Lecture topic: «differential diagnosis of arterial hypertensions, therapy, care and prevention»

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эмблема тма

(for the students of medical-pedagogical faculty)




эмблема тма


Dean of medical-pedagogical faculty,

professor Khamraev A.A.


____ _____________ 2016 y



(for the students of medical-pedagogical faculty)

Lecturer: professor Gadaev A.G.

Tashkent – 2016


Amount student

Time - 2 hours

Form of the scholastic occupation

Lecture - a visualization

Plan to lectures

Determination term arterial hypertension and hypertension disease
1.Reasons and factors of the risk bring about ascent of the arterial pressure
2. Different patogenetik mechanisms ascent of the arterial pressure

3. Categorization of hypertension disease

(rates of the arterial pressure , stage, degree, stratification of the risk)

4. General differential-diagnostic signs of symptomatic AG and hypertension disease

5.Clinical manifestations and current of the diseases running arterial hypertension.

6. Diagnostics of the diseases being accompanied with arterial hypertension.

7. Principles of the treatment, preventive maintenances and dispanserization sick with arterial hypertension

Purpose of the scholastic occupation: acquaint student with ethiology, patogenesis of the diseases, being accompanied arterial hypertension, introduce with modern categorization hypertension disease, train principle of the diagnostics, treatments, preventive maintenances and dispanserization of the diseases, being accompanied AG

The Pedagogical problems

1. Consolidate and deepen knowledges a student about disease, being accompanied increasing of the arterial pressure

2. Teach student it is correct to install diagnosis in accordance with modern categorization

3. Train student to skill to differentiate diseases, being accompanied AG

4. Acquaint student a stage preventive maintenances sick with AG

The results of the scholastic process:

the general practitioner must know:

  1. The factors of the risk bring about increasing arterial hypertension

  2. The diseases , being accompanied of arterial hypertension

3.The principles of the differential diagnostics of the diseases, being accompanied arterial hypertension

4.The principles of the treatment.

5.Principles of the undertaking the preventive maintenance and dispanserization sick with AG

Methods of teaching

Text to lectures, video film, questions, technology "yes-no"

Form of the education

Lazer projector, visual material, special technical equipment, show thematic sick

Facilities of the education


Conditions of the undertaking the scholastic process



Stages, time




1 stage

Introductory part

(5 mines)

1. Tells about subject of the lectures, her purposes and plan

  1. Listen

2 stages

Actualization (increasing to value ) of the knowledges

(20 mines)

2.1. In purpose of increasing to actualizations (increasing to value) of the knowledges student will assign the questions:
1. Give the determination a term symptomatic arterial gipertension disease? What the difference?

2. Enumerate the diseases, being accompanied arterial gipertension

3. Enumerate the factors of the risk, bring about increasing AG?

4. Enumerate the groups a preparation, using for treatment gipertension disease?

Conducts questioning

    1. Showing on screen, offers to get acquainted the student with purpose and problem to lectures

    1. Slid №1,2

2.1. Answer givenned questions

2.2 Study slide 1

2.3. Study slide 2

3 stages

Main part (information)

(55 mines)

3.1. Introduces the student with lecture material, value of the subject and principle of the shaping intelegent cultural personality, in particular squall-teacher.
In purpose of increasing to actualizations of the knowledges conducts quick questioning a student:

  1. On 1 point of the plan to lectures: Give the determination a term arterial gipertension and hypertonic deаsise

  1. On 2 points of the plan to lectures: Enumerate reasons and factors of the risk bring about ascent of the arterial pressure

  1. On 3 points of the plan to lectures: Enumerate the different patogenetik mechanisms ascent of the arterial pressure?

4.On 4 points of the plan to lectures: tell main moments to categorizations gipertension disease (rates AG, stage, degree, stratification of the risk)

5.On 5 points of the plan to lectures: Enumerate general differential-diagnostic signs symptomatic AG and hypertension disease
6.On 6 points of the plan to lectures: Enumerate main clinical manifestations and current of the diseases, running arterial gipertension
7.On 7 points of the plan to lectures: Name main methods of the diagnostics of the diseases, being accompanied arterial gipertension

8.On 8 points of the plan to lectures: Enumerate cardinal principles of the treatment, preventive maintenances and dispanserization sick with arterial gipertension

Stopping for important moment of the lectures, offers to write main positions in copy-book

3.1. Together analyse heard lecture material, will assign questions

Main moments write in copy-book

4 stages

final (10 mines)

4.1. Will assign questions:

1. Enumerate most often meeting diseases, being accompanied increasing of the arterial pressure

2. Tell modern categorization an hypertension disease

3. Name cardinal principles of the treatment, preventive maintenances sick with arterial hypertension.

4.2. Gives task for independent work student: Symptomatic arterial hypertension, connected with pathology kidney.

4.1. Answer questions

4.2. Listen, write

Hypertension (HT) is one of the major risk factors for cerebral stroke, myocardial infarction, and also cardiac and renal failure. The prevalence of hypertension is 20-40% among adults in many developed countries of the world and its frequency among the elder people exceeds 50%. Currently, there is no doubt for the necessity of a long, essentially a lifelong drug therapy of hypertension. When blood pressure (BP) decreases to only 13/6 mm hg. art., risk of cerebral stroke reduces by an average of 40%, and myocardial infarction - 16%. Essential hypertension (EH) or essential hypertension - a disease in which increasesblood pressure which is not associated with primary organic lesion of organs and systems. This is very common disease that is most common among elder people. Distinguish: оptimal blood pressure <120/80 mm Hg. Art.,normal blood pressure <120-129/80-84 mm Hg. Art. Increased  normal BP 130-139/85-89 mm Hg. Art.

The diagnosis of hypertension made on finding blood pressure above 140/90 mm Hg, at least two timesrepeated visits to the doctor

Classification of hypertension in stages (WHO, 1996)

Stage 1, At this stage there is no objective evidence of damage in target organ. The only demonstration of the disease is a syndrome of hypertension. Stage 2 At least one sign of end-organ damage: left ventricular hypertrophy (LVH), 30-300 mg/day proteinuria, creatinine 115-133mkmol / L (for men and 107-124 mkmol / L for women.generalized or focal narrowing of the retinal arteries,atherosclerotic vascular disease.Stage 3.At this stage, there are found, except symptoms of hypertension and evidence of target organ damage, associated clinical conditions: angina pectoris, myocardial infarction, heart failure, SBBB, stroke, encephalopathy, dementia, chronic renal failure, changes in the eye ground (hemorrhage, edema of the papilla drive, exudation, atrophy)

Today, there are three degrees of AH:

1 degree of AH: 140-159/90-99 mm Hg. Art.

2 degree of AH: 160-179/100-109 mm Hg

3 degree of AH: more than 180/110 mm Hg. Art.

Isolated simpt. AH> 140 <90 mm Hg

In presence of 1 degree of AH in the patient, except degree of increase, the degree of risk is also assessed.

In determining the degree of risk is considered:Gender, Age, The numbers of cholesterol in blood, Obesity, The presence of AH in relatives, Smoking, Lack of physical activity, The defeat of target organs.

Risk stratification of AH

factors of the risk

AH 1 degree

AH 2 degree

AH 3 degree


Low risk

Moderate risk

High risk

1-2 FR

Moderate risk

Moderate risk

Very high risk

More than 3 FRorPOM

High risk

High risk

Very high risk

associated clinical conditions s.diabetes

Very high risk

Very high risk

Very high risk

Etiology: not defined. But there are factors that contribute to the development of HD.

1. Neuro - psychological trauma. Emotional stress.

2. Heredity - constitutional features.

3. Professional harmfulness, constant voltage of eyesight, attention.

4. Characteristics of feeding (abusing sodium chloride)

5. Age restructuring of hypothalamic - pituitary axis.

6. Skull injury.

7. Intoxication (smoking, alcohol).


1. Increased activity of the sympathetic-adrenal system.

2. Inclusion of the renin-angiotensin mechanism

3. Increase in prostaglandin F2 and cyclic nucleotides.

4. Increased production of antidiuretic hormone.

Clinical picture: Complaints of patients depends on the stage and form GB. At the beginning of the disease there may appear subjective feelings of the patient in the form of headaches, dizziness, general weakness, fatigue, irritability and insomnia. Sometimes patients do not show any complaints, and only occasional BP measurement shows its increase. Later, when blood pressure is stable and higher, the complaints are more prominent, shortness of breath when walking, feeling pain in the heart, palpitations, and headaches occur more frequently. In case of sharp rise in pressure that occur after the stress, pressure at work, patients may develop cerebral phenomena crisis, demonstrated in a feeling of heaviness and pressure in the head or severe headaches accompanied by dizziness, nausea, vomiting, and sometimes damage of eye sight. The cause of this crisis is a sharp spasm of cerebral vessels. Pain in the heart can occur in the form of strokes and cerebral crisis. This happens when at GB develops atherosclerosis of the coronary vessels of the heart. In the later stages, when it is the phenomenon of heart failure, patients complain of pronounced shortness of breath, which is manifested in the form of typical attacks of cardiac asthma. Their origin is related to failure of the left ventricle. In severe forms of GB, patients often geteye sight damage, caused by vascular changes of the retinal of eye ground. Appearance of the patient is diverse. In some cases, the skin and mucous membranes are normal, in others - the patient's face becomes red (hypertension), and often pale, due to a sharp spasm of arterioles (pale hypertension). On palpation of the heart,there is determined enhanced apical impulse which indicates about left ventricular hypertrophy. In the early stages of the disease for a long time there is marked only left ventricular hypertrophy without significantly expanding the boundaries of the heart. Later, when the hypertrophy joins LV dilatation, increased apical impulse is displaced laterally from the mid-clavicular line, sometimes reaching to the anterior axillary line. Percussion and radiographically in these cases the left border of the heart increases. Auscultation of the heart in the early stages of the disease usually only focus of the second tone of the aorta, in the future with the development of sclerotic processes, there is heard small systolic murmur inaortic. In the later stages, when LV expands, at the top is heard systolic noise arising due to functional insufficiency of mitral valve. Usually increases both systolic and diastolic blood pressure, but particular importance is given to the numbers of diastolic pressure, a significant increase of which indicates the severity of the GB. On an electrocardiogram there are revealed signs typical of left ventricular hypertrophy, often coupled with symptoms of coronary insufficiency. In the eye ground there is observed narrowing of the arteries and veins (symptom Salus). In severe forms of GB, often appear hemorrhage and degenerative changes in the corpus luteum and the optic nerve, which can lead to serious disturbances of the vision, including blindness. Complications:

1. Cardiac: development of chronic ischemic heart disease. Acute heart failure.Development of aortic aneurysm.

2. Cerebral: Reduction of view, the development of atherosclerosis of cerebral vessels, dynamic and organic cerebral circulation.

3. Kidney: hypertonic nephroamosklerosis.Chronic renal failure.

Differential diagnosis

Symptomatic arterial hypertension in 6-9% of all cases is increase of BP. Differential diagnosis of symptomatic hypertension is important, because of the correct position of the diagnosis depends on the nature of therapeutic measures, determining prognosis. Syndrome of malignant hypertension: pale skin; AD 240/130- 300/170 mm Hg and above; ineffectiveness of antihypertensive drugs; III-IV degree of retinopathy (swelling of the optic nerve and hemorrhage); the rapid deterioration of the general condition of the patient, the rapid development of organic changes in the brain, heart and renal arteries; neutrophilic leukocytosis in the blood, increase of erythrocyte sedimentation rate, thrombocytopenia, anemia, moderate; aggressive type of renal failure; proteinuria, hematuria, cylindruria, izostenuriya in the urine sample, elevated levels of residual nitrogen, creatinine, and indican in the blood.

Signs by which one can assume the presence of symptomatic hypertension:

age <40 years; ineffectiveness of antihypertensive therapy; malignant or progressive nature of hypertension; tolerability hypertension, the small number of complaints; stable blood pressure, diastolic blood pressure increase. Troubling history:- Nephropathy, cystitis, edema, renal colic.- "Non-program" violation:

  • muscle weakness, vascular noise, paroxysms of increase of blood pressure;

  • paradoxical reaction to certain drugs.

Atherosclerotic lesions of the renal arteries - the most common cause of renovascular hypertension (70%). Usually develops in men over 50 years old. The diagnosis is based on the detection of prolonged systolic or sistolodiastolicheskogo noise above the projection of renal arteries (epigastric 2-3 cm above the navel, and at this level on the right and left of the midline of the abdomen). Noise is detected in approximately 50-60% of patients. Diagnosis is verified by objective methods of research: isotope renography, excretory urography, CT, abdominal aortography, renal vein catheterization - elevated levels of renin in the venous blood of the affected kidney. This aortography - decisive, not only in the final diagnosis, but also in the choice of treatment (balloon angioplasty, surgical correction of the stenosis). It is believed that correction of angioplasty or surgical is shown in case of: 1) difficult to treat hypertension, and 2) the deterioration of renal function with medical treatment, and 3) intolerance of drugs, and 4) young patient. In cases of non-functioning kidney - nephrectomy. Therapeutic tactic is no different from that in GB. Fibromuscular dysplasia of the renal arteries occurs in 10-20% of patients with renovascular hypertension. This disease is common in women 4-5 times more often than men, and hypertension usually occurs at a young age (under 40 years). Most often, this is congenital abnormality. The diagnosis is performed by the same methods and based on the same characters as in the atherosclerotic arterial hypertension. Only in cases of angiographic stenosis of the renal arteries, there are identified in the form of a string of beads or pearls. Treatment.Balloon angioplasty - a method of choice (a high probability of success and a low risk of re-stenosis). Nonspecific aortoarterium (panarterium, pulseless disease, Takayasu'ssyndrome, etc.) leads to stenosis of the aorta and the main arteries and ischemia of the affected organ. Renovascular hypertension syndrome occurs in half of patients and is due to the involvement in the process of the mouths of renal arteries. This increases the predominantly diastolic pressure of 100-160 mm Hg. Art. and systolic - up to 180-250 mm Hg. Art.

Blood pressure was measured both at the upper and the lower extremities. The asymmetry of the blood pressure, as well as the presence of noise above the projection sistolodiastolic renal arteries are the typical clinical signs of the disease. The final diagnosis of renovascular hypertension syndrome is set by aortography. Treatment of hypertension is the same as in GB. With the development of stenosis and occlusion of the arteries, which greatly damages hemodynamics of organ or region, there is shown vascular reconstructive surgery. Chronic glomerulonephritis. Hypertensive form of chronic glomerulonephritis - one of the most common causes of symptomatic renal hypertension (about 30-40%).On basis of pathogenetic mechanisms of AH in this disease there are the activation of the renin-angiotensin system, reducing the ability of the kidneys to produce vasodilatory and natriuretic substance that increases the reabsorption of sodium and water. In the progression of nephrosclerosis, renoprival pathogenesis of hypertension become together. In chronic glomerulonephritis, there is marked stabilization of blood pressure at high levels, and in the absence of adequate therapy - the outcome in malignant hypertension. The diagnosis of chronic glomerulonephritis is established on the basis of anamnestic indications previously deferredacute glomerulonephritis or nephropathy pregnant, repeated tonsillitis and other diseases caused by streptococcus, pain in the lumbar region. During the examination of such patients found pale face. The most informative is re-urine, and the changes in the urine are detected in increased blood pressure or at very moderate hypertension. Most often they appear with insignificant proteinuria (98% of cases), rarely –with red blood cell (60%) and with cylindruria (in 40-50% of cases). Further information can be obtained in the diagnosis of renal ultrasonography - the restriction of the cortical layer in intact pyelocaliceal system. Diagnosis is verified by needle biopsy of the kidneys. Treatment. Along with the treatment of the underlying disease, there are appointed some drugs: loop diuretics, ACE inhibitors, calcium antagonists. With resistance-a-blockers and / or labetalol. In cases of more intensive treatment can be addedminoxidil. To lower blood pressure in end-stage renal failure it may require dialysis or kidney transplantation.Chronic pyelonephritis - the most common cause of SAG. During the autopsy revealed chronic pyelonephritis in 6% in the presence of hypertension guidelines in life. The pathogenesis of hypertension in pyelonephritis is not significantly different from that of glomerulonephritis. The preferential localization of morphological changes in the renal medulla suggests a greater role in reducing the occurrence of hypertensive renal depressor. Hypertension in chronic pyelonephritis proceeds relatively benign. On making diagnosis should be paid attention to the identification of risk factors for chronic pyelonephritis, indications of a history of dysuric disorders, including childhood and adolescence, pain, lumbar region or blunt aching nature, unmotivated fever. Patients with chronic pyelonephritis attract attention with pallor of the skin, swelling and paraorbital "cyanotic" circles under the eyes. Often, these patients have nicturia. In laboratory studies of urine, the most frequently reported gipoizostsenuriya, moderate proteinuria (in 75% of cases), pyuria (50% of cases), rarely hematuria (in 30% of cases). However, many patients with acute stump any changes in the urine are not available. When posspah urine is considered diagnostically significant growth over 100,000 colonies per 1 ml of urine or release of the same pathogens in cases of repeated crops, even if the number of colonies less than 100 000 per 1 ml of urine. Pyelonephritis often dominate unilateral changes, so some diagnostic information can be obtained from radiorsnograficheskogo study. Methods of verification of diagnosis are ultrasound of the kidneys and excretory urography infuzionnai, less kidney biopsy.

Treatment. Adequate treatment of chronic pyelonephritis is conducted. Drug treatment is the same kick and chronic glomerulonephritis. Must be avoided the use of non-steroidal anti-inflammatory drugs (inhibit the synthesis of renal vasodilator prostaglandinop), potassium-sparing diuretics and potassium preparations. Fiohromotsitoma - a tumor, consisting of chromaffin cells and produce catecholamines (adrenaline and noradrsnalin). In 90% of cases,pheochromocytoma is localized in the adrenal medulla, usually on the right. Paraganglioma - extraadrenalchromaffin tissue - may be at the gate of the kidneys, the bladder, in the course of the aorta (thoracic and abdominal). The pathogenesis of hypertension in pheochromocytoma is due to the release of significant amounts kateholaminon, which leads to increased peripheral resistance. In some cases arterialyshyagipsrteshiya with pheochromocytoma is paroxysmal in nature. It is believed that the inclusion of the renin-angiotensin-aldosterone system promotes permanent form of hypertension. During crisis situations with pheochromocytoma, within a few seconds blood pressure rises suddenly, up to a very high level (250-300/150-130 mm Hg. Cent.) Appear pronounced tachycardia, pallor, cold sweats, disturbed vision. There is thirst, urination, increased levels of blood sugar. In the blood - leukocytosis. Crises can be triggered by cold test, deep palpation of the abdomen, bringing the lower extremities to the stomach, taking dopegita, reserpine, clonidine. The latter can be used for differential diagnosis. When receiving 0.3 mg of clonidine in patients without pheochromocytoma catecholamine levels in the blood (2-3 h) and urine (while taking the drug at 21 h urine is collected in a range of from 21 to 7 hours) is significantly reduced. In patients with a tumor,catecholamines in blood and urine are unchanged. The assumption about the presence of pheochromocytomais confirmed by defininingincreased urinary catecholamines in blood and their metabolites in the daily urine: epinephrine (50 micrograms), noradrenaline (more than 100-150 mg), vanilmindalnoy acid (more than 6 micrograms), including during 3 hours after a crisis . Verified diagnosis by CT scan, ultrasound. In recent years, there is more widely used scintigraphy with labeled 131J - guanethidine analog that selectively captured by the tumor. Treatment. Prompt treatment is carried out by phentolamine (Radical treatment - surgical removal of the tumor. If surgical removal is not possible, there is used a permanent cure phenoxybenzamine (a-blocker for oral) or a-metiltirozinom (catecholamine synthesis inhibitor for oral administration).

Primary Aldosteronizm (Conn's syndrome) is manifested with clinically stable hypertension, mostly diastolic blood type due to increased synthesis of aldosterone in the glomerular layer of the adrenal cortex. At the core of this disease in most cases there is a solitary adrenal adenoma (aldosteronoma). The disease is more common in women. As a result of increased secretion of aldosterone, there is defined sodium retention (the ions) in the renal tubules and the accumulation of interstitial fluid –occurspolyuria. Simultaneously, there is increased excretion of potassium ions in the renal tubules, and in the intestine, salivary glands and sweat glands. There is an extracellular alkalosis, suppressed the secretion of renin. There is developed volume (sodium), high sensitive hypertension, especially with bilateral lesions of the adrenal gland. Hypertension is associated with such an important diagnostic feature as muscle weakness, especially in the muscles of the legs. Sometimes there are attacks of paralysis of the leg muscles, lasting from a few hours to several days, spasms and contractions in the muscles of the legs, paresthesia, and numbness. The diagnosis of primary aldosteronism and its differential diagnosis should consider the level of potassium (hypokalemia), and serum sodium, the state of acid base balance, the daily urine output, which can range from 2 to 7 liters per day, urine density is usually much reduced, nocturia, izostenuriyu , alkaline urine. Reduced or zero plasma renin activity and increased urinary excretion of aldosterone are hallmarks of primary aldosteronism. Hypokalemia can be confirmed by testing hydrochlorothiazide. Among pharmacological tests to confirm the diagnosis,there may be used aldosterone antagonists (veroshpiron 100 mg / day for 4-5 weeks) as a result occurs decrease in diastolic blood pressure at least 20 mm Hg. Art. Diagnostics are done by using computed tomography or scintigraphy SM "cholesterol.

Treatment. In bilateral adrenal hyperplasia there are shown potassium-sparing diuretics (spironolactone, amiloride or triamterene) with nifedipine or without. Adrenal adenoma - surgical resection after preoperative treatment with spironolactone (veroshpiron, Aldactone).

Hypertension is often observed with endocrine diseases such as Cushing's syndrome (treatment - hypophysectomy, irradiation of heavy particles, adjuvant therapy mibotanom, Parlodel), hyperthyroidism (treatment - surgical or medical - merkazolil, (B-blockers), hypothyroidism (treatment a-thyroxine), acromegaly (treatment - transsphenoidal removal of eosinophilic pituitary adenoma, radiation or adjuvant bromocriptine).

Hemodynamic arterial hypertension (coarctation of the aorta, aortic valve) is treated surgically with vascular surgical correction of the defect.

In neuroendocrine form of hypothalamic syndrome, hypertension is treated by Peritol (12 mg daily) or Parlodel (5 mg per day). Non-pharmacological treatment: Lifestyle change,exercise stress ,weight loss, reduce consumption of salt to 4.5 grams per day,diet, reduce alcohol intake to 20-30 g of pure ethanol per day, quit smoking, auto training, medical therapy:b-blockers,calcium channel blockers, diuretics, ACE inhibitors,central alpha2-agonists,Alpha-blockers,Angiotensin II receptor antagonists, рotassium channel activators.

  • monotherapy may be a start treatment with a moderate increase in blood pressure, with a low or moderate risk of complications.

  • A combination of two drugs at low doses is suitable as seed treatment, if blood pressure increased to 2 or 3 degrees, and if the patients have moderate increase in blood pressure, but there is a high or very high risk of complications.

  • In some cases, the control of blood pressure is not reached during treatment with the two drugs. In these cases, a combination of three or more means.

  • In uncomplicated hypertension or elderly patients, antihypertensive therapy should be done step by step

Mechanisms of action of main antihypertensive drugs


Mechanisms of action


inhibits ACE, which facilitates reducing the effect of angiotensin II on the blood vessels

Angiotensin of receptor of antagonists

weakening effects of angiotensin II, which are mediated by angiotensin AT1-receptor

Calcium antagonists

reduces the flow of calcium in vascular smooth muscle cells


competitive inhibitor binding mediator of sympathetic nervous system with beta-adrenergic receptors.


natriuresis - the volume of fluid

Agonists of imidazoline receptors

central action. Excitation of imidazoline receptors suppresses the activity of the sympathetic neurons in the spinal cord, which is accompanied by inhibition of the activity of the sympathetic nervous system with a reduction of release of catecholamines, a decrease of sympathetic impulses to the vessels and heart.


 blocks alpha adrenoretseptors in the muscular wall of blood vessels, causing them to expand

Drug treatment with inhibitors of ACE can be assigned at:

  • AG + diabetes

  • AG high risk and very high risk of diabetes +

  • AG high risk and very high risk + NC

  • CHF

  • AG high risk and very high risk of LV hypertrophy +

  • AG high risk and very high risk of CRF +

  • AG high risk and very high risk + dislipedemiya

  • AG high risk and very high risk of diabetic nephropathy +

  • Renovascular hypertension ("kidney" AH)

  • Asymptomatic left ventricular dysfunction after myocardial infarction

Drug treatment with calcium antagonists can be assigned at:

  • AG + CHD

  • AG high risk and very high risk + NC

  • AG high risk and very high risk + LV hypertrophy - when combined with ACE inhibitors

  • AG high risk and very high risk dislipedemiya + in combination with ACE inhibitors

  • Pulmonary Hypertension

  • AG pregnant

Primary prevention of hypertension

  • Activities aimed at increasing the educational level of the population, make people to set healthy life style and creating the conditions for its implementation: avoiding harmful habits, nutrition, adherence to rest,prevention of inactivity, prevention of stress, Prevention of obesity and its treatment, correction dislipedemy.

Secondary prevention of hypertension

  • Inspection and tonometry

  • Fight against identified risk factors of hypertension among the population;

  • Taking on the "D" registration for newly diagnosed patients;

  • The treatment of AH drugs of proven efficacy, with group and individual selection of doses, while following the continuity and duration of antihypertensive drugs.

  • Maintain target of BP

  • Maintaining the quality of life.

Tertiary prevention of hypertension

-Prevention of complications

- Prevention of diabetes and coronary heart disease

- Psychological support

List of the literature
1. I.S.Cohen -Regenerating the Heart Stem Cells and the Cardiovascular System

2. ABC of Interventional Cardiology - Ever D. Grech, 2004

3. Cardiovascular Disease in the Elderly - Wilbert S.Aronow, Jerome L.Fleg,

4.www. gypertonia.com/...ag-prichiny

5. www. Medlinks.ru / article

6. www. kardiologia.poliklinica. ru
: syllabus -> 3-sonli-ichki-kasalliklar-kafedrasi-2017 -> МАЪРУЗА%2016-17
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