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Symptoms and syndromes in a rterial hypertension

Symptoms and syndromes in a rterial hypertension.

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Symptoms and syndromes in a rterial hypertension

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  1. Symptoms and syndromes in arterial hypertension

  2. Arterial hypertension is defined as rising of arterial blood pressure excess of 140 mm Hg systolic one (SBP), and/or excess of 90 mm Hg diastolic blood pressure (DBP). Recommendations from the Joint National Committee on the Prevention, Detection, Evaluation and treatment of High Blood Pressure (JNC-VI report) now regard a BP of 140/90 mm Hg as high normal and 130/85 mm Hg as normal.

  3. Epidemiology • Hypertension is one among the most wide-spread among all cardiovascular diseases. • 15 – 25 % of people in the population have hypertension + 15 % have bordeline hypertension. • Primary hypertensionoccupies 80 – 95 % of all arterial hypertensions and 10 % of them are secondary hypertensions.

  4. Essential, primary, or idiopathic hypertension is defined as high BP in which secondary causes forms are not present • Aetiology and pathogenesis: • Overstrain of the central nervous system • nervous-functional disorder in regulation of the vascular tone • vegetative-endocrine disorders and changes in the renal regulation of the vascular tone • vasopressor adrenal reaction by which arterioles of internal organs are narrowed • production of rennin, stimulation of rennin-angiotensin system and systemic vasodilatation • activation of aldosterone secretion.

  5. Pathogenesis of AH

  6. Risk-factors • Non-modified • Age • Genetics and family history • Sex( male or female) • Family and personal history of hyperlipidaemia • Family and personal history of diabetes • Race • Modified • Cigarette smoking, alkohol • Environment (stress, sedentary lifestyle) • Weight (obesity and metabolic syndrome) • Dietary habits (high alcohol intake, high sodium intake, low potassium intake) • Hypodinamia • Personality

  7. An assessment of dietary and lifestyle factors is important. Excessive alcohol use (more than three or four drinks per day) and a high sodium intake (typically defined by a urinary sodium excretion of more than 150 mmol per day) may contribute to resistant hypertension; the frequency of salt sensitivity is increased among patients who are at least 60 years of age, patients who are black or obese, and patients with renal impairment.

  8. Classification • According to blood pressure: - normal: SBP< 130 andDBP< 90 mm of Hg. - Bordeline hypertension: SBP = 140-160 andDBP = 90-95 mm of Hg; • Arterial hypertension:SBP> 160 andDBP> 95mm of Hg.

  9. WHPO classification of arterial hypertension (1993) Stage I – no evident signs of target organ damage Stage II – presence of at least one of the following signs of target organ damage: Heart: LVH (diagnosed radiologically, on ECG or by Echocardiography) Retina: generalized or focal narrowing of retinal arteries Kidney: microalbuminurua, proteinuria, creatinine<2mg/dl (176 µmol/l) Vessels: increased IMT or plaques in carotid, iliac, or femoral arteries Stage III – signs of severe target organ damage: Heart: angina pectoris, myocardial infarction, heart failure Brain: stroke, TIA, vascular dementia Retina: haemorrhages, exudates, papilloedema Kidney: renal insufficiency (creatinine>2mg/ml) Vessels: dissecting aortic aneurysm, symptomatic occlusive peripheral arterial disease

  10. Past medical history • Duration and previous level of high BP • Indications of secondary hypertension • Family history of renal disease (polycystic kidney) • Renal disease, UTI, haematuria, analgesic abuse (parenchymal renal disease) • Drug/substance intake: oral contraceptives, liquorice, nasal drops, cocaine, steroids, NSAID’s, erythropoietin, cyclosporin • Episodes of sweating, headache, anxiety, palpitation (phaeochromocytoma) • Episodes of muscle weakness (aldosteronism) • Risk factors • Symptoms of organ damage • Previous antihypertensive therapy (drugs used, efficacy, adverse effects) • Personal, family, environmental factors

  11. Manifestation of hypertension depends on: Course of the disease Its stage; Presence of complications and crises; Pathogenetic variant(benign and maligant). Clinical manifestation • The main objective sign of the disease is elevated arterial pressure (over 140/90 mm Hg) . Blood pressure is liable in early stage of the disease but later stabilizes.

  12. I stage Complaints: • may be abcent • patients would usually complain of neurotic disorders: general weakness, impaired work capacity, inability to concentrate during work, deranged sleep, trancient headache, e feeling of heaviness in the heart, vertigo, noise in the ears, and sometimes palpitation, hain in heart region. Exertional dyspnoea develops later. Data of objective examination • Signs if lesions of internal organs are abcent • Stable or trancient elevation of BP

  13. II stage Complaints • headache • Dizziness • Pain in heart region • Exertional dyspnoea • Presence of hpertonic crises • Data of obyective examination: rddness of skin, sweating, decreased tolerance to physical load. • Palpation: Ps – firm and tense, fast. Apex beatis expanded and displaced leftward and downward. • Percussion: widened vascular bundle, displacement of the left border of relative cardiac dullness. • Auscultation: The second heart sound is accentuated over the aorta. Systolic murmur over heart apex • There are signs of internal ograns without functional disorders: • Hypertrophty of the left ventricle (according to data of ECG and X-ray, ultrasound examination). • Generalized or focal narrowing of retinal vessels. • Microalbumiuria, proteinuria and/ormild elevation of blood plasma creatinin (up to 177 mkm/l).

  14. III stage • High, stable elevation of BP • Development of complications: • Myocardial infarction • Heart failure • Insult • Trancient ischemic attack • Retinal hemorrhage • Dissecting aortic aneurism

  15. The set if obvious examinations: • Complete blood count; • Urinalyses; - Biochemical blood serum tests; • Urine analyses ny Nechyporenco and Zymnitsky; - ECG, ultrasound of a heart; - ultrasound of kidneys; - chestX-ray; - Ophthalmoskopy.

  16. Complete blood count and biochemical lab tests: - In I stage there are no changes; • During crisis – trancient leucocitosis, dys- and hyperlipidemia, elevated level of K+, creatinin and urea • In III stage – stable changes, azotaemia. • Examination of urine: • In III stage isohyposthenuria, nicturia

  17. ECG • І st. – specific signs are abcent. • ІІ – ІІІ st . – hypertrophy of the left ventricle, heart electrical axis is deviated leftward, Rv5-6>Rv4, elevation of ST, biphasic Т (+-) Increased amplitude of Rin left leads and S - in right leads.

  18. ECG in hypertrophy of the left ventricle

  19. Ultrasoung examination of hypertensive heart (B- and M-modes)

  20. Left-ventricular hypretrophy on X-ray

  21. Symptoms of organs damage • Heart: palpitations, chest pain, shortness of breath, swollen ankles • Brain and eyes: headaches, vertigo, impaired vision, TIA’s, sensory or motor deficit • Kidney: thirst, polyuria, nocturia, haematuria • Peripheral arteries: cold extremities, intermittent claudication • Brain: murmurs over neck arteries, motor or sensory deficits • Eyes: funduscopic abnormalities • Heart: location and characteristics of apical impulse, abnormal cardiac rhythms, ventricular gallop, pulmonary rales, peripheral oedema • Peripheral arteries: absence, reduction, or asymmetry of pulses, cold extremities, ischaemic skin lesions

  22. Damage to internal organs • The adverse effects of hypertension principally involve the blood vessels, the central nervous system, the retina, the heart and the kidneys, and can often be detected by simple clinical means. • Blood vessels • In larger arteries (over 1 mm in diameter) the internal elastic lamina is thickened, smooth muscle is hypertrophied and fibrous tissue is deposited. The vessels dilate and become tortuous and their walls become less compliant. • Central nervous system • Stroke is a common complication of hypertension and may be due to cerebral haemorrhage or cerebral infarction. Hypertensive encephalopathy is a rare condition characterised by high blood pressure and neurological symptoms, including transient disturbances of speech or vision, paraesthesiae, disorientation, fits and loss of consciousness. • Kidneys • Long-standing hypertension may cause proteinuria and progressive renal failure by damaging the renal vasculature.

  23. I degree: Arteriolar thickening, tortuosity and increased reflectiveness ('silver wiring') II degree: plus constriction of veins at arterial crossings ('arteriovenous nipping') III degree: plus evidence of retinal ischaemia (flame-shaped or blot haemorrhages and 'cotton wool' exudates) IV degree: plus papilloedema HYPERTENSIVE RETINOPATHY

  24. Hypertensive retinopaty

  25. Heart • The excess cardiac mortality and morbidity associated with hypertension is largely due to a higher incidence of coronary artery disease. High blood pressure places a pressure load on the heart and may lead to left ventricular hypertrophy with a forceful apex beat and fourth heart sound. • Atrial fibrillation is common and may be due to diastolic dysfunction caused by left ventricular hypertrophy or the effects of coronary artery disease. • Severe hypertension can cause left ventricular failure in the absence of coronary artery disease, particularly when renal function, and therefore sodium excretion, is impaired.

  26. Secondary hypertensionCAUSES OF SECONDARY HYPERTENSION • Alcohol • Pregnancy (pre-eclampsia) • Renal disease • • Renal vascular disease • • Parenchymal renal disease, particularly glomerulonephritis • • Polycystic kidney disease • Endocrine disease • Phaeochromocytoma • Cushing's syndrome • Primary hyperaldosteronism (Conn's syndrome) • Hyperparathyroidism • Acromegaly • Primary hypothyroidism • Thyrotoxicosis • Congenital adrenal hyperplasia due to 11 -p-hydroxylase or • 17-hydroxylase deficiency

  27. Classification of secondary hypertension • Renoparenchimatous (pyelonephritis, glomerulonephritis) or renovascular (renal artery stenosis) disease • Endocrine disease (Phaeochomocytoma, Cusings syndrome, Conn’s syndrome, Acromegaly and hypothyroidism etc.) • Due to disorders of emodynamics (coarctation of the aorta, heart valvular diseases, atherosclerosis) • Neurogenic (brain commotion, tumor etc.) • Induced by exogenic factors (noise, heat etc.) • Complication of pregnancy • Iatrogenic: • hypertensions induces by surgical treatment • Hormonal / oral contraceptive, corticosteroids etc.

  28. Differential features of symptomatic hypertension • Age less than 20 years or more than 60; • quick elevation of BP and its stable high level • very high BP (> 220/120 mm of Hg); • - malignant course of hypertension; • - sympathoadrenal crisesеs; • - renal diseases in anamnesis; • - development of hypertension during pregnancy; • - appearance of changes in patient’s urine.

  29. Features of secondary hypentensions • Renoparenchimatous: - acute and chronic pyelonephritis, glomerulonephritis - nephritis in collagenoses (endarteriiris nodosa, lupus erytematodus, scleroderma etc); - Development of AH is possible in unilateral lesion (nephrolothiasis, hydronephris, cancer) Special appention is paid for anamnesis and data of objective examination • Endocrine hypertension • Develops in 2- 3 % of cases. • They are combined with: • Sympathoadrenal crises; • myasthenia; • changes in urine; • abecity; • thyrotoxicosis.

  30. Hemodynamic hypertensions • Are combined with dieases of heart and vessels. Main causes: • Atherosclerosis of aorta; coarctation of aorta, aortal incompetence, open aortal duct; • Complete AV block; • erhthraemia, • Bronchial asthma; • Heart failure • There AH are easly diagnosed whe the patient is exemined completely.

  31. Hypertensive crisis • Essential hypertension is characterized by periodically recurring trancient elevations of arterial pressure (hypertensive crisis). Development of such crises is preceded by psychic traumas, nervous overstrain, variations in atmospheric pressure, etc. • Hypertensive crisis develops with a sudden elevation of the arterial pressure that can persist from a few hours to several days. The crisis is manifested by sharp headache, feeling of heat, perspiration, palpitation, giddiness, piercing pain in the heart, sometimes by deranged vision, nausea, aid vomiting. In severe crisis, the patient may lose consciousness. The patient is excited, haunted by fears, or is indifferent, somnolent, and inhibited. Auscultation of the heart reveals accentuated second sound over the aorta, and also tachycardia. The pulse is accelerated but can remain unchanged or even decelerated; its tension increases. Arterial pressure increases significantly. ECG shows decreased S-T interval and flattening of the T wave. In the late stages of the disease, with organic changes in the vessels, cerebral circulation may be deranged during crisis; myocardial infarction and acute left-ventricular failure may also develop.

  32. Complications of hypertonic crisis • Cardial: - acute or chronic heart failure; - accelerated development of atherosclerosis of caoronary arteries followed by symptoms of angina pectoris and myocardial infarction; - arrhythmias. • Aortal: - atherosclerosis ; - dissecting aortal aneurism.

  33. Cerebral: - atherosclerosis of cerebral vessels and impaired cerebral circulation (encephalopathy); - dynamic and organic disorders of brain circulation і органічні Ocular: - retinal hemorrhage and its separation; - decreased vision (edema of ophthalmic nerve).

  34. TreatmentModification of life-style • Diet (Decreased salt intake to 4-6 g/day, alkohol, animal fats). • Decreased body weight. • Avoiding of smoking. • Dynamical physical examinations. • Phytotherapy, acopuncture, psychtherapy, authotrening • Influence of modification of life-style of the course of the disease: • Decreased body weight - 5-20 mm of Hg/10 kg of lost weight • Diet – 8-14 mm of Hg • Decreased salt intake (6 g per day) – 2-8 mm of Hg • Physical activity (30 min per day) – 4-9 mm of Hg • Decreased alkohol consumption (to 1 ounce per day) – 2-4 mm of Hg

  35. Appropriate lifestyle measures may obviate the need for drug therapy in patients with borderline hypertension, reduce the dose and/or the number of drugs required in patients with established hypertension, and directly reduce cardiovascular risk. • Correcting obesity, reducing alcohol intake, restricting salt intake, taking regular physical exercise and increasing consumption of fruit and vegetables can all lower blood pressure. Moreover, quitting smoking, eating oily fish and adopting a diet that is low in saturated fat may produce further reductions in cardiovascular risk.

  36. Aims of antihypertensive medicamentous therapy • Immediate:achieve target BP levels • Intermediate: prevent target organs disfuction (TOD) or regression of TOD • Final: improve long-term prognosis

  37. Main groups of hypertensive drugs • Diuretics • -blockers • Ca- channels antagonists • Angiotensine-converting enzyme inhibitors • Blockers of angiotensine-II receptors • ά1-adrenoblochers

  38. Long-acting CCB Beta-blocker* Thiazide diuretic ACE-I ARB TARGET <140 mm Hg systolic and < 90 mmHg diastolic Lifestyle modification therapy Dual Combination Triple or Quadruple Therapy * Not indicated as first line therapy over 60

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