dosed out preparations and technology organic pharmaceutical preparations Lenin pharmaceutical institute. Doctors pharmaceutical B.A.Brodsky's sciences (1872-1937) and M.G.Volpe (1894-1940) rather fruitfully worked in the field of perfection of technology galena preparations and chemist's technology. The big erudition professor L.F.Iljin (1871-1937) possessedThe chief of faculty of pharmacy of army medical college. To number L.F.Iljina's technological jobs it is necessary to attribute it

Dissertational job « About the pressed medicines and Tablets » - the first extensive and original research on Russian about tablets. To G.L.Kogan has made the first domestic manual on « Technologies Pharmaceutical (galena) preparations », issued in 1939году in Leningrad. The big contribution to development of technology medicinal forms as scientific discipline professor S.F.Shubin has brought (1898-1942), managing faculty in Kharkov pharmacological Institute. S.F.Shubinym has been written the tutorial on technology Medicinal forms for pharmacological institutes.

Fast becoming technology of medicinal forms as scientific disciplines appeared possible only due to numerous to researches which were actively spent in created (simultaneously with pharmacological high schools) Research establishments. The special attention is deserved with activity of the largest scientific the center - All-Union research pharmaceutical institute created in 1920. The basic structure of institute - synthesis medical products and allocation in the pure state biologically active substances from natural products. In Ukraine the basic research center in area technologies galena preparations and ready medicinal forms Was, arisen in 1920, HNIHFI (VNTSLS) VNTSLS is the main thing a scientific research institute on industrial technology Medicinal forms also spends the big job in area received galena preparations from glycoside-and alkaloid plants, creation of new type suppositories and ointment bases, and also perfection different stages of manufacture solutions, tablets, Aerosols and other medicinal forms.

Manufacture of medical products is carried out in 2 Departments - in Ministry of Health and the Ministry The medical industry. In Ministry of Health this function is carried out with drugstores and Pharmaceutical factories. In the Ministry of the medical industry it is concentrated Manufacture almost all groups of medical products. Original groups of some preparations are delivered the enterprises of other ministries - miasmal, chemical food the industry, and also the Ministry of Agriculture. Medical products of industrial production Act in a chemist's network through chemist's warehouses.

Занятие № 4.

1.Тема: «The Diseases of Cardiovascular System»

2.Значение изучения темы – смертность по причине сердечно-сосудистых заболеваний повышается в современном мире. Поэтому очень важно проследить причинно-следственные связи этих актуальных заболеваний.

3.Цели занятия: на основе теоретических знаний и практических умений обучающийся должен уметь определять и употреблять в речи структуру «сложное дополнение», извлекать из текста запрашиваемую информацию, уметь находить английские эквиваленты для словосочетаний

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4. План изучения темы:

4.1. Исходный контроль знаний.

Индивидуальный устный опрос (диалогическое высказывание). 4.2.Изучение нового материала.

1.Введение нового грамматического материала: стр. 308-309 (сложное дополнение

- complex object) I-Б стр.187, ynp.II, III стр. 187, VI стр. 188

2.Введение нового лексического материала через упражнения: упр.VII стр.188, X

стр.189.

3.Речевое - изучающее чтение Text A стр. 189 «Rheumatic Endocarditis». Найти эквиваленты. Закрепление материала через систему языковых упражнений: ynp.IV,V стр188, IX стр.189

- изучающее чтение текста Atherosclerosis (см Приложение1)

5.Основные понятия и положения темы:

Тема: «The Diseases of Cardiovascular System»

The patient usually complains of a general malaise, early fatigue on exertion, cardiac discomfort and palpitation. The puis rate is irregular and accelerated. The electrocardiogram shows the changes in the most important readings. The doctor finds a soft systolic murmur to be heard at the heart apex. It's evidence of an inflammatory process in the valves. The doctor determines the organic changes in the mitral, aortic and tricuspid valves to be clearly marked.

6.Задания для уяснения темы занятия, методики вида деятельности:

6.1. Вопросы для самоподготовки:

1.What most characteristic clinical manifestation has rheumatic endocarditis?

2.What readings does the electrocardiogram show in case of rheumatic endocarditis?

3.How can a therapeutist determine the enlargement of the heart?

4.How can systolic and diastolic heart murmurs be revealed in patient with R.E?

5.What regimen must a patient with R.E follow? Ю.Тестовые задания по теме.

6.2.Тестовые задания по теме.

1.Выберите правильный ответ.

1.What disease may the onset rheumatic endocarditis be preceded by? a) It may be preceded by tonsillitis.

b) It may be preceded by lung abscess.

2.What examination can the enlargement of the heart be determined by? a) It can be determined by percussion and X-ray examination.

b) It can be determined by electrocardiogram.

3.What must the diet of a patient with rheumatic endocarditis contain? a) It must contain much salt.

b) It must contain many vitamins.

6.3.Ситуационные задачи по теме: упр. XV стр. 191.

7. Список тем по УИРС, УИР:

«Группы риска» (сердечно-сосудистые заболевания)

Приложение1 Atherosclerosis is a syndrome affecting arterial blood vessels. It is a chronic inflammatory response in the walls of arteries, in large part due to the accumulation of

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macrophage white blood cells and promoted by low density (especially small particle) lipoproteins (plasma proteins that carry cholesterol and triglycerides) without adequate removal of fats and cholesterol from the macrophages by functional high density lipoproteins (HDL), (see apoA-1 Milano). It is commonly referred to as a hardening or furring of the arteries. It is caused by the formation of multiple plaques within the arteries.[1]

The atheromatous plaque is divided into three distinct components:

1.The atheroma ("lump of porridge", from Athera, porridge in Greek,), which is the nodular accumulation of a soft, flaky, yellowish material at the center of large plaques, composed of macrophages nearest the lumen of the artery

2.Underlying areas of cholesterol crystals

3.Calcification at the outer base of older/more advanced lesions.

The following terms are similar, yet distinct, in both spelling and meaning, and can be easily confused: arteriosclerosis, arteriolosclerosis, and atherosclerosis. Arteriosclerosis is a general term describing any hardening (and loss of elasticity) of medium or large arteries (from the Greek Arterio, meaning artery, and sclerosis, meaning hardening); arteriolosclerosis is any hardening (and loss of elasticity) of arterioles (small arteries); atherosclerosis is a hardening of an artery specifically due to an atheromatous plaque. Therefore, atherosclerosis is a form of arteriosclerosis.

Atherosclerosis, though typically asymptomatic for decades, eventually produces two main problems: First, the atheromatous plaques, though long compensated for by artery enlargement (see IMT), eventually lead to plaque ruptures and clots inside the artery lumen over the ruptures. The clots heal and usually shrink but leave behind stenosis (narrowing) of the artery (both locally and in smaller downstream branches), or worse, complete closure, and, therefore, an insufficient blood supply to the tissues and organ it feeds. Second, if the compensating artery enlargement process is excessive, then a net aneurysm results.

These complications of advanced atherosclerosis are chronic, slowly progressive and cumulative. Most commonly, soft plaque suddenly ruptures (see vulnerable plaque), causing the formation of a thrombus that will rapidly slow or stop blood flow, leading to death of the tissues fed by the artery in approximately 5 minutes. This catastrophic event is called an infarction. One of the most common recognized scenarios is called coronary thrombosis of a coronary artery, causing myocardial infarction (a heart attack). Even worse is the same process in an artery to the brain, commonly called stroke. Another common scenario in very advanced disease is claudication from insufficient blood supply to the legs, typically due to a combination of both stenosis and aneurysmal segments narrowed with clots. Since atherosclerosis is a body-wide process, similar events occur also in the arteries to the brain, intestines, kidneys, legs, etc.

Yet, many infarctions involve only very small amounts of tissue and are termed clinically silent, because the person having the infarction does not notice the problem, does not seek medical help or when they do, physicians do not recognize what has happened.

Causes

Atherosclerosis develops from low-density lipoprotein molecules (LDL) becoming oxidized (ldl-ox) by free radicals, particularly oxygen free radicals (ROS). Blood in arteries contains plenty of oxygen and is where atherosclerosis develops. Blood in veins

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contains little oxygen where atherosclerosis rarely develops. When oxidized LDL comes in contact with an artery wall, a series of reactions occur to repair the damage to the artery wall caused by oxidized LDL. The LDL molecule is globular shaped with a hollow core for carrying cholesterol throughout the body for making brain tissue, vitamin D, etc. Cholesterol does not dissolve in water. Blood is 70% water. The only way cholesterol can move in the bloodstream is to be carried by LDL.

The body's immune system responds to the damage to the artery wall caused by oxidized LDL by sending specialized white blood cells (macrophages and T-lymphocytes) to absorb the oxidized-LDL. Unfortunately, these white blood cells are not able to process the oxidized-LDL, and ultimately grow then rupture, depositing a greater amount of oxidized cholesterol into the artery wall. This triggers more white blood cells, continuing the cycle.

Eventually, the artery becomes inflamed. The cholesterol plaque causes the muscle cells to enlarge and form a hard cover over the affected area. This hard cover is what causes a narrowing of the artery, reduces the blood flow and increases blood pressure.

Some researchers believe that atherosclerosis may be caused by an infection of the vascular smooth muscle cells. Chickens, for example, develop atherosclerosis when infected with the Marek's disease herpesvirus.[2] Herpesvirus infection of arterial smooth muscle cells has been shown to cause cholesteryl ester (CE) accumulation.[3] Cholesteryl ester accumulation is associated with atherosclerosis.

Symptoms

Atherosclerosis typically begins in early adolescence, and is usually found in most major arteries, yet is asymptomatic and not detected by most diagnostic methods during life. The stage immediately prior to actual atherosclerosis is known as subclinical atherosclerosis. The majority of the process leading to subclinical atherosclerosis can happen without our knowing it, especially given the large variety of risk factors.[4] Autopsies of healthy young men who died during the Korean and Vietnam Wars showed evidence of the disease.[5][6] It most commonly becomes seriously symptomatic when interfering with the coronary circulation supplying the heart or cerebral circulation supplying the brain, and is considered the most important underlying cause of strokes, heart attacks, various heart diseases including congestive heart failure, and most cardiovascular diseases, in general. Atheroma in arm, or more often in leg arteries, which produces decreased blood flow is called peripheral artery occlusive disease (PAOD).

According to United States data for the year 2004, for about 65% of men and 47% of women, the first symptom of atherosclerotic cardiovascular disease is heart attack or sudden cardiac death (death within one hour of onset of the symptom).

Most artery flow disrupting events occur at locations with less than 50% lumen narrowing (~20% stenosis is average). [The reader might reflect that the illustration above, like most illustrations of arterial disease, overemphasizes lumen narrowing, as opposed to compensatory external diameter enlargement (at least within smaller arteries, e.g., heart arteries) typical of the atherosclerosis process as it progresses, see Glagov[7] and the ASTEROID trial,[8] the IVUS photographs on page 8, as examples for a more accurate understanding. The relative geometry error within the illustration is common to many older illustrations, an error slowly being more commonly recognized within the last decade.]

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