Download The Tashkent Medical Academy Chair: Normal, pathological

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.