Ulcer Atherosclerotic

Atherosclerotic ulcer

Atherosclerotic ulcer is a chronic persistent superficial ulcer that develops due to circulatory disorders in the arteries of the lower extremities. It manifests itself as spontaneous night pain in the calves and chilliness of the legs. Rarely may lead to gangrene. It is believed that varicose veins, lymphatic stasis in the superficial veins, impaired blood supply to the nerves, and bone erosions can also contribute to the development of ulcers. It can often be combined with diabetic polyneuropathy, inguinal hernia, acute thrombophlebitis of the deep veins of the leg, chronic obliterating diseases of the arteries of the lower extremities and Raynaud's syndrome. Osteoarthrosis of the joints is more often detected in patients with a long history of atherosclerotic ulcers, even in the absence of complaints.

Pathogenesis

The development of ulcers during arterial ischemia is associated with three stages of the pathological process. In stage I, ischemia does not lead to an increase in reperfusion disorders; in stage II, the rate of restoration of blood flow is insufficient for normal healing of the revascularization zone. After normalization of blood flow in phase III, the ulcerative defect disappears as a consequence of a decrease in sympathetic activity due to a decrease in tissue hypoxemia, and destruction induced by hypoxia disappears. The basis of the pathogenesis of ulcers is considered to be disruption of blood flow in the coronary and coronary arteries (venous blood during prolonged contact with cold tissues, hemic carbon dioxide), the development of trophic disorders of the subcutaneous tissue and skin, microcirculatory disorders, which in turn are caused by the development of atherosclerosis in the abdominal branches cavities, in the system of deep anterior and posterior large access on the sole, deep subcutaneous canals of the foot, vascular interruptions, thrombosis, impaired ulcer resorption rate, intimal damage, leading to a sharp increase in the adhesion of blood cells to the vascular endothelium. One of the main links in pathogenesis is considered to be a change in nervous influences in the form of increased permeability of the basement membranes of the capillaries of the skin and mucous membranes, impaired reabsorption of the liquid part of the intercellular substance from them and the involvement of microcapillaries. These changes develop water retention in the epidermis, changes in the biological properties of the skin, changes in the nervous regulation of blood vessels in the ischemic zone, and increased sweating. Dysproteinemic and microcirculatory disorders of vascular tone, the formation of atherosclerotic plaques and their disintegration, damage to the vascular intima with a sharp increase in the adhesion of leukocytes and platelets to the walls of blood vessels and other processes are important. The acute part of the pathogenesis is the development of inflammation in the vessels, blood stagnation, vascular spasm, perivenular edema, increased plasma toxicity and deficiency of coagulation factors with transient thrombocytopenia (lipemia and leukocytosis), loss of water due to edema of the muscles and subcutaneous tissues. Vitamin C and K deficiency increases the risk of bleeding. In addition, acute thrombosis can lead to the formation of venous thrombi, which form foam in the veins. Prolonged persistence of such blood clots can lead to