What Is Benign Hypertension?

Benign hypertension (also known as chronic hypertension), which accounts for about 95% of primary hypertension, has a long course and a slow process, which can reach more than ten years or decades.

Benign hypertension

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Benign hypertension (also known as chronic hypertension), which accounts for about 95% of primary hypertension, has a long course and a slow process, which can reach more than ten years or decades.

Western Medicine Name

Benign hypertension

English name

benign hypertension

Other name

Chronic hypertension

Affiliated Department

Internal Medicine-General Medicine

The main symptoms

dizziness

Contagious

Non-contagious

Whether to enter health insurance

Yes

1. The dysfunction period is the early stage of hypertension. Intermittent spasm of small arteries in the whole body is contracted and blood pressure rises. Because there are no organic lesions in the arteries, blood pressure can return to normal after the spasm is relieved. Arterioles refer to arteries with only 1 to 2 layers of smooth muscle cells in the median membrane, and vessel diameters <1 mm. Clinical manifestations of elevated blood pressure, but often fluctuating, may be accompanied by dizziness, headache, after proper rest and treatment, blood pressure can return to normal.

Eri Arteriolosclerosis: It is the main pathological feature of hypertension, manifested as arteriolar hyaline degeneration. The arteriolar vitreous changes most easily affect the renal bulbar and retinal arteries.

Due to long-term spasm of arterioles, and vascular endothelial cells are stimulated by long-term hypertension, endothelial cells and basement membranes are damaged, endothelial cell gaps are enlarged, permeability is enhanced, and plasma proteins penetrate into the blood vessel walls. At the same time, smooth muscle cells secrete a large amount of extracellular matrix, and smooth muscle cells degenerate and necrosis due to hypoxia. The vascular wall is gradually replaced by repairing collagen fibers and proteoglycans produced by plasma proteins, extracellular matrix and necrotic smooth muscle cells. The wall structure disappeared and gradually solidified into a red-stained, unstructured, homogeneous glass-like substance, which caused thickening of the arterial wall, shrinkage of the lumen, and even occlusion.

(2) Muscular arteriolar sclerosis: It mainly involves renal interlobular arteries, arcuate arteries, and cerebral arteries. Arterial intimal collagen fibers and elastic fibers proliferate, and the inner elastic membrane is divided. The median smooth muscle cells proliferate, hypertrophy, and collagen fibers and elastic fibers proliferate to varying degrees. Vessel walls thickened and lumen narrowed.

(3) Aortic sclerosis: If the aorta and its main branches are complicated by atherosclerosis.

(1) Heart: As blood pressure continues to increase, peripheral resistance increases, myocardial load increases, and compensatory hypertrophy of the left ventricle. Heart weight increases to more than 400g. Macroscopically, the left ventricular wall thickened to 1.5cm to 2.0cm (normally within 1.0cm). The papillary muscles and meat columns are thickened, and the heart cavity is not dilated, and is relatively small, which is called concentric hypertrophy (Figure 6-12). Myocardial cells became thicker and longer under light microscope, with more branches. Cardiac cell hypertrophy, round or oval, deep stained nuclei. In the later stage, when the left ventricle is decompensated, the myocardial contractility decreases, and heart cavity dilation gradually appears, which is called eccentric hypertrophy. Heart failure can occur in severe cases.

The above-mentioned lesions of the heart are called hypertensive heart disease. Patients may have palpitations, electrocardiograms show left ventricular hypertrophy and myocardial strain, and severe cases have symptoms and signs of heart failure.

(2) Kidney: In hypertension, due to the vitreous degeneration of the arteriolar arteries and the hardening of the muscular arterioles, the wall thickens and the lumen is narrowed, resulting in fibrosis and glass in the glomerular ischemia in the diseased area Like degeneration, the corresponding renal tubules shrink and disappear due to ischemia, and interstitial fibrous tissue and lymphocyte infiltration appear. Relatively mild glomerular compensatory hypertrophy, and corresponding tubule compensatory dilatation. Macroscopically, bilateral kidneys have reduced symmetry, the texture has become harder, the surface of the kidneys is uneven, and the particles are fine-grained. Unilateral kidneys can be less than 100g (about 150g in normal adults). cm 0.6cm). The cortex and medulla boundaries are blurred, and the renal pelvis and adipose tissue around the kidneys increase. Renal failure can occur in severe cases. Lesions above the kidney are known as primary granular atrophy of the kidney.

(3) Brain: Due to cerebral ischemic arteriosclerosis, ischemia and increased capillary permeability, a series of lesions can occur in the brain. There are three main types: Hypertensive encephalopathy: due to cerebral arteriosclerosis and spasm, local tissue ischemia, increased capillary permeability and cerebral edema. Clinical manifestations include headache, dizziness, dizziness, vomiting, and visual impairment. Sometimes the blood pressure rises sharply. Patients may experience severe headaches, disturbances of consciousness, and convulsions. This is called a hypertensive crisis. This crisis is seen in various stages of hypertension; softening of brain: due to the small arteries of the brain sclerosis and spasm, the brain tissue in the blood supply area ischemia and most small necrotic lesions occur, that is, microinfarct. Liquefaction and necrosis of the infarcted tissue under the light microscope, forming a loose-texture sieve-like lesion, and the late necrotic tissue is absorbed and repaired by glial fiber hyperplasia. Cerebral hemorrhage: It is the most serious complication of hypertension. Is a fatal complication. Cerebral hemorrhage often occurs in the basal ganglia and inner capsule, followed by white matter, pontine and cerebellum. More common in the basal ganglia area (especially the bean-shaped nucleus area is most common),

It is because the striatum of arteries supplying this area branches at right angles from the middle cerebral artery, and is directly impacted and pulled by the blood pressure of the middle cerebral artery, which causes the striatum to rupture and bleed. Bleeding is often large, with regional brain tissue completely destroyed, forming cystic lesions filled with blood and necrotic brain tissue. When the range of bleeding is enlarged, it can break into the lateral ventricle. The cause of cerebral hemorrhage is due to the thin cerebrovascular and arteriolar sclerosis, which makes the blood vessel wall brittle. When the blood pressure suddenly rises, it causes rupture bleeding. It can also cause small bulging to form small aneurysms and micro aneurysms due to the decreased elasticity of the blood vessel wall. When the blood pressure suddenly rises, it causes small aneurysms and micro aneurysms to rupture and bleed. Clinical manifestations: Cerebral hemorrhage often has different clinical symptoms due to different bleeding sites and different amounts of bleeding. Internal capsule hemorrhage can cause hemiparesis of the contralateral limb and feel disappeared; when the bleeding breaks into the lateral ventricle, the patient becomes comatose and even dies; left cerebral hemorrhage often causes aphasia; pontine hemorrhage can cause paralysis of the ipsilateral nerve and contralateral upper and lower limbs; Cerebral hemorrhage can cause intracranial hypertension due to hematoma occupancy and cerebral edema, and the formation of cerebral hernia.

(4) Retina: Arteriosclerosis occurs in the central retinal artery. Fundus examination showed tortuous blood vessels, enhanced reflection, and indentations at the intersection of arteries and veins. Severe cases of papillary edema, retinal hemorrhage, and vision loss.