Hyalinosis of connective tissue in the scar, microslide. Pathological anatomy: Hyalinosis. The meaning of hyalinosis and its consequences

Hyalinosis is an irreversible degeneration in which homogeneous dense masses that resemble hyaline cartilage are formed in the histion.

HYALIN is a complex fibrillar protein, which includes:

blood plasma proteins
fibrin
lipids
components of immune complexes

Hyaline is stained red by eosin and fuchsin.

Causes:

Fibrinoid swelling
Inflammation
Angioedema reactions
Necrosis
Sclerosis

Pathogenesis:

Increased vascular permeability will play a leading role. Proteins and GAGs accumulate. Denaturation and protein precipitation occurs.

Hyalinosis - two types:

Vascular hyalinosis
Connective tissue hyalinosis

According to the prevalence of the process:

General
Local

VASCULAR HYALINOSIS

Lesions mainly affect small arteries and arterioles.

PLASMORRAGY phenomena occur in the vessels.

Hyalin accumulates UNDER THE ENDOTHELIUM and eventually occupies the entire wall of the vessel.

Hyalinosis 3 types of vessels , depending on the chemical composition of hyaline:

simple hyaline - occurs under the action of angioneurotic factors (spasm or vasodilation)  plasmorrhagia  hyalinosis. (hypertension, atherosclerosis, hemolytic anemia, Werlhof's disease)
lipohyalin – HYALIN + LIPIDS, -LIPOPROOTEIDS (diabetes mellitus)
complex G. – GTHALIN + IMMUNE COMPLEXES (rheumatic diseases)

HYALINOSIS OF CONNECTIVE TISSUE

Occurs due to fibrinoid swelling. At the same time, blood plasma proteins and polysaccharides are layered onto the destructively altered connective tissue, and subsequently - protein denaturation and precipitation (chronic ulcer, adhesive disease, tumors, burn disease).

Macro: Organ deformation. If an organ has a capsule, it thickens (“glaze” capsule)

Meaning:

An irreversible process, but some hyaline masses can resolve on their own.

Leads to a sharp disruption of organ function (heart valve leaflets  heart failure; kidney  renal failure)

Amyloidosis

Amyloidosis is a mesenchymal dysproteinosis, characterized by the appearance of abnormal fibrillar protein with the subsequent formation of a complex protein-polysaccharide complex - AMYLOID.

Rokitansky, 1844

Amyloid is a glycoprotein, the main component of which is fibrillar protein - F component.

F-component: there are 4 types:

AA-bilok – not associated with IG

AL protein – associated with IG

AF protein – synthesized from prealbumin

ASC 1 protein - synthesized from its precursor - prealbumin

The second component is P-component(plasma component). These are blood polysaccharides.

AMYLOID = F-component + P-component + GAG + FIBRIN + IMMUNE COMPLEXES

Amyloid is a fairly stable substance. Immune cells do not recognize amyloid.

Pathogenesis:

4 theories of amyloid origin.

The theory of dysproteinosis (with a profound disorder of protein metabolism)
Immunological theory
Theory of cellular local secretion
Mutagenic theory - according to the theory, a cell mutation occurs and this cell begins to synthesize an abnormal protein. The immune system does not recognize these cells.

According to this theory, amyloid develops in 4 stages:

1. Pre-amyloid – cellular transformation occurs  the cell turns into an AMYLOIDOBAST. As a rule, these are RES cells - macrophages, plasmablasts.
2. Synthesis of abnormal protein by amyloidoblasts - F-component
3. Formation of amyloid substance. The F component forms the amyloid scaffold.
4. Amyloid synthesis.

Amyloidosis classification.

Primary (idiopathic) – is generalized; synthesis of AL protein (mainly affected: cardiovascular system, skeletal muscles, skin, nerves).
Hereditary - most common in those ethnic groups where consanguineous marriages occur; AF protein (nerve fibers, kidneys).
Age (senile) – ASC 1 protein (heart, arteries, brain, pancreas).
Secondary - occurs as a result of the synthesis of AA protein (diseases that are purulent-destructive in nature: tbc, bronchiectasis, osteomyelitis, paraproteinemic leukemia, tumors, rheumatoid arthritis).

Macro: in the early stages the organ remains unchanged (over time the organ increases in size, dense, easily breaks, lightning appearance (“greasy”)

Micro: METACHROMASIA

What is hyalinosis

Hyalinosis is a proteinaceous extracellular degeneration, which is characterized by the formation of homogeneous, translucent, dense masses resembling hyaline cartilage. This pathological process can manifest itself as an independent disease, or it can occur with the underlying disease and be one of the symptoms of its severe course.

Etiology
Classification
Symptoms
Diagnostics
Treatment
Possible complications
Prevention

Dystrophy can spread and affect most tissues and organs of the human body. The disease occurs quite often in adults, regardless of gender. The reasons for the appearance have different origins.

The disease is diagnosed after a comprehensive study, and in severe cases the prognosis is unfavorable.

Causes of the disease

This pathological process is a collective concept that combines various biological processes.

The main causes of pathological processes in tissues or organs are:

systemic diseases (diabetes, vascular, heart, joint diseases);
protein metabolism disorders.

Pathology can manifest itself in a local form, or it can affect the entire system.

Hyalinosis of the spleen capsule, like other forms, causes destruction of the fibrous structures of connective tissues, and also leads to changes:

in metabolism;
in the immune system;
tissue impermeability is impaired;
causes protein accumulation;
leads to an increase in the fibrous structure of tissues.

During the process of dystrophy, hyaline fibrillar protein is formed, which accumulates in tissues and is stable:

to the effects of alkalis;
does not oxidize;
it is not affected by enzymes.

However, under the influence of eosin and fuchsin, it changes color to yellow or red.

The disease can be asymptomatic and not manifest itself in any way, or it can have a severe course and cause various disorders in the tissues or organs where it is localized. Excessive formation of hyaline causes compaction, pallor, and can lead to deformation changes and shrinkage of organs.

Classification

Pathology has two forms of existence in connective tissue and blood vessels; it can be both local (focal) and systemic in nature. The local character includes hyalinosis of the heart valves, which contributes to the enlargement of the organ, dilates the ventricles, the mitral valve becomes dense, with a whitish tint, and is deformed.

Vascular hyalinosis is of three types:

simple - formed due to the release of plasma from its bed due to expansion and decrease in the density of vascular walls, often this picture is observed with hypertension and atherosclerosis;
lipohyalin – its structure contains lipids and beta-lipoproteins, found in diabetes mellitus;
complex – consists of immune complexes, fibrin and degradable components, found in rheumatic immunological diseases.

The pathological process in blood vessels develops due to increased blood pressure and decreased vascular permeability or prolonged vascular spasm.

Pathology of connective tissue occurs after its damage and disorganization under the influence of immune complexes. It manifests itself in rheumatic lesions of the valves of the heart, their patency and mobility decrease, they become denser. The accumulation of homogeneous substance causes an increase in the distance between cells.

Stromal hyalinosis is quite common. The stroma consists of connective tissue, which performs the supporting function of the supporting structures of the organ, and if it is damaged, the functional abilities and functioning of the organ are disrupted.

The pathological process of serous membranes is one of the variants of the outcome of fibrous inflammation, which is characteristic of peritonitis, pericarditis, and pleurisy. In this case, fibrin is deposited on the membrane. Most often, hyalinosis of the spleen capsule is observed, which manifests itself locally and causes a milky-white thickening of the capsule: it seems to be covered with glaze. The same picture is observed in the liver, heart, and lungs. The distance between the shell increases due to the accumulation of matter.

Hyalinosis of the spleen capsule

Symptoms of hyalinosis

Signs of the disease will directly depend on in which organ or tissue the pathological processes are observed:

vascular hyalinosis - patency and elasticity are impaired, bleeding, frequent headaches and inflammation are possible, vascular patency may be impaired, which reduces the supply of oxygen and nutrients to organs and tissues;

hyalinosis of the pleura - causes a chronic process of pulmonary adhesions due to a disorder of protein metabolism or as a result of tuberculosis, in this case pulmonary ventilation is limited, but when the process is mild, the course of the disease does not manifest itself in any way;
protein dystrophy in organs - causes their deformation and wrinkling, contributes to pain, sclerosis, partial loss of functionality, nutrition deteriorates and the supply of nutrients and oxygen is disrupted;
pathology of the mammary gland - causes compaction and heaviness in the breast, can resolve on its own and not cause any complications due to failures in protein formation;
hyalinosis in fibroids - observed during inflammatory processes or tumor-like formations, can manifest as painful sensations, discharge from the genitals.

Local hyalinosis is amenable to therapeutic measures, but systemic hyalinosis has adverse consequences.

When hyalinosis of the spleen capsule appears, its functionality is most often disrupted, which leads to dire consequences: blood flow and metabolism are disrupted, and infected blood cells are filtered out.

In this case, a person experiences severe ailments, pain, bleeding occurs, and immunity deteriorates.

Diagnostics

The diagnosis is made only after a comprehensive examination.

The patient is referred for the following studies:

A general and biochemical blood test is taken;
urine is examined;
prescribe ultrasound examination of blood vessels, internal organs or tissues;
Magnetic resonance imaging may be prescribed;
smears are taken and an ultrasound of the female genital organs is performed;
X-ray examinations of the lungs.

The macropreparation may have adhesions, compactions, and a whitish enveloping of the organ is observed. After research, the cause and type of the disease are determined, and depending on the diagnosis, treatment will be prescribed.

Treatment of hyalinosis

After establishing the main diagnosis, the doctor determines the tactics of therapeutic measures. First of all, the main pathological process is eliminated.

Means may be prescribed to improve performance:

spleen;
hearts;
vessels;
liver;
lungs.

For inflammatory processes, antibiotics and non-steroidal anti-inflammatory drugs are prescribed. In very severe cases, surgical intervention is prescribed, which is aimed at eliminating the pathological process.

Possible complications

Such a disease can be provoked by an existing disease, being one of its symptomatic manifestations and aggravating the clinical picture.

The consequences of the pathology are as follows:

the functioning of organs, systems, tissues is disrupted;
deformation occurs in places where hyalines are localized;
contributes to the appearance of heart disease, worsening diabetes, and impaired vascular patency;
causes inflammatory processes.

At the first deviations from the norm and the appearance of the above symptoms, you should contact the clinic for help, since hyalinosis of the spleen capsule, like any other form, leads to serious consequences.

Prevention

The best prevention is to maintain a healthy lifestyle, timely treatment of all diseases, proper nutrition and preventive medical examination.

What to do?

If you think that you have Hyalinosis and symptoms characteristic of this disease, then doctors can help you: therapist, pediatrician.

Diseases with similar symptoms:

Shingles (overlapping symptoms: 3 of 9)

Shingles, which is also defined as herpes zoster or herpes zoster, is a disease in which the skin is affected, and the lesion is more pronounced and massive in appearance than the traditional version of herpes of the lips. Shingles, which can affect both men and women, is particularly common in people over the age of fifty, although it may occur in younger people.

Problem Definition

Hyalinosis is a pathology in which hyaline (fibrillar protein) is deposited in the walls of blood vessels and connective tissue in the form of dense translucent masses. Hyalin, which is a protein, contains fibrin, plasma proteins, lipids and immunoglobulins. It is not affected by acids, enzymes and alkalis. Currently, hyalinosis is a disease that is very common and is observed in most elderly people who have hypertension, hypertension or diabetes. The vessels are affected to a greater extent, the connective tissue is affected to a lesser extent. With this pathology, the tissue becomes denser, so the disease is classified as a type of sclerosis.

The emergence and development of pathology

The morphogenesis of hyalinosis is very complex and depends on the type of pathology (vessels, connective tissue or serous membranes). The main thing in its formation is the destruction of cells of fibrous structures and leakage of blood vessels as a result of pathological processes in the immune and nervous systems, metabolism. In this case, hyaline is formed from the smooth muscle cells of the vessel walls. In most cases, vascular hyalinosis can appear as a consequence of various diseases: hypertension, rheumatism, inflammatory processes, necrosis or sclerosis. As a result of sclerosis, this pathology forms in scars and adhesions, vessel walls, or is involved in the formation of blood clots. This happens due to metabolic disorders in connective tissue. There is also hyalinosis of the spleen capsule, in which the capsule increases in volume and becomes saturated with proteins.

Vascular hyalinosis

Small arteries and areolas are affected by this pathology. It occurs as a result of the destruction of the endothelium and cell membranes that line the walls of blood vessels. In this case, the membranes of the vessels become thinner, they turn into thickened tubes with a narrowed or closed lumen. This process is most often observed in the brain, kidneys, pancreas and retina. This manifestation is typical for hypertension, diabetes mellitus and disorders of the human immune system. As a physiological process, arterial hyalinosis occurs in the spleen in elderly people.

Types of vascular hyalinosis

In medicine, it is customary to distinguish three types of vascular hyalinosis:

Simple, characterized by the occurrence of plasma leaving the bloodstream. This phenomenon is often observed in atherosclerosis and hypertension.
Lipohyalin, which contains lipids and is characteristic of people who suffer from diabetes.
Complex hyalinosis, which consists of immunoglobulin, fibrin and is typical for people with diseases of the immune system, rheumatism.

As a result of hyalinosis, nephrosclerosis develops in hypertension, the kidneys become wrinkled and have a fine-grained surface.

Consequences

With vascular hyalinosis, the consequences are irreversible, so the prognosis is unfavorable. Pathology leads to deformation and atrophy of the organ, as a result of which its failure develops and hemorrhages (stroke) appear. In the case of connective tissue hyalinosis, partial resorption of hyaline is possible, so to some extent the pathological process may be reversible. This applies, for example, to the mammary glands. This pathology can also lead to organ failure. As for scars, there are no special disorders observed here, but only a cosmetic defect.

Clinical picture

Vascular hyalinosis does not manifest itself clinically, with the exception of damage to the vessels of the fundus, which can be determined using ophthalmoscopy. Small arteries appear thickened and curved. The connective tissue affected by this disease is dense, inelastic, and cream-colored. This is clearly visible in keloid scars and heart valves. When the serous membranes are damaged, the tissue thickens and acquires a milky tint. If there is hyalinosis of the spleen or liver, then these organs will look as if they were doused with sugar icing. In this case, the disease will be called glaze spleen or glaze liver.

The invisible picture of pathology

With this pathology, thickening of the walls of the arteries is observed due to the accumulation of hyaline masses in them, which partially or completely close the lumen. In this case, the renal tangles are replaced by this mass. In pathologies of connective tissue and serous membranes, the presence of hyaline masses with blood glycoproteins is visible. The narrowing of the lumen of the vessels leads to barotrauma, which is not prevented by contraction of the areola, since it will lose this ability. This leads to the saturation of tissue areas that are supplied with blood by plasma, so it loses its function. Thus, hyalinosis of the renal tangles gradually develops, chronic renal failure and retinopathy appear, which leads to complete blindness. Since hyalinosis is also a pathology in connective tissue, if it occurs in the heart valves, this contributes to their deformation and leads to their insufficiency. Pathology of the serous membranes is most often detected during operations or autopsy. If it is found in the spleen or liver, this can lead to the filling of these organs with blood, stretching of their capsule and the appearance of pain. Lipids and salts are quite often deposited in the tissue as a result of its breakdown into simple chemical compounds.

Diagnostics

To identify hyaline, eosin staining is performed, and it will have a pink color. Van Gieson stain will have a result depending on the age of the patient (from yellow to red). The dyes used here are fuchsin and picric acid. The appearance of hyaline in dead tissue is indicated by casts in the urine, thrombotic masses and inflammatory exudate. For diagnostic purposes, histological studies are carried out, and hyalinosis is observed in the intercellular substance of the connective tissue. Tissue necrosis occurs, which is often accompanied by rupture of the vascular wall, the appearance of hemorrhages and thrombosis. Under a microscope, you can detect swelling of collagen fibers, cell atrophy, loss of vascular elasticity, hardening of organs, and changes in their color. Externally, the tissues affected by hyalinosis are not changed.

Differential diagnosis

It is necessary to distinguish between physiological hyalinosis, which appears as a result of aging of the body, and a pathological process. This disease is also similar to the transformation of dead tissue and secretion products. It must be remembered that pathological processes in the uterus and mammary glands are reversible, since the functions of these organs are enhanced.

Forecast

The outcome of segmental hyalinosis is renal failure. In rare cases, nephrotic syndrome occurs, which is inherited. Nephritis is often combined with pathologies of kidney development. Children mainly die due to failure of this organ.

Thus, hyalinosis is changes in connective tissue that lead to pathologies and are a consequence of various diseases. This process is also observed during the aging of the body and is physiological in nature.

Currently, all sorts of diseases are not encountered in medicine. Connective tissue diseases, in particular hyalinosis, are no exception. This is the growth of hyaline in the connective tissue, forming dense masses that resemble cartilage. This pathology is observed in various diseases, for example, hypertension, lupus erythematosus, atherosclerosis, diabetes mellitus, and so on. It is characterized by an increase in the permeability of blood vessels and body tissues, as well as the impregnation of tissues with plasma proteins. In this case, human vessels have a narrowed lumen and resemble dense tubes in their structure. This process is irreversible, but in some cases partial resorption of hyaline is possible. In some cases, this pathology can be attributed to the physiological process of the body in old and mature age. This could be, for example, hyalinosis of the vessels of the spleen, etc.

Problem Definition

The emergence and development of pathology

Morphogenesis of hyalinosis is very complex and depends on the type of pathology (vessels, connective tissue or serous membranes). The main thing in its formation is the destruction of cells of fibrous structures and leakage of blood vessels as a result of pathological processes in the immune and nervous systems, metabolism. In this case, hyaline is formed from the smooth muscle cells of the vessel walls. In most cases, it can appear as a consequence of various diseases: hypertension, rheumatism, inflammatory processes, necrosis or sclerosis. As a result of sclerosis, this pathology forms in scars and adhesions, vessel walls, or is involved in the formation of blood clots. This happens due to metabolic disorders in connective tissue. There is also a method in which the capsule increases in volume and is saturated with proteins.

Vascular hyalinosis

Small arteries and areolas are affected by this pathology. It occurs as a result of the destruction of the endothelium and cell membranes that line the walls of blood vessels. In this case, the membranes of the vessels become thinner, they turn into thickened tubes with a narrowed or closed lumen. This process is most often observed in the brain, kidneys, pancreas and this manifestation is typical in hypertension, diabetes mellitus and disorders of the human immune system. How the physiological process occurs in the spleen in older people.

Types of vascular hyalinosis

In medicine, it is customary to distinguish three types of vascular hyalinosis:

Simple, characterized by the occurrence of plasma leaving the bloodstream. This phenomenon is often observed in atherosclerosis and hypertension.
Lipohyalin, which contains lipids and is characteristic of people who suffer from diabetes.
Complex hyalinosis, which consists of immunoglobulin, fibrin and is typical for people with diseases of the immune system, rheumatism.

As a result, hyalinosis develops and hypertension becomes wrinkled and has a fine-grained surface.

Consequences

Clinical picture

Vascular hyalinosis does not manifest itself clinically, with the exception of damage to the vessels of the fundus, which can be determined using ophthalmoscopy. Small arteries appear thickened and curved. The connective tissue affected by this disease is dense, inelastic, and cream-colored. This is clearly visible in keloid scars and heart valves. When the serous membranes are damaged, the tissue thickens and acquires a milky tint. If there is a liver, then these organs will look as if they were doused with sugar icing. In this case, the disease will be called glaze spleen or glaze liver.

The invisible picture of pathology

Diagnostics

To identify hyaline, eosin staining is performed, and it will have a pink color. Van Gieson stain will have a result depending on the age of the patient (from yellow to red). The dyes used here are fuchsin and picric acid. The appearance of hyaline in dead tissue is indicated by thrombotic masses and inflammatory exudate. For diagnostic purposes, histological studies are carried out, and hyalinosis is observed in the connective tissue. Tissue necrosis occurs, which is often accompanied by rupture of the vascular wall, the appearance of hemorrhages and thrombosis. Under a microscope, you can detect swelling, cell atrophy, loss of elasticity of blood vessels, hardening of organs, and changes in their color. Externally, the tissues affected by hyalinosis are not changed.

Differential diagnosis

Forecast

Hyalinosis is a type of dysproteinosis in which homogeneous translucent dense masses (hyalin) are formed in the tissue, resembling hyaline cartilage. Hyaline consists of 1. fibrillar protein; 2. plasma proteins; 3. immune complexes; 4. lipids. Staining: 1. acid dyes (eosin, acid fuchsin); 2. picrofuchsin according to van Gieson - red or yellow; 3. positive CHIC reaction. Types of hyalinosis: 1. intracellular (Roussell's bodies in chronic inflammation, formed from plasma cells in the mucous membranes); 2. physiological (uterine vessels after childbirth, ovarian tissue in old age); 3. dead materials (hyaline blood clots, hyaline cylinders in the kidney tubules) 4. hyalinosis (hyaline dystrophy) of the walls of blood vessels (hyalinosis of arterioles is of greatest importance in hypertension) and connective tissue. Types of hyaline: 1. simple (for hypertension); 2. complex (with rheumatism); 3. lipohyalin (for diabetes mellitus). Causes: develops as a result of 1. plasma impregnation; 2. fibrinoid swelling; 3. sclerosis and necrosis.

Morphogenesis and significance: arterioles 1. neurogenic spasm of arterioles; 2. damage to the endothelium, argyrophilic membranes (a type of connective tissue fibers capable of binding silver salts) and smooth muscle fibers; 3. increasing the permeability of the vessel wall; 4. plasmorrhagia – saturation of the vessel wall with plasma proteins; 5. coagulation and compaction of protein with the formation of a dense hyaline-like substance. Significance - Causes significant impairment of renal function - the development of chronic renal failure, uremia. Connection: 1. destruction of collagen; 2. impregnation of tissue with plasma proteins and polysaccharides; 3. transformation of connective tissue bundles into a homogeneous dense cartilage-like mass. Meaning: Significant functional impairment, loss of elasticity, deformation.

Hyalinosis can be a manifestation of general disorders of protein metabolism, but most often it is a local focal or systemic (in blood vessels) dystrophic process; Hyalinosis manifests itself in both physiological and pathological conditions.

The concept of “hyalinosis” combines different origins, development mechanisms and biol. essence processes. The main thing in the development of hyalinosis is the destruction of fibrous structures of connective tissue and an increase in tissue-vascular permeability due to angioedema (dyscirculatory), metabolic, inflammatory and immunopathological processes (see Plasmorrhagia). As a result of a violation of permeability, tissue is impregnated with plasma proteins and their unchanged fibrous structures are absorbed, followed by precipitation. The resulting hyaline has different chemical properties, depending on the nature of the disease. composition (for example, hyaline for diabetic microangiopathy and hyaline for so-called immune complex diseases).

Hyalinosis refers to extracellular (mesenchymal) dysproteinosis. The appearance of hyaline droplets (hyaline droplet dystrophy) or spheres (hyaline balls) in the cytoplasm is not associated with hyalinosis. Hyalin is a fibrillar protein (Figure 1), in the construction of which plasma proteins, in particular fibrin, take part. Immunohistochemical studies reveal not only fibrin in hyaline, but also components of immune complexes (immune globulins, complement fractions). Hyaline masses are resistant to acids, alkalis, enzymes, are easily painted with acidic paints (eosin, acid fuchsin), and are painted yellow or red with picrofuchsin; Lipids and calcium salts can be deposited in hyaline masses. The appearance of organs and tissues during hyalinosis depends on the stage of the process; More often, hyalinosis does not manifest itself in any way and is detected only by microscopic examination. In cases where the process is pronounced, the tissues become pale, dense, and translucent. Hyalinosis, in particular of arterioles, can lead to deformation and shrinkage of organs (for example, the development of arteriolosclerotic nephrocirrhosis, valvular heart disease).

Hyalinosis is observed in connective tissue, organ stroma and vessel walls (Figure 2) as a result of plasma impregnation, fibrinoid swelling, sclerosis, chronic inflammation, necrosis. As a result of plasma impregnation, vascular hyalinosis occurs, most often in the arterial system. The most common is Hyalinosis of small arteries and arterioles (see Arteriolosclerosis). Hyalinosis of arterioles occurs as a result of damage to the endothelium, argyrophilic membranes and smooth muscle fibers and impregnation of the vessel walls with blood plasma proteins, which are then enzymatically affected, coagulated and compacted, turning into a hyaline-like dense substance. Hyaline masses push outward and destroy the elastic lamina, which leads to thinning of the middle shell; as a result, the arterioles turn into thickened, dense tubes with a sharply narrowed or completely closed lumen. Hyalinosis of small arteries and arterioles, which is systemic in nature, but most pronounced in the kidneys (Figures 3 and 4), brain, retina, pancreas, skin (Figure 5), is especially characteristic of hypertension (hypertensive arteriolohyalinosis). Often, systemic hyalinosis of arterioles and small arteries is observed in chronic vascular glomerulonephritis and symptomatic arterial hypertension of any origin. Widespread hyalinosis of arteries of elastic and elastic-muscular types is constantly observed in atherosclerosis, diabetes and reflects the processes of plasmorrhagia and insudation characteristic of these diseases. Local arterial hyalinosis as a physiological phenomenon occurs in the spleen of adults and elderly people, reflecting the functional and morphological characteristics of the spleen as a blood deposition organ.

As a result of fibrinoid swelling, leading to the destruction of collagen and saturation of the tissue with plasma proteins and polysaccharides, the connective tissue bundles swell, lose fibrillarity and merge into a homogeneous dense cartilage-like mass; cellular elements are compressed and undergo atrophy. A similar mechanism of development of hyalinosis of the connective tissue itself and the vascular wall is especially often observed in diseases with immune disorders. Thus, systemic hyalinosis of connective tissue and vessel walls is expressed in collagen diseases: Hyalinosis of the heart valves, myocardial stroma - in rheumatism, Hyalinosis of synovial membranes - in rheumatoid arthritis, Hyalinosis of the skin - in scleroderma, Hyalinosis of the vascular walls - in arteritis nodosa and systemic lupus erythematosus. The same is the mechanism of widespread glomerular hyalinosis in immune complex glomerulonephritis. In these cases, hyaline is built on immune complexes, which confirms the role of immunological mechanisms in the development of hyalinosis. Local hyalinosis can result in fibrinoid changes in the bottom of a chronic gastric ulcer, in the tissue of the appendix with appendicitis, as well as in the focus of chronic inflammation.

Hyalinosis as a result of sclerosis is mainly local in nature. This is Hyalinosis in scars (Figure 6), fibrous adhesions of serous cavities, Hyalinosis of the vascular wall in atherosclerosis, involutional sclerosis of the arteries, in the organization of a blood clot, Hyalinosis of the capsule surrounding any pathological focus, tumor stroma. Hyalinosis in these cases is based on local metabolic disorders of the connective tissue; Hyalinosis of necrotic tissues, fibrinous deposits and other organic substances has a similar mechanism.

In most cases, the process is irreversible, but resorption of hyaline masses is also possible. Thus, hyaline in scars, the so-called keloids (see), can undergo loosening and resorption. Let's reverse Hyalinosis of the mammary gland, and the resorption of hyaline masses occurs in conditions of hyperfunction of the gland. In some cases, hyalinized tissue becomes mucus.

The functional significance of hyalinosis varies depending on the location, degree and prevalence of the process. For example, hyalinosis in small skin scars usually does not cause any particular distress. Widespread hyalinosis leads to significant functional disorders, as is observed, for example, with rheumatism, scleroderma, hypertension, and diabetes.

Hyalinosis is one of the types of protein metabolism disorders. It leads to the accumulation in tissues of homogeneous, dense and translucent masses of the organic substance hyaline - a complex protein that is resistant to alkalis, acids, and enzymes.

What is hyalinosis

Hyalinosis is characterized by increased permeability of the vascular walls and tissues of the body, due to which they are impregnated with plasma proteins. Normally this should not happen. As a result, the vessels narrow and become like dense tubes. The phenomenon is considered irreversible, but in some cases partial resorption of hyaline accumulations is possible.

Classification

There are three forms of pathology, which differ in the mechanism of development and other characteristics:

Vascular hyalinosis. It develops when blood pressure rises and the walls become excessively permeable.
Hyalinosis of connective tissue. This type occurs due to mucoid or fibrinoid swelling, when the tissue is impregnated with plasma proteins and polysaccharides;
Hyalinosis of serous membranes. Its cause is the appearance on the surface of the membrane of an organizing inflammatory fluid with a high content of fibrinogen.

According to prevalence, hyalinosis is divided into:

systemic (common);
local.

In this case, the pathology of blood vessels and connective tissue occurs in both variants, and hyalinosis of the serous membranes is exclusively local.

Causes of pathology

The reasons for the development of pathology associated with the accumulation of hyaline in blood vessels and tissues are:

diabetes;
diseases of the cardiovascular system;
joint damage;
disturbances in protein metabolism processes;
inflammatory pathologies.

Vascular hyalinosis in most cases is systemic in nature, but more often affects:

kidney structures;
brain;
organs of vision;
pancreas;
skin tissue.

It is one of the signs:

hypertension;
diabetic microvascular damage;
immunity disorders.

Hyalinosis of connective tissue occurs as a result of its disruption due to the action of immune complexes. This happens, for example, with rheumatic changes in the heart valves.

Hyalinosis of the serous membranes is considered one of the likely outcomes of the fibrotic inflammatory process, for example, with:

peritonitis (inflammation of the peritoneum);
pericarditis (inflammation of the pericardial sac);
pleurisy (inflammation of the pulmonary membranes).

Among the causes of hyalinosis are not only pathological, but also physiological processes that are considered normal, for example, in an aging organism.

Symptoms

The set of signs of pathology is determined by its location:

Hyalinosis of blood vessels narrows their lumen, impairs patency and reduces the elasticity of the wall, which is why bleeding and periodic headaches are likely. Arteries with a disturbed structure lead to a deficiency of oxygen, as well as nutritional components in tissues and organs.
Hyalinosis of the pleura triggers the adhesive process in the lungs. Ventilation becomes worse, but when the disease is mild, the person does not notice it.
Hyalinosis, which affects organs, leads to their deformation and sclerosis, as well as partial loss of performance. Among other things, it causes discomfort and pain. So:
- with the phenomena of protein dystrophy in the mammary gland, the organ becomes denser, causing a feeling of heaviness;
- with hyalinosis in uterine fibroids, pain in the lower abdomen is manifested, which is accompanied by vaginal discharge.

In case of pathology affecting the spleen capsule, general malaise develops against the background of pain, and bleeding is possible.

What is the danger

Hyalinosis is the result and one of the symptoms of various diseases, so its main danger is that it can aggravate the course of pathologies. As a result:

the functioning of organs is disrupted;
tissues are deformed in places of hyaline deposits;
heart disease develops;
the course of diabetes is aggravated;
vascular patency worsens;
inflammation develops.

Hyalinosis in pregnant women can lead to arrest of fetal development. This occurs when, due to pathology, blood clots form in the capillaries through which oxygen and nutrition are delivered to the tissues. As a result, blood flow is disrupted and the embryo dies.

Hyalinosis in children can take dangerous forms. For example, there is an infantile type of systemic hyalinosis, which is considered a rare but dangerous condition. Babies with this congenital pathology die before the age of two, and those who survive become deeply disabled.

Diagnostics

Hyalinosis is detected after a set of diagnostic measures, which include:

general and biochemical blood test;
urine test;
ultrasound scanning of blood vessels, as well as organs and tissues;

Depending on the probable causes of the disease, the doctor may additionally prescribe:

smears and ultrasound of the female genital organs;
X-ray of the lungs.

Based on the diagnostic results, the cause of hyalinosis and its type are identified, and then therapy is prescribed.

Treatment

The development of hyalinosis can be influenced in the process of eliminating the pathologies that became its causes. Thus, for diseases of internal organs and systems, medications are prescribed to improve their functioning. Inflammatory processes are eliminated with antibacterial and non-steroidal anti-inflammatory drugs. As a radical measure in particularly severe cases, the surgical method is used.

Forecast

The prognosis largely depends on the localization and degree of development of the process. For example, hyaline accumulations in scars are not dangerous for serious disorders and can resolve. The systemic version of the disease, on the contrary, leads to serious disruptions in the body and is dangerous with adverse consequences, as happens, for example, with rheumatic lesions, hypertension, diabetes and other diseases.

Hyalinosis is sometimes asymptomatic, so it is not immediately detected. To avoid illness and related disorders, it is recommended to lead a healthy lifestyle, periodically check your health and promptly treat identified pathologies.

1. Hyalinosis of the vessels of the spleen- in the central arteries of the follicles in the thickened vascular wall among the fibrous connective tissue there are homogeneous masses of hyaline, intensely stained with eosin (specimen No. 38).

2. Hyalinosis of the spleen capsule- in the thickened capsule, among the fibrous connective tissue, there are lumpy homogeneous masses of hyaline, intensely stained with eosin (specimen No. 54).

3. Amyloidosis of the spleen, sago type (Congo mouth stain)- homogeneous pink masses of amyloid are selectively deposited in the follicles of the spleen, leaving the red pulp free (specimen No. 42).

4. Amyloidosis of the spleen, "sebaceous" type (Congo mouth stain)- homogeneous pink masses of amyloid are deposited in the red pulp of the spleen along the basement membranes of the sinuses, the latter being separated by amyloid masses. In addition, amyloid in the form of pink corollas is deposited along the vessels. In the follicles of the spleen, amyloid deposits are insignificant (specimen No. 41).

5. Liver amyloidosis (hematoxylin-eosin stain)- homogeneous pale pink masses of amyloid are deposited in the spaces of Disse between the basement membranes of the sinusoids and hepatic beams. Hepatocytes, compressed by amyloid, are reduced in size; in their cytoplasm in the perinuclear zone there are grains of lipofuscin, colored golden yellow (preparation No. 40).

6. Amyloidosis of the kidney (Congo mouth stain)- homogeneous masses of amyloid, colored red, are visible in the glomeruli. Amyloid is also deposited along the basement membranes of the epithelium of the tubules and arterioles (specimen No. 44).

7. Amyloid nephrosis with wrinkling– in the glomeruli along the vascular loops and in the tubules along the basement membranes, homogeneous masses of reddish-brown amyloid are visible. In places, connective tissue grows between the convoluted tubules. In the lumen of part of the tubules there are red blood cells and pinkish protein masses. Lymphoid infiltration is noted (preparation No. 20).

8. Adrenal amyloidosis (hematoxylin-eosin stain)- pink masses of amyloid are deposited in the adrenal cortex, compressing epithelial cells and blood vessels. The zonal structure of the adrenal cortex is difficult to trace (specimen No. 51).

9. Fatty infiltration of the myocardium or simple fatty heart- muscle fibers are separated by fatty tissue that penetrates the myocardium, right up to the endocardium. The muscle fibers in the area of fatty infiltration are thinned (specimen No. 153).

ISSUES OF PROGRAMMED CONTROL.

1. Indicate what mesenchymal dystrophies you know that develop depending on the type of impaired metabolism.

2. Indicate what mesenchymal dysproteinoses you know.

3. Define the concept of “metachromasia”.

4. Define the concept of “fibrinoid swelling”.

5. Indicate which components are included in fibrinoid.

6. Specify the outcomes of fibrinoid changes.

7. Indicate the manifestation of which reactions is the development of systemic fibrinoid changes.

8. Indicate what components are included in hyaline.

9. Indicate which processes are leading in the development of hyalinosis.

10. Indicate as a result of which processes hyalinosis develops.

11. Indicate the different types of hyalinosis.

12. Indicate which vessels are predominantly affected by hyalinosis.

13. Indicate which diseases are most characterized by the formation of vascular hyaline.

14. Specify the types of arteriolohyalinosis.

15. Specify the types of vascular hyaline.

16. Indicate what type of vascular hyaline occurs in diabetes mellitus (a); hypertension (b); rheumatic diseases (c).

17. Define the concept of “amyloidosis”.

18. Indicate the components of amyloid.

19. Indicate the types of fibrillar amyloid proteins.

20. Indicate by what criteria amyloidosis is classified.

21. Indicate the types of amyloidosis depending on the possible cause of the development of the process.

22. Indicate, as an example, in which diseases secondary amyloidosis develops (5 diseases).

23. Indicate which organ damage is most typical in senile (a, b, c, d) and hereditary (e) amyloidosis.

24. Indicate the etiological forms of AL- (a, b), AA- (c, d), AF- (e), ASC 1 - amyloidosis (f).

25. Indicate which organs are predominantly affected by AL- (a, b, c), AA- (d), AF- (e), ASC 1- (f, g) amyloidosis.

26. Indicate what type of amyloid is formed in primary (a), hereditary (b, c), secondary (d, e), senile (f) amyloidosis.

27. Indicate the types of amyloidosis depending on its prevalence.

28. Indicate the types of amyloidosis depending on the uniqueness of clinical manifestations.

29. Indicate which cells can perform the function of amyloidoblasts in generalized forms of amyloidosis.

30. Indicate the types of amyloidosis depending on the characteristics of amyloid formation in relation to connective tissue fibers.

31. Indicate along which connective tissue fibers parenchymal (a) and mesenchymal (b) amyloidosis develops during the formation of amyloid.

32. Indicate which proteins are precursors of fibrillar amyloid protein in AA - (a) and AL - (b) amyloidosis.

33. Indicate the development of what type of amyloidosis is characterized by a large role of macrophage (a) and lymphoid (b) cellular systems.

34. Indicate where amyloid deposition occurs during the development of the “sago” (a) and “sebaceous” (b) spleen.

35. Indicate the name of the spleen when amyloid is deposited in the pulp (a) and in the lymphatic follicles (b).

36. Indicate the principles by which types of obesity are classified.

37. Indicate the forms of obesity and the reasons for their development.

38. Specify the types of secondary obesity.

39. Indicate what type of obesity develops with physical inactivity (a), Itsenko-Cushing syndrome (b); Gierke's disease (c), brain tumors (d).

40. Indicate the types of obesity according to its external manifestations.

41. Indicate the types of obesity depending on excess body weight.

42. Indicate what indicators are taken into account when characterizing morphological changes in general obesity.

43. Indicate the types of general obesity depending on its morphological characteristics.

44. Indicate what nature of the process is typical for hypertrophic (a) and hyperplastic (b) types of obesity.

45. Define the concept of “lipomatosis”.

46. Define the concept of “obesity.”

STANDARDS OF ANSWERS.

1. a) protein (dysproteinoses); b) fat (lipidoses); c) carbohydrates

2. a) mucoid swelling; b) fibrinoid swelling; c) hyalinosis; d) amyloidosis

3. Metachromasia is a phenomenon based on a change in the state of the main interstitial substance with the accumulation of chromotropic substances

4. Fibrinoid swelling is a process of deep, irreversible disorganization of connective tissue, which is based on the destruction of the main substance and fibers, accompanied by a sharp increase in vascular permeability and the formation of fibrinoid

5. a) fibrin; b) tissue proteins; c) polysaccharides; d) blood plasma proteins; e) nucleoproteins

6. a) necrosis; b) sclerosis; c) hyalinosis

7. a) infectious-allergic; b) allergic (autoallergic; c) angioneurotic

8. a) blood plasma proteins; b) fibrin; c) immune complexes; d) lipids

9. a) destruction of fibrous structures; b) plasmorrhagia

10. a) plasmorrhagia; b) fibrinoid swelling; c) inflammation; d) necrosis; e) sclerosis

11. a) vascular hyalinosis; b) connective tissue hyalinosis

12. a) small arteries; b) arterioles

13. a) hypertension (hypertensive conditions); b) diabetes mellitus; c) immune disorders

14. a) hypertensive; b) diabetic

15. a) simple; b) lipohyalin; c) complex

16. a) lipohyalin; b) simple; c) complex

17. Amyloidosis is a stromal-vascular dysproteinosis, accompanied by a profound disturbance of protein metabolism, the appearance of abnormal fibrillar protein and the formation of amyloid in the interstitial tissue and walls of blood vessels

18. a) fibrillar protein; b) plasma component; c) hematogenous additives; d) chondroitin sulfates

19. a) AA protein; b) AL protein; c) AF protein; d) ASC 1 protein

20. a) due to development; b) by type of fibrillar protein; c) by the prevalence of the process; d) according to clinical manifestations

21. a) primary (idiopathic); b) hereditary (family, genetic); c) secondary (acquired); d) senile

22. tuberculosis, COPD, osteomyelitis, paraproteinemic leukemia (myeloma, Waldenström disease, Franklin disease), cancer, rheumatoid arthritis

23. a) heart; b) arteries; c) brain; d) islets of Langerhans of the pancreas; d) kidneys

24. a) primary (idiopathic); b) secondary; c) secondary; d) hereditary; e) hereditary; f) senile

25. a) heart; b) lungs; c) vessels; d) kidneys; e) peripheral nerves; e) heart; g) vessels

26. a) AL-amyloid; b) AA-amyloid; c) AF-amyloid; d) AL-amyloid; e) AA-amyloid; f) ASC 1 – amyloid

27. a) generalized; b) local

28. a) cardiopathic; b) nephropathic; c) neuropathic; d) hepapathic; e) epinephropathic; f) mixed; g) APUD – amyloidosis

29. a) macrophages; b) plasma cells; c) myeloma cells; d) fibroblasts; e) reticular cells; e) endothelial cells

30. a) pericollagenous; b) perireticular

31. a) reticular; b) collagen

32. a) SAA; b) L – chains of immunoglobulins

33. a) AA – amyloidosis; b) AL – amyloidosis

34. a) lymphatic follicles; b) pulp

35. a) “greasy” spleen; b) “sago” spleen

36. a) according to the etiological principle; b) by external manifestations; c) by the degree of excess body weight; c) by the nature of morphological changes

37. a) primary; b) secondary

38. a) nutritional; b) cerebral; c) endocrine; d) hereditary

39. a) nutritional; b) endocrine; c) hereditary; d) cerebral

40. a) symmetrical (universal); b) top; c) average; d) lower

41. I degree (20 – 29%); b) II degree (30 – 49%); c) III degree (50 – 99%); d) IV degree (100% or more)

42. a) number of adiposocytes; b) size of adiposocytes

43. a) hypertrophic; b) hyperplastic

44. a) high-quality; b) benign

45. Lipomatosis is a pathological process characterized by a local increase in the amount of fatty tissue

46. Obesity is a pathological condition characterized by a general increase in the amount of neutral fats in fat depots

LESSON 5. Violation of calcium and phosphorus metabolism. Stone formation. Rickets. Diseases of the skeletal system.

OBJECTIVE OF THE LESSON: To study morphological changes in tissues due to impaired calcium and phosphorus metabolism, the pathological anatomy of cholecystitis and kidney stones, the mechanism of stone formation, the pathogenesis of rickets and major diseases of the skeletal system.

QUESTIONS TO PREPARATE FOR THE CLASS

1. Conditions for the occurrence of hyper- and hypocalcemia, hyper- and hypophosphatemia in the body.

2. Impaired calcium metabolism with hyper- and hypocalcemia.

3. Disorders of calcium metabolism due to hyper- and vitamin deficiency D.

4. Changes in calcium and phosphorus metabolism due to excess or deficiency of calcitonin. The role of alkaline phosphatase in dystrophic calcification.

5. Disorders of calcium metabolism in intestinal and kidney diseases. Pathogenesis of nephrogenic osteopathy and osteogenic nephropathy.

6. The concept of dystrophic calcification and calcareous metastases. Conditions for their occurrence.

7. Conditions for stone formation. Types of stones. Complications of urolithiasis and cholelithiasis.

8. Calculosis of the gallbladder and calculous cholecystitis. Causes of occurrence. Morphological changes. Outcomes.

9. Rickets. Kinds. The mechanism of development of damage to the skeletal system.

10. Parathyroid osteodystrophy. Etiology, pathogenesis, pathological anatomy.

11. Osteomyelitis. Kinds. Causes and mechanism of development of changes in bone tissue.

12. Fibrous dysplasia. Osteopetrosis. Paget's disease. Etiology, pathogenesis, morphological changes in bone tissue.