Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
The Tashkent Medical Academy Chair: Normal, pathological physiology and pathological anatomy Subject: Pathological anatomy Lecture № 1 The lecturer: Academician M.S.Abdullahodzhaeva Theme: the GENERAL DOCTRINE About ILLNESS CAGE ALTERATION 2011-2012 The purpose: to acquaint with illness definition, an etiology, pathogenesis and classification of illnesses. The basic structural displays of alteration of a cage, compensatoradaptive reactions of a cage to damage. Pedagogical problems: 1. To acquaint with definition «That such illness» and its biological essence. 2. To give an etiology, pathogenesis and classification of illnesses. 3. To open an etiology, pathogenesis cage alterations, to give classification and morphological displays of alteration of a cage. 4. To acquaint with values and outcomes of each kind of a dystrophy and necrosis cages. Expected result: 1. Make illness definition. 2. Know classification of illnesses, their etiology and pathogenesis. 3. List mechanisms of development and kinds of a cellular dystrophy and necrosis. 4. Know macro-and microscopic displays of a dystrophy and necrosis cages. 5. Know value and outcomes of a dystrophy and necrosis cages. 6. Know adaptive reactions of cages to damage. Training methods: lecture. THE SUMMARY In lecture the general concept about illness is given: definition, an etiology, pathogenesis and classification. The biological essence of illness speaks. The reasons, the mechanism of development of alteration of a cage reveal. Kinds of adaptive reactions of a cage are specified in damage. Morphological displays of alteration are allocated. Definition and classification parenchymatous dystrophies is made. Are described macro-and microscopic changes in parenchymatous bodies. Outcomes and value parenchymatous dystrophies speak. THE GENERAL PATHOLOGY ILLNESS DEFINITION Illness of the person concerns the difficult socially-biological phenomenon in which basis reaction of a complete organism to the pathogenic factor lays. In the literature there are various definitions of the illness which generalisation allows to consider illness as infringement of normal human life owing to damage of structure and infringement of function of an organism under the influence of external and internal pathogenic factors. Each illness is accompanied by proof infringements of a homeostasis, loss by an ability organism to adapt to changing conditions of an environment, easing of protective mechanisms. All it leads to development of local and general structural changes. Illness display is closely connected not only with damage, but also with development protective, compensatory and adaptive processes as illness is the adaptation of an organism characterised by specific forms and levels of adaptive certificates (Davydovsky And. В, 1966). The considerable number of illnesses proceeds in the beginning asymptomatic (preillness), and only at any stage of the development it starts to be accompanied by clinical displays. This moment marks that stage of development of illness when it is long accruing structural changes cease to be stopped protective, compensatory and adaptive reactions. In illness development allocate three basic stages: 1) illness formation (preillness, the illness beginning); 2) the developed clinical picture of illness; 3) recover. The parity of structural changes and clinical displays of illness during the different periods are various (Sarkisov D. With, 1988). Aetiology Aetiologies are rather various. Thus can matter not only natural factors (bacteria, viruses, carcinogens, a trauma), but also artificial, caused by activity of the person. The last concern escalating application in a life, foodstuff, pharmacology of synthetic organic connections; wide use of toxic substances (for example, pesticides) in agriculture, the industry etc. In occurrence of illnesses risk factors, that is presence of the contributing conditions promoting disease matter also: a condition of reactance of an organism and it immunobiological mechanisms, senile age, various adverse conditions of an environment, smoking, stresses. For example, in pneumonia development play a role not only infection activators (pneumococcus, staphylococcus, a virus, etc.), but also a condition of reactance of an organism, cooling. In atherosclerosis occurrence smoking, age, the excessive use of alcohol, a motionless way of life matter not only exchange infringement lipids, but also. Eiological factors divide all on external (exogenous) and internal (endogenous). To exogenous to factors influence of microbes, viruses, mushrooms etc. concern mechanical, chemical, thermal. A heredity, age, constitutional features of an organism are considered as endogenous factors. These two groups etiological factors are interconnected, as an organism heredity, its constitution, features of the higher nervous activity were formed under the influence of environment factors on an extent filo - and ontogenetic developments of the person. PATHOGENESIS Pathogenesis is a mechanism of development of illness in whole and its private displays. Studying most the general laws of occurrence, development, a current and an outcome of diseases makes the maintenance of the general doctrine about pathogenesis. The knowledge pathogenesis, no less than aetiologies, is important not only from the theoretical point of view, but also in practical activities of the doctor. Into concept «pathogenesis» enter not only functional shifts, but also the primary morphological changes dated, as a rule, to certain structures. Thus the great value in illness development is got by mutual relations between damage and protection (adaptation, indemnification), that is especially accurately traced on an inflammation example. So, along with occurrence in the centre of an inflammation of pathological processes (alteration, venous stagnation, a blood stop - стаз, the hypostasis, metabolism infringement, formation of toxic substances) develop protective and compensatory processes (the strengthened inflow of arterial blood, increase of intensity of exchange processes to the fabrics surrounding the centre of an inflammation; immune reactions, migration lymphocytes, phagocytosis etc.) . However it is necessary to underline, that protective and compensatory processes in some cases can become the reason of development of pathological processes. For example, immune reactions, protective by the nature, can become the development reason autoimmune illnesses (system red lupus, rheumatic an arthritis etc.). Clinical displays of illness are defined by a parity of processes damages (alteration), protective, compensatory and adaptive reactions of an organism (adaptation). As it was already marked, illness begins with any primary damage ("half-ohm") at influence of the pathogenic factor. And this "floor" can occur at any level, including molecular level of the organisation. From these positions damage (alteration) should be considered as change of structure not only subcellular or-ganell, cages, fabrics, bodies, but also structure of molecules, and also as recombinationaly transformations (regrouping) at level of the molecular organisation. All these structural changes irrespective of level are accompanied by functional infringements. In biology one of most vivid examples of occurrence of qualitative changes owing to a structural regrouping of systems are gene mutations (a disposition of a site of chromosomes, an exchange of fragments between different chromosomes, inversion of separate sites of chromosomes on 180 °). These mutational shifts, not influencing quantity of synthesised fiber, change it confarmation, enzymatic activity, speed of synthesis, that finally leads to development various enzymophatis. The combination recombinational transformations with quantitative changes of the chromosomal device (aneuploidly, poliploidy) plays the important role both in kompensatornoadaptive reactions of an organism, and in occurrence of some hereditary illnesses (Sarkisov Д. With, 1994). Recombinational transformations are the important mechanism of adaptive reactions of the organism which is carrying out its adaptation to constantly varying conditions of existence in an environment. Adaptation at development of pathological processes has essential value in expansion various compensatory changes in an organism, the protective mechanisms counteracting illness. Compensatory PROCESSES Compensatory processes represent certain type of adaptable reactions of an organism on damage. As a result of their development the infringements of function caused by damage are liquidated, connected with what they are one of recover factors. The important role in recover other adaptable reactions of an organism providing destruction or restriction of the damaging factor - development of antibodies, фагоцитоз play also, an inflammation etc. Compensatory processes can develop on molecular, subcellular, cellular, organs and system levels. The primary damage which has arisen on органном level, is accompanied compensatory by reactions at level of body, systems, a complete organism. So, at heart diseases indemnification of the broken blood circulation is carried out at the expense of a hypertrophy of that department of heart which tests the raised loading. This compensatory hypertrophy provides normal blood circulation in an organism. At destruction of a part nephron in a kidney (amyloidosis, not-froskleroz) inner organ indemnification occurs at the expense of strengthening of function remained nephrons, that causes their hypertrophy. At damage at cellular level compensatory reactions are expressed in the form of endocellular regenerations. CLASSIFICATION OF ILLNESSES Illnesses of the person are numerous, but they can be united on following parametres: I. On an aetiology (infectious and uninfectious). II. By a principle of a generality of the socially-mediated action on a human body of natural and artificial factors (professional illnesses, a military pathology etc.). III. To an anatomo-topographical sign of localisation of the basic centre of defeat (illness of lungs, heart, kidneys, a liver etc.). IV. On an accessory to a certain sex, age (female illnesses, children's, illnesses of an old age). V. On the basis of a generality of forms of their development and a current (sharp, acute, chronic). VI. On similarity of pathogenetic mechanisms (autoimmune diseases, hereditary etc.). Biological value of displays of illness variously. One illnesses are accompanied by infringements of function and fabric or body structures. For example, punching of a thin gut at a belly typhus, a hemorrhage in a brain at hypertensive illness, etc. These changes are rather dangerous to the person as represent "floor" - qualitatively new sign, characteristic for the given illness. Other displays of illness is only reaction of an organism to action of the pathogenic factor or to the structurally functional changes caused by "half-ohm". These reactions are considered as protective, compensatory and adaptive, having morphological lines (for example, an inflammation, immune reactions, an atrophy, a hypertrophy). The protective role of an inflammation consists in restriction of distribution of infectious process with its subsequent liquidation and full restoration of structure and function of systems, body, a fabric. Compensatory value of a hypertrophy, for example, stomach walls at a stenosis of the gatekeeper consists in maintenance of normal process of digestion. Outcomes of illnesses happen different. In one cases at a favorable outcome there come recovers, that is full restoration of structure and function of those systems which have been damaged during illness. At an illness failure the proof pathological condition which changes structure can develop and breaks body function: for example, narrowing of a target part of a stomach in an outcome of scarring of kissing ulcers in this area; wrinkling kidneys with its reduction and function infringement in an outcome of various pathological processes in it (for example, glomeronephritis). In some cases illness comes to the end with the death of the patient connected with irreversible infringement of function of the central nervous system and the termination of activity of all vital bodies. One of remarkable properties of an organism is a presence of the limited number of standard protective reactions by means of which various combinations the organism answers the diversified external influences. Evolution has created a set from a small number socalled typical general pathalogic processes - inflammations, a thrombosis, regeneration, a hypertrophy, immunity, an atrophy, meeting at all illnesses. By means of every possible combinations from these elementary units of "the pathoanatomical alphabet» the organism quite successfully manages in rather various "external relations" (Sarki-owls Д. With, 1994). Taking into account stated studying of pathological anatomy of illnesses of the person is expedient for beginning with consideration general pathologic the processes making in various combinations a basis of illness, and also protective, compensatory and the adaptive processes developing in reply to damage. ALTERATION AND CAGE ADAPTATION From positions of a cellular pathology of R.Virhova (1855) first and major element of a life in normal and pathological conditions is the cage, in which substance operate under physics and chemistry laws. The normal cage as elementary structural and a metaphyte functional unit is a being which eats, digests, moves, allocates. The cage is unruly and constantly changes the structure and function in reply to various exogenous and endogenousfactors. By means of electronic microscopy it was possible to open in cages difficult system organells, each of which plays a part in work of the endocellular conveyor. Organells the same properties live, as a cage are inherent. They possess ability to continuous self-updating, damage under the influence of adverse factors, to regeneration, prolifiration etc. Cellular organells are numerous. This kernel, a kernel, митохондрии, ribosomes, polycatfishes, lamellar complex Гольджи, гранулярная and a smooth cytoplasmatic network. They differ not only on a structure, but also localisation in them of various biologically active substances. So, in a kernel are localised RNK - polimerasis, that is enzymes, catalyze formation РНК. In a kernel the enzymes participating in processes of replication dezoksiribo-nucleinic acid (DNA) contain. In a nuclear cover the enzymes participating in detoxication, and also providing hormonal management (adenylate cyclase, insulin receptors) come to light. With mitochondrion enzymes of a chain of biological oxidation (fabric breath) and oxidising phospholized, and also enzymes of piruvat-degidrogenaz th complex, a cycle threecarbonic acids are connected, synthesis of urea, oxidation of fat acids, etc. In ribosomes enzymes of albuminous synthesis, in endoplazmatic networks - synthesis enzymes lipids, and also the enzymes participating in reactions of hydrooxygination are localised. In lyzosoms contain basically hydrolitic enzymes. With a plasmatic membrane first of all are connected to adenosys three phosphotasis(AtF-aza), transporting ions of sodium and калия, аденилатциклаза. In cytoashes (gialoplazm) enzymes glycolysis pentophosphate a cycle, synthesis of fat acids are localised, etc. There is exist combination fermental systems to certain sites of a cage (компартментализация) provides division and integration of endocellular functions, and also corresponding regulation of processes of a metabolism and energy in a cage. For example, with mitochondrion breath, power stocks and calcium transport are connected. In ribosomes and granular a cytoplasmatic network there is a fiber synthesis. Smooth endoplazmic the network carries out accumulation and transport lipids and glycogen, and also detoxication function. In lamellar complex Goldji synthesis of products and their secretion are observed. Whether-zosomam endocellular digestion and protective function are inherent. Besides, in cages the specialised meta-plasmatic educations which are carrying out private functions are had. So, tonofibbrils carry out basic function of a cage, miofibrills - the reduction of a cage promoting its movement. Microfibers, щеточная a border participate in processes of aspiration etc. All органеллы are among themselves connected. Therefore damage any of them attracts damage of all cage. (Fig. 1) the cage answers stressful influence with three kinds of reactions:/) adaptation, 2) reversible damage and 3) irreversible damage (death). Cage adaptation is its reaction to action of stimulusthe various nature. It has first of all protective character and is directed on the cage adaptation to new conditions of environment, on alignment of a metabolism, structural and functional shifts which are caused by the operating factor. Damage (alteration) of a cage is too reaction of a cage to influence of various pathogenic factors which is accompanied by infringement of a metabolism, structures of a cage and its functional condition. Processes of adaptation, damage and death of a cage are defined not only the nature and force of stress, but also a condition of blood supply, a metabolism, a previous condition of a cage, degree of its differentiation and sensitivity. In some cases cages to those or other influences it is easy to explain special sensitivity. For example, four-chloride carbon what by it would not enter into an organism, metabolyses in a liver. Free radicals formed thus are more toxic, than SSTS-THAT IS WHY hepatocytis, taking up the basic blow, are quickly damaged by free radicals. cardiomiocytis are characterised by extremely high level of an exchange, as causes their very high sensitivity to hypoxia. At the same time it is difficult to explain, why a poliomyelitis virus, getting into an organism through a digestive path, damages impellent neurons forward horns of a spinal cord. All stressful and pathogenic factors have the an effect in the beginning at molecular level after which submicroscopic shifts at level cellular organells develop, microscopic changes at level of a cage, a fabric, body. In the subsequent changes and at anatomic level are found out. Possibility of revealing of the described morphological changes is defined by an applied method. For example, at ischemic damage of a myocardium with the help histochemical methods and electronic microscopy of change in penalties-diomiotsitah it is possible to reveal in some minutes, at anatomic level - in some hours. CAGE ALTERATION From modern positions cage alteration represents infringements of structure which can occur at molecular, submicroscopic and microscopic levels, that finally leads to infringement of its ability to live, development of pathological process and illness. THE REASONS AND THE MECHANISM OF DAMAGE OF THE CAGE Chemical compounds and medicines, physical and biological factors, immune reactions, genetic mutations, food infringements, ageing can be principal causes of alteration of a cage hypoxia. The action mechanism on an organism of the specified factors is combined, as many molecules, enzymes, biochemical systems, органеллы cages are so closely connected among themselves, that at times it is difficult to differentiate, that is a primary target of damage, and that secondary alteration. At the same time it is known by pathogenes cage damages by some pathogenic factors. Hypoxia Hypoxia - the most frequent reason of alteration of a cage. To the factors causing hypoxia, it is possible to carry: 1) Reduction of blood supply owing to pathological process in a vascular wall (atherosclerosis) or closings of a gleam of a vessel (obturation of blood clot or embolia); 2) Insufficient saturation of blood by the oxygen, observed at infringements of the certificate of breath, at reduction of quantity of oxygen in air (hypoksemic hypox ia); 3) Anaemia, changes of a condition of haemoglobin, for example its transformation in methemoglobin (at a poisoning with potassium chloride) or in carboxyhemoglobin(at a poisoning with carbonic oxide). In these cases haemoglobin function as oxygen carrier is broken. Depending on degree of hypoxia in a cage changes, characteristic for adaptation, reversible and irreversible damage can develop. For example, at narrowing of a femoral artery of a cage of skeletal muscles of the bottom finiteness will atrophy (decrease in volume). This atrophy reflects their adaptation to blood supply reduction. The reduction of cellular weight provides balance between requirement of oxygen and level of exchange processes for muscular cages. Increase гипоксии leads to alteration and death of these cages. The first target on which operates hypoxia, aerobic breath of a cage, that is oxidising fosfori-lirovanie at level of mitochonrion in this connection formation adenozinthreephosphate acids (АТФ) is slowed down or stops is. Decrease in its level influences many endocellular processes:/) decreases ATF - азная activity in cellular membranes; 2) activity of cellular pumps (kalij-natrievogo the pump) decreases; 3) the water exchange in the damaged cages that leads to a sharp endocellular hypostasis is broken; 4) activity phosphofruitkinaesis is stimulated, that causes increase of speed анаэробного гликолиза. It in turn supports a source of cellular energy and formation АТФ from glycogen, promotes accumulation of dairy acid and inorganic phosphorus in the course of hydrolysis фосфорнокислых aethers that reduces рН the endocellular environment (ацидоз cages). Other phenomenon caused by hypoxia, consists in striking off of ribosomes from granular endoplazmic reticulum's and disassociation the policy on monocatfishes. If hypoxia proceeds, destruction of organells accrues, that reflects infringement of permeability of membranes and decrease in their functional activity. On a cellular surface vials are formed. In cytoplasm and out of a cage appear pseudomielinic the structures formed of membranes organells. During this period mitochondrisies can have a usual structure, be exposed to swelling or condensation (increase of osmiofilness). Endoplazmatichesky ретикулум extends. As a whole the cage is in a swelling condition. All described changes can be reversible if supply of a cage by oxygen is restored. If the ischemia proceeds, there are irreversible damages of a cage. Морфологически it is expressed in vasculation of mitochondrias and them крист, in деструкции a plasmatic membrane. In last new channels of ionic conductivity that does a membrane of even more nontight for Са2 + are formed. Mass occurrence of calcium (инфлюкс) in cytoplasm with its initial adjournment in mitochondras begins. Матрикс them becomes dense. In kardiomi-otsitah these changes appear through 30-40 mines from the beginning of an ischemia and testify to irreversible damage of cages of a cardiac muscle. In connection with the raised permeability of a membrane loss by cages of the fiber, necessary coensims, ribonucleic acid proceeds. Cages start to pass in environment of metabolits, vital for restoration АТF, that reduces relative density of endocellular high-energy phosphates even more. The further decrease рН cages (that is increase of acidos) damages a membrane of lyzosoms. It causes liberation of their enzymes in cytoplasm, activation sour a hydromanhole, enzymatic digestion of cellular components. In these conditions the maintenance ribo-nukleoproteidov, dezoxycarbonucleoproteids and glycogen sharply decreases. After death of a cage of its structure intensively are exposed destruction with an exit of enzymes in intercellular space. Emission of endocellular enzymes in intercellular space with the advent of them in blood whey in connection with infringement of permeability of a plasmatic membrane has the important clinical value as trouble-shooting test of death of a cage. For example, in a cardiac muscle a number of enzymes contains: пируваттрансаминаза, лактатдегидрогеназа, креатинкиназа. Increase of level of these enzymes and especially isoenzymes in blood whey is clinical criterion infarkt of myocardium, that is focal, local некроза cardiomyocytes in a cardiac muscle. In parallel with this process in the lost cages from interstitional spaces get macromolecules. As a result the lost cage is replaced with the weight consisting from phospholipids in shape pseudomielins of structures which are absorbed by phagocytes and break up to fat acids. At the heart of irreversible damage of cages two phenomena lay:/) impossibility of restoration of function mitochondrial, absence oxidising phosphorilation and generation ATF at reperfusion and reoxygenation; 2) development of deep infringements of function of membranes. The central factor in pathogenesis irreversible damage of a cage is alteration of a cellular membrane that promotes to influx calcium from extracellular spaces where it is in high concentration. If besides the ischemic fabric is exposed reperfusion influx calcium amplifies. Calcium occurrence is observed not only in the conditions of an ischemia, but also at toxic damage. The calcium grasped mitochondrium after reoxygenation, damages and ingibiescellular enzymes, denaturate fiber and causes changes, characteristic for coagual necrosis. CHEMICAL COMPOUNDS AND MEDICAL PRODUCTS The reason of damage of a cage often are chemical substances and medicines. Actually each chemical substance and a medicine can become the pathogenic factor that depends on a dose and a way of its introduction. Even such harmless medicine as glucose, at introduction in the big con- centration can have on a cage pathogenic an effect, breaking osmotic pressure of environment surrounding it. The majority of chemical compounds and medicines have the target. So, barbiturate cause changes exclusively in hepathocyts because they metabolises in a liver, and end-products of their exchange have on liver cages direct damaging an effect. Corrosive sublimate is soaked up through a stomach, and damages kidneys and a thick gut. Last years the central role of oxygen in damage of cages is proved. Its lack, as is known, has great value in development of ischemic damage of cages. However its surplus breaks normal chains of biological oxidation that causes formation of a considerable quantity of free radicals, which, strengthening repussycats th oxidation lipids, is damaged by the vital structures of cages. The mechanism of damage of membranes is connected with formation of free radicals. Free radicals (atoms or the groups of chemical atoms possessing free valencies) provide normal functioning of cages. So, at the heart of destruction of microbes by phagocytes lays freeradical oxidation. The most simple on a structure free radicals of a live cage are анион - a radical supeoxyd (Ог ") and a neutral radical hydroxil (IT) - gidro-ksilnyj a radical. Last enters interaction with all basic chemical components of a cage: fibers, the nucleinic acids much coenzyms, lipi-dami, as underlies its cytotoxic action. Radicals can be formed in cages: 1) at stressful influences, 2) absorptions of radiating energy (ultra-violet and X-rays), 3) influence exogenic chemical substances, 4) in the course of ageing. Free radicals possess the expressed pathogenic property. In the presence of oxygen they cause repussycats th oxidation липчдов in membranes cellular органелл. As a result are damaged of endoplasmatic reticulum, in mitochondrions and others microsomal cage components. Illustration stated is damage gepato-tsitov at introduction in an organism of four-chloride carbon. In the course of its metabolism in a liver free radicals in smooth endoplasmatic networks with participation ok-sidaz are formed, that causes autooxydation the fat acids which are a part mambrane of phospholipids. Whether-pidnyh decomposition of membranes leads to fast destruction of structure and function endoplasmatic reticulum. After its alteration are damaged mitochondrions. In connection with increase of permeability of a plasmatic membrane progress swelling of cages and инфлюкс calcium, that as a result leads to death a cage. For a long time it is known, that easy and other fabrics are damaged at influence by oxygen of high concentration that is connected with formation of the free radicals arising at «an oxygen intoxication». The similar mechanism underlies damage of eyes at the newborns who were in an incubator with the raised maintenance of oxygen. The damage rate of cages free radicals depends on presence and activity of antioxidants, enzymes supeoxydimutasis, catalasis, "glytationperoxidaze, protective mechanisms of cages making a basis and an organism from. Free radicals. PHYSICAL FACTORS The trauma, high and low temperatures, sudden changes of atmospheric pressure, radiation, the electric power, acoustic energy, laser radiation influence cages different ways. The low temperature causes narrowing of vessels with reduction of inflow of blood to the freezed site of a fabric. Paralyze vasoconstrictors, promotes expansion of vessels, delay of a current with the subsequent intravascular coagulation of blood. In the described cases arises gipoksicheskoe damage of cages. Besides, at very low temperature there can come crystallisation of endocellular water with the expressed infringement of a metabolism in a cage. The heat can incinerate a cage. Autolysis, arising at extensive burns, promotes formation of toxic substances which, being soaked up in blood, damage a cage. The heat strengthens a metabolism in a cage (hypermetabolism) that causes balance infringement between intensity of an exchange and blood supply level. Besides, the intensification of exchange processes leads to accumulation sour метаболитов, reducing рН the cellular environment to critical level (not compensated acidosis cages). Sudden changes in atmospheric pressure worsen cage blood supply. Divers and the miners working in the conditions of raised atmospheric pressure, have a saturation of blood by gases, basically nitrogen and oxygen. At sudden decrease in atmospheric pressure that can be observed at fast lifting of the diver on a surface, gases leave the dissolved condition, forming in blood gas vials. Oxygen is again dissolved in blood, and nitrogen as less soluble forms the vials breaking microcirculation. Blockade microcirculation channels (gas embolism) causes hypooxycal damage of cages. Radiating energy. In defeat of cellular structures and macromolecules the important role is played by radicals of water, peroxide, hydroperoxide chinona and other substances formed in a cage at an irradiation in the presence of oxygen. The "hot" radicals appearing as a result of ionisation of water, damage a cage, again co-operating with endocellular structures. The irradiation causes also infringement of structure and DNA metabolism which defeat underlies a cage mutation. Electric energy at passage through a body generates a heat, causing thereby a burn. Thus degree of alteration of cages depends on force of a current, pressure, resistance of fabrics, ways of an input and a current exit. So, at transmission a current of low frequency arises эelectrolysis which leads to polarisation of cellular membranes. On one sites of fabrics there is a sour reaction (a congestion of positively charged ions), to others - alkaline (a congestion of negatively charged ions). In a zone of sour reaction it is observed denaturation fibers with development koagulation (dry) necrosis, in a zone of alkaline reaction - колликвационный (damp) necrosis. BIOLOGICAL FACTORS Biological factors are rather various, as well as the fauna, plants and the microbes, surrounding the person is various. Pathogenic effect parasites can render allocation of venomous snakes and fishes, microbes, viruses, mushrooms. Toxic action of snake poisons is connected with presence in them lipolitic and proteolitic the enzymes damaging membranes of cages and them organels. The mechanism of pathogenic action of viruses and microbes is ambiguous, as their interaction with a cage of the owner has the different form. So, many viruses, parasitizing in cages, do not damage them. They name "viruses-passengers". Other viruses cause alteration of cages. Bacteria, as well as viruses, are unpredictable in the actions. One of them concern to harmless commensal, that is do not harm to an organism (commensalism), others even are necessary for ability to live of an organism (symbiosis). For example, the intestinal stick living in intestines of the person, is a source of formation of vitamin K However in some cases the same intestinal stick can cause a sharp intestinal infection at the newborn deprived of immunity, or at the adult with the expressed got immunodeficiency. Contrary to it, for example, pale treponem always pathogenic. The mechanism of action of bacteria on cages is not absolutely clear. It is known only, that some microorganisms develop ectotoxin, capable to cause alteration of the cages located even on a considerable distance from a place of introduction of bacteria. For example, ectotoxin a diphtheritic stick which takes root through the top respiratory ways, amazes cardiomyocites, cages of adrenal glands, peripheral nerves. Other bacteria develop endotoxin or the enzymes, having pathogenic an effect at their disintegration. So, lecitiasa, allocated anaerobic bacterium Clostridium perfringens, it is capable to destroy a membrane of cages. hemolysin, developed beta-gemoliticheskim a streptococcus, lysisis erythrocyte. Other potential mechanism of damage of a cage bacteria is development of hypersensitivity of the immediate or slowed down type. The mechanism of action of parasites is to a lesser degree studied. It is established, that the activator amebiasis (parasitic disease) develops enzyme, lysisis cages in a place of the introduction. Malarial plasmodium, taking root in erythrocyte, destroys haemoglobin with formation toxic metabolite (a malarial pigment), damaging cellular organels. Viruses on the action mechanism on a cage are divided into two kinds: 1) cytopathogenic (cyto- lytic); 2) oncogenic, stimulating replication cages with possible development of a tumour. In a basis the cytoliytic effect of a virus direct infringement by a virus of a metabolism of a cage (fig. 2) lays. Using for the replication cellular ATP, ribosomes, enzymes and other biosynthetic processes, viruses thereby break a cage metabolism. Many viruses break synthesis of macromolecules by cages of the owner. For example, the poliomyelitis virus suppresses formation of the active complexes participating in synthesis of fibers. Some viruses cause cytoskeleton alteration: rupture intermediate filaments, infringement in the organisation of microtubules. Ordinary respiratory viruses change number of microtubules in cilia epithelia cages, reducing that their impellent activity and breaking removal of alien particles from respiratory ways. To a virus of a measles and a cage herpes react formation cinticial or multinuclear cages. Other mechanism of damage of a cage a virus consists in an induction of the immune answer against an antigene of a virus or an antigene of the cage infected with a virus (fig. 3). Thus destruction cages occurs or antibodies, or at direct influence on a cage of cytotoxic immune cages. For example, damage of cages of a liver at a virus hepatitis can occur by cytolysis, induced T - lymphocytes («a death kiss»). Many cytopathogenic viruses have certain specific an effect on cages (the trophy a virus). It is connected with presence of receptors on membranes of cages of the owner which co-operate with specific structures of viruses that allows a virus to be attached in the beginning to a membrane, and then to get into a cage with its subsequent damage. Character of reaction of a cage on replication a virus depends from virulence a virus, a kind of cages of the owner, resistance of an organism. The described changes at virus infections are one party of a spectrum of interaction of a virus with cages. On the other hand, oncogenic viruses cause replication cages with tumour development. IMMUNE REACTIONS Immune reactions as humoral, and the cellular nature, with direct influence humoral antibodies and sensitize lymphocytes on a cage can be the reason of alteration of a cage also. Besides, as a result of formation of immune complexes (antitelo+anti-gen+komplement) enzymes neutrophiles and other toxic substances damaging cages are liberated. GENETIC INFRINGEMENTS For a cellular homeostasis the great value has presence of the normal genetic device in this connection suddenly arising changes of the genetic information which have been written down in molecules of nucleinic acids cages (mutation), can lead to alteration. These mutations are accurately shown at cellular level by infringement of normal synthesis of enzymes. For example, absence of activity galaktozo - 1-fosfat-uridil-transferazy (illness Lesh - Nikhen), insufficiency gljkozo - 6 phosphate-degidrogenazy at some hemolytic anemias. The mutations, whatever origin they were, can appear the reason not only hereditary illnesses of a metabolism, but also development of tumours and a cellular immune pathology. The mutation can arise in process haemathogenesis, at an early stage of a zygote or at the differentiated cages (a somatic mutation). In the latter case transformation of a normal cage, in tumoral (malignization) can be observed. As is known, genetic infringements can be descended, that is to be family suffering (for example, an is crescent-cellular anaemia). FOOD INFRINGEMENTS In damage of cages albuminous insufficiency, avitaminosises, a lack or surplus of microcells in a diet (microelementosis) have great value. So, insufficient receipt of copper with food accelerates ageing process mitochondrion, leads to the raised permeability mito-hondrialnoj membranes, breaks transport АТP through an internal membrane. Surplus of free copper oppresses activity of oxidising enzymes that causes destruction of cages. Avitaminosises, as well as the superfluous use of vitamins, often meet in developing countries and damage of cages can cause. So, at an avitaminosis And alterations are exposed cages epithelium conjuctiva an eye and corneas (xerophthalmia). The atrophy of cages of salivary glands develops also. At insufficiency of vitamins of group In and nicotinic acid there is an atrophy of cages of a mucous membrane of an intestines, a stomach, a liver, dystrophic changes in cages of nervous system. A superfluous food is paradoxical, that, characteristic for people with a high standard of living, too is the important reason of morbidity and death rate in which basis alteration of cages lays. AGEING At damage of a cage in the course of ageing two mechanisms matter: 1) progressing accumulation alternative processes in a cage which conducts to its irreversible damage, and 2) decrease in ability of a cage to answer damage protective and compensatory with reactions. There is also a representation, that each cage has the limited genetically determined period of a productive life. the morphologic old cages become larger, sometimes multinuclear and are more inclined to damage. In their cytoplasm appear vacuole the different sizes. In the central nervous system are observed reduction of number of nervous cages and neurofibrillar a degeneration especially expressed at senile demencia and an Alzheimer's disease. Factors of an environment, to which old individuals in an increasing order are exposed (ultra-violet beams, medicines, X-rays, a foodstuff etc.), are capable to cause both somatic mutations, and various changes in cytoplasmatic components. The proof of this thesis is accumulation in cages of different fabrics lipofuscin - a pigment of yellowy-brown colour. In the course of ageing it appears in different fabrics, more often in heart, a liver, a brain. The pigment represents a complex lipids and the fibers arising at with peroxygen oxidation lipids in cellular membranes. In the literature lipofuscin name a wear process pigment. MORPHOLOGY OF REVERSIBLE AND IRREVERSIBLE DAMAGE OF THE CAGE The basic structural expressions of alteration are a dystrophy and некроз which consideration should be begun with submicroscopic changes. At influence of pathogenic factors of alteration can be exposed all органеллы cages. Before all there is a damage of a plasmatic membrane of the cage, reflecting infringements in regulation of ionic balance. Cage swelling, formation of cytoplasmatic vials, shortening and deformation of microfibers, formation psev-domielinovyh structures, wear process and loss of intercellular contacts are marked. These changes arise quickly and have reversible character. In later stages of irreversible damages membranes not only cages, but also all organell collapse. Alteration of mitochondriums develops very quickly in the conditions of an ischemia and more slowly at influence of some chemical substances. At an early stage of an ischemia of a mitochondrium are condensed, then very quickly are exposed to the swelling arising in connection with ionic shift in internal partitions of mitochondriums. Through 30 mines after an ischemia in a matrix of mitochondriums there are the dense osmiophilic formations consisting of lipids of lipoproteidis complexes and testifying to the beginning of irreversible processes. At реперфузии and chemical damage these dense granules are rich with calcium. For irreversible damage more expressed swelling of the mitochondriums, full rupture of mitochondrial membranes with their subsequent Calcification are characteristic. Expansion of an endoplazmatic reticulum is observed in early terms after influence of the pathogenic factor that is caused by shifts in moving of water and ions. Then striking off of ribosomes from a rough endoplazmatic reticulum, a disassociation by the policy on monocatfishes is ob- served. Fiber synthesis thus decreases. The described reactions are reversible, but if the pathogenic factor continues to operate, the endoplazmatic reticulum will divide (breaks up), forming pseudomielinum structures. In a stage of reversible damage of a lysosome light, bulked up, without signs of liberation of lysosomic enzymes. With the beginning of lethal damage of a lysosome are broken off and can disappear from a skeleton of a dead cage as distinguishable structures. CAGE DYSTROPHY As it was already marked, to structural changes in a cage, underlying damage, infringements exchange and enzymatics of processes in a cage, having various morphological expression precede. For example, swelling of mitochondriums, shortening their crist, an enlightenment matrik-sa reflect insufficiency of an adenozinthreephosphate and infringement of oxidising processes in a cage, arising as a hypoxia direct consequence. In a classical pathology infringement of a cellular metabolism can be considered as the dystrophic processes accompanied by accumulation in a cage of various products of an exchange which chemical nature defines a dystrophy kind. So, if there are inclusions of the albuminous nature speak about infringement of an albuminous exchange (albuminous regeneration) if in a cage inclusions of fats are found out, lipids - about a fatty dystrophy (fatty regeneration). Accordingly in a cage infringements of a pigmentary, carbohydrate exchange can develop, etc. Thus, the dystrophy is the difficult pathological process accompanied by expressed structural shifts in a cage in which basis infringements of a cellular metabolism lay. Developing dystrophic process causes infringement of function of a cage. Aetiology and pathogenesis. The dystrophy reasons, as well as damage of cages, are various. Proceeding from aetiologic factors, allocate dystrophies in which basis lay dis-tsirkuljatornye, endocrine and cerebral infringements, gene mutations, and also immunopathological processes. In all cases irrespective of a dystrophy kind it is a question of those or other changes exchange and enzymatics of processes in a cage, physical and chemical shifts in it, as underlies endocellular accumulation of various substances. In one cases these endocellular accumulation do not influence a functional condition of a cage, in others - this process causes damage of a cage and its dysfunction. Accumulation of endocellular inclusions connect: With increase in a cage of superfluous quantity of the metabolits meeting in norm. For example, endocellular accumulation of a glycogen at sick of a diabetes at long high level of glucose in blood; With accumulation of some unmetabolizes of products that is observed at congenital infringements of a metabolism (illness of accumulation); With superfluous endocellular synthesis of some substances, for example a melanin pigment at аadrenalдреналовой insufficiency. Dystrophic processes are more often observed in highspecialised functionally active cages (a liver, kidneys, heart). Thus at the heart of the same dystrophy developing in various on structure and functions cages, different mechanisms lay. So, in a liver at the heart of a fatty dystrophy of hepatocyts accumulation triglitse-ridov lays; in Cardiomiocyts at a diphtheria - ability of exotoxin a diphtheritic stick to join in a carnitin metabolism - кофактора oxidations of fat acids. Morphogenesis of dystrophies. Infiltration - superfluous penetration of products of an exchange from blood and a lymph in cages in cages or intercellular substance and-or infringement of their inclusion in a metabolism with the subsequent accumulation. Decomposition - (phanerosis) disintegration of difficult substances in the chemical relation. Disintegration of polisaharidno-albuminous complexes underlies phibrinoid changes of a connecting fabric at rheumatic illnesses. Transformation - transition of one substance in another. Transformation of carbohydrates in fats is that, for example, at a diabetes, the strengthened polymerisation of glucose in a glycogen, etc. the Perverted synthesis is a synthesis in cages or fabrics of the substances which are not meeting in them to norm. To concern: synthesis of abnormal fiber of an amiloid in a cage and formation abnormal belkovo-polisaharidnyh amiloid complexes in intercellular substance, synthesis of an alcoholic gialine by a hepatocyt, glycogen synthesis in an epithelium of a narrow segment of a nephron at a diabetes. Depending on a kind of infringement of a metabolism in a cage allocate albuminous, fatty, carbohydrate, pigmentary, mineral dystrophies. ALBUMINOUS DYSTROPHY The exchange of albumens underlies functional displays of cellular structures. For example, with an exchange of fibers, in particular sulfur-bearing, nervously-reflex activity of neurons is closely connected. Thanking to aktimiozinum muscular cages possess contractile ability. From here becomes obvious, what deep structural and functional changes can arise in fabrics at infringements of an albuminous exchange. The albuminous dystrophy is divided on hydropic, gialinovo-drop and horn, differing on the mechanism of the development. Hydropic dystrophy. One of the important indicators of a dystrophy of a cage and first sign of all forms of its damage is the swelling of a cage observed at increase of permeability of membranes, infringement of diffusive osmotic mechanisms and activity of cellular pumps. In these conditions the cage loses ability to support an ionic and water homeostasis, as a result from ekstratselljuljarno th space in a cage the liquid starts to arrive. If liquid receipt in a cage proceeds, in its cytoplasm appear small vacuols, representing expanded and секвестрированные segments endoplazmaticheskogo a reticulum, filled with a liquid. This kind of damage of a cage name vacuolic, or hydropic, a dystrophy characterised by sharp increase in cytoplasm of water with formation вакуолей of various size. Vacuoles can be plural or, merging to occupy all cytoplasm, pushing aside a kernel to periphery. Appearance of bodies thus does not vary. A number of authors prefer to consider this kind of a dystrophy as «a drivingnochno-albuminous dystrophy». The vacuolic dystrophy is observed in muscular and nervous cages, leukocytes, in cages of an epithelium of a skin and nephritic tubules, in hepatocyts, cages of a bark of adrenal glands. The most demonstrative hydropic regeneration is marked in an epithelium of nephritic tubules (hydropic нефроз) at exhausting diarrheas. In a liver the vodjanochno-albuminous dystrophy of hepatocyts is observed at a virus hepatitis. At height of the development all forms of a vodjanochnoalbuminous dystrophy lead цитолизу. Functions of bodies are thus broken. The reasons of the given kind of a dystrophy - infectious, infectious-toxic processes, gipopro-teinemija, infringement vodnoelektrolitnogo balance. The cytoplasm vacuolization can be observed and in physiological conditions as display секреторной activity. In particular, it is marked in ganglions of the central and peripheral nervous system, especially in hypothalamus neurons. The gialinovo-drop dystrophy is characterised by occurrence in cytoplasm of the large gialinelike albuminous drops merging among themselves. They are formed at merge of lysosomes to the pinocytic vials containing re-absorbed fiber. At the heart of development of a gialinovo-drop dystrophy the perverted synthesis of fiber in a cage can lay also. Most often this kind of a dystrophy meets in cages of a liver and kidneys. In a liver it is observed at an alcoholic hepatitis, primary billiarбилиарном a cirrhosis, a children's Indian cirrhosis. In cytoplasm of hepatocyts at an alcoholic hepatitis there are gialinelike little bodies Маллори (an alcoholic gialine). In kidneys at various нефропатиях in the conditions of the expressed pro- teinuria and реабсорбции a fiber considerable quantity in an epithelium of wiggle tubules are found out гиалиновые inclusions in the form of vitreous pink droplets. Occurrence of albuminous inclusions in a cage can be observed and in norm. For example, the albumin small amount reabsorbates in proximal wiggle tubules also can be found out in cages of their epithelium. At the infringements promoting a heavy proteinuria, the squirrel is marked pinotsitoznaja реабсорбция. At the proteinuria termination albuminous grains metabolize and disappear. At certain virus infections are described гиалиновые virus inclusions in cytoplasm of the amazed cages. The gialinovo-drop dystrophy is defined only микроскопически. The outcome of a gialinovo-drop dystrophy is adverse. Process, being irreversible, causes serious functional infringement of a cage and it некроз. The horn dystrophy is characterised by superfluous formation of horn substance in cages ороговевающего an epithelium - a hyperceratosis, a callosity or formation of horn substance there where it in norm does not meet (a leukoplakia in mucous membranes, cancer pearls in epithelial tumours). This kind of a dystrophy is observed at a chronic inflammation, an infection virus th, avitaminosises, hormonal infringements, infringements of development of a skin. The horn dystrophy underlies such pathological processes, as a hyperceratosis, ихтиоз, a leukoplakia. Convertibility of this process can be observed only in an initial stage of a dystrophy at elimination of the aetiologic factor. Congenital ихтиоз it is incompatible with a life. The leukoplakia is considered as precancer process which can be a source of development of a malignant tumour from an epithelium. FATTY DYSTROPHY In cages lipids which concern фосфатиды, ste-ridy, стерины, cholesterol, цереброзиды, forming with fiber lipoproteidis complexes, participate in construction мембранных structures. In norm in the form of inclusions they are not found out in cages. An exception cages эндотелия capillaries, an epithelium of direct tubules of kidneys make, macrophages in which lipids meet and in norm. In the adrenal glands representing to depot of mobile lipids (cholesterol), it is possible to define their presence macroscopic on intensively-yellow colour. The fatty dystrophy in cages can be expressed in following forms: 1) increase or reduction of the maintenance of lipids in cages of adrenal glands, hepatocyts, an epithelium of loops Генле and direct tubules of kidneys, in эндотелии brain capillaries in which they meet and in norm; Qualitative infringements, for example occurrence of lipids in an epithelium of direct tubules of kidneys where in norm only neutral fat is found out; Occurrence of lipids in cages паренхимы bodies where in norm they морфологически are not defined; резорбтивное adiposity mainly cages monotsitarno-makrofagalnoj systems in process resorption them of products of fatty disintegration. The mechanism of development of a fatty dystrophy is various, but in all cases occurrence in a cage fatty вакуолей, large or small, specifies in absolute increase in the maintenance of endocellular lipids. It is preceded in some cases by swelling of a cage which is the indicator of its reversible damage. Accumulation of fatty inclusions can sometimes be a harbinger of destruction of a cage. In many situations they appear in cages, прилежащих to a zone necrosis. In mostly degrees the mechanism of development of a fatty dystrophy in a liver (fig. 8) is studied. In normal conditions in a liver lipids arrive from a fatty fabric and foodstuff. From a fatty fabric they are liberated and transported only in one form - in the form of free fat acids. Lipids of foodstuff are delivered in a liver as in a kind липидных particles (consisting of threeglycerids, fosfoli-pidov, the squirrel), and in the form of free fat acids. The part of fat acids is synthesised in the liver. The most part of fat acids irrespective of their origin eterifitsi-ruetsja to threeglycerids, a part is converted in cholesterol which joins in phospholipids or is oxidised in mitochondriums before ketonic connections. For deducing from a liver endocellular threeglycerids should комплексироваться with molecules specific апопротеина (an albuminous acceptor of lipids) with formation of lipoproteids. For superfluous accumulation of the threeglycerids causing a fatty dystrophy of a liver, following factors matter: 1) superfluous receipt of free fat acids in a liver. For example, at starvation from fatty клетчатки neutral fats will strenuously be mobilised. As a result of it the considerable quantity of fat acids arrives in a liver where they are synthesised in threeglycerids. Mobilisation of lipids from fatty клетчатки is promoted also by introduction kortikosteroi-dov; The raised synthesis of fat acids from acetate; Decrease in intensity of oxidation of fat acids that leads to increase этерификации them in threeglycerids; Strengthening eterification fat acids in the threeglycerids, caused by increase of the maintenance an alpha-glitserofosfata. In development of this reaction plays a role surplus of alcohol; 5) synthesis decrease apoprotein - the fiber necessary for conversion (transformation) of threeglycerids in lipoproteids, the unique form, in which lipids экскретируются from a liver. In this connection maintenance decrease апопротеина conducts to accumulation of threeglycerids. The described mechanism of development of a fatty dystrophy of a liver is observed at influence on an organism четыреххлористо^о carbon, at an insufficient food, easing of secretion of lipoproteids in a liver. In industrially developed countries the most frequent reason of a fatty dystrophy of a liver is an alcoholism as alcohol is among gepatotoksiche-skih the substances breaking function of mitochondriums and a micro-catfish. Thus, in a pathogenesis of a fatty dystrophy of a liver play a role:/) the raised mobilisation of free fat acids; 2) decrease in recycling of threeglycerids; 3) reduction of intensity of oxidation of fats; 4) strengthening eterification; 5) the block экскреции lipoproteids; 6) direct damage of an endoplazmatic reticulum by free radicals. The fatty dystrophy of easy degree does not render influence on function of the cages, more expressed - can break liver function, but can be and reversible. Therefore if the alcoholic at whom the cirrhosis has not developed yet, stops to take alcohol it has a return development of process to full restoration of structure and body function. Irreversible fatty hepatoz a liver it is observed at deep damage of the vital endocellular structures. The fatty dystrophy is more often observed in a liver and heart, but can develop and in other bodies. Fatty dystrophy of a liver. At moderately expressed fatty dystrophy macroscopic the liver does not change. With progressing of accumulation of fats in hepatocyts the liver increases, gets yellow, yellowy-brown Colour. Its weight can reach 3-6 kg, the consistence becomes soft, the surface on a cut has a grease appearance. The earliest changes in a liver at elektronno-microscopic level is a formation of liposomes (the formations limited to a membrane). Probably, that the origin of liposomes is connected with an endoplazmatic reticulum. At light microscopy at early stages of a fatty dystrophy there are fat droplets in cytoplasm of a cage round a kernel. At process progressing вакуоли merge and displace a kernel to cage periphery. Microscopic the fatty dystrophy of a liver can look in the form of "goose" or ложномускатной a liver. «The goose liver» is an diffusion adiposity of body at which all hepatocyts are replaced with fat droplets. At such adiposity of a liver even the remained hepatocyts look not базофильными, as in norm, and эозинофильными. It is connected by that in liver cages ribonucleic acid disappears. The is false-muscat liver is characterised by non-uniform adiposity of the hepatocyts located only on periphery of segments. In this connection in the centre of segments usual colour remains, and on periphery there is a yellowy-brown colouring in this connection the liver takes a motley form. The reasons of a fatty dystrophy is an anaemia, food infringement, long illnesses, a poisoning, infectious processes. An outcome it is long proceeding fatty dystrophies (cirrhosis) is diffusion growth of a connecting fabric in a liver. The fatty dystrophy of kidneys is macroscopic characterised by increase in volume of kidneys and occurrence of small yellow specks, specks at a pale background утолщенного коркового a layer. During the first periods of illness of a kidney big, and then they are wrinkled at the expense of growth of a connecting fabric (the again-wrinkled kidneys). Микроскопически in an epithelium of wiggle tubules and in строме body are visible numerous lipid inclusions. The reason of a fatty dystrophy of kidneys is the syphilis is more often. The fatty dystrophy of heart is observed mainly at a hypoxia and shown in two variants. At the first variant arising at moderated, but a long hypoxia, non-uniform adjournment of lipids in the form of drops in Cardiomiocyts owing to what alternation of the fibres containing lipids is marked, with inactive fibres (fig. 9) is found out. It creates the motley drawing reminding a skin of a tiger («тигровое heart»). It is most expressed on papilar muscles and трабекулах ventricles hearts (fig. 10). Especially massive fatty dystrophy arises in most functionally burdened sites of a myocardium. If there is a defect aortal the valve the greatest loading tests left ventricles. In it the picture so-called «тигрового hearts» develops. The myocardium of other chambers of heart can remain not changed. The isolated fatty dystrophy of the nervous device and spending system of heart which is observed at syndrome Шагаса is described. Last represents a version of tripanosomoz, extended in Argentina and Brazil. As a rule, the fatty dystrophy of heart in the field of spending system - process irreversible also involves a heart paralysis. At the second, a variant a fatty dystrophy arises at a deep hypoxia or some forms миокардита (for example, parenximatozic miocarditis at a diphtheria), and fatty inclusions are defined in all Cardiomiocyts. Accumulation of lipids is observed at some pathological processes, for example, in smoothmuscular cages and macrophages intims of an aorta and large arteries at an atherosclerosis. The described cages take a foamy form. Gathering in an intim of vessels, they form атеромы, characteristic for this serious suffering. Foamy cages, being overloaded with lipids, are broken off with liberation in строму intims of lipids. In macrophages endocellular accumulation of cholesterol is observed at гиперлипидемическом a condition with formation in a subepithelial connecting fabric of a skin and in sinews опухолевидной weights. Fatty inclusions collect and in physiological conditions. For example, macrophages in process phagocytosis fatty necrotic detritis cages are filled with the big number small вакуолей, containing lipids that gives them a foamy kind (foamy cages). CARBOHYDRATE DYSTROPHY From carbohydrate dystrophies the greatest value have sugar urineemaciation and glycogenosis. Sugar urineemaciation (diabetes) is characterised by increase of the maintenance of sugar in blood (hyperg;ykemia) and in urine (glycozuria)., the diabetes mechanism the diversified factors can be starting:/) nervous stresses, mental affects, tumours and traumas of nervous system; 2) exchange factors; 3) endocrine shifts (базедова illness, pregnancy). In a pathogenesis insufficiency инсулярного the device matters. Diabetes - a vivid example of infringement of an exchange of glucose. At this disease the glycogen is found out in epithelial cages distal parts of wiggle tubules of kidneys, is more rare in a descending part of loop Генле, in liver cages, beta cages of islets Langengars of a pancreas, in muscular cages of heart. The glycogen in cages appears in the form of accurate глыбок in cyto- plasm that gives it vacuolizeda kind, thus cages look light. For not clear reasons glycogen adjournment in hepatocyts at light microscopy is found out and in kernels which bulk up and become light. However such accumulation of a glycogen in kernels has no clinical expression. Accumulation of a glycogen in cages is observed at a number of the genetic diseases united by the general name «glycogenosis». This group of illnesses is connected, on the one hand, with absence of one or several enzymes (for example, 1,4-gljukozidazy), participating in a metabolism of a normal glycogen, and with another - with synthesis of abnormal forms of a glycogen which is not capable to metabolize. At various syndromes of the hereditary nature superfluous endocellular accumulation of a glycogen is observed mainly in cages of a myocardium, skeletal muscles. A liver, kidneys. In all cases the glycogen comes to light in the form of light vacuols in cytoplasm. Superfluous accumulation of a glycogen results in secondary damage of a cage and it necrosis. At exchange infringement glycoproteids in cages accumulation of mucous substances (муцинов and mucoids) is observed. At a mucous dystrophy two processes develop: 1) strengthening of formation of slime and 2) change of its physical and chemical properties. Excessive secretion of slime causes destruction of a cage, it is torn away, output channels are closed (ob-turirujutsja) by slime with development retention cist. Epithelial tumours can be exposed also to a mucous dystrophy (ослизнение tumours). The Principal cause of this kind of a dystrophy - an inflammation. At an unsuccessful outcome the atrophy and a sclerosis of mucous membranes are observed. The mucous dystrophy underlies hereditary system disease - муковисцидоза. Necrosis Necrosis cages (from. гр. nekros - dead) is mortification, destruction of a cage in a live organism. Changes, characteristic for necrosis, cause two competing processes: enzymatic digestion of a cage and денатурация fibers Whether-zosom Katalitichesky enzymes appear in a cage or from a dead cage, or from lysosomes of migrating leukocytes In the first case process of digestion of a cage is considered as аутолиз, in the second - as heterolisis. Depending on that prevails - enzymatic digestion of a cage or денатурация the squirrel, allocate two principal Necrosis: colliquative and coagulative. In case of progressing denaturation cellular structures develops коагуляционный некроз. Process of the enzymatic of digestion органелл underlies a cage kollik-vatsionnogo некроза. The enzymes which are carrying out digestion of cellular structures appear in cytoplasm at infringement of a membrane of lysosomes. They not only "bodies" of internal digestion but also original "murderers" of a cage with which help it is carried out heterophagocytosis and аautophagocytosis. Lysosomes contain various hydrolitic the enzymes promoting destruction englobed of a material within 1-2 days. Гетерофагоцитоз. At the given phenomenon of phagocytic the object arrives from environment in a cage by ek-dotsitoza. Capture of a material in the form of particles is called phagocytosis, and in the form of the dissolved small macromolecules - pi-notsitozom. Гетерофагия it is carried out by "professional" phagocytes (нейтрофилы, macrophages), but it can be observed and in other types of cages. An example гетерофагоцитоза is capture and digestion of bacteria нейтрофилами, removal некротизированных cages macrophages, reabsorb-tsija pinocytic vials of fiber in проксимальных departments of wiggle tubules of kidneys. Dissolution in lysosomes фагоцитированных вакуолей occurs, probably, by digestion of the absorbed material. Autophagocytosis. The lysosomes which are carrying out autoperevari-vanie (selfdigestion), are called autolysosome, and process - аутофагией. In many cases it is observed очаговое damage separate органелл with their subsequent digestion. The normal functional condition of cages thus remains. Enzymes of lysosomes are capable to split the majority of fibers and carbohydrates, but some lipids remain, not being exposed to digestion. The lysosomes which have absorbed detritis, can exist in cages as residual little bodies or can be pushed out from a cage. Some pigments, such as the coal inhaled from atmosphere, or a pigment, inokuli-rovannyj in a skin at a tattoo, can long remain in фаголизосомах macrophages (decades). Lysosomes are also «a basket for papers», where cages секвестрируют the substances, not capable to metabolize. Signs of death of a cage. The death of a cage is characterised by certain structural changes in cytoplasm and a kernel. At irreversible damage of a cage of change to a kernel it is possible to divide into three kinds: кариолизис, кариопикноз, кариорексис. Кариолизис, accompanied by loss базофилии kernels, it is connected with enzyme activationdezoxyribonucleasis which splits DNA on phosphatic acid and the nucleinic bases which are not perceiving nuclear colourings. Кариопикноз it is characterised by loss of usual structure of a kernel and its reduction. The kernel starts intensively and dif-fuzno to be painted owing to water and condensation loss хромchromatin. The last is connected with condensation of DNA and smorShivaniem базофильной weights. Кариорексис is a fragmentation of a pincnotic kernels. The kernel in necrotic to a cage irrespective of a kind does not disappear in 1-2 days (fig. 12). The cytoplasm deprived of a kernel, turns in dense, opaque a (eozinofilic) weight that is caused, on the one hand, denaturation cytoplasmatic fibers, with another - activation sour ribonucleasis, destroying cytoplasm-ticheskuju RNK - Thus, necrotic the cage turns in acidofilic a denuclearized skeleton. Finally in a live organism dead cages and them детрит disappear. Even coagulated cages leave as a result of a process combination enzymatic digestion and phagocytosis of its leukocytes. If the lost cages and cellular детрит collapse and reabsorbites not completely they are exposed of petrification (calcification). This phenomenon named a dystrophic Calcification, it is possible to observe at a tuberculosis, an atherosclerosis. Apoptosis («the programmed death of a cage») a-unusual morphological version некроза, covering a cage part, individual cages. It is regulated by two genes: proto-onkogenom BCL2 and a gene-supressorom р53. Aptosis comes to light in the form of roundish or oval eozinophilic weights in cytoplasm with expressed cariorexis. Aptosis it is necessary for: Programmed distruction cages during the period embriogenesis; Gormonalno-dependent involution, for example endometrium; Death Immuncomponentic cages after emission of cinins; Phenomenon of negative selection of autoreactive T-cages. In a pathology of apoptosis it is observed in a liver at a toxic or virus hepatitis (little body Каунсилмена), in tumours various генеза, participating in their development and a progression. CAGE ADAPTATION The cage constantly adapts to changes which occur in its microenvironment, therefore ояа cannot exist, if its structure and function constantly do not vary. At influence of stressful and pathogenic factors the cage adapts by shifts in a metabolism and structure that gives the chance to it to achieve changed, but the steady condition allowing it to survive in the conditions of changed environment. Example of such adaptation is hyperplazii of granular an endoplazmatic reticulum which is observed in the conditions of a hypoxia, superfluous receipt of medical products, excessive functional overstrain. Thus on lightoptic level in cytoplasm there are albuminous grains which give it the bulked up kind. At electronic microscopy these albuminous grains reflect hyperplazia organells cag- es. Muddy swelling of cages - adaptive process, easily reversible and in most cases is not accompanied by functional infringements of a cage. Except the described process, to cage adaptation the atrophy and a hypertrophy concern. ATROPHY The atrophy is a reduction of the sizes of a cage at the expense of loss of a cellular substance. The most important reasons of an atrophy are:/) decrease in functional activity of a cage (an atrophy from inactivity); 2) infringement иннервации; 3) decrease in level of blood supply; 4) an inadequate food; 5) infringement of endocrine regulation as hormones, especially insulin, tiroksin, glucocorticoids, justglandins, influence speed of an exchange of fiber. Irrespective of the caused reason of a cage decrease in such a manner that keep ability to survive. The cages subjected to an atrophy, are characterised by a small number of mitochondriums and miofilaments, reduction of volume of an endo-plasmatic reticulum. At an atrophy concentration hydrolitic proteasis raises. However these энзимы are not simply released in cytoplasm as it can lead uncontrollable cellular деструкции, and join in autophagosomic vacuols. Thus, in many situations the atrophy is accompanied by appreciable increase in number Autophagosomic vacuoles. HYPERTROPHY The hypertrophy is an increase in a cage in sizes. At involving in this process of considerable number of cages there is a body hypertrophy. The hypertrophy can be caused increase of functional activity of the cage, specific hormonal stimulation. It can be observed at physiological and pathological processes. At the heart of physiological increase in a uterus during pregnancy the hypertrophy of cages (increase in their sizes) and hyperplazia (increase in number of cages) lays. The hypertrophy of muscular cages of a uterus is stimulated with an estrogen (female sexual hormones) by means of receptors of the estrogen which is settling down on smooth muscular cages. These receptors promote interaction of hormones from nuclear DNA, raising thus fiber synthesis in smooth muscular cages. Increase of processes of albuminous synthesis leads to a hypertrophy of cages. It is an example of a physiological hypertrophy of the cages connected with hormonal stimulation. As example of a hypertrophy of adaptive character the increase in volume of cages in the conditions of the raised physical activity can serve. Cages of a myocardium and skeletal muscles as they cannot adapt for increasing level of exchange processes by division (mitosis) especially hypertrophy. So, the hypertrophy of Cardiomiocyts is stimulated with high arterial pressure. Cages of skeletal muscles hypertrophy in the conditions of the raised physical activity. It is thus synthesised more enzymes and philaments. To reach balance between requirement and functionality of a cage. The number increase miophilaments allows to carry out the strengthened physical activity at a high metabolism. If the factors which have caused an adaptive hypertrophy of Cardiomiocyts, continue to operate, it can lead to failure of their adaptive possibilities. Processes decompensation in muscular fibres in which basis lays лизис and reduction miofibrilar contractile elements thus develop. Principal causes decompensation can be:/) reduction of blood supply of the hypertrophied cages; 2) decrease in oxidising processes; 3) alteration and degradation of albuminous synthesis. I ULTRASTRUCTURAL BASES OF ILLNESS By means of electronic microscopy there was possible a studying of a pathogenesis and морфогенеза of some the illnesses connected with alteration specific organells of a cage, such, as lysosomes, microlittle bodies and cytoskeleton components. Lysosomes. A number of hereditary illnesses is caused lizo-somalnoj enzymopaties, the leader to accumulation in a cage of some initial or intermediate products of an exchange. Therefore hereditary lysosomic enzimopaties make group of illnesses of accumulation, or tezaurismozes. Into it enter glycogenoses (illness to the Pomp), gangliozids (illness Тея - the Saxophone), etc. So, at insufficiency of the enzymes splitting mucopolysaccharides, there is their superfluous accumulation in cages of all organism, especially in neurons, that causes gross infringements. Microlittle bodies (peroxysomes). At primary defeat of microlittle bodies there is «paroxisome illnesses» which concern uncatalemia, tserebro-gepato-renalnyj syndrome Целлвегера and system insufficiency of a carnitin. Aktalazemiait is caused by thermostability decrease catalasis, that leads to reduction of its maintenance. A clinical syndrome of this disease concern gangrenous pitting oral cavities. At absence пероксисом in hepatocyts synthesis of bilious acids that leads to development cerebrohepatorenal syndrome of Cevelger is broken. Catalic activity of a liver is sharply lowered (to 20 %). At system insufficiency of a carnitin its deficiency is especially expressed in skeletal muscles, a liver, blood plasma. Clinically this «peroxysomic illness» is characterised miopatia with periodic infringements of function of a liver and a brain. Cytoskeleton. Cytoskeleton components are considered as specific органеллы, carrying out basic, transport, contractil and impellent functions.