Hyalosa: how bad is the pathology. Hyalios and Guial Distrophy

Definition.Hylia - This is a vascular-stromal dystrophy characterized by extracellular accumulation in the tissues of a non-existent protein substance - hyaline1.

The hyaline is not a chemical concept, but only a convenient conditional designation of any protein sediments of a certain appearance.

Massage. Hyaliosa vessels - the phenomenon is extremely common due to the high incidence of the population hypertensive disease and secondary hypertension, in which it is most often observed. Other forms of hyalinosis are less common.

Classification.Three forms of hyalinosis distinguish between the mechanism of occurrence, morphological manifestations and clinical significance are distinguished:

1) hyaliosis vessels;

2) hylia connective tissue ;

3) hylia serous shells.

The hyaline vessels and connective tissue can be common or local, the hyaline serous shells is only local.

Conditions of occurrence. Hylinose in vessels develops under conditions of increasing blood pressure in them and / or increase their permeability. An additional condition can be a long vessel spasm.

Hylinose the connective tissue should precede its preliminary damage and disorganization under the action of immune complexes or other factors.

The s servos of serous shells develops as one of the outcome of the exudative fibrinous inflammation - peritonitis, pericarditis, pleuritis, in which fibrin is deposited locally on the shell.

Mechanisms of occurrence.For vessel hyalinosis, the main mechanism is infiltration. The hyalos is developing in small arteries and arteriols. For arterial hypertension blood plasma proteins under pressure seep into the wall of the vessel, which is called plasmatic impregnation. The wall of the vessel at the same time thickens and stains basophilic. In the future, the components of the plasma penetrated into the wall of the vessel are connected to the components of the intermediate substance in the vessel, forming hyaline. The composition of hyaline can also include products for the destruction of smooth muscle cells Media vessels, although it is not necessary. This process is a multi-step nature, while the severity of the hyalinosis gradually increases.

In addition to the arteries and arterioles, the hypinosa may be subjected to kidney balls. With an elevated blood pressure in the opposing arteriol, the plasma components penetrate into the mesangium of the renal gunpowder (Fig.14.1) and, connecting with the components of the mesangium matrix of the renal glove, turn into hyaline. Probably, in the implementation of this mechanism, the local increase in the magnifier's capillari permeability plays a certain role, since the hyalos is usually initially developing only in some segment of the glorifying (Fig.14.2.) And only then all the balls are affected. As you accumulate in Mesangia, the hyaline capillary loops of the glorula are squeezed and start, and the tangle from vascular formation turns into a lump of homogeneous protein. This contributes to the developing parallel hyaline bringing and incidental arterioles and their narrowing, which contributes to the local increase in blood pressure in the glorifying capillaries and more intensive infiltration.

With vasculitis and glomerulonephritis of infiltration of the walls of the vessels and mesangia kidney glomers contributes, first of all, the increased permeability of the walls of the arteriole and / or capillaries under the action of immune complexes and biologically active substancesexcreted by cells of inflammatory infiltrate and Mesangi macrophages. Due to repeating episodes alcoholic intoxicationaccompanied by an increase in the permeability of arterioles and plasma impregnation of their walls, hyaline vessels in chronic alcoholism develop.

The causes and mechanisms of the often observed in sectional material of the Hyalinose arterioles of the spleen are not clear (Fig.14.3a).

The basis of the hitch of the connective tissue lie infiltration and decomposition. The most studied mechanisms for the development of hyalinose during rheumatism, in which immunoglobulins, which are antibodies against antigens hemolytic Streptococca, begin to cross-react with connective tissue antigens, leading to its disorganization in the form of mucoid and fibrinoidswelling1. The changed components of the connective tissue matrix are attached to the blood plasma proteins, including fibrinogen, which is associated with an increased permeability of microgsudes or, as a special case, sash, feeding their blood-worn blood valves. The compound of these substances leads to the formation of hyaline.

The mechanism of the Hyalinosis of Rubtsov as a whole remains unclear (Fig.14.4a). It is possible to assume infiltration from immature newly emerging vessels, but it is unclear why this is not observed in all cases. It is also impossible to exclude the role of excessive or perversion synthesis: it is known that, for example, that high content in the body of vitamin C contributes to the formation of hyalinosis in the refue, and the suppression of the function of the fat cells is prevented.

The practical mechanism of the formation of hyalinose in tumors occurring in a number of both benign and malignant tumors.

Galyina serous shells is associated with transformation Fibrin, not resolved after the release of fibrinogen from blood vessels during inflammation. In the development of such a transformation, the role is played by some unexplained local factors, since in most cases (including serous shells) unprofitable fibrin is exposed to germinating with a connecting cloth or observation.

Macroscopic pattern. The hyaline vessels is visible only at ophthalmoscopy, and then using a magnifying glass. Arterioles of the eye dna with hypertension or sugar diabetes They look thickened, convulsions - such a picture ophthalmologists is denoted as hypertensive or, respectively, diabetic retinopathy.

The hitch of the connective tissue is most demonstrative with rheumatic lesions of the sash (flaps) of the heart valves: instead of being thin and translucent, they look like milk-white, opaque, thickened, dense, almost unshamed (Fig. 14.5).

The hyaline serous shells is impossible to confuse with anything. Most often, it is observed on the surface of the liver or spleen in the form of a local milk-white thickening of the capsule. With extensive hyaline shells of these organs describe them as "Flashing spleen" or "Flashing liver"for their similarity with a bun, covered with sugar glaze frozen on its surface (Fig.14.6, 14.7a). The focal hyalos is often observed on the front surface of a painfully enlarged heart in the region of its tops, which is associated with heart blows about the inner surface of the sternum (Fig. 14.8a). Rounded or round-star shaped milk-white plaques with a diameter of up to 1-10 cm are found as a random find at the autopsy on the surface of the pleura, less often, peritoneum. The thickness of the centers of gray-shells is usually not more than 0.5 cm, but sometimes it can reach 1 cm or more (Fig.14.9a).

Microscopic pattern.With the hyaline of small arteries and the arterioles of the walls, they look thickened by accumulating homogeneous eosinophilic masses in them, intensely staining with acidic dyes, in particular, eosin (Fig.14a). The core of smooth muscle cells among these masses is rare. In the renal gloms, the deposition of the mass of hyaline is observed in some sector of the glorula, then the entire tangler turns out to be a substituted hyaline and, having lost the capsule, acquires the type of rounded, smaller than the diameter of the normal gloring, eosinophilic homogeneous inclusion in the intertension of the kidney with single kernels in it cells (Fig.14.11A). The hyalosus is not developing in all gloms at the same time: gradually dystropically changed everything becomes more Clushing. Sleeping in vessels with hyaline hypertension is simple, with diabetes mellitus - lipogaline.

With the hyaline of the connective tissue, the distance between the cells forming it is increased due to the accumulation of a homogeneous substance, which is not always painted by eosin so intense as hyaline in the walls of the vessels. A similar picture is observed in the hyaline of serous shells (Fig. 14.12a).

Clinical meaning.Because resistive vessels are subject to hyaline, their defeat plays an unfavorable role in the progression of arterial hypertension. The kidney glukeems at a certain stage are compensated by an increase in the volume and strengthening of the function of even unchanged gloms, however, with a subtotal lesion of the glomeruli, chronic renal failure is developing, which in diabetes can be one of the direct causes of patients' death. The hypertensive and diabetics hypertensive and diabetics leads to impairment of violations until full blindness. The hyalios of the small arteries of the limbs with some systemic vasculites is accompanied by pronounced, sometimes non-supportive pains in non-sufficiently bloodstand limbs and in the end - with fingertips. Similar changes in the limbs are observed in diabetes mellitus, while the skin's arteriole hyalinosis can develop its local pathological thinning, at which the vessels and subcutaneous fatty tissue become visible through the "window". The most common outcome of such a damage is the formation of poorly healing skin ulcers.

The hyaline sash (flap) of the heart valves leads to their wrinkling, incomplete closure and development of heart defect in the form of deficiency of the corresponding valve, which ultimately ends with death from chronic heart failure. The hyaline of the articular tissues and the near-handing scars is accompanied by a violation of movements in these joints.

There is no clinical value in the volume of the hyalosa of serous shells and only indicates the preceding once fibrinous inflammation. If the spleen or liver is in a kind of shell, which prevents them with expansion with increasing blood flow, may be accompanied by pain during exercise.

The hyaline is irrelevant with the exception of the Hyalinosis of the scars, which over time or as a result of some therapeutic effects, for example, the electrophoretic administration of the lidases, may become more elastic, although in this case the hyaline does not completely disappear.

Hyalosa is an irreversible dystrophy, in which homogeneous dense masses are formed in histione, which resemble hyaline cartilages.

Hyalin - a complex fibrillar protein, which includes:

blood plasma proteins

fibrin

lipids

components of immune complexes

Hyaline is painted with eosine and fuchsin in red.

The reasons:

Fibrinoid swelling

Inflammation

Angioedema reactions

Pathogenesis:

A leading role will play increased vascular permeability. Proteins accumulate, GAG. Denaturation arises, protein precipitation.

Hylinose - two species:

Hyaliosis vessels

Hylinose connecting fabric

According to the prevalence of the process:

Hyaliosis vessels

Defeasure predominantly small arteries, arterioles.

In the vessels there are phenomena of plasmoreragia.

Gialin accumulates under the endothelium, over time it takes the entire wall of the vessel.

Hylia vessels 3 species , depending on the chemical composition of Hyalin:

simple hyaline - occurs under the action of angioedema factors (spasm or extension of vessels)  Plasmoria  hyaline. (hypertensive disease, atherosclerosis, hemolytic anemia, Vergood's disease)

lipogaline - Hyalin + Lipids, -Lipoproteins (diabetes)

complex G. - Gtalin + Immune Complexes (Rheumatic Diseases)

Hylinose connecting fabric

Arises due to fibrinoid swelling. At the same time, proteins of blood plasma and polysaccharides are layered on destructively altered connecting tissue, and in the future  denaturation and precipitation of protein (chronic ulcer, adhesive disease, tumor, burn disease).

Macr.:Deformation of the organ. If the organ has a capsule - it thickens ("Flashing" capsule)

Value:

Irreversible process, but some hyaline masses can solve themselves.

Leads to a sharp violation of the function of the organ (sash valve valves  lack of heart; kidney  renal failure)

Amyloidosis

Amyloidosis is a mesenchymal dispennosis, characterized by the appearance of anomalous fibrillar protein, followed by the formation of a complex protein-polysaccharide complex - amyloid.

Rokitansky, 1844g.

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

F-component: distinguish 4 types:

AA-BILK - not associated with IG

Al-protein - associated with IG

AF protein - synthesized from the prehalation

ASC 1-protein - synthesized from predecessor - prehalation

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

AMYLOID = F-component + R-component + Gag + fibrin + immune complexes

Amiloid is a rather resistant substance. Immune cells do not recognize amyloid.

Pathogenesis:

4 Theories of the emergence of amyloid.

Disprotein theory (with deep violation of protein metabolism)

Immunological theory

Theory of cell local secretion

A mutagenic theory - according to the theory, the cell mutation arises and this cell begins to synthesize the anomalous protein. The immune system does not recognize these cells.

According to this theory, amyloid develops in 4 stages:

Doamiloid - Cellular transformation occurs  The cell turns into an amyloidoblast. As a rule, these are RES cells - macrophages, plasmoblasts.

Synthesis amyloidoblasts anomalous protein - F-component

The formation of amyloid substance. The F-component forms the carcass of amyloid.

Synthesis of amyloid.

Classification of amyloidosis.

Primary (idiopathic) - is generalized; Al-protein synthesis (mostly amazed: cardiovascular system, skeletal muscles, leather, nerves).

Hereditary - most frequent in those ethnic groups, where relative marriages occur; AF protein ( nerve fiberskidney).

Age (senile) - ASC 1-protein (heart, artery, brain, pancreas).

Secondary - arises due to the synthesis of aa-protein (diseases that carry purulent-destructive character: TBC, bronchiectatic disease, osteomyelitis, paraprotehemic leukemia, tumors, rheumatoid arthritis).

Macr.: In the early stages, the organ without change (with time the organ increases in size, dense, easily breaks, lightning view ("Silen")

Mikr.: Metachromasia

Hyalosa arterioles is a characteristic phenomenon in the pathological picture of hypertension.

Hyalin masses are deposited in the inner sheath of arterioles under the endothelial cover between the inner and outer leaflets of the elastic plate; The average muscle membrane of the vessels is pushed by the hyaline masses of the dust. The deposition of the hyaline masses leads to a strong thickening of the vessel walls, narrowing the vascular lumen, and sometimes to its full closure. It is possible that hyaline is formed in the walls of the vessel as a result of coagulation of liquid protein mass flowing into the inner layers of the blood vessel. From this point of view, the hyalos can be considered as the outcome of protein impregnation. Hyalin masses are more homogeneous and dense. Jet phenomena around the vessels accumulated in the walls of the Hyalin masses is usually not observed.

Hyalosa arteriol is found not only in patients with hypertension. In a large number of cases and in a weak form, it can be found in the people of elderly who did not suffer from hypertension. Hyalosa arteriole strikes various vascular areas far from equally. The most extent is expressed in the arteries of the spleen, moreover, not only in patients with hypertension, but also in the elderly with normal pressure. Very often and in pronounced degree it occurs with hypertension in the kidney vessels, adrenal glands, pancreas. If the hyalos of the kidney arterioles during hypertension occurs in 97% of cases, then among the norms it is observed only in 2%. Consequently, the kidney arteriole is a phenomenon characteristic of hypertension.

The protein masses entering the thickness of the vascular walls during hypertension may further be resorption. Thus, protein impregnation at first, if it has not achieved a large extent, there is a reversible process. This is extremely important for the circumstance shall serve as an additional stimulus for the energetic treatment of hypertensive.

But most often, protein impregnation and hyaloside arterioles in hypertension are accompanied by destructive and sclerotic changes. Arteriolosclerosis is the usual outcome of later stages. increased pressure. It leads to subsequent disorders of blood supply and nutrition of tissues and organs, even more strongly narrowing the bloodstream in addition to the narrowing, which is created as a result of hypertensive change of the tone of vessels.

Protein impregnation and hyaline arterioles can often be observed with hypertension at the same time, and in different organs these changes may be in different phases of their development, then more freshly, later. This says that plasma impregnation, hyaline and arteriolosclerosis - the forms of one process flowing in the form of repeated flashes, "and every time all new areas of the arterial network are involved in the process." In some organs, there is mainly hyaline, in others - plasma impregnation, in the third - their combination.

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The mechanisms of damage and death of the cell 1. The formation of free radicals (with insufficient oxygen intake in tissue) there are free radical peroxidation oxidation of lipids (spills). 2. Violation of calcium homeostasis. Free calcium in cytoplasm cells is contained in very low concentrations Compared to extracellular one. This state is supported by CA2 +, MG2 + -ATFAs. Ischemia, intoxication cause an increase in calcium concentration in the cytoplasm, which leads to activation of enzymes, damaging cells: phospholipase (cell membrane damage), protease (destruction of the membrane and proteins of the cytoskeleton), the ATPAZ (depletion of ATP stocks) and endonuclease (chromatin fragmentation). 3. ATP deficiency leads to the loss of plasma membrane's facilities and therefore the death of the cell. 4. Early loss of plasma membrane of selective permeability. It occurs when ATP is deficiently, and when the phospholipas is activated. The plasma membrane may be damaged by direct influence of bacterial toxins, virus proteins, complement, physical, chemical agents.

Forms of damage to cells

Distinguish: · ischemic and hypoxic damage; · Damage caused by free radicals, including activated oxygen; · Toxic damage. Ischemic and hypoxic damage. More often due to occlusion arteries. The main mechanisms of death of cells in hypoxia are a violation of oxidative phosphorylation, leading to ATP insufficiency, damage to the cell membranes. The most important mediator of irreversible biochemical and morphological changes is calcium. Cell damage caused by free radicals. It occurs under the influence of chemicals, radiation, oxygen, the aging of cells, the destruction of tumors by macrophages. Free radicals react with inorganic and organic compounds - proteins, lipids and carbohydrates. For damage to the cell, three reactions in which free radicals are entering. · Free radical peroxidation oxidation of lipids (spills) membranes leading to damage to membranes, organelles and cells themselves. · Oxidative transformation of proteins. Free radicals cause cross-binding of amino acids (methionine, histidine, cystine, lysine). Destroys the enzymes by neutral proteases. · DNA damage. Free radicals react with thimine, which is part of DNA, it leads to cell death or its malignant transformation. · Toxic damage. Chemicals (in the form of water-soluble compounds) can act directly, binding to molecules or cellullary cells. For example, mercury binds sulfhydryl groups of the cell membrane and causes an increase in the permeability of the cell membrane and the inhibition of the ATPAZ-dependent transport. If the mercury chloride is getting into the body, the cells of the gastrointestinal tract, kidneys suffer to the greatest extent. Cyanide affects mitochondrial enzymes. Antitumor chemotherapeutic preparations (including antibiotics) cause cell damage by cytotoxic action. Chemical compounds (fat soluble) are first converted to toxic metabolites, which then act on target cells. At the same time, free radicals are formed.

In classical morphology, non-measure damage to the cells is called dystrophy

8. Emergency cells. Apoptosis. Definition of concept. Morphological manifestations of apoptosis and the mechanism of their development. Physiological and pathological importance of apoptosis.

Cell death is irreversible cell damage

Apoptosis-genitically Programmir-I CL death in a living organism. For the removal (emiliation) of unnecessary structures in the process of embryogenesis.

Morphologic manifestation:

1-condensation of nuclear heterochromatin and CL wrinkling with the preservation of the integrity of the organelle and the cell membrane.

2- Cape the collapse on apoptosis, which are membrane structures with the case-and inside with organelles and kernel particles

3- Then apoptotic calves are phagocycable and destroyed with the help of a lease surrounding and cl.

Mechanism:

1-condensation of chromatin is associated with the splitting of nuclear DNA, CT occurs in the sections of the m / in nucleosomes and leads to the formation of fragments.

2- Violation of the volume and size of CL explains the activity of transglutaminase. This far-t catalysis is the recessive binding of cytoplasm proteins, an art shell under the plasma membrane.

3-phageozithosis of apoptotic taurus macrophages and dr cells.

4. The dependence of apoptosis from gene activation is one of its important features. This is ensured by protoncogenic. Apoptossecific genes are revealed, which stimulate or brake the death of the cell. 5. Oncogens and suppressor genes, play a regulatory role in induction of apoptosis (oncogen P53 in the norm stimulates apoptosis; P53 is necessary for the development of apoptosis after DNA damage to radiation).

Physiological and pathological importance of apoptosis:

1-mediate Programmer removal of CL in embryogenesis (incllantation, organogenesis and involution)

2- Hormzavis-I involution CL in adults

3-ensuring the destruction of CL in proliferating cell populations, such as crypt epithelium thin gut and death class in tumors

4- h / h apoptosis are implemented by the death of autoreactive clones of T-Ltmphocytes and pathological atrophy of hormonzavis-X TC

5- apoptosis underlies the pathological atrophy of parenchymathose-X organs after the overlap of the duct

6- with apoptosis The death of CL caused by cytotoxic and T-CL and the death of CL with certain viral diseases

7-apoptosis underlies the KL-th death caused by various and weak damaging impacts - and, CT in large doses lead to the death of CL (term-e-ie, radiation, cytotoxic, anticolum drugs and possibly hypoxia)

9. Necrosis. Definition of concept. Macroscopic and microscopic signs of necrosis.

Necrosis, death, the death of CL and TC in the living organism; At the same time, their entirely ceased to be a completely discontinued by the spectrum of morphological changes, CT developed, after the death of CL in the living TC. This is the result of destroying the action of enzymes on felly damaged CL. The actual and two competitor of the process are developing: the enzyme-E Perevar-E CL and denatourization of proteins.

Necrosis morphogenesis:

1-parangerous-like necrotic, but turn it out.

2-necrobiasis-irreversible dystrophich-e cheat, characterized by the predominance of catabolic reactions over Anabolich and

3-death CT, the time of the occurrence of CT tired-b is difficult

4-autolysis-decomposition of a dead substrate under the action of hydrolytic far-killed cells and macrophages.

Macro: Signs of necrosis can manifest themselves in different ways: they depend on the originality of the body, necrosis occurs in CT, as well as on the nature of the damaging factor.

Micro: Signs relate to both the core and CL cytoplasm, as well as the extracellular matrix.

Change the kernel incl:

Caryopic conjugation of the cores due to the condensation of chromatin;

Kariorexis decay kernels on fucking

Cryolysis- dissolution of the kernel in connection with the activation of hydrolase (RNase and DNase)

Change cyt-s:

Plasmoagulation-denaturation and coagulation of protein with the appearance in the cytoplasm of bright pink boulders

Plasmorexis decay of the cytoplasm on the boulder

Plasmolyisisiso- molten cytoplasm

MODRICS MODRICS MODRICS:

In the splitting of reticular, collagen and elastic fibers under the influence of proteases, elastaz, collagenase. Necroticas are often impregnated with fibrin with the development of fibrinoid necrosis.

Hylia This is a vascular-stromal protein dystrophy characterized by deposits in the tissues of homogeneous translucent dense masses of hyaline resembling the main substance of the hyaline cartilage. Hyalosa should not be confused with hyalinocapor dystrophy, which is intracellular dispennosis.

Classification.

The following types of hyalinose distinguish:

1. hyaline vessels;
2. hyaline connective tissue;
3. galyna serous shells.

Hylinose can be common and local.

Massage.

The hyaline walls of the vessels are very common and meets in most seniors, especially those who suffer from hypertension, symptomatic hypertension, as well as diabetes mellitus. The hyaline connecting tissue is less common, even more rarely - the hyaline serous shells.

Conditions of occurrence.

1. For vessel hyalinosis - raising arterial pressure and an increase in the permeability of the walls of small arteries and arterioles.
2. For the hyalinosis of the connective tissue - the preceding disorganization in the form of mukoidal swelling and fibrinoid changes.
3. For the hyalinosis of serous shells - the presence of an organic fibrinic inflammatory exudate on the surface of the serous shell.

Mechanisms of occurrence.

Hylia Vessels - small arteries, arterioles and glomers of the kidney - arises as a result of an increase in blood pressure, necrosis of smooth muscle cells medium shell, and infiltration of the vascular wall proteins of blood plasma. These proteins, connecting with the products of necrosis of myocytes, form hyaline. Another mechanism for the development of vessel hyalinose, for example, with vasculitis, as well as diabetes mellitus is associated with an increase in the permeability of the vascular wall and the infiltration of plasma proteins that are transformed into hyaline.

The cunning tissue hyaline is preceded by the destruction of its main substance and, in particular, mucoproteins and collagen fibers. Sour mucopolisaccharides arising from the collapse of the decay of Mukoprotein due to their pronounced hydrophilicity lead to swelling of the tissues. At the same time, there is also an increase in the permeability of local microsudes, of which albumin, globulins and fibrinogen are overlooked into the fabric, which, compacting, form hyaline. GALINO of serous shells The result of the evolution of fibrinous inflammatory exudate on the surface of organs having serous diligence.

Macroscopic pattern.

The hyaline vessels macroscopically is not determined, with the exception of the hyalinosis of the vascular bottom, which is detected with ophthalmoscopy using a magnifying glass. Microsudes look thickened and convulsions. The hyalipized connecting tissue is dense, losing elasticity, milky white or slightly creamy color. This is especially good. This is noticeable in the sash valves of the hearts, thickened and sharply deformed, and in the so-called keloid scars. With the guialinda of serous shells, the cloth in this place is sharply thickened, milky-white color, cartilaginous consistency. Authorities with a common hyaline shells - a liver or spleen - look like a touch of sugar icing and are described as a glaze liver or spleen.

Microscopic pattern.

The walls of the hyalinized small arteries and the arterioles are thickened due to the accumulation of homogeneous eosinophilic masses in them, their lumen is significantly narrowed or completely closed. Renal gloves are partially or fully substituted by such masses, in which the cells of single cells are occasionally found. With the hyaline of the connective tissue and serous shells among few fibrocytes - homogeneous eosinophilic masses characterized by a positive chic reaction, indicating the presence of blood glycoproteins in them. The colorful reactions to mucous swelling observed during the mucoid swelling becomes negative.

Clinical meaning.

A significant narrowing of the lumen of a hyalinized vessel leads to a barotraummet, which is normal to reduce the arteriole, which has now lost its elasticity and ability to reduce. The hydrodynamic shot leads to the plasma imgusting of the distal sections of blood supply to the fabric with the loss of their functions. So the hyalosine of kidney glomers is developing with hypertension with a pattern of increasing chronic renal failure. Thus develops diabetic retinopathy, the outcome of which is often full of blindness.

The hitch of the connective tissue of the flaps or the flaps of the heart valves leads to their deformation and incomplete closure, the consequence of which is valve deficiency.

Galyinos of serous shells in the overwhelming majority of cases turns out to be an unexpected find on operations or on autopsy and clinical value does not have. There may be cases of total or subtotal hyalinosis of the surface of the liver or spleen, which in conditions of increased blood flowing organs interferes with the stretching of the capsule and may be accompanied by painful sensations.