IDIOPATHIC HYPERTENSIA (grech, hyper-+ tonos tension; synonym: essential arterial hypertension, primary arterial hypertension; not recommended synonym an essential hypertension) — a widespread disease of a little studied etiology, the main manifestations a cut are: the increased arterial pressure in a frequent combination with regional, hl. obr. cerebral, frustration of a vascular tone; staging in development of symptoms, the expressed dependence of a current on a functional condition of nervous mechanisms of regulation of arterial pressure in the absence of a visible causal relationship of a disease with primary organic damage of any bodies or systems. The last circumstance would distinguish G. from so-called symptomatic, or secondary, arterial hypertension which cornerstone organic lesion of the internals or systems participating in formation or regulation of the ABP, napr, kidneys, adrenal glands, etc. (see is. arterial hypertension ). In foreign literature of G. often call essential, or primary, hypertensia as many foreign authors (J. Pikkering, E. Page, etc.) would consider G.'s etiology. obscure. According to the decision of Committee of WHO experts the terms «essential hypertensia» and «idiopathic hypertensia» should be considered identical.
Before creation of indirect methods of measurement of the ABP about his increase at people judged by such signs as intense pulse, increase in heart to the left and accent of the second cardiac sound over an aorta. A wedge, studying of arterial hypertension at the person became possible after S. Riva-Rocci in 1896 suggested to apply to measurement of the ABP the hollow rubber cuff imposed on a shoulder investigated and connected to the air pump and a mercury manometer. The method was improved by N. A. Korotkov; the auskultativny way of measurement of the ABP offered them found universal distribution and is widely applied today. The reasons of arterial hypertension long remained not clear. Folgard and Headlights (F. Volhard, Th. Fahr, 1914), based on the combination of increase in the ABP to diseases of kidneys which was often observed in clinic and at a pathoanatomical research, considered that arterial hypertension is always a consequence of these diseases. Yushar (H. Huchard, 1889) who also paid attention to communication of an arteriolosclerosis of kidneys with arterial hypertension noted that in many cases the pathoanatomical research does not find renal pathology in persons at whom increase in the ABP was observed during lifetime. Yushar assumed therefore that arterial hypertension in similar cases is caused special, not revealed neither clinically, nor morphologically by defeat of renal arterioles — «presclerosis». In the 20th 20 century questions of a role of endocrine disturbances (in particular the caused diseases of a hypophysis and adrenal glands) in developing of arterial hypertension were widely discussed. During this period of G. did not consider as an independent nosological form.
A turning point in development of ideas of G. there was an idea about a possibility of «primary» increase in the ABP who is not connected with organic pathology of any body. The big merit in development of this idea belongs to the Soviet scientist-clinical physician G. F. Lang who stated in 1922 the assumption of existence of the special nosological form of the arterial hypertension called by it an idiopathic hypertensia and which is characterized by the specific etiology and a pathogeny which are essentially distinguishing it from other forms of arterial hypertension. In 1948 F. Lang offered the original concept, according to G.'s cut. is a consequence of disturbance of functions of the highest cortical centers (neurosis) leading to disorder of activity of the hypothalamic structures responsible for regulation of the ABP. This concept gained further development in A. L. Myasnikov's works and his schools.
A. L. Butchers would be considered by G. as the arterial hypertension caused «by primary disturbances of cortical and subcrustal regulation of vasculomotor system as a result of disorder of higher nervous activity with the subsequent involvement in pathogenetic process of humoral factors». The specified concept gained wide recognition as in our country, and abroad. In 40 — the 60th 20 century the role of disturbances of nervous control of the ABP was intensively studied as experimentally, and a wedge, by methods. In the same years the majority of modern was revealed or created antihypertensives (see), acting at the different levels of system of regulation of blood circulation. The role of hereditary, social, geographical and other factors in G.'s development is widely studied.; separate value of changes of action of the heart and vessels, and also interrelation of nervous and humoral disturbances in increases in the ABP is investigated; pathogenetic mechanisms of regional frustration of a tone of arteries and veins are profoundly studied; the differentiated approach to G.'s treatment is developed. in its different stages. The essential contribution to studying of these questions was made by the Soviet scientists.
G. Given about prevalence., even the population received as a result of mass inspections, it is necessary to consider approximate. It is connected, first, with the fact that various authors used different standards of the ABP and, secondly, with impossibility at mass inspections to carry out the differential diagnosis between G. and symptomatic forms of arterial hypertension which frequency in clinic makes apprx. 20% of all cases of increase in the ABP (N. A. Ratner, 1974). However symptomatic hypertensia occur among the population, apparently, much less often (according to A. A. Alexandrova, apprx. 4% of all cases of increase in the ABP).
The committee of WHO experts offered for obtaining comparable results at mass inspections of adult population (irrespective of age) to apply criteria of arterial hypertension: The ABP is lower than 140/90 mm of mercury. — norm, from 140/90 to 159/94 mm of mercury. — «a dangerous zone», 160/95 mm of mercury. above — arterial hypertension. Since the vast majority of cases of arterial hypertension would fall on G.'s share., it is necessary to consider that mass measurements of the ABP allow to make idea of the frequency of this disease among various groups of the population.
Prevalence of arterial hypertension among women and men is approximately identical though there are instructions that at women she meets a little more often. So, according to some authors, arterial hypertension at women is noted approximately by one and a half times more often than at men. According to Gordon and Divayn (T. Gordon, B. Devine), using criteria of WHO, it is observed at 12,8% of men and 15,3% of women aged from 18 up to 79 years living in the USA and belonging to white race. Frequency of arterial hypertension sharply increases with age. I. A. Rybkin and soavt, (the age standards taking the ABP for the upper bound) found increase in the ABP only in 0,8% of 16 — 19 years inspected in an age group and in 18,5% of 55 — 59 years inspected in a group of persons.
Increase in the ABP meets at residents of the large cities considerably more often, than among country people. E.g., A. M. Andrukovich (taking 140 — 85 mm of mercury for the upper bound of norm of the ABP.) revealed among citizens of both sexes at the age of 50 — 59 years arterial hypertension in 56,7% of cases, and among similar group of inhabitants of rural areas on sex and age composition — in 15,5%. E. Yu. Abzhanov using criteria of WHO inspected inhabitants of a number of districts of the Kazakh SSR and found that the frequency of arterial hypertension among men • at the age of 30 — 59 years living in rural areas makes 5,9%; it is about 2 — 2,5 times lower, than in the corresponding age groups of residents of the cities of Kazakhstan. Rather low prevalence of arterial hypertension among inhabitants of rural areas is confirmed also by data of H. N. Kipshidze et al., according to the Crimea increase in the ABP is noted at 7,3% of men and 18 years from 1031 inspected, living in rural areas of Georgia are more senior than women (authors used criteria of WHO).
Data on the frequency of arterial hypertension in various countries are difficult comparable since until recently authors used various standards of the ABP. In Japan, on a nek-eye to data, it is observed at 26,1% of persons of both sexes 40 years (these 7000 observations),
V. I. Metelitsa and soavt are more senior, found arterial hypertension in 23,6% of men at the age of 50 — 59 years living in Moscow (1000 observations). Though all these researchers used criteria of WHO, the results received by them are a little contradictory since the different contingents of the population were inspected.
It agrees standard in our country and to representations eurysynusic abroad, the main reason for G. the acute or long emotional overstrain is (see. Emotional stress ), leading to development of neurosis. In favor of this hypothesis big prevalence of G. would testify. among the population of the large cities with inherent in them accelerated life and abundance of mental irritants, than among inhabitants of the corresponding territorial, geographical and ethnic groups living in rural areas.
As A. L. Myasnikov, G. specified. meets at the persons occupied with the work demanding steady and strong psychoemotional stress more often. Concerning the arterial hypertension which is sharply developing under the influence of extraordinary emotional pressure there would be no full unity of opinions on legitimacy of reference it to G. Numerous cases of such hypertensia were registered at residents of the besieged Leningrad in the period of the Great Patriotic War («a blockade hypertension»), however after break of the Siege of Leningrad and relative normalization of living conditions of the ABP at patients with «a blockade hypertension» was quickly and with firmness normalized without any treatment.
So far it is not clear why the neurosis caused by similar irritants in one cases would lead to G.'s development., and in others proceeds with normal or even the lowered ABP. This ambiguity equally belongs also to any other somatizations form of neurosises.
It is possible to assume that there is no specific «hypertensive» neurosis, and implementation of nonspecific neurosis in a form G. (or other «somatic» disease) certain acquired and inborn features of an organism (including and features of the personality), and also some influences of external environment promote.
In particular, the opinion about etiol was expressed, to a role in G.'s emergence. sodium salts, especially sodium chloride [Dahl (L. To. Dahl) et al., 1957; M. I. Fatula, 1969]. Other researchers [Bock (K. Vosk), 1972] did not find correlation between contents in a diet of sodium salts and the frequency of arterial hypertension.
A. M. Vikhert's data allow to assume that hypertensive effect of sodium salts on some persons is connected with hereditary features of metabolism, but this form of arterial hypertension at people could not be identified with G. At the same time G. it is impossible to carry to purely hereditary diseases since often it is possible with reliability to establish that none of close relatives of the patient had no this disease (A. L. Myasnikov, 1965). V. A. Kononyachenko assumes that to G.'s development. genetically caused features of a metabolism contribute. It is noted that among relatives of the patients suffering from G., the frequency of this disease is higher, than among the population in business. High concordance of incidence of G. is noted. at unioval twins and considerably smaller — at raznoyaytsevy. Experimental data about genetic conditionality of arterial hypertension at rats of certain breeds at long contents on the diet containing excess amount of sodium chloride are obtained.
The assumption Folgarda and Farah, and also Yushara about a causal role of damage of kidneys in G.'s development. did not find confirmation in numerous clinical and pathoanatomical trials.
Though G.'s frequency. clearly increases with age, it cannot be considered a disease of aging. Even at very old men of the ABP it is in most cases normal, and frequent and lowered. G.'s increase. with age connect with a variety of reasons. First of all duration of influence of emotional tension matters. It is not excluded that the known role in G.'s increase. with age plays development of atherosclerosis of arteries, krovosnabzhayushchy vasomotor centers. The insignificant narrowing of these vessels, insufficient to cause tserebroishemichesky hypertensia, would promote G.'s development. against the background of the existing neurosis. The decrease in depressor function of baroreceptors of an aorta and a sinocarotid zone or unsharp narrowing of a renal artery caused by atherosclerosis G.'s implementations can also promote., caused by neurosis. It is not excluded that to G.'s development. at persons of the senior age groups the decrease in a renal blood-groove which is naturally found in people contributes 40 years (D.F. Chebotaryov) are more senior. To contribute to G.'s development. also a number of hormonal disturbances can.
Especially defiantly frequent development of arterial hypertension in the period of a climax at women at whom neurotic states often develop and a «hypertensive» orientation of neurosis amplifies decrease in oestrogenic function of ovaries and compensatory increase in function of bark of adrenal glands (V. G. Baranov, 1966). Often patients with a diffusion toxic craw have a symptomatic systolic hypertensia, sometimes at them also the systolodiastolic hypertensia which is not disappearing after radical treatment of a basic disease develops. It creates premises for assumptions that endocrine frustration at a climax and a thyrotoxicosis in some cases would promote true G.'s development.
The opinion is eurysynusic that to G.'s development. also obesity contributes. Data of the special researches devoted to this question are contradictory. V. Shach found correlation between obesity and arterial hypertension, Geyger and the Adhesive tape (N. of Geiger, N. Scotch) found that the frequency of arterial hypertension at corpulent people is not higher, than among the population in general. Even if communication of arterial hypertension with obesity will be confirmed, will remain not clear whether it is necessary to carry this form of hypertensia to G. Also data on a possible role of smoking, and also an alcohol abuse in G.'s development are contradictory.
A number of foreign authors considers an etiology of an idiopathic hypertensia obscure or not quite found out what the Committee of WHO experts agreed with.
According to the neurogenic theory of G., offered by G. F. Lang, the leading link in a pathogeny of this disease — the disturbance of century of N of which is originally arising under the influence of external irritants and further leading to permanent excitement of the vegetative pressor centers (see. Pressor reactions ), as causes increase in the ABP. Already in an initial stage of G. the pathogeny joins changes from humoral pressor and depressor systems. Assume that activation of humoral mechanisms during this period of a disease has compensatory character and arises as reaction to an overstrain and disturbance of a trophicity of nervous cells of a brain.
In an initial stage of G. the hyperkinetic type of blood circulation which is characterized by increase in cordial emission at a little changed general peripheric resistance of vessels [I. K. Shkhvatsabaya, forms 1972; R. Sannerstedt, 1970, etc.]. At the same time already in initial stages of G. sometimes vascular resistance in kidneys increases. During this period when distensibility and elasticity of an aorta are still kept, there is a reconfiguration of baroreceptors of a sinocarotid zone and aortic arch which is expressed in preservation of normal activity of an aortal nerve at increase in the ABP (in fiziol, conditions increase in the ABP causes the activation of an aortal nerve leading to normalization of pressure). According to P. K. Anokhin, this «reconfiguration» of baroreceptors at G. provides problems of regulation of blood circulation, shifting its parameters on the level, optimum for new conditions. A thickening of walls of an aorta and carotid arteries, reduction of their elasticity in late stages of G. lead to decrease in sensitivity of baroreceptors, as defines reduction depressory reactions (see) on increase in the ABP.
Influence of c. the N of page on a tone of arteries and especially arterioles, and also on function of a myocardium is mediated through sympathoadrenal system (see), including vasomotor centers of a hypothalamus, a sympathetic nerve, adrenal glands, alpha and beta and adrenergic receptors of heart and vessels. Increase in activity of sympathoadrenal system leads not only to a hyperkinesia of heart, but also to a konstriktion of arterioles. It is supposed that narrowing of renal arterioles at G. causes ischemia of the juxtaglomerular device of kidneys owing to what production of enzyme amplifies renin (see) which interacts with one of fractions of alfa2-globulins of blood and turns it in angiotensin (see), possessing the expressed pressor action. Despite a nek-swarm the narrowing of renal arterioles found in many patients in initial stages of G., the renal blood stream in connection with increase in cordial emission at a part of patients even increases. It is possible that sympathoadrenal influences stimulate the juxtaglomerular device directly. Increase in a renal blood-groove leads to increase of a mocheotdeleniye and excretion of ions of sodium. Loss of sodium stimulates secretion with adrenal glands of Aldosteronum — the hormone promoting a delay of sodium in fabrics including in walls of arterioles that does them especially sensitive to pressor influences, in particular to influence of mediators of a sympathetic nervous system (see. Aldosteronum ). In turn, increase in secretion of Aldosteronum can be caused by sympathoadrenal influences. It is established that angiotensin can be a secretagogue of Aldosteronum also. During G.'s formation. the described changes in system a renin — angiotensin — Aldosteronum meet changeably, have functional character and most clearly are shown in the conditions of a stress. There would be data on existence of various options of interaction of humoral factors in G.'s pathogeny. [J. Laragh, 1973]., proceeding with increase in activity of a renin in a blood plasma, it is characterized by the expressed bent to spasms of arterioles (vasopressor hypertensia). If activity of a renin is low, increase in mass of the circulating blood is noted, as serves, perhaps, as the main pathogenetic mechanism of increase in the ABP (hypervolemic hypertensia). The assumption that hypervolemic hypertensia is connected with some changes of secretion of Aldosteronum finds confirmation at a part of patients with low activity of a renin at whom at introduction of excess amount of sodium salts secretion of Aldosteronum does not increase. Such reaction is characteristic of primary hyper aldosteronism (see). However at G. it is about a false hyper aldosteronism since secretion of Aldosteronum remains normal and the hypopotassemia, typical for primary hyper aldosteronism, is not noted. At early stages of G. at patients with high activity of a renin in a blood plasma increase in cordial emission and a stroke output of blood in combination with others a wedge, signs of a hyper sympathicotonia and increase in excretion of dopamine is observed.
At patients with normal or reduced activity of a renin increase in mass of the circulating blood and increase in the general peripheric vascular resistance is noted. Lech. the effect of blockers of beta and adrenergic receptors at patients of the first group is expressed much more accurately, than at patients of the second group.
Stability and expressiveness of arterial hypertension at G. also blood are defined not only by activity of pressor systems of an organism, but also a condition of a row of depressor systems, including kinin system of kidneys (see. Kinina ), activity of an angiotensinase (the enzyme inactivating angiotensin) and renal prostaglandins (see).
Increase in activity of depressor mechanisms at early stages of G. it is necessary to consider as reaction to arterial hypertension. In fiziol, conditions Depressor systems neutralize action of the factors causing increase in the ABP. Between pressor and depressor systems accurate interaction is traced (I. K. Shkhvatsabaya and soavt., 1971).
Period of stabilization of G. it is characterized by qualitatively new hemodynamic shifts: gradual reduction of cordial emission and increase of the general peripheric vascular resistance. The significant role during this period is played by decrease in compensatory reserves of depressor nervous and humoral mechanisms (humoral Depressor systems, sensitivity of baroreceptors of an aortic arch and sinocarotid zone). The enduring tension of the hypothalamic structures responsible for regulation of the ABP caused remaining throughout all disease and even by the amplifying disturbance of century of N of leads to the fact that originally unstable and short-term increase in a tone of arterioles (and in particular arterioles of kidneys) becomes constant. In this regard in G.'s pathogeny. during stabilization the increasing role is played by humoral factors. Functional (vasoconstriction), and further and organic (arteriologialinoz) narrowing of renal arterioles causes hyperfunction and a hypertrophy of the juxtaglomerular device and, therefore, increase in secretion of a renin. Thus, the vicious circle becomes isolated: narrowing of renal arteries — * hypersecretion of a renin — the strengthened formation of angiotensin — hypersecretion of Aldosteronum — the delay of sodium in walls of arterioles leading to increase in their sensitivity to pressor factors — vasoconstriction (narrowing of arterioles of kidneys). If during G.'s formation. the role of the specified humoral mechanisms is rather small and their participation in a pathogeny of a disease is changeable, during stabilization, especially in late stages of G., it becomes very essential. In these stages in G.'s pathogeny. quite often new links, in particular increase in pressor activity of hypothalamic structures under the influence of the ischemia connected with vasoconstriction and an angiopatiya of vessels of a brain (tserebroishemichesky hypertensia) join. At a considerable part of patients atherosclerosis of an aorta develops (see. Atherosclerosis ), leading to loss of its elasticity that promotes further increase in systolic pressure, and the destruction of barorecrptor zones nullifying in combination with their «reconfiguration», their depressor function. Atherosclerosis of arteries, vaskuliruyushchy a brain, and also renal arteries creates premises to stabilization of the raised ABP in connection with constant ischemia of a brain or kidneys.
A question of pathogenetic relationship between G. and by atherosclerosis it is not solved. A. L. Myasnikov specified that there would be two assumptions of the reasons of a frequent combination of G. with these or those displays of atherosclerosis:
1) atherosclerosis, as well as G., is an eurysynusic disease and meets in the senior age groups more often;
2) increase in the ABP creates hemodynamic premises to development of atherosclerosis (it is known that distalny the site of an arteriostenosis where pressure of blood is lower, atherosclerotic defeats, as a rule, do not develop). However G.'s combination. meets atherosclerosis considerably more often than it would be possible to expect at mere coincidence of two diseases. On the other hand, at symptomatic hypertensia atherosclerosis develops rather seldom. It gave the chance to suggest about etiological and pathogenetic proximity of both diseases in which origin, according to A. L. Myasnikov, the leading role belongs to a psychological overstrain.
Pathological anatomy of G. it is characterized by various changes of cardiovascular system, kidneys, the central and peripheral nervous system, closed glands and other bodies.
With morfol, the points of view it would be accepted to consider three periods of G.:
1) period of functional disturbances; 2) period patol, changes in arteries and arterioles; 3) the period of secondary changes in bodies owing to disturbance of blood circulation in them.
In the first, functional, G.'s period. modern methods morfol, researches do not allow to find any changes in fabrics and bodies, except for a hypertrophy of a left ventricle of heart and irregularity of caliber of small arteries and arterioles.
The brightest pathoanatomical sign of G. in the second and third periods the hypertrophy of heart, hl is. obr. left ventricle (tsvetn, fig. 1). The weight of heart can increase to 900 g, and wall thickness of a left ventricle at the basis — to reach 3 cm. Cardial cavities at the beginning of G. or are not expanded at all (a concentric hypertrophy of heart), or are expanded slightly (a tonogenny cardiomegaly). In the subsequent, in process of increase of a disease and a hypertrophy of a myocardium, development in its fibers of dystrophic changes, cardial cavities gradually extend (myogenetic expansion) that is designated as an eccentric hypertrophy of heart (see. Hypertrophy ). Such picture can be one of signs of a decompensation of cordial activity. Microscopic changes of a myocardium at G. originally also numbers of mitochondrions, to nek-rum to coarsening of an argyrophil framework of a myocardium and emergence in a stroma of collagenic fibers come down to a thickening of muscle fibers, increase in the sizes of their kernels, increase in the sizes. Owing to discrepancy between a lot of work of a myocardium and a condition of its food, in certain sites of a myocardium of a left ventricle of heart and to a lesser extent right dystrophic processes in the form of muddy swelling begin to develop (see. Proteinaceous dystrophy ), fatty dystrophy (see). There can be even small sites of a necrosis of muscle fibers. Promotes it also quite often observable at G. the expressed atherosclerosis of coronal arteries. Because of dystrophic and necrobiotic changes of a myocardium there are ochazhka of development of connecting fabric that leads to a focal and diffusion myocardiofibrosis (tsvetn. fig. 4). In small arteries of a myocardium of change are usually insignificant, but the phenomena of fibrinoid swelling can be observed (see. Fibrinoid transformation ) up to a necrosis with reactive perivascular cellular infiltration and an outcome in a sclerosis.
In an arteriovenous anastomosis of heart the hypertrophy and a hyperplasia of their walls at the expense of a functional layer are noted. In process of increase of the phenomena of G. in a wall of an anastomosis sclerous changes develop that, according to some researchers (A. V. Arkhangelsky), worsens blood supply of a myocardium; it is one of the factors promoting development of a cordial decompensation. Due to the hyponutrient and hard work of heart at G. there are considerable changes in its intramural nervous system. So, in ganglionic cells of vegetative small knots of auricles there are phenomena of a chromatolysis, pycnosis and an ectopia of kernels, wrinklings and death of cells (tsvetn. fig. 5). In nerve fibrils of different caliber coarsening, varicose swellings, glybchaty disintegration, in receptor devices of a myocardium — dystrophic and destructive processes in the form of the coarsened and reinforced fibers, fragmentations, saggings of a neuroplasm are noted. The phenomena of reactive growth of the nerve fibrils making the sensitive terminations are sometimes observed.
The described changes in an intramural nervous system of heart are not specific to G., but are quite characteristic of diseases which are followed by oxygen insufficiency. At G. there are changes in arteries of different caliber, but they are not homogeneous in character. So, these changes usually reflect development of atherosclerosis in large arteries of elastic and elastic and muscular type, and any characteristic of G. changes do not develop. In average and small arteries there are changes indicating a hyperpermeability of a vascular wall that leads to adjournment in an intima not only lipids, but also gialinopodobny proteinaceous masses. The greatest changes at G. develop in arterioles (tsvetn. fig. 12), and defeat has them more or less widespread character and is designated as arteriolosclerosis (see).
Extent of distribution and a phase of damage of small arteries, arterioles and capillaries can be unequal in various bodies and even in the same body.
Besides, there are some qualitative features of process in each body. It is connected partially with local structural features of arterial system. Along with old arteriolosklerotichesky changes (a hyalinosis, elastofibroz) fresh changes in a type of plasmatic treatment and an arteriolonekroz meet (tsvetn. fig. 10). It indicates that changes in arterioles, small arteries, and also in capillaries at G. proceed with change of the periods of attenuations and flashes of dystrophic process. Klinikoanatomichesky comparisons show that the morphology of acute dystrophic changes of walls of small arteries, arterioles and capillaries (plasmatic treatment, a necrosis of a vascular wall) is an equivalent of that a wedge, G.'s manifestations., which are designated in clinic as hypertensive crises and can arise in any piece of vascular system (I. V. Davydovsky). Changes in veins at G. are expressed as some thickening of elastic membranes and an intima.
Increase in the ABP in a big circle of blood circulation is followed by nek-ry changes as well in vessels of a small circle of blood circulation.
In small branchings of a pulmonary artery develops elastofibroz, leading sometimes to considerable narrowing of a gleam of vessels. In bronchial arteries the thickening of a muscular layer, a sclerosis of a wall and seldom a hyalinosis is noted. Argyrophil fibers are thickened and coarsen. In pulmonary veins against the background of a congestive plethora the hyperplasia of elastic membranes of an intima, accumulation in it a chromotrope-nogo of substance and development of a sclerous thickening of an internal cover meet. In vessels of the closing type the phenomena of an elastofibroz of a wall develop that, apparently, complicates their function.
It is noted that in arterial vessels of lungs change-types of an arteriolonekroz, plasmatic treatment and a hyalinosis do not meet. Density of vascular network of pulmonary fabric in experiences with «fruit liqueur» of pulmonary vessels would remain at G. without changes as in cases with a hypertrophy of a right ventricle, and without it.
Changes in various bodies and systems at G. considerably hl are defined by prevalence and weight of changes of vessels. obr. arterioles. On the basis of defeat of arterioles of kidneys a nephrosclerosis — growth of connecting fabric on site of zapustevayushchy nephrons develops (see. Nephrosclerosis ). The kidney decreases in sizes, becomes fine-grained and is called pervichnosmorshchenny (an arteriolosklerotichesky kidney; tsvetn. fig. 3). Arteriolosklerotichesky nephrosclerosis would represent manifestation of the third (last) period of G. Quite often at the persons suffering from G., kidneys remain as morphologically, and functionally intact.
M. A. Zakharyevskaya's researches showed that at G. in vascular system of kidneys the following processes develop; changes of arteries of age character, atherosclerotic changes, arteriolosclerosis. Age changes are well-marked in intra renal arteries of average caliber and consist in a thickening of an internal cover of arteries owing to stratification of an internal elastic plate on several membranes with development of a small amount of connecting fabric between them.
The specified changes never lead to development of a nephrosclerosis. Atherosclerotic changes in renal vessels are observed at simultaneous development of atherosclerosis in other parts of arterial system. In system of renal arteries atherosclerotic changes are most expressed at the place of an otkhozhdeniye of a renal artery from an aorta. In intra renal arteries atherosclerosis is shown only in the form of adjournment of lipids in an internal cover. Narrowing by atherosclerotic plaques of a gleam of a renal artery can lead to a gruboochagovy nephrosclerosis which is designated as the atherosclerotic nephrosclerosis which does not have big a wedge, values. And, at last, the third type of vascular changes in kidneys — an arteriolosclerosis — typical and most important manifestation of G.
Changes of balls at an arteriolosklerotichesky nephrosclerosis are various. Along with the normal, but increased in sizes balls balls atrophic and balls with alterativny changes are found.
The quantity of normal balls fluctuates over a wide range depending on weight of a nephrosclerosis.
Atrophic balls can have character fallen down, and in one of them the phenomena of hyalinization are available, in others are absent.
Sometimes in the hyalinized balls powdered or krupnokapelny adjournment of lipids meets. Balls with alterativny changes look variously. Among them balls meet fresh plasmatic treatment of capillary loops and walls of arterioles. In unstructured proteinaceous weight nuclear disintegration, scraps of elastic fibers, separate gemolizirovanny erythrocytes are visible. At destruction of capillary loops the proteinaceous masses and erythrocytes are found in a cavity of the capsule of a ball and gleam of tubules. Sometimes in homogeneous plasmatic masses threads of fibrin are found. In later phase of plasmatic treatment of a ball proliferation of cells occasionally joins the described changes from the remained loops, the capsule and a neck of a ball. In the result of plasmatic treatment and a necrosis of loops and necks of balls consolidation of proteinaceous and devitalized masses with development develops hyalinosis (see). Depending on prevalence of plasmatic treatment the hyalinosis can cover all ball or only its separate loops. Also changes in a type of so-called apoplectic balls (a picture of sharp overflow of loops of balls blood) and obesity of balls at which lipidic drops or grains fill cells of balls in different degree are described. Loops of the grown fat balls — thin-walled, as in normal nephrons.
In epithelial cells of the juxtaglomerular (okoloklubochkovy) device of a kidney at G. the quantity of granules of a renin increases.
In tubules at an arteriolosklerotichesky nephrosclerosis there are either atrophic, or dystrophic changes. The atrophy is observed in the tubules corresponding to the hyalinized balls. Tubules are reduced in volume, their epithelium is flattened. The intercanalicular stroma is thickened and fibrozirutsya. Dystrophic changes of tubules are found in those nephrons in which arterioles and balls alterativny changes are observed. In these cases in an epithelium of the main department of tubules the phenomena of proteinaceous and fatty or hyaline and drop dystrophy are noted. The necrosis of an epithelium is sometimes observed. In process of hyalinization of balls in the tubules corresponding to them atrophic changes with gradual substitution of a parenchyma connecting fabric begin to develop. In the remained nephrons between sites of a fibrous zapustevaniye the balls increased in sizes are noted (tsvetn. fig. 9) and tubules with an expanded gleam. In a medulla of a kidney excess of connecting fabric and a hyalinosis is observed.
Changes in the central and peripheral nervous system at G. differ in a big variety and depend on weight of a course of a disease, its duration and extent of changes of vascular system. In a brain in various stages of G. it is possible to observe hypostasis and a small thickening of a soft meninx, expansion of subarachnoid spaces, okolososudisty cellular infiltrates. In substance of a brain changes of nervous cells with the reaction of a glia expressed in a varying degree are observed acute and hron. In hard cases of G. with a rapid current from nervous cells of a cerebral cortex destructive changes are noted. On this soil it is especially frequent in II and III layers of bark of a frontal lobe and in a hippocampus extensive zapustevaniye are formed (E. JI. Gerberas). Increase in tissue of a brain of argyrophil granularity (fig. 1) is quite often noted that, according to P.E. Snesarev, reflects disturbance of the oxidation-reduction processes developing at G. as a result of fabric hypoxias (see). The hyperplasia and a hypertrophy of astrocytes, dystrophic changes in a form of a loosening of protoplasm and a thickening of shoots, amoebalike transformations of cells with disappearance of shoots and pycnosis of kernels is observed, from a microglia — some polymorphism of changes, emergence of branchy forms, and shoots of separate cells are exposed to coarsening. Sometimes it is possible to see fragmentation of shoots and cellular bodies (fig. 2). In development of structural disturbances of neurons at G. a certain value has their functional state. It becomes especially noticeable during the studying of kernels of a myelencephalon. There is a clear distinction in extent of defeat of vegetative and somatic kernels.
The most serious changes of cells meet in a dorsal kernel of a vagus nerve as on total quantity of the changed neurones, and especially on number of the nervous cells which are in a condition of a necrobiosis and a necrosis. Also considerably changes from nervous cells of vegetative kernels of hypothalamic area prevail.
As well as in other bodies, in particular in kidneys, in small arteries, arterioles and capillaries of a brain, proteinaceous subintimalny deposits are noted (tsvetn. fig. 6) with gradual development of a hyalinosis (tsvetn. fig. 7 and 11), plasmatic treatment and a loosening of all wall of an arteriole with a necrobiosis of elements of a wall or without it. At this process there are ruptures of elastic membranes, there are microaneurysms, fibrinferments of a gleam of arteries, the jump of structure of small arteries and arterioles which is followed by expansion of their gleam (K. G. Volkova, etc.).
Strokes at G. arise in the field of the central gray nodes and the internal capsule where vascular changes reach the greatest degree (see. Stroke ). In the place of hemorrhage tissue of a brain collapses completely, formed the cavity executed by the turned blood mixed with particles of the destroyed tissue of a brain. The streamed blood can break in side cerebral cavities. If the patient transferred the acute period of hemorrhage, then in the center process of disintegration and fluidifying of mass of the turned blood, formation of hemosiderin on the periphery of the center and gematoidin in its center begins. On site hemorrhages there is a cavity.
In the tissue of a brain surrounding a cavity plentiful accumulation of the granular spheres filled with a part fat, a part hemosiderin is found. Sometimes along with fresh hemorrhage cysts — the remains of earlier occurred hemorrhages are noted (tsvetn. fig. 2).
Changes of the autonomic nervous system at G. are various, are not for it specific and are found preferential in system of afferent (vistseroretseptorny) fibers and vegetative kernels of chest department of a spinal cord. Along with dystrophic and necrobiotic changes in century of N of page it is possible to find signs of regenerator processes. Here it is possible to carry a hypertrophy of a neurocyton, emergence in a kernel of two and more kernels, existence of multinucleate ganglionic cells (tsvetn, the tab. of fig. 5), figures of amitotichesky division of ganglionic cells, accumulations of neyrosimplast. Numerous collaterals which intertwine with collaterals of the next dendrites depart from some dendrites in sympathetic nodes (tsvetn, the tab. of fig. 6).
The most widespread type of changes of nervous cells sympathetic gangliyev and vegetative kernels of a spinal cord is swelling of cells, a partial or full chromatolysis (tsvetn. tab. of fig. 1 and 2); can develop kario-and plazmotsitoliz. Quite often there are phenomena of gidropichesky dystrophy especially characteristic of cells of peripheral nerve knots; glybchaty disintegration of fibers is observed. Fine amyelenic fibers usually do not change. The synoptic device sympathetic gangliyev is early enough involved in pathological process, and synoptic ringlets become is raised argyrophil and gradually turn into the rough argyrophil spheres which are coming off terminal threads. The died on the spot cells in sympathetic nodes residual small knots are formed of satellites.
In a vagus nerve and in its node reactive and dystrophic changes of thick pulpy nerve fibrils are noted.
In a knotty ganglion sharp swelling of ganglionic cells, spraying in them chromatophilous substance, karioliz is found (tsvetn, the tab. of fig. 3). Dystrophic changes are defined also in nerve terminations and fibers of a reflexogenic zone of an aortic arch (tsvetn, the tab. of fig. 4) and a carotid sine.
For G. defeats of hl are characteristic. obr. vessels of a retina of an eye (same, as in vessels of other areas), and also the secondary changes of a choroid designated as hypertensive retinopathy (see).
The most constant is the papilledema (see. Congestive nipple ) and the departments of a retina surrounding it. Also hemorrhages, amotio of a retina are observed by proteinaceous liquid (tsvetn. fig. 8) and necroses.
Focal amotio of a retina (see) the hl is shown by accumulation in subretinal space. obr.: in a circle of an optic papilla, proteinaceous liquid. Hemorrhages. in tissue of a retina can be focal or diffusion, meet in all layers of a retina> but sharper happen are expressed in its back departments. In a nerve fiber layer of hemorrhage have the form of strips, in periblasts of a retina —., rounded shape. In later stages of a retinopathy adjournment in a retina of proteinaceous masses is observed. Proteinaceous deposits at first appear in an intergranular layer of back departments of a retina, their deposits gradually extend also to front departments. Focal necroses of a retina would meet in hard cases of G. as display of far come retinopathy in the presence of hypostasis, amotio, hemorrhages and the expressed both hyperplastic, and dystrophic changes of vessels.
Nervous cells of a ganglionic layer of a retina would be exposed to changes in all stages of G. They are poorly expressed in I and II stages. In these cases in a number of nervous cells the hyperchromatosis of kernels, irregularity of the drawing and distribution of chromatophilous substance, vacuolation of protoplasm are noted. In a late stage of development of G. are noted a total chromatolysis, sharply expressed vacuolation of protoplasm we are cells, kariotsitoliz and full death of nervous cells.
Generally changes of nervous elements of a retina at G. depend on the circulatory disturbances caused in it by both functional disturbances, and organic lesions of vessels of internal covers of an eye. Exert impact of change which would be found at G. on a condition of an eye. in a semi-lunar node of a trifacial, through means to-rogo trophic influence on organs of sight is provided. In a semi-lunar node at G. changes of vessels (elastofibroz, plasmatic treatment, a hyalinosis), nervous cells and fibers are found. In nervous cells the phenomena of wrinkling, vacuolation and death of neurons meet, fibers are exposed to glybchaty disintegration.
In closed glands at G. find in different extent of change both from vessels, and from a parenchyma. Changes of vessels meet in adrenal glands, a pancreas, a front share of a hypophysis, a thyroid gland, changes of a parenchyma — generally also in these glands.
In a front share of a hypophysis the quantity of eosinophils and main cells meets standard, the number of basphilic cells quite often increases.
In adrenal glands at G. the hyperplasia cortical and marrow is defined. Changes of a medulla are changeable. In one cases its hyperplasia, in others, heavier and long on a current — atrophic and dystrophic changes is noted. In a pancreas the atrophy, a sclerosis and lipomatoz parenchyma, the centers of a necrosis are observed, and intensity of atrophic and dystrophic disturbances is in direct dependence on extent of vascular changes. In a thyroid gland at G. atrophic and dystrophic changes are observed; in certain cases activation of a colloid and existence of a large juicy follicular epithelium meets. In gonads of any characteristic changes, in addition to the vascular defeats which are found sometimes, it is not revealed.
Morfol, changes in closed glands at G. most likely have secondary character and are caused by vascular changes because of which there are dystrophic, necrobiotic and sclerous changes. An opportunity is not excluded that the known role in their development is played by the trophic disturbances connected with defeats in the central and peripheral nervous system and in the innervatsionny device of closed glands.
In a carotid glome dystrophic and sclerous changes are noted that will be coordinated with assumptions that defeat of the depressor device would play a role in a pathogeny of hypertensia in late stages of G.
In went. - kish. a path at G. only occasionally typical defeats of vessels in all phases of their development meet. In a liver they are not found.
In a spleen the heavy destructive changes of vessels complicated by thrombosis and development of the multiple centers of a necrosis (a so-called spotty spleen) sometimes develop. In similar cases quite often for the same reasons there are multiple necroses in a pancreas (a so-called spotty pancreas).
In vessels of skin at G. proliferation of all elements of a wall of vessels, fall of a gleam of capillaries and proliferation of pericytes is observed preferential.
Absence morfol. changes in bodies (except a hypertrophy of heart) in the first, functional period of G. it will be coordinated with ideas of the leading role of disturbances of the central nervous control of cardiovascular system in an origin of a disease.
Sometimes only manifestation of G. for many years increase in the ABP is. Absence or scarcity wedge, G.'s manifestations., especially in its early stages, conducts to the fact that at a part of patients the disease remains it is long not revealed. So, according to Research in-that cardiology to them. And. JI. Myasnikova of the USSR Academy of Medical Sciences, more than at 35% of men at the age of 50 — 59 years increase in the ABP was for the first time revealed at mass inspection. However most of patients addresses with complaints which in early stages of G. it is impossible to consider specific (fatigue, irritability, sleeplessness, weakness, dizziness, heartbeat).
Are not strictly specific and designated by G. F. Lang as typical for G. headaches (morning, like «the heavy head», occipital localization, amplifying in horizontal position, decreasing after walking) which are really characteristic of sick G., but are observed also at the persons which do not have increase in the ABP.
In late stages of the complaint of patients often would be defined by G.'s complications. (renal or heart failure, displays of the accompanying atherosclerosis). Exacerbations of a disease are quite often observed short-term (from several hours to several days) — crises (see) which, according to some information, would be noted at 20 — 34% of sick G.
G.'s current. it is characterized by staging in development of arterial hypertension and symptoms of regional circulatory disturbances. In the USSR G.'s classification would find broad application. on stages and phases, offered by A. L. Myasnikov. In it original positions of classifications of G. would be developed. on stages, developed by G. F. Lang and E. M. Tareev. According to this classification accepted by the All-Union conference of therapists in 1951 during G. allocate three stages, each of which is subdivided into two phases.
The I stage
the Phase A — latent, or prehypertensive. The ABP usually normal also raises more, than at healthy faces, only at the time of emotional pressure, under the influence of cold, pain and some other external irritants. A phase B — tranzitorny. The ABP raises periodically, hl. obr. under the influence of external irritants, is also returned to datum level without any to lay down. actions; vascular crises (more precisely angiodystonic, i.e. connected with frustration of a tone of vessels) are observed seldom. Sometimes in this stage narrowing of small arteries and a phlebectasia of an eyeground comes to light. Organic changes from heart, kidneys, a brain are absent.
The II stage
the Phase A — labile. The ABP is constantly raised, but his level is unstable. Under the influence of the sparing regime (rest, normalization of a dream, the rational organization of work, etc.) of the ABP time be normalized can on a nek-swarm. More often than in the I stage, there are vascular crises (see). The hypertrophy of a left ventricle of heart determined by strengthening of an apical beat, shift of the left border of a knaruzha, and also radiological and on an ECG develops. On an eyeground, except the changes revealed already in the I stage of a disease also crimpiness of arteries and «a symptom of decussation» of the I degree (narrowing of a vein in the place of its crossing with an artery), and also pallor of nipples of optic nerves quite often are found. A phase B — stable. It is characterized by substantial and permanent increase of the ABP, for decrease: to-rogo use of medicamentous therapy is necessary. Vascular crises proceed more hard. Also displays of the accompanying atherosclerosis (stenocardia, a myocardial infarction, disturbances of cerebral circulation etc.) are quite often observed. Signs of a hypertrophy of a myocardium become more expressed. The second cardiac sound over an aorta is, as a rule, strengthened, at the accompanying atherosclerosis of an aorta it can have a metal shade. Sometimes over a top of heart systolic noise is listened that speaks about the relative insufficiency of the mitral valve caused by dilatation of a hypertrophied left ventricle or reduction of a tone of papillary muscles. Systolic noise can be listened also over an aorta; such noise is connected with its expansion, a cut it is possible to reveal perkutorno and radiological. In some cases it is possible to find the retrosternal pulsation connected with lengthening of the ascending department of a chest aorta.
Angiopatiya of a retina is sharply expressed: arteries are narrowed, izvita, veins are considerably expanded; «the symptom of decussation» of the II—III degree is noted (moderate or considerable stretching of a vein distalny and proksimalny areas of decussation and sharp narrowing in the place of a crossing with an artery). The caliber of arteries becomes uneven; quite often they have an appearance of «a silver wire». Dot retinal apoplexies, thrombosis of her arteries and veins are sometimes observed. In this phase of a disease dystrophic changes of internals (first of all a brain, heart and kidneys) owing to circulatory disturbances in them can be observed.
The III stage
the Phase A — sclerous compensated. The ABP with firmness is also considerably raised, his decrease requires use of strong medicamentous means. If crises are observed, they proceed the same as in a phase B II of a stage. There are signs of an arteriolosclerosis of kidneys (decrease in concentration function, sharp reduction of a renal blood-groove, quite often small proteinuria and a hamaturia), a cardiosclerosis (a priglushennost of cardiac sounds, big, than in the previous stage, expressiveness of symptoms of its hypertrophy and dilatation), a sclerosis of brain vessels (decrease in memory, concentration of attention, faintheartedness, etc.). But function of internals is broken unsharply (there are no permanent manifestations of renal, heart and cerebrovascular failure), and working ability of some patients is at least partially kept. A phase B — sclerous dekompensirovanny. It is characterized by heavy dysfunctions of internals that does patients completely disabled (renal or heart failure; heavy cerebrovascular insufficiency, it is frequent with focal nevrol, disturbances owing to thromboses or hemorrhages; hypertensive angio-and neuroretinopathy).
In the III stage of the ABP can be slightly lower, than in II («the beheaded hypertensia» owing to decrease in propulsive function of heart or disturbances of cerebral circulation). Heavy changes of vessels and nervous structures of an eyeground are characteristic of both phases III of a stage. In addition to the symptoms typical for a phase B II of a stage, massive retinal apoplexies, «white spots» — the centers of plasmorrhagias or dystrophic changes of a retina can be observed. Some arteries have an appearance of «a copper wire» that is caused by the expressed hyalinosis of their walls.
On G.'s classification., accepted by Committee of WHO experts in 1962, during a disease three stages are also allocated: I \functional changes; II \initial organic changes and III — a stage of the expressed organic changes in bodies, first of all in kidneys.
G.'s classification. on stages, and especially on phases, it is to a certain extent conditional. Sometimes it is impossible to establish to what stage (and in particular to what phase) G. would belong. at the specific patient. Quite often arterial hypertension having labile character at early studies keeps it for many years, and any signs of progressing of a disease are absent. Sometimes, on the contrary, arterial hypertension at sick G. from the moment of its detection has stable character; in similar cases it is not possible to reveal early stages of a disease which, perhaps, really are absent. The question of a ratio between G. is not clear. The I stages and a neurangiosis with a tendency to pressor reactions. It is not excluded that it is about one disease with different forms of a current.
On the nature of progressing of symptoms of G. and its durations allocate four options of a current: 1) quickly progressing (malignant); 2) slowly progressing; 3) not progressing; 4) involution. Belonging to G. would be discussed. arterial hypertension with a malignant current * bystry progressing is characteristic Of this form, and the ABP from the very beginning of a disease with firmness keeps on high figures and is frequent, tends to further increase; very much early the organic changes inherent to final stages of G. develop. (a heavy neuroretinopathy, an arteriolosclerosis and arteriolonekroz in kidneys and other bodies, heart failure, disturbances of cerebral circulation). The disease in the absence of active treatment comes to an end with the death of patients in 1 — 2 years after emergence of the first symptoms. Treatment can slow down considerably development of a disease and even, according to a number of authors, lead to crossing of its current to slowly progressing. G.F. Lang specified that a malignant current of G. can be primary and secondary; in the latter case it would be preceded by the long period of slow progressing of G., what gives the grounds to speak about «a malignant phase» of a disease. «For the second time malignant» hypertensia at sick G. connect with development of the changes characteristic of a renal failure.
The malignant current meets at symptomatic arterial hypertension incomparably more often (see. arterial hypertension ). It allows authors to assume a nek-eye that all cases of a malignant course of arterial hypertension have secondary, symptomatic character even if its reason is not found out.
A. L. Myasnikov (1965), Shpakh (M. O. of Spach) et al. (1973), etc. consider that arterial hypertension of any etiology, including and the caused G. can get a malignant current. E. M. Tareev suggested that «malignant option» of G.'s current. represents an independent nosological form.
In spite of the fact that at G. vessels of all areas, in a wedge are surprised, to symptomatology signs of preferential damage of a brain, heart or kidneys usually prevail that E allowed. To allocate to M. Tareev three forms G. — cerebral, cardial and renal.
In clinical practice often it is necessary to meet the simultaneous expressed defeat of vessels of two or all three specified areas in this connection it is not always possible to carry a disease at the specific patient to one of these forms.
G.'s current. at many patients is complicated by hypertensive crises which A. L. Myasnikov (1965) considers as the sharp exacerbations of a disease for short term which are characterized by a number of neurovascular disturbances and the subsequent humoral reactions. Hypertensive vascular crises were described for the first time by Pal (J. Pahl, 1903). On observations N. A. Ratner et al. (1974) crises would be noted at 20 — 34% of sick G. Crises can arise in all stages of G., and sometimes serve as its only manifestation. N. A. Ratner and G. L. Spivak suggest to distinguish hypertensive crises of two types. The crises of the first type (connected with emission in blood of adrenaline) are more characteristic of early stages of a disease. Clinically they are shown by a shiver, heartbeat, a headache. Their duration is measured for hours, and sometimes and minutes. Increase in the ABP is usually small. After crisis the polyuria is quite often noted. The crises of the second type (caused by emission of noradrenaline) would meet preferential in late stages of G. Foreign authors call them hypertensive encephalopathy. Crises of the second type are shown by a severe headache, nausea, vomiting, vision disorders («the flying front sights», hulls before eyes, sometimes a short blindness). During crisis disturbance of cerebral circulation of dynamic character (with passing focal symptomatology) or a stroke can develop; stenocardia, a myocardial infarction, cardiac asthma and a fluid lungs is quite often noted. Crises proceed from several hours to several days. At coronary heart disease sudden and substantial increase of the ABP can precede a sharpening of coronary insufficiency or be combined with it even if these patients would not suffer from G. Therefore G.'s diagnosis. in similar Cases it is illegal.
In late stages of G. can become complicated renal failure (see), heart failure (see. Cardiovascular insufficiency ), cerebrovascular insufficiency. Promotes development of the complications connected with atherosclerosis such as coronary heart disease (see), ischemic and hemorrhagic strokes (see), subarachnoidal hemorrhages, the stratifying aortic aneurysm (see. stratifying ). G.'s complication. There can be also vision disorders connected with development angio-and retinopathies (see).
Clinically to allocate the mental disorders arising at G., it is extremely difficult since the prevailing majority of the observed mental changes has no specific character; on manifestations they are similar to the mental changes which are noted at other vascular diseases of a brain, In particular at atherosclerosis (see). Many psychiatrists refuse from a wedge, differentiations of atherosclerotic and hypertensive psychoses and prefer to speak generally about vascular psychoses or mental disorders at vascular damages of a brain, without differentiating them in nozol, or morfol, the relations.
About the frequency of mental disorders at G. in literature there is no consensus: one authors deny existence of independent hypertensive psychoses, others — say about their wide spread occurance. For systematization of mental disorders at G. various criteria were offered: their group was carried out on a stage of a disease, on psychopathological and (or) pathogenetic signs.
In early stages of G. are possible various nonspecific nevrozo-and psychopatholike frustration, significantly not different from similar mental disorders in initial stages of cerebral atherosclerosis. They are shown, e.g., by a pseudo-neurotic syndrome with complaints to fatigue, decrease in working capacity, easing of memory; the phenomena of irritable weakness, affective lability, dominance of alarming mood and hypochiondrial fears are noted. Also development of suspiciousness, hypochiondrial fixing on unpleasant somatic feelings is observed. Due to crises or with attacks of stenocardia hypochiondrial fears quite often accept supervaluable or phobic character. In initial stages of G. personal features earlier inherent to the patient which at some patients reach extent of psychopatholike changes amplify and pointed. At the same time there is coarsening of the personality, the thinnest individual traits and installations are gradually lost. Characteristic feature of mental changes in the initial stages of G. the expressed fluctuations of degree of their intensity — variability a wedge, manifestations are up to their total disappearance for various spans. Depending on progressing of vascular process of the loudspeaker of these nevrozo-and psychopatholike changes occurs against the background of development of more or less expressed organic psychosyndrome;; changes of the personality and different parties of intellectual activity (judgments, memory, ability to creativity, etc.).
Number of authors [E. G. Averbukh, E. Krapf, etc.] emphasized frequency acute depressive and alarming depressions in the II stage of G. Their nosological treatment is difficult. Part of them, nd-visible, it is necessary to consider as the endogenous psychoses provoked and altered by a cerebral vascular disease. Some forms of acute affective frustration can be carried to vascular psychoses. Usually it is the acute, rather short-term, quickly reaching the maximum expressiveness trevozhnodepressivny syndromes which often proceed with fears (in the form of so-called depressions of fear), it is frequent with the crazy ideas of condemnations and death, and sometimes also with stupefaction at height of psychosis. The parallelism which is found in such cases between development of passing affective frustration and dynamics of vascular process (raising of the ABP, crises, etc.), and also anamnestic data, in particular lack of phase affective frustration in the past, confirm interpretation of these forms as acute hypertensive psychoses. About same tells also strengthening of psychoorganic changes which is observed quite often after disappearance of acute mental disorders. Other acute mental disorders arising at G., proceed with syndromes of the broken consciousness (an oglushennost, twilight, delirious, oneiric and amental states). They arise preferential in connection with acute disorders cerebral circulation (see). Change of conditions of the broken consciousness is characteristic. The Oglushennost of various degree and duration passes quite often into a condition of psychomotor excitement with fears, hallucinatory and crazy frustration, and further in delirious or amental syndromes (see) from the outcome in a deep adynamy or in Korsakovsky syndrome (see). At G.'s complications. a hematencephalon stupefaction happens usually more expressed, polymorphic and long, than at purely atherosclerotic (ischemic) strokes. The phenomena of confusion and psychomotor excitement happen especially expressed at subarachnoidal hemorrhages. Arising quite often at cerebral forms G. long conditions of an oglushennost remind conditions, characteristic of tumors of a brain, of the dulled consciousness (so-called pseudo-tumorous states). At hypertensive crises also twilight states occasionally meet passing motive avtomatizm.
The acute mental disorders developing in connection with disturbances of cerebral circulation can be followed by the focal, aphotic, apraktichesky, agnostic and other symptoms which are depending on localization of vascular defeat.
In the III stage of G. various syndromes of dementia — permanent depletion and impoverishment of all parties of mental activity develop gradually or sharply (postapoplectically). Observed in these cases a wedge, forms of dementia generally correspond to dismnestichesky or lacunary, anamnestic, pseudoparalytic and pseudo-senile types of dementia, i.e. those which meet also at atherosclerosis of brain vessels. However it is undoubted more often than at atherosclerosis of brain vessels, at G. the so-called pseudoparalytic option of weak-mindedness with the expressed euphoria, carelessness and complacency, falloff of criticism, rough change of the personality and disinhibition of inclinations, but at the same time with rather less expressed dysmnesias is observed. Rather often, especially after disturbances of cerebral circulation, the anamnestic (korsakovopodobny) type of dementia or syndromes of dementia proceeding with various focal symptoms develop.
The differential diagnosis is difficult, especially at elderly patients when G. quite often complicate other mental diseases. Such combination is observed especially often at patients maniac-depressive psychosis (see). As in such cases of G. alters a wedge, a picture of affective psychosis, giving it «organic lines», the correct diagnosis is possible often only on the basis of the anamnestic data including data on a constitutional and genetic background, on Krom the disease developed. Also cases when G. are often observed. precedes, and it is possible, and provokes late demonstrating endogenous psychosis. Since the wedge, a picture and in such cases happens considerably modified, the decision differentsialno - diagnostic difficulties quite often perhaps only on the basis of overseeing by the further current. Pseudo-tumorous states are differentiated with tumoral processes generally on nevrol, and Ophthalmolum. to data taking into account results of other researches. The differential diagnosis between a pseudoparalytic form of vascular dementia and general paralysis (see) the hl is based. obr. on absence characteristic of neurosyphilis nevrol, and serol, data.
The forecast of mental changes at G. it is closely connected with the forecast of the basic vascular disease. In general, mental disorders develop most often at more progressing and in the predictive relation less favorable forms of an idiopathic hypertensia.
Diagnosis and differential diagnosis
Various approach to G.'s treatment. and symptomatic arterial hypertension demands the most exact differential diagnosis of these states. To reveal or exclude all possible reasons of symptomatic arterial hypertension only on a wedge, to symptoms and data of primary inspection it is not always possible. Difficult diagnostic methods of many symptomatic hypertensia (see. arterial hypertension ) cannot be used in each case of the raised ABP; therefore, though G. treats the most widespread diseases, in certain cases the diagnosis remains doubtful. Proceeding from practical reasons, in many cases the preliminary diagnosis of G. put in the absence of accurate symptoms of any disease, a cut could serve as the reason of symptomatic arterial hypertension at this patient. There is a number of signs which existence demands careful inspection of the patient for identification or an exception of symptomatic arterial hypertension: 1) the age of the patient is younger 20 and 60 years are more senior if arterial hypertension developed in this period of life; 2) sharply arisen and permanent increase in the ABP; 3) very high ABP; 4) malignant course of arterial hypertension; 5) existence of crises with clinic of sympathoadrenal excitement; 6) instructions on any disease of kidneys in the anamnesis, and also on developing of arterial hypertension during pregnancy; 7) existence during detection of arterial hypertension even of the minimum changes in an urocheras and insignificant proteinuria.
If data of a special research of patients with the listed signs do not reveal the disease which is the cornerstone secondary, symptomatic, hypertensia, G.'s diagnosis. it is possible to consider reliable.
Chances of a combination of G. with other diseases when (with rare exception) it is impossible to solve with confidence whether the available damage of kidneys, closed glands, etc. is a background for G.'s development. or reason of symptomatic arterial hypertension. Only when the ABP is with firmness normalized after elimination of the presumable reason of arterial hypertension (e.g., removal of the kidney affected with pyelonephritis), it is possible to come to a firm conclusion about the symptomatic nature of increase in the ABP.
In an end-stage of G. in the presence of wrinkling of kidneys the differential diagnosis with nephrogenic symptomatic arterial hypertension is especially difficult, is sometimes almost impossible.
Sick G. need acute medical aid during the developing of hypertensive crises, at an acute left ventricular failure, at displays of coronary heart disease, disturbances of cerebral circulation.
In need of emergency hypotensive treatment apply Dibazolum (8 — 10 ml of 0,5% of solution intravenously), rausedyl (1 mg intramusculary or slowly intravenously in isotonic solution of sodium chloride), hypothiazid of 50 mg inside or lasixum of 40 mg intravenously. At insufficient effect apply ganglioblokator (petrolhexonium to 20 mg intramusculary, Pentaminum to 40 mg intramusculary or kapelno intravenously), watching that decrease in the ABP was not very sharp — it can lead to development of coronary or cerebrovascular insufficiency. Many patients are helped by neuroleptics — aminazine (20 — 25 mg intramusculary), Droperidolum (to 4 ml of 0,25% of solution intramusculary or intravenously slowly). It is very effective katapresan (Haemitonum) which at crises appoint in a dose 0,15 mg intramusculary or slowly intravenously to 20 ml of isotonic solution of sodium chloride. At long crises it is reasonable to appoint alpha Methyldopa (dopegit) inside 0,25 g (to 2 g a day). The adrenolytic drugs blocking alpha receptors (Tropaphenum of 1 ml of 1% of solution in 20 ml of isotonic solution of sodium chloride intravenously slowly or 1 — 2 ml of 1 — 2% of solution intramusculary), are more efficient at sympathoadrenal crises. At symptoms of the encephalopathy connected with wet brain magnesium sulfate (sulfate magnesia) — 10 ml of 25% of solution intramusculary, diuretics, first of all osmotic diuretics is appointed (20% solution of Mannitolum in isotonic solution of sodium chloride in a dose of 1 g of nonvolatile solid to 1 kg of weight intravenously or 30% solution of urea in 10% solution of glucose in the same dose intravenously). Seldom for cerebral decompression resort to a spinal puncture. Bloodletting is ineffective. Mustard plasters on the course of a backbone, hot foot baths can give subjective relief.
The causal treatment directed to fight against the neurosis which is the cornerstone of G., it is the most effective at early (IA — IIA) stages of a disease. Events of the general character are held (normalization of a work-rest schedule, exercises under control of the doctor). If it is not enough, appoint the differentiated therapy neurosises (see) with use of sedatives (bromides, drugs of a valerian, motherwort, etc.), tranquilizers (Tazepamum, Seduxenum, Elenium, eunoktin, etc.), is more rare — neuroleptics and antidepressants to destination than the psychoneurologist. The complex of treatment joins also verbal impact on the patient who would have to know about G.'s essence. and success achieved in in fight against it. Most of patients if only they do not differ in excessive suspiciousness, should report true values of his ABP. When one doctor «diminishes» figures of pressure, and another tells the same sick their true size, it can lead to emergence at the patient of negative emotions, disbelief in success of treatment.
Inefficiency of the described treatment usually demands use actually antihypertensives (see), G. operating on various links of a pathogeny. The drugs which are slowing down carrying out nervous impulses at the level of vegetative gangliyev — ganglioblokator have the strongest effect (petrolhexonium, Pentaminum, Pyrilenum, Dimecolinum, etc.). Due to their expressed side effects, and also quickly developing tolerance to them these drugs for G.'s treatment. hl are applied seldom. obr. in cases of its malignant current at inefficiency of other means, and also at hypertensive crises.
At treatment it is necessary to measure by ganglioblokator the ABP in position of the patient lying and standing in connection with a possibility of development of an orthostatic collapse — sharp pressure drop upon transition from horizontal position in vertical (see. Collapse ). The expressed hypotensive action is peculiar a nek-eye to sympatholytic drugs, in particular Octadinum (Isobarinum). Octadinum can also cause an orthostatic collapse in this connection treatment is begun with small doses (10 mg a day), gradually increasing them to 50 — 100 mg a day. Ornidum (bretylium) is close to Octadinum on force of action and features of use. Methyldopa possesses a little smaller therapeutic action, but the best portability (dopegit); effective daily doses of this drug are extremely individual and therefore they treatment begin 0,25 g with a daily dose, if necessary gradually bringing it to 2 g (in 3 — 4 receptions). Broad use in G.'s treatment. received the drugs containing Reserpinum (Raunatinum, Rauwasanum, etc.). and also Reserpinum, the central antipsychotic action to-rogo successfully supplements actually hypotensive effect. Side effects of Reserpinum in the doses applied in practice of the therapist (as a rule, no more than 2 mg a day), are observed seldom. Possesses the expressed hypotensive action katapresan (Haemitonum), being the activator of alpha adrenoceptors in c. N of page which excitement reduces activity of the central sympathetic neurons that slows down release of noradrenaline in synapses of a brain. Blockers of beta and adrenergic receptors — anaprilin (Obsidanum, inderal) — cause bradycardia and reduce the minute volume of heart what connect generally their hypotensive action with. In connection with significant differences in individual sensitivity for achievement of therapeutic effect sometimes it is necessary to increase a dose to 250 mg of an anaprilin a day and even more though the average daily dose of drug makes 60 — 120 mg.
All above-mentioned means if necessary combine with the means reducing a myogenetic (basal) tone of vessels. Quite often apply to such combination gidrazinoftalazin (apressine). It increases cordial emission, improves blood supply of vitals. However to apressine tolerance quickly develops, and complications (psychoses, a hyperthermia, a syndrome of a system lupus erythematosus) caused by it limit its use in effective doses. Dibazolum which was widely used in the recent past would practically not have hypotensive effect during the mezhpristupny period of G., as well as the papaverine appointed sometimes for this purpose. The myogenetic tone is indirectly influenced also by the diuretics strengthening removal from an organism of ions of sodium. Most often appoint a dichlothiazide (hypothiazid) in a dose of 25 — 50 mg 2 times a day. Diuretic action of a dichlothiazide on patients who have no delay of water in an organism is practically not shown. Furosemide (lasixum) has no essential advantages before hypothiazid concerning hypotensive action. Use of the diuretic means strengthening removal from an organism of ions of sodium leads also to loss of potassium, edges shall be compensated by the corresponding diet or purpose of drugs of potassium. Hypotensive action of the antagonist of Aldosteronum of Spironolactonum (veroshpiron, Aldactonum) is shown by hl. obr. at appointment as its sick G., proceeding with the phenomena hyper aldosteronism (see).
Use of all antihypertensives at G. shall be long — months-long, and if necessary and long-term. Long decrease in the ABP to desirable level, hypersensitivity or, on the contrary, tolerance to drug and emergence of side effects can be the cause of cancellation of this or that drug; in the last cases it is necessary to select other drug.
At a combination of antihypertensives it must be kept in mind that combinations of antihypertensives are most rational, each of which would affect different levels of a pathogeny of G., napr, Reserpinum and hypothiazid, Reserpinum and Octadinum, anaprilin and apressine, etc. Use of similar combinations allows to reduce doses of each of the drugs which are their part and, thus, to weaken their side effects, without having lost hypotensive effect.
Individual selection of antihypertensives and their combinations should be carried out taking into account the leading pathogenetic mechanisms of arterial hypertension at each patient that is not always possible because of complexity of techniques of necessary inspections (definition of activity of a renin, indicators of the central hemodynamics, excretion of Aldosteronum, etc.). During formation of a disease (the I—II And stages) in most cases observe the hyperkinetic type of blood circulation which is clinically shown tachycardia and preferential systolic hypertensia. In these cases it is reasonable to appoint the blockers of beta and adrenergic receptors promoting reduction of frequency and force of cordial reductions. In later stages drugs of Rauwolfia and combination of various antihypertensives are effective. In general a question of whether it is necessary to aim to reduce pressure at all sick G. to datum level, it is disputable. At 20% of sick G. with moderate arterial hypertension the lowering of arterial pressure is followed by deterioration in health.
Especially carefully patients should use hypotensive drugs about a wedge, manifestations of the accompanying G. atherosclerosis (coronary heart disease, cerebrovascular insufficiency), and also arteriolosclerosis of kidneys. At patients with displays of atherosclerosis falloff of pressure can lead to development of focal changes in a myocardium or an ischemic stroke; reduction of blood supply of kidneys at their arteriolosclerosis promotes development of a renal failure. At initially malignant current of G. early and active hypotensive therapy certainly is shown. Except performing hypotensive therapy, if necessary symptomatic means are appointed the patient: vasoactive drugs of regional action, cardiac glycosides, koronaroaktivny, antiarrhythmic and other means.
Sharp restriction of content of sodium salts in a food allowance (to 1 g of sodium chloride a day) approximately in 1/3 cases leads to normalization of arterial pressure at patients with arterial hypertension. However patients hard transfer such diet; in certain cases it leads to development hyponatremias (see). Moderate restriction in a diet of sodium chloride can be recommended to all patients.
Efficiency of treatment of G. at corpulent patients increases treatment for obesity.
Surgical treatment of sick G. — bilateral thoracolumbar sympathectomy (see) — it is applied very seldom in connection with instability of its results and existence of a big arsenal of powerful antihypertensives.
Sick G. usually badly adapt to changes of climatic conditions in this connection it is the most reasonable to treat them in local sanatoria. Treatment of patients in early (IA — IIA) stages of a disease in the resorts of the Crimea and the Caucasus (except for mountain) in not hot season is possible. Are not subject a dignity. - hens. to treatment sick G. with a malignant current, and also sick G. The III stages, with frequent crises or the expressed displays of a coronary, cerebrovascular and renal failure.
Physiotherapeutic, actions come down to fight against the neurosis which is the cornerstone of a disease.
The physiotherapy exercises are applied to prevention, treatment and at sick G.' rehabilitation. Justification to use of LFK at G. the counterbalancing influence is physical. exercises on processes of excitement and braking in a cerebral cortex, improvement of functions of neurohumoral regulatory mechanisms and approval of activity of the main systems of an organism. Especially expressed beneficial effect is exerted by physical. exercises on a condition of a hemodynamics: improve processes of exchange in a cardiac muscle, normalize reactivity of vascular system of patients along with improvement of functions of external respiration, digestion and a metabolism, in particular lipidic exchange; they normalize also processes of hemocoagulation and promote reduction of subjective displays of a disease.
LFK is shown all by sick G.: for patients with a disease of I and II stages it is Method of functional, pathogenetic therapy and prevention; for patients with G. The III stages, complications having a row, physical. exercises are appointed as a type of symptomatic therapy.
LFK in the following forms is applied: the morning exercises (charging) / to lay down. gymnastics, the dosed walking, terrainkur (ascension on the hilly terrain), swimming, tourism, rowing, outdoor games (volleyball, badminton, towns), ski walks. The beneficial effect on patients is exerted by moderate work in the fresh air — in a garden, a kitchen garden. The LFK main form is to lay down. the gymnastics, edges is carried out daily from 20 to 3.0 min. The all-developing exercises alternating with respiratory — static and dynamic character are recommended/. Exercises are carried out at quiet speed, without efforts and a pressure of zheniye. Special exercises for - sick G. 6. are: exercises on relaxation of various/muscular groups, respiratory, on a training of a vestibular mechanism; and on coordination (fig. Z). Y With success is used swimming in the pool. The patient in the III stage of a disease at development of complications is generally applied to lay down. gymnastics (in prone positions, sitting), the dosed walking. In the presence at sick headaches, dizzinesses use of massage occipital * areas of the head and a shoulder girdle according to
V. N. Moshkov lasting 10 — 15 min. every other day is reasonable.
Patients shall be engaged in LFK regularly and a long time after consultations with the doctor; it supplements complex therapy of patients and is well combined with a dietotherapy, various balneoprotsedura and physical therapy.
there are messages on a possibility of long remission and even involution of G. at timely begun (in the I—II stages of a disease) and regularly carried out treatment. Sometimes at this ABP it is normalized for years and changes of an eyeground regress patol. Nek-ry authors [Page (J. N, Page), 1966; E. M. Volynsky, 1967; T. Ya. Sidelnikova, 1971] separate cases of recovery of sick G. are described., the Crimea at early stages rational therapy was appointed. However most often G. has slowly progressing current. The correct use of hypotensive drugs would promote increase in life expectancy of sick G., to considerable reduction of frequency of complications, delay of progressing of a disease. Moyer and Brest (J. The N of Moyer,> A. N Brest, 1966) would compare life expectancy of sick G., regularly receiving antihypertensives, and similar group of the patients who were not receiving treatment. In 5 years of observation 72% of treated and only 24% of uncured patients survived.
Sick G.' death. can be caused by the changes caused by the most arterial hypertension (a renal failure, heart failure), but more often complications of the accompanying G. are a cause of death. atherosclerosis (myocardial infarction, disturbances of cerebral circulation). As a result of broad use of active antihypertensives structure of lethal outcomes at G. considerably changed. More slowly the hypertrophy and an overstrain of a myocardium, change in arterioles of kidneys progress, the frequency of development of a renal failure sharply decreased; the number of hemorrhagic strokes decreased though the number of ischemic strokes relatively increased [T. Ya. Sidelnikova, 1971; It is thin (V. Hood) and soavt, 1966; Smerk (F. N of Smirk), 1972] that, perhaps, d by reduction of perfused pressure at patients is connected with atherosclerosis of vessels of a brain. In structural change of a lethality at G., apparently, also increase in life expectancy of patients, the majority of whom lives up to that age, plays a role, in Krom complications - the accompanying G. are most often shown. atherosclerosis.
The forecast at G. worsens nearby, factors:
1) permanent increase in the ABP at young men;
2) the constant of diastolic pressure is higher than 110 mm of mercury.;
3) significant increase in heart;
4) existence on an ECG of signs of the expressed overload of a left ventricle of heart;
5) heart failure;
6) existence of functional insufficiency of kidneys;
7) existence of signs of disturbance of cerebral or coronary circulation;
8) a heavy retinopathy (at an azotemic retinitis of the III degree of 80% of patients perishes within 5 years since the beginning of its identification even if function of kidneys at them during this period is kept). The forecast at moderated changes of an eyeground is defined by hl. obr. extent of damage of heart (hypertrophy and especially overload). Some wedge, signs define the next forecast. So, the expressed renal failure and hypostasis of nipples of optic nerves point to a possibility of a lethal outcome in the next weeks or months.
Sick G.' working capacity. depends on a number of subjective and objective factors. Between changes of the ABP and health of patients there is no obligatory parallelism: many patients feel well and work even at very high figures of the ABP. Patients are completely disabled during hypertensive crises and within several days after their termination though during the mezhkrizovy period the vast majority of these patients are able to cope with the professional duties successfully. Permanent decrease or full disability at i sick with. comes at emergence of complications of the most arterial hypertension (renal or heart failure, a heavy retinopathy) or the accompanying atherosclerosis (a myocardial infarction, disturbances of cerebral circulation etc.).
Proceeding from the concept, according to a cut G.'s reason. disturbances of century of N of serve, assume that primary prevention of G. the prevention of neurosises is. The prevention of progressing of a disease and development of its complications is promoted by normalization of a work-rest schedule, a rational diet and individually picked up therapy.
A big role in the prevention of progressing of G. play the night sanatoria (dispensaries) created in the USSR at many industrial enterprises where employees of these enterprises receive medical treatment on the job (see. Sanatorium dispensary ).
Bibliography: Averbukh E. S. Mentality and idiopathic hypertensia, L., 1965; Lang G. F. Idiopathic hypertensia, L., 1950; Moshkovv. H. Physiotherapy exercises at an idiopathic hypertensia, M., 1950, bibliogr.; Myasnikova. L. Idiopathic hypertensia, M., 1954, bibliogr.; it, Hypertension and atherosclerosis, M., 1965, bibliogr.; P e-ro in Yu. L. Structurally functional aspects of the concentrating activity of a kidney, Arkh. patol., t. 35, JsTs 7, page 75, 1973, bibliogr.; P about with t of N about in Yu. V., P ER about in Yu. L. and r and at N about in Yu. P. Skleroz of a medulla of a kidney at an idiopathic hypertensia, in the same place, t. 36, No. 7, page 48, 1974; Ratner N. A. Arterial hypertension, M., 1974, bibliogr.; To a container e in E. M. Idiopathic hypertensia, M., 1948, bibliogr.; At sh to and l about in A. F. and Vikhert A. M., Morphology of the juxtaglomerular device of kidneys, Arkh. patol., t. 34, No. 9, page 3, 1972, bibliogr.; Sh x in and c and and I am I. K. Some voprosvd pathogeny of an idiopathic hypertensia, Cardiology, t. 12, Jsft 8, page 5, 1972; Sh x in and c and and I am I. K., Nekrasova A. A. iserebrovsky Yu. A. Gumoralnaya пре^сорно-депрессор-ная function of kidneys in a pathogeny of experimental renal hypertensions, in the same place, t. 11, No. 11, page 25» 1971; Erina of E, B, Treatment of an idiopathic hypertensia, M., 1973, bibliogr.; L a r a g h J. H. Vasocon-striction-volume analysis for understanding and treating hypertension, Amer. J. Med., v. 55, p. 261, 1973; O w e n S. G. S t r e t-ton T.B. a. Y an of 1 1 a n with e-O w e n J. Essentials of cardiology, L., 1968; P a g e L. B. a. S i d d J. J. Medical management of primary hypertension, Boston, 1973; Pickering G. Hypertension, Edinburgh — L., 1974, bibliogr.; SmirkP. H. High arterial pressure, Oxford, 1957; Die zerebralen Durchblutungsstorungen der Erwachsenen alters, hrsg. v. J. Quandt, S. 723» B., 1969.
I. K. Shkhvatsabaya, V. A. Bogoslovsky; A. I. Strukov (stalemate. An.), I. I. Hitrik (to lay down. physical.), E. Ya. Shternberg (psikhiat.).