascular wall of the vessels of the glomerulus, then the process extends to the tubular apparatus, which leads to atrophy of the tubules, glomeruli and their replacement with a homogeneous mass of amyloid.

In amyloidosis of vessels the formation of tissue couplings is noted by the type of hyalinosis.

Outcome and importance for organism: depends on the localization and distribution process. Irreversible.

Feature: specific color – Congo-rot (Congo red), with the mass of amyloid painted in a very beautiful ruby color.

Mixed disproteinosis

Mixed disproteinosis – they are protein dystrophies, which are characterized by abnormalities of protein metabolism in the parenchyma and in the stroma of the organ. These dystrophies develop in violation of the metabolic processes of complex proteins, such as:

1.Nucleoproteins

2.Glycoproteins

3.Chromoproteins (pigments)

4.Lipoproteins

Metabolic imbalance of nucleoproteins

Nucleoproteins are complex proteins built on the principle of "protein + nucleic acid (DNA or RNA)". The final products of nucleoprotein metabolism are uric acid and its salts, as well as water. These products are normally excreted through the kidneys. In case of violation of the exchange of nucleoproteins, the final products (primarily uric acid and its salts, which are practically insoluble in water) are deposited into tissues. The basic pathology is manifested in the form of uric acid diathesis (in a man – gout), and uric acid infarct.

Etiology: for all these processes the main etiological factor are:

1.Severe metabolic disorders

2.Severe forms of inflammation

3.Violation of feeding (nutrition - for human)

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4. Heavy alteration of the tissues (primarily necrosis).

The essence of these processes is the deposition of uric acid and its salts in the tissues, on the surface of the joints, as well as in natural cavities with the formation of foci of inflammatory reaction.

Uric acid diathesis (gout)

This is the deposition of uric acid salts on the articular surfaces of the limbs in tendons, cartilages, serous membranes, in the form of whitish-gray-yellow overlays, similar to powder. After removal of these overlays areas of inflammation, necrosis focuses, connective tissue growth are exposed.

Micro: basophilic mass (the salt of uric acid) and foci of severe inflammation, necrosis, perifocal zone (border) of inflammation, retract connective tissue at different stages of maturation.

The outcome and value for organism: depends on the amount and the severity of the process. In far-severe cases, there is a powerful growth of connective tissue, the process becomes irreversible.

Most often carnivores (cats, dogs) and poultry suffer from the consumption of a large number of protein products.

Uric acid heart attack

This is a physiological condition in some newborns, especially in the first days of life and a pathological condition in adult animals, characterized by the deposition of uric acid salts and the acid itself in the form of yellow crystals in the tissues of organs, primarily kidneys. There is infiltration of the kidneys.

Macro: a cluster of red and yellow stripes in the renal tissue, which give the kidneys radial striations. This pathology can be observed in the form of inclusions, inlays, accumulations of salts in the dead and inflamed tissue.

The outcome and value for organism: depends on the volume of the lesion. If the volume of the lesion is large, it leads to severe organ failure. As a rule, this pathology causes perifocal inflammation and connective tissue growth, which leads to sclerosis of the organ.

Metabolic disorders of glycoproteins – mucous dystrophy

Glycoand mucoproteins are complex protein compounds with sugars, hyaluronic acid and its salts. These substances are contained in

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mucins and mucoids. Mucins are complex substances, the basis of mucus, which are secreted by the epithelium of the mucous membranes and individual glands. Mucins perform a protective function against mechanical damage and chemical agents and are carriers of digestive enzymes.

Mucoids are mucoid-like substances that are part of various tissues and have an alkaline reaction. Their main role is the medium for performing chemical reactions, for example, thyroid colloid – iodine atoms are attached to the protein-based thyroid hormones.

In case of metabolic disorders of these substances parenchymal and stromal vascular dystrophies develop.

Parenchymatous mucous dystrophies

The essence of this process is:

1.Hypersecretions of mucus

2.The change in the qualitative composition of mucus

3.Death of mucus producing cells.

Etiology: these dystrophies develop in:

1.Inflammation of mucous membranes

2.Mechanical damage and the action of chemicals on the mucous membranes

3.In the pathology of the glandular organs (thyroid, adrenal glands,

etc.).

Pathomorphology: degeneration of the mucosa of exposed mucous membranes and glandular organs.

Feature: in catarrhal inflammation (i.e., inflammation of the mucous membranes), usually develops mucosa epithelial dystrophy.

Macro: mucous membrane is swollen, dull, covered with a thick layer of thick, viscous, turbid or opalescent slime. The surface of the mucous is reddened (in acute process), compacted (in chronic process).

Micro: a marked inflammatory hyperemia, congestion of the mucous surface over the light pink mass with an abundance of desquamated (descended) epithelium. The surviving epithelial cells of the mucosa are in a state of granular or vacuolar degeneration, many cells have lost the kernel.

A type of mucosa is the degeneration colloid degeneration of the thyroid gland. It is a severe endemic disease associated with iodine deficiency in soil and water.

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The essence of the process: due to lack of iodine compensatory hypertrophy and hyperplasia of secretory cells of the thyroid follicles develop. They begin to produce an increased amount of colloid, which, accumulating in the follicles, overflows them, which leads to atrophy of the secretory apparatus and the merging of nearby follicles.

Macro: developing colloid (endemic) goiter. The thyroid gland is sharply increased in volume, lumpy, well contoured under the skin, with palpation – tested consistency. On the cut from it an abundance of cloudy, gelatinous liquid flows.

Micro: there is a sharp increase in the volume of follicles that merge with each other, as well as atrophy of the interfollicular partitions with their rupture and atrophy of the secreting cells, with desquamation.

Outcome and importance for the body: the disease has serious consequences for metabolism, when iodine-containing drugs are given, the situation is normalized and the morphology of the gland comes to normal.

Colloidal dystrophy also develops in the adrenal glands, kidneys and other glandular organs.

The extracellular (stromal-vascular) mucous degeneration

This is the impregnation of the mucus of the connective tissue, as well as its replacement of individual parenchymal elements.

Etiology:

1.Exhaustion (cachexia)

2.Serious chronic disease

3.Deep metabolic disorders (including the structure of connective tissue).

Macro: penetration of the components of connective tissue, fatty tissue, mucoid substance are observed, which dissolves the collagen and connective tissue turns into a mucoid mass. The fabric is swollen, flabby, gelatinous.

Micro: the abundance of homogeneous light-pink mass with fragments of broken cells and fibers.

The outcome and value for organism: the process is usually irreversible. It is typical for extreme exhaustion.

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Disorders of pigment metabolism

Pigments are substances that have their own coloring. Most of these substances refer to the chromoproteids. All pigments are divided into 2 large groups:

1.Endogenous pigments: formed and present in the body. Violation of their exchange is most important. Divided into:

A. Hemoglobinogenic – derived from hemoglobin B. Anemoglobinogenic

2.Exogenous pigments: enter the body from the outside. Hemoglobinogenic pigments are derived from hemoglobin and may

contain iron (ferrum). From hemoglobin synthesized:

1.Ferretin.

2.Hemosiderin

3.Bilirubin

4.Hematin

5.Gemin et al.

These hemoglobinogenic pigments have the highest value.

Violation of hemosiderin metabolism

Hemosiderin is a brown-yellow pigment formed from iron compounds that are parts of hemoglobin. When deposited in tissues hemosiderin gives them the color of rust.

Micro: on hematoxylin-eosin can be seen in the form of rusty clumps in the cytoplasm of the reticulum and endothelial cells. It accumulates mainly in the cytoplasm of macrophages (another name - siderocytes, siderophages or cells of heart disease).

Etiology:

1.Venous congestion

2.Hemolysis

3.Mechanical injuries and limited hemolysis of red blood cells

The essence of the process: under the influence of pathogenic factors, the destruction of red blood cells, from which hemoglobin comes. Hemoglobin is utilized by macrophages (in this case – siderophages), in which hemosiderin is formed.

Pathomorphology: under pathological conditions, general and local hemosiderosis develops.

General hemosiderosis is observed in intravascular hemolysis and capture of iron components by siderocytes, followed by infiltration of

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the surrounding tissues. Intravascular hemolysis is observed in sepsis, anthrax, swine erysipelas, toxemia, blood parasitic diseases, poisoning.

Organs and tissues, depending on the intensity of hemosiderosis, are painted in different shades of rusty-brown-yellow.

Micro: in tissues when stained with hematoxylin-eosin a large number of cells reveal, filled with rusty clumps. This is the smiles of hemosiderin.

A specific color is the color of Perls on the formation of the berlin azure. Hemosiderin thus is painted in a beautiful azure color.

Local hemosiderosis develops in the foci of hemorrhages, bruises. This is the so-called local ferritization.

Violation of bilirubin metabolism

Bilirubin is a green-yellow bile pigment formed from the protein part of hemoglobin – globin. The formation of bilirubin can be expressed as follows. Erythrocyte, disintegrating, gives rise to hemoglobin. Verdobilin is formed, then free bilirubin, which, falling into the liver and binding to glucuronic acid turns into associated bilirubin. It is then excreted in the feces (in the form of stercobilinogen) and urine (in the form of urobilinogen). Oxidizing, these substrates are converted into stercobilin and urobilin.

In case of pathology, the organism accumulates both free and bound bilirubin.

The process of accumulation of bilirubin in the body leads to the formation of a symptom complex called jaundice.

Jaundice is a complex set of symptoms, characterized by the accumulation in the body of free and associated bilirubin above the norm, followed by yellow (icteric) staining of visible mucous membranes, sclera of the eyes, serous membranes, internal organs, muscles.

Jaundice can be of three types:

1.Mechanical (stagnant, subhepatic)

2.Parenchymal (hepatic)

3.Hemolytic (cythemolytic icterus, suprahepatic)

Mechanical jaundice (subhepatic)

Blockage of the biliary tract in concrement (calculus) forming, parasites, inflammation, cancer.

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The essence of the process: the bile accumulating in excess breaks the thin walls of the bile passages and enters the blood. In this case, there are all signs of jaundice (icterus).

Parenchymal jaundice (hepatic)

Etiology: develops when severe lesions of the liver present. These are phosphorus poisoning, a number of infectious diseases (leptospirosis, septic infections).

Essence: damaged hepatocytes are not able to give bile to the bile capillaries and bile directly diffuses into the blood.

Hemolytic jaundice

Feature: this jaundice is not associated with liver disease, as the formation of bilirubin is not associated with the flow of bile into the blood, and is associated with the function of cells of the macrophage system.

Etiology: all kinds of pathologies that lead to powerful hemolysis of red blood cells: toxicosis, anthrax, blood parasitic diseases, etc.

The essence of the process is that the cells of the mononuclear phagocyte system are able to synthesize bilirubin from the components of hemolysed red blood cells (i.e. from hemoglobin).

Among the pathological forms of hemoglobin pigments of great importance is hematin. It is a pigment formed when chemicals effect on hemoglobin. For example, hydrochloric acid hematin. It is formed at the bottom of stomach ulcers and has a black color.

Metabolic anemoglobinogenic pigments

The most important here is the pigment melanin and lipofuscin.

The metabolism of melanin

Melanin is a protein pigment, of tyrosinetryptophan nature, of black or dark brown color. It is formed by specialized cells of epithelial origin-melanocytes. The metabolism of melanin is manifested either in its lack or its excess.

Lack of melanin formation is manifested in the form of:

1.Albinism is a hereditary form of deficient melanin synthesis.

2.Vitiligo is a local congenital depigmentation.

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3. Leucoderma is a local acquired lack of melanin pigment, especially wounds of various parts of the body, syphilis.

Excessive accumulation of melanin is characterized as melanosis. This is the deposition of melanin in unusual places, most often in the liver.

Macro: organ changes its color depending on the intensity of deposition of pigment. The liver can either not change its color, or acquire a slate-like color.

Micro: pigment accumulates in intercord space, as well as in the interlobular connective tissue, in the cytoplasm of melanocytes.

A metabolic lipofuscin

Lipofuscin is a golden brown pigment, a protein of fatty nature. It is deposited in organs and tissues that undergo hypoxia, that is, in atrophied tissues, in tissues during aging. Therefore, lipofuscin is called the pigment of aging, wear.

It is deposited in the cytoplasm of parenchymal cells in the form of small, golden-brown rounded granules. The main places of deposition are liver, skeletal muscles, myocardium, skin. The first three tissues are interconnected (liver, myocardium, skeletal muscle). "Freckles of death" – dark spots on the skin of the elderly – lipofuscin deposition.

Exogenous pigmentation

These are pigments that enter the body from the outside – dust, soot, cement, silica, mercury salts, silver salts. At the same time anthracosis of the lungs develops (in contact with coal, soot), pneumoconiosis (if dust, cement, silica), argeros of the kidneys ("steel kidney" - in cases of poisoning by salts of silver), "large mottled kidneys" – in cases of poisoning by salts of mercury.

Violation of fat metabolism. Fat dystrophy. Lipidosises

All lipids in the body are divided into two large groups:

1.Neutral fats

2.Lipoids

Neutral fats are the basis of the fat depot. They are located in the subcutaneous tissue, mesentery, omentum, form the basis of epicardial fat. In violation of the exchange of neutral fats extracellular, i.e. stromal and vascular fat dystrophy develops.

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Lipoids are complex fats, which are phosphatides, steroids, cerebroside, wax. They are part of the cytoplasmic fat, strongly associated with proteins, form complex but unstable fat-protein complexes. When the metabolic cellular lipids present parenchymal fatty dystrophy develops.

Fat dystrophies are divided into parenchymal (true) and stromal vascular (extracellular).

Stromal-vascular (extracellular) fatty dystrophies

These are fat dystrophies, arising from violation of the exchange of neutral fats. In the conditions of pathology, they are manifested in the form of exhaustion and obesity. These processes can be both local and general character.

Exhaustion (cachexia) is a decrease in the total amount of fat in the fat tissue.

Etiology: starvation, chronic infections, infestations, oncology, chronic gastroenterocolitis, chronic pneumonia.

Macro: adipose tissue loses fat, reduces in volume, becoming soft, moist, gelatinous, becomes of yellowish-grey color. On the cut, the gelatinous liquid flows, with the chronization of the process, the connective tissue grows. The measure of extreme exhaustion is serous atrophy of epicardial fat. The process is accompanied by brown atrophy of the liver, and myocardium.

Micro: adipocytes in fat depots abruptly disappear or dramatically decrease in volume, marked eosinophilic homogeneity in adipose tissue and retract connective tissue are registered.

Local depletion – lipodystrophy – a decrease in the amount of fat in the adipose tissue, which is local, limited.

Etiology: mainly diseases of the endocrine system. Pathomorphology: macroscopically, focal fat destruction with the

formation of cysts, cavities, granulomas are noted.

A cyst is a newly formed cavity filled with liquid. Granuloma – the growth of new tissue. Cavity - has no content.

Obesity is an increase in the amount of fat in the fat tissue, as well as its deposition in unusual places for the norm.

Etiology: overfeeding, lack of exercise, diseases of endocrine system, disease of the nervous system, metabolic diseases.

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Macro: a marked increase in the number of fat in the fat depot with the appearance of excess deposits of fat about the kidneys, liver, epicardium, and also the deposition of fat in intermuscular space are noted.

Micro: there is hypertrophy and hyperplasia of adipocytes (lipocytes), they increase in volume, fatty tissue occupies a larger space, and there is the appearance of lipocytes in the intermuscular space, as well as the appearance of columns of fat cells between sarcomere.

The outcome and value for organism: for farm animals it is very good: good quality meat. For small pets obesity (I, II degree) develops, which leads to a serious complication in the form of CF, RF, cardiac tamponade and metabolic disorders of all kinds of substances.

Local obesity is an excessive limited accumulation of fat in the tissues. Lipopathy. The essence of the process lies in the vacant (replacement) obesity. It is the emergence of lipocytes in the place of the atrophied or disabled tissues and organs. For example, the appearance of fat on the site of a disabled thymus, on the site of nonpermanent lymph nodes, or on the site of atrophied muscles.

Lipidoses

They develop as a result of lipid metabolism disorders. The mechanism of development consists of three main processes:

1.pathological infiltration

2.decomposition

3.transformation Etiology:

1.general obesity

2.protein starvation

3.intoxications

4.infectious disease

5.metabolic disorder

6.severe forms of inflammation

Pathomorphology. Most often, fatty dystrophy affects the liver, kidneys, myocardium. Less often – other organs and tissues.

Feature: fatty liver dystrophy (macrovesicular hepatic steatosis) is a stencil response of the liver to the effects of pathogenic factors.

Macro.

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