141. Hypertension: etiology, pathogenesis, pathological anatomy, causes of death.

Hypertension is a chronic disease, the main clinical sign of which is a long-term and persistent increase in blood pressure (hypertension).

Etiology.

Increased consumption of table salt

Excessive nervous tension, leading to a disorder of autonomic nervous activity

Pathogenesis. A number of factors are involved in the mechanism of development of hypertension:

1) nervous - overstrain (nervous factor) leads to depletion of the centers of vascular regulation with the involvement of reflex and humoral factors in the pathogenetic mechanism;

2) reflex possible shutdown of depressive effects of the carotid sinus and aortic arch, as well as activation of the sympathetic nervous system;

3) hormonal enhancement of pressor effects of the pituitary-encephalic region (hyperplasia of cells of the posterior and anterior lobes of the pituitary gland), excessive release of catecholamines (hyperplasia of the adrenal medulla) and activation of the renin-hypertensive system as a result of increasing renal ischemia;

4) renal impairment of the mechanisms of reabsorption, secretion in convoluted tubules; improper functioning of the renin-angiotensin-aldosterone system, impaired secretion of kinins and prostoglandins that alter the tone of arterioles. Kidney pathology may cause the absence of vasopressin receptors.

5) hereditary

Pathological anatomy.

In malignant hypertension (144 questions), manifestations of a hypertensive crisis, i.e. a sharp increase in blood pressure due to arteriole spasm, dominate. The morphological manifestations of a hypertensive crisis are quite characteristic and presented

-corrugation and destruction of the basement membrane of the endothelium

- arteriole spasm

-plasma impregnation or fibrinoid necrosis of its wall

- thrombosis

In benign hypertension (question 143), taking into account the duration of the disease, there are three stages with certain morphological differences: 1) preclinical; 2) common arterial changes; 3) organ changes due to arterial changes and impaired intraorgan circulation.

1. The preclinical stage of hypertension is spoken of in cases where episodes of temporary increase in blood pressure (transient hypertension) appear. At this stage, hypertrophy of the muscular layer and elastic structures of arterioles and small arteries, morphological signs of arteriole spasm or deeper changes in cases of hypertensive crisis are found. There is moderate compensatory hypertrophy of the left ventricle of the heart.

2. The stage of widespread arterial changes characterizes the period of persistent increase in blood pressure.

-Changes in arterioles - are expressed in plasma impregnation and its outcome - hyalinosis, or arteriol sclerosis. Plasma impregnation of arterioles and small arteries develops due to hypoxic damage to the endothelium, its membrane, muscle cells and fibrous wall structures, which is caused by vessel spasm. The elements of wall destruction, as well as the proteins and lipids impregnating it, are resorbed with the help of macrophages, however, this resorption is usually incomplete. Similar changes appear in small muscle-type arteries.

-Changes in the arteries of elastic, musculoelastic and muscular types are represented by elastofibrosis and atherosclerosis. Elastofibrosis is characterized by hyperplasia and cleavage of the internal elastic membrane, developing compensatorily in response to a persistent increase in blood pressure, and proliferation between the split membranes of connective tissue, i.e. sclerosis. With persistent and prolonged arterial hypertension, pronounced atherosclerosis develops, which differs in some way: atherosclerotic changes are more common, "descending" into muscle-type arteries, which is not observed in the absence of hypertension.

At this stage, the degree of myocardial hypertrophy increases, the heart mass reaches 900-1000 g, and the wall thickness of the left ventricle is 2-3 cm. Due to stenosing atherosclerosis of the coronary arteries, myocardial hypoxia occurs, which leads to the development of dystrophic and necrobiotic changes in muscle fibers and myogenic expansion of the cavities of the hypertrophied heart. The outcome is diffuse small-focal cardiosclerosis

3. Changes in organs: Malignant GB – heart attacks and hemorrhages Benign GB – dystrophy of the parenchyma of organs, vascular hyalinosis, sclerosis.

Causes of death:

Acute heart failure

Acute renal failure (arteriol necrosis – death of cells of the bearing arteriole, inflammation in the loops of the glomeruli, edema, cellular reaction, sclerosis of the glomerular stroma, protein dystrophy in the epithelium of the tubules).

Cerebral infarction, stroke.