142. Clinical and morphological forms of hypertension, pathological anatomy, causes of death.

Clinical and morphological forms of GB.

Based on the predominance of vascular, hemorrhagic, necrotic and sclerotic changes in the heart, brain or kidneys in GB, its cardiac, cerebral, renal and mixed forms are distinguished.

1. The cardiac form of hypertension, as well as the cardiac form of atherosclerosis, is the essence of coronary heart disease. Hypertrophy of the myocardium of the left ventricle of the heart ( "bull's heart") with small-focal cardiosclerosis as a result of chronic tissue hypoxia due to relative insufficiency of blood supply to the hypertrophied heart muscle

2. The brain shape is the basis of cerebrovascular diseases. Hemorrhages in the brain are the most characteristic. They can be small, arising by diapedesis, or large with the destruction of brain tissue - hematomas. Hematomas usually develop when microaneurysms rupture, which occur, as a rule, due to hyalinosis and fibrinoid necrosis; they are especially often found in small arteries of the brain, mainly subcortical nuclei and subcortical layers. As a result of hemorrhages, rusty cysts form in the brain tissue.

3. Renal form. It is characterized by both acute and chronic changes.

a) Acute:

- arteriol necrosis, usually leading to acute renal failure;

- kidney infarctions due to thromboembolism or arterial thrombosis.

b) Chronic: the development of arteriol-sclerotic nephrosclerosis (primary shrunken kidney).

4. Mixed form.

It is observed when the previous forms are combined.

Causes of death:

Most patients with benign GB die from heart failure, myocardial infarction, cerebral infarction (hemorrhagic or ischemic), cerebral hemorrhage or intercurrent diseases, less often from renal failure caused by arteriosclerotic renal wrinkling.

With malignant hypertension, death can occur from kidney failure, heart failure, cerebral hemorrhage, and cerebral edema.

143. Pathological anatomy of benign hypertension, 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

Pathological anatomy.

In benign hypertension, 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 manifested by episodes of temporary increase in blood pressure — transient hypertension. At this stage, hypertrophy of the muscle layer and elastic structures of arterioles and small arteries, morphological signs of arteriole spasm or deeper changes in their hypertensive crisis are found. Moderate compensatory hypertrophy of the left ventricle of the heart is noted.

2. The stage of widespread arterial changes is characterized by periods of persistent increase in blood pressure. Characteristic changes are determined in the arterioles, arteries of elastic, musculoskeletal and muscular types in the heart. Changes in arterioles (the most typical sign of hypertension) plasma impregnation and its outcome — hyalinosis, or arteriol sclerosis. Plasma impregnation of arterioles and small arteries develops in connection with hypoxia of 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 by macrophages, however, this resorption is usually incomplete. Hyalinosis of arterioles, or arteriosclerosis, develops.

3. The last stage of hypertension is secondary organ changes due to changes in the arteries and impaired intraorgan circulation. These secondary changes appear catastrophically quickly due to spasm, thrombosis of the vessel, completing plasma impregnation or fibrinoid necrosis of its wall. Then they manifest as hemorrhages or heart attacks.

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.