slide 2
Hypertension is high and constant blood pressure: 140/90 and above.
The ideal level is when the upper number of blood pressure is kept below 120 (systolic pressure). The bottom number should be below 80 (diastolic).
slide 3
Hypertension is the most common disease of the XXI century (WHO). Approximately 600 million people worldwide suffer from high blood pressure.
slide 4
Stages of hypertension
Stage 1 (mild) is characterized by relatively small rises in blood pressure in the range of 160-179 (180) mm Hg. Art. systolic, 95-104 (105) mm Hg. Art.-diastolic. The level of blood pressure is unstable, during the rest of the patient it gradually normalizes, but the disease is already fixed, the increase in blood pressure inevitably returns. Some patients do not experience any health disorders. Others are concerned about headaches, noise in the head, sleep disturbances, decreased mental performance. Occasionally, non-systemic dizziness, nosebleeds occur. Usually there are no signs of left ventricular hypertrophy, the ECG slightly deviates from the norm, sometimes it reflects a state of hypersympathicotonia.
slide 5
Stage 2 (middle) differs from the previous one in a higher and more stable level of blood pressure, which at rest is in the range of 180-200 mm Hg. Art. systolic and 105-114 mm Hg. Art. diastolic. Patients often complain of headaches, dizziness, pain in the heart. Signs of target organ damage are revealed: left ventricular hypertrophy, ECG signs of subendocardial ischemia. From the side of the central nervous system, various manifestations of vascular insufficiency are noted, cerebral strokes are possible. In the fundus, in addition to narrowing of the arterioles, compression of the veins is observed. Renal blood flow and glomerular filtration rate are reduced, although urinalysis shows no abnormalities.
slide 6
Stage 3 (severe) is characterized by a more frequent occurrence of vascular accidents, which depends on a significant and stable increase in blood pressure and the progression of atherosclerosis of larger vessels. BP reaches 200-230 mm Hg. Art. systolic, 115-129 mm Hg. Art. diastolic. Spontaneous normalization of blood pressure does not happen. The clinical picture is determined by damage to the heart (angina pectoris, myocardial infarction, circulatory failure, arrhythmias), brain (ischemic and hemorrhagic infarcts, encephalopathy), fundus, kidneys (decreased renal blood flow and glomerular filtration). Some patients with stage III hypertension, despite a significant and sustained increase in blood pressure, do not experience severe vascular complications for many years.
Slide 7
Cause of hypertension
Statistics: 90% of hypertension diseases are caused by lifestyle and bad habits. Conclusion: we become hypertensive in most cases by our own choice.
Slide 8
Lifestyle factors are the cause of hypertension
Excess body weight Each kilogram of fat requires 15 km of additional tiny blood vessels. Therefore, more pressure is required to push blood through them. Statistics: people who have a body weight of 20% above normal are 5 times more likely to suffer from hypertension than people with normal body weight. Obesity was the cause of the disease in 70% of men and 61% of women with hypertension.
Slide 9
Too Much Salt, Too Much Dietary Sodium High blood pressure has been found to be rare in regions of the world where the salt content of food is very low. Salt consumption is on the rise in many countries. As a result, hypertension, like an epidemic, affects half of the adult population. Excess salt in the body often leads to spasm of the arteries, fluid retention in the tissues and, as a result, to the development of arterial hypertension. It is estimated that every kilogram of excess weight means an increase in pressure by 2 mm. rt. Art.
Slide 10
Smoking The components of tobacco smoke, getting into the blood, cause vasospasm. Substances contained in tobacco contribute to mechanical damage to the walls of arteries, which predisposes to the formation of atherosclerotic plaques in this place. Smoking one cigarette raises blood pressure. The elevated pressure is maintained for at least 30 minutes.
slide 11
Alcohol The result of scientific research: moderate alcohol consumption (no more than 5 times a year) leads to hypertension in 15% of cases. Daily use of strong alcoholic beverages increases blood pressure by 5-6 mm. rt. Art. in year.
slide 12
Coffee, tea The result of scientific research: one cup of coffee or tea can increase blood pressure by 5-6 divisions.
slide 13
Inactivity The result of scientific research: a person who does not exercise will sooner or later suffer from high blood pressure.
Slide 14
Stress and mental overstrain The stress hormone adrenaline makes the heart beat faster, pumping more blood per unit of time, resulting in increased pressure. If stress continues for a long time, then the constant load wears out the vessels and the increase in blood pressure becomes chronic.
slide 15
Atherosclerosis Excess cholesterol leads to a loss of elasticity in the arteries, and atherosclerotic plaques narrow the lumen of the vessels, which makes it difficult for the heart to work. All this leads to an increase in blood pressure. However, hypertension, in turn, spurs the development of atherosclerosis, so that these diseases are risk factors for each other.
slide 16
Heredity Heredity plays an important role in the development of hypertension, mainly in young people, less in the elderly. It has been established that hypertension in families where the closest relatives suffer from high blood pressure develops several times more often than in members of other families. In parents with hypertension, children are 3.5 times more likely to suffer from it compared to other children. It is not hypertension itself that can be genetically inherited, but only a predisposition to it, this is due to the peculiarities of the metabolism of certain substances (in particular, fats and carbohydrates), as well as neuropsychic reactions. However, the implementation of genetic predisposition is largely due to external influences: living conditions, nutrition, adverse factors.
Slide 17
Prevention of the development of hypertension Prevention of arterial hypertension is divided into primary and secondary. Primary prevention is needed for healthy people - those whose pressure does not yet exceed normal numbers. The following set of wellness measures will help not only keep your blood pressure normal for many years, but also get rid of excess weight and significantly improve your overall well-being.
Slide 18
Physical exercise Any physical exercise in individuals with mild to moderate arterial hypertension contributes to an increase in physical performance. Exercises aimed at training endurance (general developmental, breathing exercises, training on simulators, swimming, brisk walking, running) lead to a noticeable antihypertensive effect. However, during strenuous exercise, systolic pressure increases dramatically, so it is best to do a little (30 minutes) every day, gradually increasing the load from light to moderate.
Slide 19
Restriction of animal fats Gradually replace butter, cheeses, sausages, sour cream, lard and fried cutlets from your diet with additional vegetables and fruits, vegetable oil and lean fish. Prefer low-fat dairy products. Thus, you can control the content of cholesterol in the blood (prevention of atherosclerosis), normalize weight and at the same time enrich your diet with potassium, which is very useful for hypertension.
Slide 20
Low salt diet Quantity table salt should be limited to 5 grams (1 teaspoon) per day. It should be noted that many products (cheeses, smoked meats and pickles, sausages, canned food, mayonnaise, chips) themselves contain a lot of salt. So, remove the salt shaker from the table and never add salt to ready meals. Replace salt with herbs, garlic. If you find it difficult to go without salt, you can purchase salt with a reduced sodium content, which tastes almost the same as regular salt.
slide 21
Psychological unloading Stress is one of the main causes of high blood pressure. Therefore, it is so important to master the methods of psychological relief - auto-training, self-hypnosis, meditation. It is important to strive to see in everything positive sides, find joy in life, work on your character, changing it in the direction of greater tolerance for other people's shortcomings, optimism, balance. Hiking, sports, hobbies, and pets also help to maintain mental balance.
slide 22
Non-Drug Therapy In addition to the hypertonic diet, therapy may include breathing exercises, light massage, acupuncture, acupuncture, reflexology, normalization of sleep, adherence to a daily routine, intake of natural and synthetic vitamins, antioxidants, nutritional supplements and general strengthening herbs. In a word, it is necessary to "improve" your lifestyle as much as possible. Measurement of blood pressure Do this daily, and write down the received figures in a special notebook. If your pressure is close to 140/90, or higher than this figure, then it is high and you should consult a doctor.
Authors: Prof. Fazlyeva R. M. Assoc. Mukhetdinova G. A. Ufa,
Arterial hypertension (AH) is a condition in which systolic blood pressure is 140 mm Hg. Art. and above and / or diastolic blood pressure - 90 mm Hg. Art. and higher.
The prevalence of hypertension affects 20-30% of the adult population Among people over 65 years old - 50-65% The rule of half - half of the patients know about the presence of hypertension, half of those who know are treated, no more than half of those treated reach normal blood pressure levels.
Hypertension (essential or primary hypertension) is a chronic disease, the main manifestation of which is arterial hypertension syndrome in the absence of a primary cause for its increase. Frequency 90-95%.
HBetiology and pathogenesis Obesity Stress Genetic factors Excessive salt intake Membrane disorders Baro- and chemoreceptors. Endothelin RAAS Violation of sodium excretion. Increased SAS activity
Secondary hypertension (symptomatic) EG must be differentiated from secondary (symptomatic) hypertension, which is understood as such forms of increased blood pressure, which are caused by diseases of the organs and systems involved in the regulation of blood pressure.
The main groups of secondary hypertension: 1. Renal (nephrogenic) - 18% or 70-80% of symptomatic hypertension; 2. Endocrine; 3. Hemodynamic, caused by lesions of the heart, aorta, its large branches; 4. Centrogenic, caused by organic lesions of the central nervous system; 5. Exogenous, due to medication (GCS, hormonal contraceptives), alimentary (tyramine). A special form of hypertension is an increase in blood pressure due to an increase in blood viscosity, for example, with polycythemia.
Classification of symptomatic hypertension (according to Arabidze (1992) 1 Renal arterial hypertension 1) Congenital anomalies of the kidneys and blood vessels (hypoplasia, dystopia, hydronephrosis, polycystic, horseshoe kidney, pathological mobility, atresia and hypoplasia of the renal artery, aneurysms. 2) Acquired kidney disease ( diffuse glomerulonephritis, amyloidosis, Kimelstil-Wilson syndrome, systemic vasculitis, tumors). 3) Acquired lesions of the main renal artery (atherosclerosis, calcification, thrombosis, embolism, fibromuscular dysplasia, Takayasu's disease, aneurysm, endarteritis, hemangiomas, vascular compression, stenosis and thrombosis of the renal vein.
2. Arterial hypertension caused by damage to large vessels 1) Coarctation of the aorta 2) Atherosclerosis 3) Stenosis of the vertebral and carotid arteries 4) Complete AV blockade
3. Arterial hypertension in endocrine diseases 1) Pheochromocytoma 2) Itsenko-Cushing disease and syndrome 3) Primary hyperaldosteronism 4) Toxic goiter 5) Congenital adrenal hyperplasia 6) Acromegaly 7) Hyperparathyroidism
4. Arterial hypertension in diseases of the central nervous system 1) Encephalitis 2) Poliomyelitis 3) Tumors and injuries of the brain
features of hypertension in CGN and kidney disease: > Young age of patients; > Lack of "vegetative neurosis"; > The course of the disease without crises; > Dependence of exacerbations on tonsillitis and SARS, and not on psycho-emotional factors; > Patients with renal hypertension do not feel their high blood pressure, in contrast to patients with EG, in which even a slight increase may be accompanied by an abundance of symptoms; > Edema occurs in 1/3 of patients with CGN, but may also occur in EG, especially in the volume-sodium-dependent variant.
laboratory and instrumental studies: > Presence of urinary syndrome; > During the period of exacerbation - the acceleration of ESR, the appearance of acute phase proteins, often anemia; > In the presence of chronic renal failure - a decrease in glomerular filtration, an increase in residual nitrogen and urea, creatinine; > In the fundus - hypertensive retinopathy, usually more pronounced than in EG, transudates in the fundus can be observed even with moderate hypertension; > Needle biopsy of the kidneys.
Vasorenal hypertension Causes of vasorenal hypertension: > In old age - atherosclerosis; > In the young - FMD, less often nonspecific aortoarteritis (Takayasu's disease); > Rare causes are hypoplasia, thrombosis, post-traumatic aneurysm.
General signs of vasorenal hypertension 1. Stably high nature of hypertension from the very beginning; 2. Preferential increase in DBP; 3. Systolic murmur over the projection area of the renal arteries (with unilateral lesion, the murmur is audible in 50-70% of patients, with bilateral - in almost all); 4. Resistance to conventional antihypertensive therapy; 5. Frequent malignant course of hypertension (with unilateral lesion in 30%, with bilateral 50-60%); 6. Concomitant lesions of other arterial systems; 7. Asymmetry of pulse and blood pressure.
Primary hyperaldosteronism (Conn's syndrome) Characteristic signs (four "G"): 1. Hypertension; 2. Hypokalemia (potassium below 3.0 mmol/l); 3. Hyperaldosteronism; 4. Hyporeninemia.
Primary hyperaldosteronism (Conn's syndrome) o Severe muscle weakness resembling myasthenia gravis; o Convulsive muscle twitching, parasthesia, numbness and flaccid paralysis type disorder, often with hanging head symptom; o Persistent left ventricular hypertrophy does not develop, P-Q shortens, electrical systole lengthens, S-T segment shifted down, the T wave flattens and merges with a significantly enlarged U wave. o Polyuria (up to 3 l / day); o Nocturia; o Isosthenuria (1007-1015, and in diabetes insipidus 1002-1005).
Pheochromocytoma The main clinical manifestation of pheochromocytoma is a paroxysmal instantaneous increase in blood pressure to significant numbers (up to 250/140 - 300/160 mm Hg), accompanied by tachycardia up to 100-130 beats per minute, fever, dizziness, throbbing headache, trembling, pain in the epigastric region, limbs, pallor, increased respiration, dilated pupils, blurred vision, hearing, thirst, urge to urinate.
Pheochromocytoma In the blood and urine during an attack - leukocytosis, hyperglycemia, glucosuria; Urinary excretion per day more than 30 mcg of adrenaline, more than 100 mcg of noradrenaline and more than 6 mg of vanillindelic acid; CT - topical diagnostics.
Itsenko-Cushing's syndrome The disease occurs 3-4 times in women and in 80-90% of cases occurs with hypertension. In 30% of patients, the syndrome is due to primary adenoma or carcinoma of the adrenal cortex.
Itsenko-Cushing's syndrome Clinical symptoms: Obesity according to the "upper type": red and shiny face, powerful torso and neck and abdomen with thin legs; There are purple-violet striae on the abdomen and thighs, petechiae and telangiectasias are detected on the extensor surfaces of the forearms; Oligo- or amenorrhea, impotence and gynecomastia in men; Hair loss under the armpits, on the pubis, dry skin, nail dystrophy, acne; Acute steroid ulcers in the gastrointestinal tract, prone to bleeding; Insomnia, euphoria, fatigue and weakness;
Itsenko-Cushing syndrome Laboratory data: polycythemia, eosinopenia, lymphopenia, hypercortisolemia, aldosteronemia, hypernatremia, hypomagnesemia, metabolic alkalosis, hypercholesterolemia, triglyceridemia, increased excretion of 17-OKS and 17-KS.
ISAH: isolated systolic hypertension o Increase in SBP above 140, with DBP below 90 mm. rt. Art. (high pulse pressure (“jumping” pulse, accent of 2 tones over the aorta, rough systolic murmur conducted into the interscapular space. Aortic seal can be established using X-ray and Echo. KG examination.
Coarctation of the aorta Narrowing or complete break in the isthmus at the border of the arch and the descending aorta. It can be isolated, and can also be combined with patent ductus arteriosus or other congenital heart defects. It is 4 times more common in men.
Coarctation of the aorta When examining adult patients, a good development of the chest, shoulder girdle and neck is revealed with a noticeable lag in the development of the lower extremities. The pulsation of the intercostal arteries is determined, the apex beat is strengthened, systolic trembling is often palpated in the 2-3 intercostal spaces to the left of the sternum. A systolic murmur is heard over the entire surface of the heart, which is carried out to the vessels of the neck and into the interscapular space. II tone on the aorta is accentuated. Systolic blood pressure in the upper extremities in all patients is significantly increased, while diastolic blood pressure rises slightly or remains normal. As a result, the pulse pressure increased. Blood pressure in the lower extremities is much lower than in the upper ones.
Coarctation of the aorta On the ECG in adults, signs of hypertrophy and overload of the left sections are revealed, in 70% of the plain chest radiographs, usuration of the ribs arising from the pressure of the intercostal arteries is determined. Two-dimensional echocardiography visualizes the site of narrowing of the aorta. Using Doppler echocardiography, systolic turbulent blood flow and pressure gradient above and below coarctation can be determined. The final diagnosis is made using aortography.
Target organ damage Heart left ventricular hypertrophy (LVH) heart failure Brain acute cerebrovascular accident (stroke, transient ischemic attack); chronic disorders of cerebral circulation (hypertensive encephalopathy, lacunar infarcts) Kidneys Hypertensive nephropathy Hypertensive nephrosclerosis Eyes Hypertensive retinopathy
Target organ damage Effects on the heart Left ventricular hypertrophy (LVH) Heart failure
Damage to target organs Effect on the brain acute cerebrovascular accident (stroke, transient ischemic attack); chronic disorders of cerebral circulation (hypertensive encephalopathy, lacunar infarcts)
Laboratory and instrumental research methods General analysis blood Complete urinalysis Biochemical blood test (potassium, sodium, creatinine, glucose, cholesterol levels) ECG - left ventricular hypertrophy (Sokolov-Lyon index SV 1 + RV 5, 6> 35 mm in persons over 40 years old; >> 45 mm in persons younger than 40 years) 24-hour BP monitoring (ABPM) Echocardiography - left ventricular hypertrophy (LVLH >> 1.2 cm; TMZHP >> 1.2 cm; increased LVML), impaired diastolic, late systolic function of the left ventricle Fundus examination of kidney ultrasound, adrenal glands, renal arteries to detect secondary hypertension
The location of the moment vectors of ventricular depolarization in the horizontal plane in the norm (a) and with LV hypertrophy (b) ECG with left ventricular hypertrophy
Treatment of hypertension Non-drug measures to reduce blood pressure Stop smoking Reduce excess body weight Reduce alcohol consumption Limit the intake of salt to 5-2 g / day Complex diet modification - increase the consumption of fruits and vegetables, foods rich in potassium, magnesium, calcium, fish and seafood, restriction of animal fats Increased physical activity
Drug treatment of hypertension 2. Main groups of antihypertensive drugs β-blockers Diuretics Calcium antagonists ACE inhibitors α-blockers of angiotensin receptors III drugs of central action
Group of drugs Representatives Indications Contraindications Diuretics Hypothiazid 12.5-50 mgmg Indapamide 1.25-2.5 mg Furosemide 40-240 mg Spironol kton 25-100 mg CHF, elderly, systolic AH Gout a
Group of drugs Representatives Indications Contraindications β-adrenergic blockers Propranolol 40-240 mgmg Atenolol 50-100 mg Metoprolol 50-400 mg Bisoprolol 2, 5-20 mg Angina pectoris, myocardial infarction, tachyarrhythmia syndrome m, m, AV block adade 2-3 degree
Group of drugs Representatives Indications Contraindications Calcium antagonists Verapamil 120-480 mg Diltiazem 180-360 mg Amlodipine 5-10 mg Nifedipine SRSR 30 mg diltia zema)
Group of drugs Representatives Indications Contraindications ACE inhibitors Captopril 25 mg, Enap (5, 10 mg), Diroton (10 mg) Arterial hypertension, chronic heart failure Pregnancy, bilateral renal artery stenosis, hyperkalemia
Group of drugs Representatives Indications Contraindications Angiotensin IIII receptor blockers Losartan 25-50 mg Valsarta n 80-320 mgmg Cough when taking ACE inhibitors Pregnancy, bilateral renal artery stenosis, hyperkalemia
Group of drugs Representatives Indications Contraindications Centrally acting drugs Clonidine 0.2-0.8 mg Methyldopa 500 mg-2g Moxonidine n Broncho-obstructive syndrome, hypersymptomatic aticotonia Bradycardia, heart block, depression
Group of drugs Representatives Indications Contraindications α-adrenergic blockers Doxazosin 1-16 mg Prazosin 2, 5-20 mg Prostate adenoma Orthostatic hypotension
Drugs for the relief of hypertensive crisis drug at dose Special indications Furose mid 20-120 mg IV bolus Pulmonary edema, hypertensive encephalopathy Clonid inin (Clonidine) 0.075-0.150 mg IV slowly In the syndrome withdrawal of clonidine
Medicines for the relief of hypertensive crisis drug at dose Special indications Labeto Lol 20-80 mg IV bolus Stroke, dissecting aortic aneurysm Captopril 6, 25-50 mg orally, sublingually Nifedi pin 10-30 mg sublingually
Complications of hypertension: Myocardial infarction Stroke Renal failure Heart failure Hypertensive encephalopathy Retinopathy Dissecting aortic aneurysm
Description of the presentation on individual slides:
1 slide
Description of the slide:
2 slide
Description of the slide:
HYPERTENSION LESSON PLAN: Definition of "Hypertension", prevalence and relevance for the paramedic. 2. Etiology and pathogenesis of hypertension. 3. Clinical manifestations of the disease. 4. Classification of GB. 5. Diagnosis of GB. 6. Complications of GB. 7. Hypertensive crises. 8. Principles of treatment. 9. Prevention of GB.
3 slide
Description of the slide:
4 slide
Description of the slide:
RELEVANCE OF THE TOPIC STUDY AH is the most important cause of disability and premature mortality in the world. Hypertension is a risk factor in the development of atherosclerosis and coronary artery disease (myocardial infarction). Hypertension is followed by atherosclerosis and myocardial infarction. PROVEN!!! Regular measurement of blood pressure and keeping it normal reduces the development of myocardial infarction by 19-20%; the number of strokes by 43-45%
5 slide
Description of the slide:
In Russia, 42% of the population is diagnosed with Hypertension (25% of the adult population; 50% of persons over 60 years old) Russian hypertensive 34% do not know how to treat correctly 12% know, but do not want to be treated 32% know, but are treated incorrectly 22% are treated right
6 slide
Description of the slide:
RISK FACTORS UNCORRECTED (IRREVERSIBLE) CORRECTABLE (REVERSIBLE) AGE AND GENDER men - over 55 years old women - over 65 years old
7 slide
Description of the slide:
In medicine, the term “CHARACTER OF HYPERTENSION” is already firmly rooted - a lover of going to bed late - exhausted to the limit at work - relieves stress with a cigarette or a lot of alcohol - a lover of tasty food - a master of sorting things out mainly by shouting - always excited and striving to "break through the walls with his forehead" - afraid of being late for something and not being able to do something
8 slide
Description of the slide:
The main symptom of hypertension is an increase in blood pressure. Subjective sensations or complaints appear after damage to the target organs. TARGET ORGANS HEART RETINA EYES BRAIN KIDNEY VESSELS
9 slide
Description of the slide:
HEART - left ventricular hypertrophy. Diagnosis: percussion increase in the boundaries of the heart, auscultatory - deafness of the first tone, accent of the second tone on the aorta. Additional research methods: ECG, R-graphy of the chest organs, ultrasound of the heart. BRAIN - cerebrovascular accident (motor and sensory disorders, speech disorders, swallowing, consciousness, etc.) KIDNEY - hypertensive nephropathy: sclerosis of the kidney vessels, leading to a decrease in the concentration function of the kidneys (nocturia, hypoisostenuria), in erythrocytes, protein. Subsequently, chronic renal failure may develop (delay in the body of metabolic products, namely toxic substances that are excreted in the urine, uremia develops). For diagnosis: additional research methods (urinalysis, biochemical blood test, Zimnitsky test (polyuria, oliguria anuria), nocturia, hypoisostenuria. Biochemical blood test: increased urea, creatinine. RETINA OF THE EYE - hypertensive retinopathy. Narrowing and tortuosity of the retinal arteries and veins develops , hemorrhages in the fundus.Later, degeneration of the optic nerve papilla develops in the form of white spots.All this can lead to complications such as retinal detachment and optic nerve atrophy with loss of vision.VESSELS - atherosclerosis.
10 slide
Description of the slide:
CLASSIFICATION OF ARTERIAL HYPERTENSION IN STAGES Stage I No objective signs of target organ damage Stage II At least one of the following manifestations of target organ damage is present: Left ventricular hypertrophy (according to x-ray, ECG or echocardiography); generalized or focal vasoconstriction of the retina; microalbuminuria, proteinuria and/or creatinimia 1.2-2.0 mg/dl; atherosclerotic changes (plaques) according to ultrasound examination or angiography (in the carotid arteries, aorta, iliac and femoral arteries). Stage III In addition to the listed signs of target organ damage, there are the following clinical manifestations. Heart: angina pectoris, myocardial infarction, heart failure. Brain: stroke, transient cerebrovascular accident. Hypertensive encephalopathy. vascular dementia. Retina: hemorrhages or exudates with or without edema of the optic nerve. These signs are characteristic of malignant and rapidly progressive arterial hypertension. Kidneys: Plasma creatinine more than 2 mg/dl. Renal failure. Vessels: exfoliating aortic aneurysm, occlusive lesions of the arteries with clinical manifestations.
11 slide
Description of the slide:
BP classification by BP level BP category systolic (mm Hg) BP diastolic (mm Hg) Optimal< 120 < 80 Нормальное < 130 < 85 Высоко нормальное 130 - 139 85 - 89 ГИПЕРТЕНЗИЯ: Степень 1 140 - 159 90 - 99 Степень 2 160 - 179 100 - 109 Степень 3 >180 > 110 ISOLATED SYSTOLIC HYPERTENSION > 140< 90
12 slide
Description of the slide:
RISK STRATIFICATION BP (mmHg) Other risk factors Grade 1 140-159 / 90-99 Grade 2 160-179 / 100-109 Grade 3 > 180 / > 110 COMPLICATIONS I - no RF Low risk< 15% Средний риск 15 – 20% Высокий риск 20 – 30% II – 1 -2 ФР (кроме диабета) Средний риск 15 – 20% Средний риск 15 – 20% Очень высокий риск >30% III - 3 or more RFs or target organ involvement or diabetes High risk 20 - 30% Moderate risk 15 - 20% Very high risk > 30% IV - AD clinical manifestations Very high risk > 30% Very high risk > 30% Very high risk > 30%
13 slide
Description of the slide:
14 slide
Description of the slide:
COMPLICATIONS OF ARTERIAL HYPERTENSION Chronic heart failure Acute left ventricular failure Myocardial infarction Dissecting aortic aneurysm Angina pectoris Visual impairment Blindness Renal failure Stroke
15 slide
Description of the slide:
TREATMENT OF HYPERTENSION Goal of therapy: The main goal of treatment is to achieve the target level of blood pressure.< 140/90 мм.рт.ст. АД < 130/85 мм.рт.ст. (при сахарном диабете) АД < 125/75 мм.рт.ст. (при ХПН) Достижение целевого уровня АД должно быть постепенным и хорошо переноситься пациентом. Если пациент отнесен к высокому и очень высокому риску, то незамедлительно начинают медикаментозную терапию. При низком и среднем риске рекомендуется изменение образа жизни в течение 3-4 месяцев; при неэффективности начать медикаментозное лечение.
16 slide
Description of the slide:
Reduce elevated blood pressure levels to TARGETS Improve quality of life, reduce changes in target organs Final goal- reduce the risk of complications
17 slide
Description of the slide:
18 slide
Description of the slide:
MEDICATIONAL THERAPY It is necessary to reduce blood pressure to the target gradually over 4-6 weeks, otherwise the quality of life worsens and complications from the target organs occur (the brain suffers, blood circulation is disturbed) They are well treated: severe arterial hypertension, women, high level of education, high income, a high level of culture, married. Poorly treated: smokers, alcoholics, repeated treatment, consuming a lot of salt.
19 slide
Description of the slide:
HYPOTENSIVE DRUGS Diuretics Hypothiazid, Veroshpiron ß - blockers Atenol, Concor Calcium antagonists Verapamil, Corinfar (Nifedipine) ACE inhibitors Enalapril, Kapoten, Enap adrenoblockers Prazosin Angiotensin II receptor antagonists Losartan Centrally acting drugs Clonidine, Clonidine
20 slide
Description of the slide:
INDICATIONS FOR HOSPITALIZATION - Uncertainty of the diagnosis and the need for special research methods to clarify the form of arterial hypertension - Difficulty in the selection of drug therapy (frequent crises, resistance to ongoing therapy).
21 slide
Description of the slide:
INDICATIONS FOR EMERGENCY HOSPITALIZATION - Hypertensive crisis that does not stop at the prehospital stage - Complications of arterial hypertension requiring intensive care and constant medical supervision (stroke, acute visual impairment, myocardial infarction, pulmonary edema, etc.)
22 slide
Description of the slide:
HYPERTENSION CRISIS (HC) is a pathological condition that manifests itself as a sharp deterioration in well-being against the background of an increase in blood pressure, accompanied by the appearance or aggravation of existing cerebral and (or) cardiac symptoms and requires urgent treatment.
23 slide
Description of the slide:
ETIOLOGY OF HYPERTENSION CRISIS I. Diseases causing II. Endogenous Exogenous critical hypertensive provoking factors of the condition Primary (essential) arterial hypertension (AH) or hypertension (EH) Exacerbation of concomitant diseases (osteochondrosis, etc.) Stress and exercise Pheochromocytoma Excessive release of renin Salt abuse Diencephalic syndrome Acute or chronic ischemia of the brain Alcohol excess Acute and chronic glomerulonephritis Transient increase in secondary aldosteronism with sodium and water retention during the period of hormonal adjustment Meteorological changes Chronic pyelonephritis Discontinuation of antihypertensive treatment Colds Influence of other drugs
24 slide
Description of the slide:
MAIN HAZARDS of GC Local cerebral ischemia due to arteriolospasm Increased cerebrovascular permeability Increased intravascular pressure Increased risk of ischemic stroke Hypertensive encephalopathy Increased risk of vascular rupture (cerebral hemorrhage, aortic dissection, nosebleeds, etc.) Increased afterload (afterload), increased myocardial consumption oxygen, activation of the reninangiotensin system Increased risk of cerebral edema Decreased renal blood flow (arteriolospasm) Increased risk of acute left ventricular failure, heart rhythm disturbances, myocardial ischemia (focal necrosis) Increased risk of kidney failure
25 slide
Description of the slide:
IN THE PATHOGENESIS OF GC, the following is distinguished: vascular mechanism - an increase in total peripheral resistance as a result of an increase in vasomotor (neurohumoral influence) and basal (with sodium retention) arteriolar tone; cardiac mechanism - an increase in cardiac output, myocardial contractility and ejection fraction in response to an increase in heart rate (HR), circulating blood volume.
26 slide
Description of the slide:
CLASSIFICATION GK CLASSIFICATION I. AN Golikova II. M. S. Kushakovsky III. A. L. Myasnikov - N. A. Ratner IV. I. N. Bokareva Hyperkinetic Eukinetic Hypokinetic Neurovegetative Water-salt Convulsive (hypertensive encephalopathy) The first type (adrenal) The second type (noradrenal) uncomplicated complicated Cerebral Cardioischemic With acute left ventricular failure With dissecting aortic aneurysm With eye structures damage With kidney damage
27 slide
Description of the slide:
CAUSES OF CRISES Stress Excessive exercise Alcohol and tobacco abuse Abrupt withdrawal of antihypertensive drugs Inadequate therapy in women crises occur 6 times more often than in men
28 slide
Description of the slide:
COMPLAINTS OF PATIENTS WITH GC Cerebral Cardiac Symptoms of neurotic and autonomic dysfunction intense headache dizziness nausea, vomiting visual impairment, transient blindness, double vision, flickering of "flies" before the eyes development of focal cerebral symptoms: numbness and / or decrease in pain sensitivity of the tongue, lips, skin of the face and hands, a feeling of crawling, the appearance of weakness in the limbs transient hemiparesis (up to one day), short-term aphasia convulsions pain in the heart area palpitations feeling of interruptions shortness of breath chills a feeling of fear, irritability sweating, sometimes a feeling of heat thirst at the end of a crisis - rapid, profuse urination with clear urine
29 slide
Description of the slide:
TYPE I CRISIS (HYPERKINETIC) - acute rapid development of a crisis - duration of a minute, hours (rarely up to a day) - complaints of headaches, palpitations, tremors throughout the body, excessive sweating, cold extremities, dry mouth - on examination - hand tremor, skin integuments of increased humidity, extremities are cold to the touch - heart rate is 80 per minute, blood pressure is predominantly increased systolic, pulse pressure increases - abundant urination at the end of the crisis - develops in the early stages of arterial hypertension - complications are not typical
30 slide
Description of the slide:
CRISIS TYPE II (HYPOKINETIC) - gradual development of a crisis - the duration of the crisis is long (from several hours to several days) - complaints of severe headaches, heaviness in the head, nausea, vomiting, transient visual disturbances, noise, ringing in the ears, constricting pain in areas of the heart, drowsiness, lethargy - disorientation, confusion - heart rate 60-80 per minute, blood pressure is dominated by an increase in diastolic pressure, pulse pressure decreases - in the later stages of hypertension develops against the background of the initial high blood pressure - possible complications: stroke, myocardial infarction, angina pectoris , cardiac asthma, etc.
Definition of GB;
Reasons for the development of GB;
Risk factors for developing GB;
Clinical picture of GB;
Complication of GB;
Definition of HA;
Clinical picture of GC;
Complications of GC;
Diagnosis of GB;
GB treatment;
Prevention of GB;
Classification of blood pressure;
terms;
Download:
Preview:
To use the preview of presentations, create an account for yourself ( account) Google and sign in: https://accounts.google.com
Slides captions:
Hypertonic disease
Hypertension is a pathology of the cardiovascular apparatus that develops as a result of dysfunction of the higher centers of vascular regulation, neurohumoral and renal mechanisms and leads to arterial hypertension, functional and organic changes in the heart, central nervous system and kidneys, characterized by a persistent increase in blood pressure from 140/90 mm Hg. Art. and higher.
Causes of GB development: CNS overstrain; Heredity.
Risk factors for developing GB: Smoking; alcohol consumption; The use of table salt in large quantities; Lack of sleep; CNS injury; stress; Obesity; Physical inactivity.
Clinical picture of GB: Headache (usually in the occipital region); Dizziness; Noise in ears; palpitations; visual impairment; Sleep disorder; Weakness; Unpleasant sensations in the region of the heart; Nausea; Shortness of breath on exertion.
Complication of GB: Hypertensive crisis
A hypertensive crisis is an urgent serious condition caused by an excessive increase in blood pressure, manifested by a clinical picture of target organ damage (in the case of a complicated crisis) and involving an immediate decrease in blood pressure to prevent damage to third-party organs.
The clinical picture of GC: Increased systolic blood pressure> 140 mm Hg. Art. -> 200 mmHg Art.; Sharp headache; Dyspnea; Dizziness; Pain in the chest; Redness of the face, chest; "Mushki", flashing before the eyes; Noise, ringing, squeaking in the ears, deafness; Neurological disorders: vomiting, convulsions, impaired consciousness, in some cases clouding of consciousness, strokes and paralysis. A hypertensive crisis can be fatal.
Complications of GC: Stroke; heart attack; Cardiac and renal failure;
Diagnosis of GB: Control of blood pressure; Collection of anamnesis; Physical examination; Electrocardiogram; Echocardiogram; arteriography; Dopplerography; Blood chemistry; General urine analysis; Ultrasound of the thyroid gland.
Treatment of HD: ATS diet 1 (restriction of salt, liquid, alcohol, smoking; elimination of fatty, fried foods); Optimal working and rest conditions (work only during the day shift, without exposure to noise, vibration, excessive stress); Acupuncture; Physiotherapy; Phytotherapy; Beta-blockers; Diuretics; Ca antagonists; ACE inhibitors.
Prevention: Primary: Elimination of risk factors for the development of GB; Restriction in food of salt and fats; healthy image life; 2. Secondary: Phytotherapy; exercise therapy; Spa treatment.
BP classification: Optimal BP: SBP
Terms: GB - hypertension; AH, arterial hypertension; HC - hypertensive crisis; BP - blood pressure; SBP - systolic blood pressure; DBP, diastolic blood pressure; SG - systolic hypertension.
References: https://ru.wikipedia.org/wiki/%C0%F0%F2%E5%F0%E8%E0%EB%FC%ED%E0%FF_% E3%E8%EF%E5%F0 %F2%E5%ED%E7%E8%FF BF%D0%B5%D1%80%D1%82%D0%BE%D0%BD%D0%B8%D1%87%D0%B5%D1%81%D0%BA%D0%B8%D0%B9_% D0%BA%D1%80%D0%B8%D0%B7 Lectures.
Performed by a student of group 1-III MSO GBOU SPO "MU No. 1 DZM" Vedyaeva Evgenia
Thank you for attention!
On the topic: methodological developments, presentations and notes
The presentation presents the issues of general epizootology in fish diseases. The definition of epizootology, the manifestation of the epizootic process, the occurrence and course of epizootics, sources, factors are given.
Presentation for the Methodological development of the lecture: "Nursing care for hypertension" 12. 2016
Presentation to methodological development lecture session "Nursing care for hypertension" was prepared in accordance with work program section interdisciplinary course: "Sisterly...
Presentation on the topic "treatment of blood diseases in children" for conducting theoretical classes on MDT 02.04. Treatment of pediatric patients...
Arterial hypertension is a symptom of many diseases. There are primary arterial hypertension, or hypertension (essential hypertension), as well as secondary (symptomatic) hypertension, for example, arterial hypertension with glomerulonephritis and nephrotic syndrome (renal hypertension), with narrowing of the renal arteries (renovascular hypertension), pheochromocytoma, hyperaldosteronism, etc.
In all cases, seek to cure the underlying disease. But even if this fails, arterial hypertension should be eliminated, since arterial hypertension contributes to the development of atherosclerosis, angina pectoris, myocardial infarction, heart failure, visual impairment, and impaired renal function. A sharp increase in blood pressure - a hypertensive crisis can lead to bleeding in the brain (hemorrhagic stroke). In different diseases, the causes of arterial hypertension are different. and we will consider these reasons in this article.
Definition
Arterial hypertension (AH) is a persistent increase in blood pressure (BP) - systolic up to 160 mm. rt. Art. and above, diastolic up to 95 mm. rt. Art. and higher.
Systolic blood pressure in the range of 140-159 mm Hg. and diastolic blood pressure 90-94 mm Hg. refer to "transitional" pressure.
Types of arterial hypertension:
I. according to the initial mechanism of development:
A. general (systemic) hypertension:
- Neurogenic:
a) centrogenous
b) reflex
- Endocrine - due to endocrinopathies:
a) adrenal glands
b) thyroid gland
- Metabolic (hypoxic, ischemic):
- ischemic (renal and cerebroischemic)
- venous congestive
- hypoxic (without primary disturbance in organs and tissues)
- Hemic - due to an increase in the volume and / or viscosity of the blood
- mixed
B. Local (regional) AGs (in individual main vessels or regions of the vascular wall of the body)
II. Change in cardiac output:
- hyperkinetic - hypertension with increased cardiac output with normal or reduced tone of resistant vessels.
- hypokinetic - arterial hypertension with reduced cardiac output, but a significantly increased tone of resistant vessels.
- eukinetic - hypertension with normal cardiac output and increased vascular resistance.
III. By type of predominant increase in blood pressure:
- "Systolic" AH
- "Diastolic" AH
- "Systolo-diastolic" AH
IV. By the nature of the clinical course:
- "benign" hypertension - with slow development, an increase in both systolic and diastolic blood pressure, as a rule, eukinetic
- "Malignant" hypertension - rapidly progressive, with a predominant increase in diastolic blood pressure, as a rule, hypokinetic, less often - hyperkinetic (especially at the initial stage).
Etiology and pathogenesis of arterial hypertension
1.Centrogenic hypertension
Cortical and subcortical neurons, nerve centers involved in the regulation of blood pressure, are a complex functional association consisting of two multicomponent neuronal systems: pressor-hypertensive and depressor-hypotensive.
The main structure that regulates the level of systemic blood pressure in the body is the cardiovasomotor (vascular-motor) center.
Its efferent influences alter both vascular tone and heart function.
The number of "pressor" neurons in the cardiovasomotor center is approximately 4 times greater than the number of "depressor" neurons.
Causes of hypertension of central origin:
- functional disorders of higher nervous activity,
- organic lesions of brain structures that regulate systemic hemodynamics
The mechanism of development of hypertension associated with a violation of the GNA - neurosis:
The action of a causative factor (stressor) → overstrain and often disruption of cortical nervous processes - excitation and inhibition, disturbances in their balance and mobility → development of a neurotic state (neurosis) → formation of a cortical-subcortical excitation complex (excitation dominant) with the involvement of the sympathetic nuclei of the posterior hypothalamus , adrenergic structures of the reticular formation and the cardiovasomotor center → increased sympathetic influences on organs and tissues, manifested by the release of excess adrenaline and noradrenaline → increased tone of the walls of arterial vessels + stimulation of the heart, increased shock and minute blood output → increased systolic and diastolic blood pressure.
At the same time, the excitation of the subcortical centers causes excessive activation of other systems, in particular, the hypothalamus-pituitary-adrenals system.
This is accompanied by an increase in the production and concentration in the blood of physiologically active substances with a hypertensive effect: vasopressin, ADH, corticosteroids (mineral and glucocorticoids), catecholamines. The action of these substances causes narrowing of arterioles, an increase in cardiac output, which leads to an increase in blood pressure.
2. Centrogenic hypertension - as a result of organic damage to brain structures involved in the regulation of blood pressure levels.
The reasons:
- tumor compression of the brain
- trauma (concussion),
- hemorrhage,
- inflammatory process (encephalitis)
These factors can directly damage the structures involved in the regulation of blood pressure levels (sympathetic nuclei of the hypothalamus, structures of the reticular formation, cardiovasomotor center) and cause their ischemia.
The hypothalamus-pituitary-adrenals system can also be activated, which leads to an increase in vascular tone, heart function and the formation of hypertension.
3. Conditioned reflex hypertension
The repeated combination of the action of indifferent ("conditional") agents with irritants that cause hypertension.
4. Unconditioned reflex hypertension
- as a result of chronic irritation of the extero- and interoceptors or nerve trunks (damage or inflammation of the trigeminal, facial, sciatic nerve)
- due to the cessation of afferent impulses, which normally has an inhibitory effect ("depressor") effect on the tonic activity of the cardiovasomotor (pressor) center
Normally, even slight fluctuations in blood pressure cause an increase (with an increase in blood pressure) or a decrease (with a decrease in blood pressure) of "depressor" impulses.
Restraint receptors that respond to their stretch are located in various regions of the vascular system.
To the greatest extent - in the region of the aortic arch and branching of the carotid artery - the carotid sinus.
A long-term decrease or cessation of "depressor" impulses "releases" the cardiovasomotor center from restraining influences and can lead to the development of hypertension.
The reasons:
- damage to the baroreceptors of the aortic arch and / or carotid sinus (as a result of intoxication, trauma, infection)
- decrease in the extensibility of the walls of the aorta or carotid artery (with the functional safety of baroreceptors) due to atherosclerotic changes in them, calcification
- disturbances in the conduction of afferent impulses as a result of damage to the nerve trunks (tumor, trauma, inflammation)
- adaptation (“addiction”) of baroreceptors to a long-term elevated blood pressure, which they begin to perceive as normal.
5. Endocrine hypertension
Mechanisms:
- are implemented in connection with an increase in the production and (or) activity of hormones with a hypertensive effect,
- due to an increase in the sensitivity of blood vessels and the heart to their influences
6. AH in adrenal endocrinopathies
- "corticosteroid" caused by overproduction of mineralocorticoids or glucocorticoids
- "catecholamine" adrenal hypertension develop in connection with a significant chronic increase in blood levels of catecholamines - adrenaline and norepinephrine, produced in the adrenal medulla.
Cause- tumor of the adrenal medulla - pheochromocytoma
The mechanism of hypertensive action of excess catecholamines: increase under their influence of vascular tone and heart function.
Norepinephrine stimulates mainly α-adrenergic receptors, and, to a lesser extent, β-adrenergic receptors, leading to an increase in blood pressure due to a vasoconstrictor effect.
Adrenaline acts on both α- and β-adrenergic receptors.
In this regard, not only vasoconstriction is observed, but also the work of the heart increases significantly (due to the positive chrono- and inotropic effect).
- "Mineralocorticoid" AG due to overproduction of aldosterone
Cause hyperplasia or tumor of the adrenal cortex
The development of hypertension in hyperaldosteronism is based on the implementation of its effects: renal (renal) and extrarenal (extrarenal)
Renal effect of aldosterone:
Hyperproduction of aldosterone → reabsorption of excess sodium ions (in exchange for K ions) from provisional urine in the distal tubules of the kidneys → increase in sodium concentration in blood plasma → its hyperosmia → activation of vascular osmoreceptors → stimulation of the process of neurosecretion of ADH in the nuclei of the hypothalamus and its release into the blood → proportional to hyperosmia reabsorption of fluid in the tubules of the kidneys → normalization (temporary) of osmotic homeostasis + increase in the volume of circulating and extracellular fluid + increase in cardiac output → increase in blood pressure.
Extrarenal effect of aldosterone:
Hyperproduction of aldosterone → increase in the permeability of cell membranes for sodium ions → accumulation of excess sodium in the cells of tissues and organs, combined with a decrease in their level of K and an increase in its concentration in the extracellular fluid → cell swelling, incl. walls of blood vessels + narrowing of their lumen + increase in their tone + increase in the sensitivity of blood vessels and the heart to the action of agents with a hypertensive effect (catecholamines, vasopressin, AT-II, prostaglandides) → AD.
- "Glucocorticoid" AG- a consequence of hyperproduction of glucocorticoids (cortisone, hydrocortisone), which is combined, as a rule, with an increase in the level of aldosterone in the blood.
The reasons:
- hyperplasia or hormonal tumors of the adrenal cortex - corticosteromas - Itsenko-Cushing's syndrome
- a consequence of prolonged administration of large doses of glucocorticoids to patients (after transplantation of a homotransplant, in the treatment of diffuse lesions of the connective tissue of immuno-allergic genesis: systemic lupus erythematosus, scleroderma).
The mechanism of development of hypertension in Itsenko-Cushing's syndrome:
- Glucocorticoids have a direct hypertensive effect (without changing sodium in the blood and cells of organs and tissues),
- at high concentration in blood plasma, there is an increase in the sensitivity of blood vessels to the vasoconstrictor action of catecholamines
- have a mineralocorticoid (aldosterone-like) effect
7. AH in hyperthyroid states
A prolonged increase in the blood levels of iodine-containing thyroid hormones (thyroxine, triiodothyronine) and / or an increase in the sensitivity of tissues to them is accompanied by the development of arterial hypertension.
The development of hypertension in hyperthyroid states is based on the cardiotonic effect of thyroxine and triiodothyronine, which is manifested by a significant increase in cardiac output.
This is achieved due to pronounced tachycardia (due to a positive chronotropic effect), an increase in stroke output (due to the positive inotropic effect of thyroid hormones).
In this regard, AH in hyperthyroid states are hyperkinetic in nature.
Along with high systolic blood pressure, normal or even low diastolic pressure is often observed.
This is due to:
- compensatory effect (in response to an increase in cardiac output) expansion of resistant vessels,
- direct damaging effect of excess thyroid hormones on the vascular walls.
It is manifested by a weakening of vascular tone and a decrease in the resistance of resistant vessels.
8. Hypertension in disorders of the function of the hypothalamic-pituitary system
An increase in the production and incretion of ACTH by the cells of the anterior pituitary causes the development of Itsenko-Cushing's disease, one of the components of which is arterial hypertension.
The reasons:
- hyperplasia or tumor of the basophilic cells of the anterior pituitary gland,
- an increase in the production of corticotropin-releasing factor by hypothalamic neurons, which is accompanied by hypersecretion of ACTH.
- The development of hypertension with an increase in the blood level of ACTH is the result of hyperproduction of gluco- and mineralocorticoids by the adrenal cortex
9. Metabolic hypertension ("hypoxic", "organ-ischemic" hypertension)
Pathogenesis: a metabolic disorder that occurs with circulatory disorders and hypoxia of various internal organs.
Activation of the processes of synthesis of metabolites with a pressor effect, combined with a violation of the production of metabolites with a depressant effect, as well as, as a rule, an increase in the sensitivity of heart and vascular receptors to pressor effects.
Metabolites with hypertensive effect: biogenic amines (catecholamines, serotonin), vasopressin, angiotensin II, group F prostaglandins, aldosterone, thyroxine.
Metabolites with hypotensive action: histamine, γ-aminobutyric acid, acetylcholine, bradykinin, kallidin, prostaglandins groups A, E, J, adenosine
10. Renal hypertension
The kidneys take part in the work of the pressor-hypertensive and depressor-hypotensive systems of the body.
In this regard, chronic renal disease is often accompanied by the development of hypertension.
- Vasorenal (renovascular, renal ischemic)
The reason is a decrease in blood perfusion pressure in the vessels of the kidneys due to:
- compression of the main renal arteries from the outside
- narrowing or completely closing them from the inside
- hypovolemia (posthemorrhagic, burn disease)
- compression of the branches of the renal artery in the kidney itself during inflammatory processes in its parenchyma (glomerulonephritis).
Mechanism:
A decrease in the volume of flowing blood is perceived by specialized receptors - volume receptors of the JGA cells of the kidneys → an increase in the production of renin in JGA cells → angiotensin I → angiotensin II
AT II has a number of effects leading to an increase in blood pressure:
- directly causes smooth muscle contraction of arterioles
- activates the release of catecholamines from vesicles of axons of sympathetic neurons
- increases the sensitivity of the vascular wall to catecholamines and other vasoconstrictor agents.
AT II stimulates the production and release into the blood from the cells of the adrenal cortex - aldosterone → activates the process of reabsorption of sodium ions from the primary urine in the distal tubules of the kidneys and excretion into the urine → osmoreceptors of the vascular bed are activated, neurosecretion of ADH and its release into the blood → increased permeability of the renal wall tubules for fluid → an increase in its volume in an already narrowed vascular bed → an increase in diastolic blood pressure → an increase in venous blood flow to the heart → an increase in stroke output → systolic blood pressure → arterial hypertension.
- Renoprivnaya
The reason is a decrease in the mass of the kidney parenchyma, which produces compounds with an antihypertensive effect, which are components of the depressor system of the body.
Depressor system components:
- vasodilating prostaglandids (groups I2 and E)
- kinins (bradykinin, kallidin)
Causes of a decrease in the mass of the kidneys:
- removal of part of the kidneys, one kidney
- necrosis,
- total nephrosclerosis,
- hydronephrosis,
- polycystic
Mechanism
- a decrease in the synthesis and release of prostaglandides and kinins into the blood.
11. Cerebroischemic hypertension
The reasons:
- violation of the blood supply to the brain, especially the oblong, in which the vasomotor center is located.
Mechanism
- increase in sympathetic pressor impulses
12. AH associated with an increase in blood volume and/or viscosity (hemic).
- wakez disease,
- polycythemia,
- erythrocytosis,
- hyperproteinemia
A persistent increase in blood pressure occurs due to an increase in the mass and volume of circulating blood, as well as blood viscosity.
Activation of the contractile function of the heart contributes to an increase in cardiac output and the development of hypertension
Conditions contributing to the development of hypertension (risk factors)
I hereditary predisposition
- systemic membranopathies - accumulation of excess calcium and sodium in myocytes
- receptor dysfunction - dominance of the effect of hypertensive agents
- violation of gene expression of endothelial cells - a decrease in the synthesis of vasodilators
II environmental factors
- excess salt in food
- intoxication
- occupational hazards
- brain injury
- accommodations
III Individual characteristics
- age after 30-40 years
- dominance of hypertensive reactions to various influences
- hypercholesterolemia
- male gender
- overweight
The main links of hypertension - 1
The main links of hypertension - 2
Stage I - the development of neurosis.
Activation of the centrogenic neurogenic link of pathogenesis, which includes the formation of a cortical-subcortical complex of stable excitation (sympathetic nuclei of the hypothalamus, adrenergic structures of the reticular formation, vascular-motor center).
Strengthening of pressor influences on the cardiovascular system through two channels:
1. neurogenic effects (activation of sympathetic nerve influences
2.humoral hypertensive effects (ADH, adrenaline, ACTH, gluco- and mineralocorticoids)
- increase in OPSS,
- venoconstriction
- increase in BCC,
- increase in cardiac output
Stage II - stabilization of blood pressure at a high level.
Mechanisms:
- Reflexogenic - a decrease in depressor impulses from baroreceptors of the aortic arch
- Endocrine - stimulation of the production of hormones with a hypertensive effect
- Metabolic - renal hypertensive mechanisms
- Hemic - polycythemia (due to hypoxia) and increased blood viscosity
Stage III - organic changes and damage to internal organs.
- atherosclerosis - heart attack, stroke
- sclerotic kidney disease
- dystrophic changes in other organs (brain, retina, heart)
You can download the presentation on this topic here>>> 