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II. ХИРУРГИЯ
SURGICAL FACTORS OF DEVELOPMENT OF w 616-132"007-64 SYMPTOMATIC ARTERIAL HYPERTENSION
(REVIEW ARTICLE)
Khanchi M.Kh.1, Abzaliev K.B.2, DemeuovT.N.1, Khakimov M.K.3
1Science center surgery A.N. Syzganov 2Kazakh Medical University of Continuing Education 3Semey state medical university
Abstract
A huge amount of material and compelling statistics have been accumulated, Indicating that the lethality of patients and the development of such severe, often fatal complications as cerebral vascular lesions, myocardial infarction, circulatory insufficiency, aortic aneurysm of any site, rates of atherosclerosis development and others, mainly depend on the level of arterial pressure in the surveyed contingents. First, - the task, how can early verification of the diagnosis. It is the increase in blood pressure or the subjective sensations and objective changes associated with its presence that make the patient go to the doctor and are found most often in dispensary examinations or when they are diagnosed with concomitant diseases. Secondly, regardless of the nature of the disease, the hypertensive syndrome itself becomes the most important factor determining the further fate of the patient.
Симптоматикалык артериалык гипертензиясы дамуыньщ хирургиялык факторлары (шолу макала)
Ханчи М.Х.1, Абзалиев К.Б.2, Демеуов Т.Н.1, Хакимов М.К.3
1А.Н. Сызанов атында™ Улттык, ™лыми хирургия орталь^ы, 2Уздшз бЫм беруд1 Казак медицина университет! 3Семей каласыньщ мемлекеттк медицина университет!
Ацдатпа
Бас миыньщ кантамыр закымданулары, миокард инфарктыньщ, канайналымыныц жетк/л/кс/зд/г/, кез-келген жерде орналаскан аорта аневризмасы, атеросклероздыц даму кезецдер/ жэне де езгелер/ сиякты жи/ ауыр аскынулардан аурулар¥а катысты ел/м-ж/т/м о^аларын дэлелдейт/н сен/мд/ статистикалык деректер/ жэне айтарлыктай жинакгал€ан тэж/рибе, ец бастысы, тексер/лет/н контингенттерд/ц артериалдык кан кысымыныц децгей/не байланысты. Б/р/нш/ден, ал¥а кой€ан максаты: диагнозды барынша ерте аныктау. Эс/ресе, артериалды кан кысымыныц (АК) кетер/лу/ немесе оныц болуына субъективт/ сез/нулер мен объективт/ езгер/стер/н/ц салда-рынан ауру дэр/герге жуг/нуге мэжбур болады, сонымен ертерек диспансерл/к тексерулер кез/нде немесе /леспе ауруларына катысты аныкталады. Ек/нш/ден, аурудыц салдарына катысы жок, гипертензиялык синдром аурудыц алдаш тащырын айкындайтын мацызды факторлар болып табылады.
ABOUT THE AUTHORS
Khanchi M.Kh. - surgeon of the department of angiosurgery, can.med., a high level certificate physician. e-mail: khanchi.mead@yahoo.com
Abzaliev K.B. - head of the Department of Cardiovascular Surgery of the Kazakh Medical University of Continuing Education, doctor of Medical Sciences, professor
Demeuov T.N. - director of vascular surgery department, doctor of higher category.
Keywords
aortic aneurysm, mortality, atherosclerosis
АВТОРЛАР ТУРАЛЫ
Ханчи M.X. - А.Н.Сызранов aTbiHfiafbi Улттык рыылыыми хирургия оpтaлыыFыы кан-тамыр хирургиясы бвл1мшесшщ дар!гер1, M.F.K. e-mail: khanchi.mead@yahoo.com
Абзалиев К.Б. - Уздшз бШм беру Казак медицина университетi, Журек- кантамыр хирургиясы кафедрасымыщ менгеpушiсi, профессор, м.ьд.
Демеуов Т.Н. - А.Н. Сыжанов aтыlндaFЫl Улттык Fыlлыlми хирургия орталым! кантамыр хирургиясы бeлiмшесiнiн менгеpушiсi, мя.к.
Туйш сездер
аорта аневризмасы, eлiм-жiтiм о/иасы, атеросклероз.
Хирургические факторы развития симптоматической артериальной гипертензии (обзорная статья)
Ханчи М.1, Абзалиев К.Б.2, Демеуов Т.Н.1, Хакимов М.К.3
Национальный научный центр хирургии им. А.Н. Сызганова, 2Казахский Медицинский университет непрерывного образования Государственный Медицинский университет города Семей
Аннотация
Накоплен огромный материал и убедительные статистические данные, свидетельствующие, что летальность больных и развитие таких тяжелых, нередко смертельных осложнений, как сосудистые поражения головного мозга, инфаркт миокарда, недостаточность кровообращения, аневризмы аорты любой локализации, темпы развития атеросклероза и другие, зависят главным образом именно от уровня артериального давления у обследуемых контингентов. Во-первых, - задачей, как можно ранней верификации диагноза. Именно повышение АД или связанные с его наличием субъективные ощущения и объективные изменения заставляют обратиться больного к врачу и ранее всего обнаруживаются при диспансерных осмотрах или выявляются при обследовании по поводу сопутствующих заболеваний. Во-вторых, независимо от природы заболевания сам гипертензионный синдром становится важнейшим фактором, определяющим дальнейшую судьбу больного.
ОБ АВТОРАХ
Ханчи M.X.- врач - хирург отделения ангиохирургии АО ННЦХ им. А.Н. Сызганова, к.м.н., врач высшей категорий. e-mail: khanchi.mead@yahoo.com
Абзалиев К.Б. - заведующий кафедрой сердечнососудистой хирургии Казахского Медицинского Университета непрерывного образования, профессор, д.м.н.
Демеуов Т.Н. - Заведующий отделением сосудистой хирургии Национального научного центра хирургии им. А.Н. Сызганова, к.м.н.
Ключевые слова
аневризма аорты, летальность, атеросклероз
As early as the beginning of the 20th century, clinicians knew that most patients with arterial hypertension even in later stages of the development of the disease, changes in the kidneys are modest and do not act as the root cause of the disease. This disease, characterized by an increase in blood pressure, was named by Frank in 1911 as "essential hypertension" (EG). In the twenties of the 19th century, G.F. Lang opened a new page in the study of AG, suggesting and substantiating the neurogenic theory of the development of hypertensive syndrome. At the same time, the term "hypertonic disease" is proposed. Later in 1948. G.F. Lang established the central-nervous theory of etiology and pathogenesis of hypertensive disease, which later was developed and detailed by AL Myasnikov.
At the stage of the specialized survey, the principle "from simple to complex" is preserved, i.e. Consistent application of increasingly accurate and direct diagnostic methods. This stage of the purposeful diagnosis of surgical forms of symptomatic hypertension should be conducted in specialized departments (angiologic, cardiological, urologi-cal, endocrinological, etc.). It is quite obvious that this division of complex diagnostics is conditional, since in some cases diagnostic methods can be performed at other stages of diagnosis.
In this presentation, we briefly touch on the obvious signs of only those diseases in which an increase in blood pressure, if not the only, but leading symptom, and when the disease is similar to essential hypertension, and the differential diagnosis is difficult.
Undoubtedly, the result of further progress in medicine will be a gradual decrease in the number of patients suffering from essential hypertension and, correspondingly, an increase in the number of symptomatic forms of hypertensive syndrome. The frequency and variety of surgical forms of symptomatic hypertension caused the researchers' ubiquitous interest in this problem, especially in the 70s of the last century. Many aspects of it have received wide coverage in the works of domestic and Western authors [1,2,3,4,5,6.]
The key point and the necessary condition for solving any clinical problem has always been the improvement of diagnostics. A large number of works devoted specifically to the diagnosis of symptomatic hypertension have been published. Among them we mention dissertational works. [7,8,9,10,11].
In the recommendations of World Health Organization (WHO )1999, arterial hypertension (AH) is the level of systolic blood pressure (BP), equal to 140 mm Hg. Or more, and (or) the level of diastolic blood pressure, equal to 90 mm Hg. Or more, in people who do not receive antihypertensive drugs. Given the significant spontaneous fluctuations
in blood pressure, the diagnosis of hypertension should be based on the results of repeated measurement of blood pressure during several visits to the doctor.
Depending on the degree of organ changes AH is divided into the following stages:
I stage. There are no objective signs of organ changes.
II stage. There is at least one of the following signs of organ damage:
- hypertrophy of the left ventricle (X-ray, ECG, echocardiography;
- widespread and localized narrowing of the arteries;
- proteinuria and / or a slight increase in plasma creatinine concentration (1.2-2.0 mg / 100 ml);
Ultrasonic or radiological confirmation of the presence of atherosclerotic plaques (carotid arteries, aorta, iliac and femoral arteries).
III stage. Heart - angina pectoris, myocardial infarction, heart failure;
The brain - transient disorders of cerebral circulation, hypertensive encephalopathy, stroke;
The ocular fundus - hemorrhages of the retina and exudates with edema of the optic nerve disk or without it;
Kidneys - plasma creatinine concentration above 2.0 mg / 100 ml;
Vessels - stratification of the aortic aneurysm, occlusive arterial lesion.
Modern medical science uses terms, or lexical elements, most of which are borrowed from a special vocabulary of two classical ancient languages -Greek and Latin. However, in the past two centuries, there has been a fairly active introduction of terms derived from modern Anglo-American, European and Oriental languages into professional medical vocabulary. Terms are the language of science, a necessary condition for communication and understanding between scientists of different countries and peoples. Now, before our eyes, active integration of new ideas, discoveries and achievements of scientific and technological progress in the medical science of different countries in the interests of all mankind, a single professional terminology acquires special significance. Therefore, medical terms should not be locked in the same language, but should be of an international character, not only in sound, but equally treated and bear a single semantic load.
It is also necessary to determine the competing names of "hypertension" and "hypertension". Already in the mid-seventies of the nineteenth century, it was recognized necessary to streamline the scope of the two widely used. These are medical terms that are close in meaning: "hypertension"
(from ancient Greek "tonos" - tension, tension) and "hypertensio" (from latency tensio - tension, pressure). The first of these was recommended only for the designation of an increased tonus of smooth muscles, including arterial walls; The second - for the denotation of short-term and long-term increases in the pressure of liquids in vessels and closed cavities, including for increased arterial blood pressure. Consequently, both in primary and secondary blood pressure increase, it is necessary to use the term "arterial hypertension" rather than "arterial hypertension" and, accordingly, "hypertensive crisis", and not "hypertensive crisis".
Indirect signs of an increase in blood pressure in humans and traces of the destructive activity of high blood pressure remained in the evidence of apoplexy attacks that have been observed throughout the history of mankind, about the intense pulse of Hippocrates and Avicenus (Ibn Sina, XI century) who noticed that people consuming a lot Salt, the pulse became hard; The facts of hypertrophy of the "heartless" heart, aneurysms and aortic ruptures, observed by anatomists since the beginning of autopsy. R.Bright (R.Bright, 1789-1858), after studying the pathologoanatomical picture of 100 dead patients who had been diagnosed with albuminuria during their lifetime, noted (1836) that these individuals often develop hypertrophy of the left ventricle of the heart. The earlier assumption by Bright that "the less the kidney works, the more the heart should work", in fact, established a causal relationship between the pathology of the kidneys and the increased work of the heart, ie. "Nephrogenic form of Symptomatic arterial hypertension SAG" in modern interpretation. However, Bright believed that the reason for the intensified work of the heart, which causes its hypertrophy, in jade are changes in the chemistry of the blood, because there were no ideas about hemodynamic factors yet. In this respect, a completely separate group of SAGs is represented by the so-called. Hemodynamic hypertension. The classic pathogenetic model is the most vivid representative, which is congenital coarctation of the aorta (CA). Also, the coarctation syndrome of acquired genesis, observed with stenosing nonspecific aortoarteritis of thoraco-abdominal localization, in which regional or coarctation hypertension (CG) develops. The principal interest of the CG is that the complexity of the relationship between regional and general mechanisms of blood pressure regulation is especially bright here, which excludes the possibility of compensating hemodynamically significant aortic narrowing with the help of universal mechanisms Of systemic blood pressure regulation.
Hemodynamic features of the pathology in most of these patients, regional hypertension of the up-
per trunk acts as a dominant symptom. Initially, an increase in blood pressure and cardiac output in patients with CA is one of the effective mechanisms of compensation for congenital aortic defect, which provides a quite adequate level of blood flow (mainly through the collateral network) required by the lower half of the body. However, as the incompatibility between blood circulation regimes increases higher and lower, the constrictions become more and more important, and gradually, in view of the decrease in perfusion pressure in the kidneys, the renal pressor mechanism acquires undoubted significance. Thus, with age, regional hypertension of the organs of the upper humeral girdle in CA is transformed into the same pathogenic factor as Systemic. hypertension in other diseases. Diagnosis of surgical forms Symptomatic arterial hypertension (SAG) - In the method of examination of patients with suspicion of the symptomatic nature of hypertension there is a certain stereotype, consisting in the separation of the complex of diagnostic measures into separate stages.
I."outpatient" - a detailed analysis of complaints, anamnesis, measurement of blood pressure (BP) on all 4 limbs, auscultation of the heart, all parts of the aorta, brachiocephalic arteries and lowerlimbs;
II. "Stationary" - analysis of laboratory data (general blood and urine tests, biochemical blood tests, Zimnitsky, Adissa-Kakovski, Reberg assays), ECG, ultrasound, Echo KG, radiological examination data, ophthalmological and neurological status indicators;
III. "Specialized" - radioisotope studies (re-nography and scintigraphy), functional intravenous urography, studies of catecholamines, carbohydrate metabolism, contrast aortography, kidney biopsy;
IV. "Intraoperative stage" - intraoperative revision of a specific pathology with carrying out all the necessary additional diagnostic measures.
Basic forms: Renovascular (vasorenal) hypertension is a systolodiastolic AH caused by the pathology of the renal artery and resulting as a result of kidney ischemia. The most common causes of renovascular hypertension are atherosclerosis of renal vessels, nonspecific aortoarteritis and fibro-muscular dysplasia of the renal arteries. Atherosclerosis of the renal arteries is the most common cause of renovascular hypertension. It causes 7075% of all stenoses of the renal arteries. Most often the disease develops in men older than 40 years. The most typical localization of stenosis in the area of the vessels from the aorta and / or the proximal third of the renal artery to the right, in 7-10% of cases, it can be complicated by thrombosis. At half of patients simultaneously signs of an atherosclerotic
lesion of other localization with corresponding clinical symptomatology (ischemic heart disease, obliterating endarteritis, acute disturbance of cerebral circulation, transient ischemic attack) are noted simultaneously.
With stenosing lesion of the renal artery, the blood pressure is consistently high. When it is measured, asymmetry is often seen on both hands, that is, a difference of more than 20 mm Hg. St., Which is due to atherosclerotic lesion of one of the subclavian arteries. A characteristic feature of re-novascular hypertension is the steady increase in diastolic pressure, resistant to multicomponent antihypertensive therapy.
Nonspecific aortoarteritis (Takayasu's disease) is a chronic granulomatous vasculitis with a predominant lesion of the aorta and large arteries. Characterized by fever, pain and weakness in the muscles of the legs when walking (syndrome of intermittent claudication), progressive reduction in visual acuity, weight loss, arthralgia, asymmetry or lack of pulse on the hands or feet, increasing ischemia of the affected organ. With a high activity of the pathological process, the rate of increase in blood pressure can be rapid. The main reasons for the increase in blood pressure can be ischemia of the kidneys, central nervous system, heart. When examining the blood, symptoms of immunocomplex pathology are noted (an increase in the content of immunoglobulins, immune complexes, increased sedimentation rate of erythrocytes, C-reactive protein, gamma globulins, fibrin, fibrinogen). The diagnosis is established on the basis of the clinical picture, the detection of pronounced immune shifts. Angiographic examination reveals characteristic changes: constriction of the lumen or complete occlusion of the aorta, renal artery (one or both), carotid artery, its large branches in the proximal parts of the upper and lower extremities.
Fibromuscular dysplasia of kidney vessels is an anomaly of the development of the wall of the renal artery. The etiology of the disease is unknown.
Fibromuscular dysplasia of kidney vessels is more often observed in women 20-40 years old. There are thickenings, fibrosis, aneurysms, disorders of the elastic layer, multiple muscular densi-fications ("spurs") protruding into the lumen of the artery, narrowing its lumen. Vessels reveal areas of extensions and narrowing in the form of beads. More often the process is bilateral, with lesions of the vessels outside and inside the kidneys. In 30% of patients, changes are unilateral. Fibromuscular dysplasia often combines with atherosclerosis of renal vessels.
Aneurysms of the renal arteries and arteriovenous fistulas are the most rare causes of renal vessel lesions. Of the malformations of renal vessels,
multiple arteries, hypoplasia of the renal arteries. Nephroptosis. The increase in blood pressure during nephroptosis is caused by the kink of the renal vessels and ureter. Clinical manifestations are noted in asthenic women after physical exertion. Important tools for the diagnosis of renovascular hypertension are instrumental methods of assessing the asymmetry of the size, shape and function of the kidneys, in particular ultrasound. The difference in the size of the kidneys, exceeding 1.5 cm, is a characteristic sign of a vasorenal hypertension. Duplex scanning with color Doppler mapping of the renal arteries allows us to identify stenoses of the renal arteries, especially those localized at the mouth of the vessel. For the same purpose, radioisotope studies are used. Informative methods for the diagnosis of vasorenal hypertension are magnetic resonance angiography and spiral CT. "Golden" standard.
Diagnosis of stenosis of the renal arteries is recognized as abdominal angiography. Angiography is contraindicated in cases of intolerance to radi-opaque preparations and with progressive chronic renal failure. The main treatment for vasorenal hypertension consists of medical therapy, angioplasty and stenting of the affected renal arteries. Combined antihypertensive therapy includes calcium antagonists, diuretics, and preparations that block RAAS. The appointment of angiotensin converting enzyme inhibitors or angiotensin II receptor blockers is contraindicated in stenosis of the renal arteries. In the case of atherosclerotic etiology, vasorenal hypertension is associated with ongoing therapy with statins and aspirin in small doses.
Arterial hypertension in endocrine diseases. Diseases of the adrenal glands. The adrenal gland is a paired organ that looks like a triangular plate. Their lower edge is slightly bifurcated and embraces the poles of the kidneys ("Napoleon's hat"), located along with the kidneys in the total fatty tissue. Adrenal dimensions vary greatly in man, but on average their length is 45 mm, width 25-30 mm, thickness 6-10 mm. The weight of both adrenal glands reaches 10-12 g. They consist of cortical (cortex) and cerebral part. The adrenal cortex is divided into a glomerular, fascicular and reticular zones, each of which produces strictly specific hormones. In the glomerular zone, mineral corticoids (aldosterone) are formed, in the fascicle - gluco-corticoids (cortisol, corticosterone), and the main role in the production of sex hormones (androgens, estrogens, progesterone) is attributed to the reticular zone. However, for all relative independence, individual zones retain structural unity and functional interaction, being an integral system. Brain (medullary) part of the adrenal gland produces adrenaline and norepinephrine. By their chemical nature,
these hormones are able to vigorously restore salts of heavy metals, so when treating the adrenal with a solution of potassium dichromate, the medullary part becomes brown due to the fallout of the lower chromium oxides. In connection with this, the cells of the cerebral part are called chromaffinic, or pheo-chromic. Cortical and medullary tissues can sometimes be found in the body in isolation in the form of the so-called accessory adrenals. An isolated cluster of chromaffin cells exists in the form of paraganglia, both free and within the sympathetic ganglia of the border pillars. Strengthening the function of the adrenal glands (cortex or medulla) leads to the appearance of diseases, as a rule, well clinically outlined. With the strengthening of the function of the glomerular zone, the phenomena characteristic of aldosteronism (Conn's syndrome) are increasing. With the intensification of the function of the beam zone only, phenomena that are characteristic of excessive production of glucocorticosteroids (the Itenko-Cushing syndrome) develop, and when the function of the adrenal medulla or chromaffin tissue of other localization increases, symptoms that are characteristic of hyperproduction of Catecholamines (pheochromocytoma).appear. Primary aldosteronism (Connes syndrome) is a syndrome that develops as a result of excessive aldosterone formation in the glomerular layer of the adrenal glands. The cause of this in 85% of cases is a hormonal-active tumor, originating from the glomerular zone of the adrenal cortex (aldosteroma), less often bilateral diffuse hyperplasia of the adrenal cortex (9%) or carcinoma (6%). Increased secretion of aldosterone leads to an increase in sodium reabsorption in the distal renal tubules, a decrease in its excretion and hypernatremia. Excessive release of potassium in the renal tubules, intestines, salivary and sweat glands, increase the secretion of hydrogen ions leads to the development of hypokalemia, hypochloraemia and extracellular alkalosis. The increase in blood pressure is due to an increase in the volume of plasma and circulating blood, va-sospastic reactions due to the accumulation of sodium ions in the vessel wall. Isolation of aldosterone in the urine is usually increased, but in some patients with severe symptoms, its normal excretion is noted. Hyperaldosteronuria is combined with a decreased (often up to 0) activity of plasma renin.
Primary aldosteronism (Connes syndrome) is a syndrome that develops as a result of excessive aldosterone formation in the glomerular layer of the adrenal glands. The cause of this in 85% of cases is a hormonal-active tumor, originating from the glomerular zone of the adrenal cortex (aldosteroma), less often bilateral diffuse hyperplasia of the adrenal cortex (9%) or carcinoma (6%). Increased secretion of aldosterone leads to an increase in
sodium reabsorption in the distal renal tubules, a decrease in its excretion and hypernatremia. Excessive release of potassium in the renal tubules, intestines, salivary and sweat glands, increase the secretion of hydrogen ions leads to the development of hypokalemia, hypochloraemia and extracellular alkalosis. The increase in blood pressure is due to an increase in the volume of plasma and circulating blood, vasospastic reactions due to the accumulation of sodium ions in the vessel wall.
Isolation of aldosterone in the urine is usually increased, but in some patients with severe symptoms, its normal excretion is noted. Hyperaldosteronuria is combined with a decreased (often up to 0) activity of plasma renin. Connes syndrome is a rare disease that occurs mainly in women 30-45 years old, but it happens in children and the elderly. Symptoms of primary hyperaldosteronism can be divided into three groups: neuromuscular, renal and associated with AH. Muscular weakness, convulsions, paresthesia are related to neuromuscular symptoms. Muscle weakness has the character of recurring seizures, in 39% of patients, flaccid paralysis lasts from several hours to 3-4 weeks. Pares-thesia and sharp pain in the muscles are observed. In a number of patients, convulsions occur at normal levels of calcium and phosphorus in the blood serum, but with positive symptoms of Khvostek and Tissaur. A tetany can be generalized or local. Its development is explained by extracellular alkalosis and intracellular acidosis. The defeat of the kidneys is manifested by polyuria, nicturia, hypostenuria, which is accompanied by increased thirst and polydipsia. The majority of patients with AH, resistant to drug therapy and manifested almost constant headache, dizziness, a feeling of heaviness in the heart. The ECG shows changes that are typical of hypokalemia.
In the diagnosis of Conn's syndrome, the following research data are helpful:
1) hypokalemia (however, in the early stages of the disease, the potassium content may be normal), including transient(<3.6mmol/l);
2) extracellular alkalosis (blood pH more than 7.46); Bicarbonate of plasma (27-50 meq / l, norm 21-27 meq / l);
3) hypochloremia (norm 96-108 mmol / l);
4) increased plasma aldosterone content;
5) reduced renin activity in blood plasma (<1 ng / ml / h);
6) alkaline reaction of urine, increase in the release of potassium and the amount of urine to 2-7 l/day, specific gravity less than 1016, moderate proteinuria;
7) low plasma renin content. To visualize changes in the adrenal glands and to clarify the side of tumor localization, CT and MRI are
performed. Surgical removal of aldosterol in 50-70% of patients normalizes or significantly reduces blood pressure. Prior to surgical removal by the aldosterone, as well as patients with bilateral hyperplasia, the adrenal cortex is prescribed spironolactone, with an insufficient antihypertensive effect, the addition of calcium antagonists is possible. Patients with familial form of hyperaldosteronism are shown therapy with glucocorticosteroids (dexameth-asone), which leads to normalization of blood pressure.
Disease and Itenko-Cushing syndrome. Disease Itenko-Cushing is a complex multi-symptomatic disease characterized by impaired function of the hypothalamic-pituitary-adrenal system and, above all, by the defeat of the centers of hypotha-lamic regulation. The leading part of this system is the pituitary gland, in the nuclei of which a specific corticotropin-activating factor (CRF) is formed, which contributes to the release of adrenocortico-tropic hormone (ACTH) from the pituitary gland. Excessive stimulation with this hormone causes an increase in the function of the adrenal cortex and the development of secondary hypercorticism. Disease of Itenko-Cushing is relatively rare, but among other forms of hypercorticism, it ranks first. In this disease, microadenomatosis of the pituitary gland is often noted. The Itenko-Cushing syndrome is caused by adenoma or hyperplasia of the adrenal cortex. In recent years, attention has been drawn to the development of a similar syndrome in bronchogenic cancer, thymus, thyroid, pancreas, uterus, and ovarian cancer (paraneoplastic syndrome). It is impossible to distinguish clinically from the syndrome from Isenko-Cushing's disease. The syndrome occurs mainly in women (79%) and develops at any age, but more often from 18 to 42 years. Patients complain, mainly, on progressive obesity, hirsutism, menstrual irregularity, unstable mild headache, which does not have any typical localization, pain in the lumbar region, drowsiness. Most patients experience increased fatigue and weakness. Sometimes asthenia is expressed significantly. Appearance of the patient is extremely characteristic: round, moon-shaped, purple-red, sometimes with a cyanotic face (matronism). In the clinical picture of the disease there is a characteristic redistribution of fatty tissue with its predominance in the upper part of the trunk ("buffalo type"), on the neck ("fatty hump"), on the abdomen ("frog stomach"). Limbs with Isenko-Cushing syndrome are thin. The skin of the trunk and especially of the face has a purple-red color, and is scaly. On the back, breasts appear acne, on the anterolateral surfaces of the hips, abdomen, breasts - atrophic bands stretching crimson or cyanotic-red color (striae). Subcutane-
ous hemorrhages are common. The appearance of stretch marks on the skin is the result of its atrophic changes down to the deep layers.
The reddish-violet color of the striae is caused by blood vessels directly lying under the stretched and thinned horny layer of the skin. Sometimes there is hyperpigmentation of the skin. One of the frequent symptoms of this disease in women is hypertrichosis - a profuse growth of hair on the face and trunk (mustache, beard), often requiring daily shaving. Often there is a loss of hair on the head, a low coarse voice, atrophy of the mammary glands, amenorrhea, moderate atrophy of the uterus and the vagina. Men rarely develop viril traits, but almost all patients show signs of demasculinization of varying degrees (hair loss on the face and trunk, gynecomastia, decreased libido, testicular hypoplasia). Significantly, the cardiovascular system suffers. More than 90% of patients experience sys-tolic-diastolic hypertension with secondary changes in the blood vessels, heart, kidneys, often developing myocardial infarction, angina pectoris, and impaired cerebral circulation. Many patients have mental disorders, depression, sometimes agitation, intolerance to others. In this regard, patients avoid contact with people, express suicidal thoughts. Against the background of deep disturbances in the metabolism of phosphorus and calcium, osteoporosis is observed in most patients. The process of decalcification involves, first of all, the spine (the picture of "fish vertebrae"), pelvic bones, ribs. Osteoporosis can lead to pathological compression fractures of the vertebrae, which causes a decrease in the height of the spine. Rib fractures are frequent. Violation of carbohydrate metabolism, observed in 50-90% of patients with Isenko-Cushing syndrome, manifests itself in a decrease in glucose tolerance or in the development of diabetes mel-litus (steroid diabetes). To clarify the diagnosis and determine the etiology of the disease, topical diagnostic methods are used: examination of the pituitary and adrenal glands using CT or MRI, and chest X-ray examination to detect a tumor or its possible metastases. In malignant tumors of the thoracic organs, ACTH-ectopic syndrome may occur.
The blood increased the content of ACTH and cortisol, in the urine - 17-oxycorticosteroids and 17-corticosteroids. Depending on the established etiology, there are surgical, radiotherapy and medical methods for treating hypercortisy. Pheochromo-cytoma is a tumor that originates from cells of the adrenal medulla or in the adenocarpal chromaffin tissue. Their main property is the ability to produce an excessive amount of catecholamines. Vnenado-coccal tumors are called paragangliomas. They occur in 0,04-1,3% of patients with AH. In 85-95% of cases pheochromocytomas are located in the adre-
nal glands, more often in the right. In 10% of cases, the tumors are bilateral. Paragangliomas are usually located in the sympathetic chain near the abdominal aorta. The size of the tumor is from 1 to 15 cm, rarely up to 25-40 cm. The pathogenesis of AH in pheochromocytoma is well studied.
The increase in blood pressure is caused by excessive release of adrenaline, noradrenaline or dopamine. Most often stand out the first two, rarely only adrenaline or norepinephrine. Tumors that release only adrenaline or dopamine do not lead to a significant increase in blood pressure. The clinical picture consists of the symptoms of cardiovascular damage under the influence of catecholamines. The majority noted a rise in blood pressure. There are the following forms of the course of the disease: with a crisis increase in blood pressure, with a constantly elevated blood pressure and the presence of crises against the background of a constant increase in blood pressure. In 10-15% of cases, pheochromocytoma AH has a constant, not a crisis character, which creates additional difficulties in diagnosis.
Normotenzivnye variants of the disease are associated with a dopamine-secreting tumor, which has a hereditary (family) character. If the tumor secretes mainly adrenaline, then the hypertension can be replaced by periods of arterial hypotension with syncope caused by hyperactivation of beta-adrenoceptors and subsequent vasodilation. These features of hypertensive mechanisms in pheochro-macytoma cause the instability of blood pressure, poor control of drugs, including possible paradoxical reactions - increasing blood pressure to the administration of beta-blockers. The features of crises in pheochromocytoma include: severe headache, palpitations, severe sweating, pale skin, lowering the temperature of the hands, legs, tremor, vomiting, pain in the heart, abdomen, heart rhythm disturbances, acute left ventricular failure. Patients may have visual and hearing impairment, mydriasis, lacrimation, exophthalmos. In the blood there is leukocytosis, lymphocytosis, eosinophilia, hyper-glycemia. In urine there is a glycosuria, erythrocy-turia. Increasing blood pressure more often lasts about an hour, but can be several days. Complications include: cerebral blood flow disorders, acute encephalopathy, fiber detachment, hemorrhagic necrosis of the tumor (which is accompanied by severe abdominal pain, nausea, vomiting, shock). After a sharp increase in blood pressure, there is a pronounced decrease in blood pressure. The instability of AH, orthostatic hypotension is noted in 70% of patients and is an important diagnostic sign. In 10% of patients there are uncontrolled changes in hemodynamics - demonic increases and decreases in blood pressure. With prolonged illness, myocar-
dial hypertrophy is observed, almost all patients have heart rhythm disturbances. In some patients, conduction disorders are recorded. The development of spasm of peripheral vessels can lead to parasthesias, pains in limbs, intermittent claudication, gangrene, ischemic enteritis and colitis, intestinal infarctions, intestinal obstruction, bleeding. Kidney damage is accompanied by proteinuria (90%), moderate erythrocytic activity, cylindruria (30%). There may be pain in the lower back, nocturia. The narrowing of the renal arteries is caused by compression of the tumor or fibromuscular dyspla-sia. In rare cases, paraganglioma is localized in the bladder. The clinic is characterized by crises after urination. Diagnosis is based on the detection of increased catecholamines (in the blood) and their metabolites (in the blood and urine). Usually, the rates are increased by 5-10 or more times. The adrenal gland is detected with the help of ultrasound, CT, MRI. , Detected in the adrenal gland in CT or MRI, diagnose tumors from chromaffin tissue in the adenadalocular localization, as well as metastases, since in 10% of cases there are malignant pheo-chromocytomas. The only radical treatment for this disease is surgical removal of the tumor. Before the operation for correction of blood pressure, alpha-adrenoblockers are used according to indications, and in the future, beta-blockers can be added to them. Monotherapy with beta-blockers without sufficient blockade of alpha-adrenergic receptors can lead to a sharp increase in blood pressure.
Arterial hypertension with coarctation of the aorta. Coarctation of the aorta is a congenital organic narrowing of the aorta, more often in the isthmus and arc zone. Coarctation of the aorta is more often found in childhood, but can be diagnosed later. Patients survive without surgery until 30-33 years. The reasons for increasing blood pressure for coarctation of the aorta are: a mechanical obstacle to the blood flow, a decrease in compensatory reactions due to the elasticity of the aorta, ischemia of the kidneys with a decrease in blood pressure below stenosis. Complaints depend on the severity of stenosis, AH and complications. Patients mark a headache, a feeling of heaviness in the head, weakness in the legs, rapid fatigue when walking.
On examination, there is a greater development of the musculature of the shoulder girdle and less - of the lower limbs. On the radial artery, the pulse is not changed, but on the arteries of the lower extremities, the pulsation is weakened. There may be pulsation of intercostal spaces. Systolic murmurs are heard on the basis of the heart and in the in-terscapular space on the left. The diagnosis is confirmed by angiography, MRI. Surgical treatment should be carried out by all patients. It consists in resection of the aorta site and prosthetics of the af-
fected area. In most patients after surgery, blood pressure decreases steadily.
Thus, arterial hypertension is a polyethological disease with an extremely diverse nosological structure, united by a single sign, high arterial pressure (BP). The clinical forms of diseases included in this group refer, in fact, to a wide variety of medical specialties - therapy, surgery, endocrinology, neurology, nephrology, urology, etc. Nevertheless, at present, all these various diseases should be considered together, in mutual comparison. This need is dictated by several reasons. First, - the task, how can early verification of the diagnosis. It is the increase in blood pressure or the subjective sensations and objective changes associated with its presence (headaches, heaviness in the heart, shortness of
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