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Hypertension

Hypertension. Definition. Sustained elevated blood pressure in a quiet state is called- hypertension. Diagnostic criteria proposed by WHO. systolic pressure. diastolic pressure. classify. Normal BP. <140 mmHg. <90 mmHg. 140-159 mmHg. 90-99mmHg. Grade 1 hypertension.

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Hypertension

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  1. Hypertension

  2. Definition Sustainedelevated blood pressure in a quiet state is called- hypertension Diagnostic criteria proposed by WHO systolic pressure diastolic pressure classify Normal BP <140mmHg <90mmHg 140-159mmHg 90-99mmHg Grade 1 hypertension Grade2 hypertension 100-109mmHg 160-179mmHg >110mmHg >180mmHg Grade 3 hypertension

  3. Types Essential hypertension Cause Not Yet Clear Secondary hypertension Cause Clear Secondary hypertension is secondary from renal, endocrine and nervous system diseases, much as temporarily, after a good treatment of the primary disease, hypertension will fade away.

  4. Pathogenesis Blood pressure is proportional to cardiac output and peripheral vascular resistance. Any fators that can cause the above two aspectsrising may be concerned with high blood pressure

  5. Pathogenesis Genetic factors Dietary factors Major factors Environmental factors Other factors

  6. Genetic factors Familial aggregation: parents: 2-3 times, morbidity of children single-parent: 1.5 times Concentration of intracellular Na, Ca ion rise Serum hormone-like substance Inhibition of Na / k-ATP enzyme activity Contraction of small artery Angiotensin gene encoding variability Influenced by multiple genetic and acquired factors

  7. Dietary factors Excessive sodium intake sodium intake<5g/d Potassium promote sodium excretion Eat a lot of vegetables Calcium can reduce the pressor effect of sodium High calcium diet The three imbalance cause hypertension

  8. Epidemiological and clinical observations have shown there is a close relationship between salt intake and hypertension。 Extracellular fluid volume Cardiac output salt intake Vascular smooth muscle cell Na + Intracellular Ca + + Vasoconstriction (peripheral vascular resistance rise) BP

  9. Environmental factors Long term mental stress, pressure The vasoconstrictor effect is dominant Vasomotor regulation be out of control Peripheral resistance BP

  10. Other factors Overweight or obesity Smoking Age Lack of physical activity

  11. Extracellular fluid

  12. Types and pathological change benign hypertension（chronic hypertension） malignant hypertension（ accelerated hypertension）

  13. benign hypertension • Process mainly involves small arteries and arterioles，evokes spasm、hardening and affects some important organs. • Benign hypertension may be divided into three stages:

  14. Dysfunctions period • small arteries • arterioles • elasticarteries Arterial systemchanges period heart cerebrum kidney retina Visceral lesions period

  15. Dysfunctions period • The whole bodysmall arteries and arterioles spasm, no organic disease • BP increased occasionally • Clinical symptom appear occasionally, BP will return to normal after a rest

  16. Arterial systemchanges period • Hyaline arteriolosclerosis: Hyaline arteriolosclerosis is a major morphologic characteristic. • Arteriolar sclerosis • Elastic arteries appear AS.

  17. Hyaline arteriolosclerosis：The arteriolar wall is hyalinized, and the lumen is markedly narrowed

  18. Arteriolar sclerosis

  19. Clinical features: May be associated with AS lesions Further raise of blood pressure, and continued at high levels. Lose Fluctuation.

  20. Visceral lesions period Heart：Left ventricle Compensatory hypertrophy Concentric hypertrophy Eccentric hypertrophy

  21. Normal heart Concentric hypertrophywall thickening, heart cavity to narrow Eccentric hypertrophywall thickening, heart cavity enlarge

  22. Microscopically features：cardiocytes are thicker、elongate, nucleus is bigger and hyperchromatic.

  23. Clinical feature myocardial ischemia，finally progress to heart failure

  24. kidney ：Primary granular contracted kidney

  25. Microscopically features： • Renal arteriolar sclerosis, hyalinization • Sclerosis and hyalinization of some glomeruluses. Visible compensatory hypertrophy of the other glomeruluses • Atrophy and disappearance of some renal tubules. Visible compensatory dilatation of the other renal tubules • Hyperplasia of interstitial connective tissue, infiltration of lymphocytes

  26. dilatation of some renal tubules compensatory hypertrophy of some glomeruluses

  27. Bilateral renalsymmetryreduction. Texture hardening, renal surface uneven, with fine granules

  28. Cerebral lesion 1）Cerebral edema: headache, dizziness, vertigo and so on 2）Hypertensive encephalopathy: the syndrome of central nervous dysfunctions caused by acute cerebral edema and intracranial hypertension. Blood pressure increased significantly, severe headache, vomiting, convulsions and coma. 3）Cerebral softening: cerebral ischemic infarction 4）Cerebral hemorrhage: known as stroke. The most serious complication of hypertension

  29. Cerebral softening: cerebral ischemia occurs anemic infarct, liquefaction, forming a loose texture mesh lesions. Necrosis of brain tissue repaired by the proliferation of glial cells, because the lesions were smaller, generally do not cause serious consequences.

  30. loose mesh lesions

  31. Hypertensive retinopathy The central artery arteriolosclerosis, ophthalmoscope see vascular tortuosity, reflecting enhancement, arteriovenous crossing compression, papilledema, retinal hemorrhages and exudates.

  32. Central retinal artery can occur hardening. ophthalmoscopeshownvascular tortuosity, pale, with bleeding

  33. malignant hypertension（ accelerated hypertension） In youth, diastolic pressure is often greater than 130mmhg, can be secondary from chronic hypertension, but often from primary. features: 1）Hyperplastic arteriolosclerosis: intima and smooth muscle cell hyperplasia, collagen fibers increased significantly, the vessel wall, a concentric lamellar thickening, called onion-skinchange. 2）Necrotizing arteriolitis: fibrinoid necrosis of the intima and medial. Patients death in a year due to uremia, cerebral hemorrhage and heart failure.

  34. Hyperplastic arteriolosclerosis (onionskinning) causing luminal obliteration, with secondary ischemic changes

  35. fibrinoid necrosis

  36. The distinction between benign and malignant hypertension • Benign Malignant • Morbidity high（90%） low（10%） • Age The middle-aged or older The young and middle-aged • BP ＞150/95mmHg Persistent diastolic pressure • 130 ~ 140mmHg • Symptom mildseverity • changes Hyaline arteriolosclerosis Hyperplastic arteriolosclerosis • Necrotizing arteriolitis • Course of disease ＞10years 1 ～2 year • cause of death Cerebral hemorrhage, Renal failure,uremia（95%）， • heart failureCerebral vascular accident

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