134. Systemic vasculitis: definition, etiology, classification, pathological anatomy, examples of diseases.

Vasculitis is a disease characterized by inflammation and necrosis of the vascular wall. Local vasculitis develops in the foci of inflammation due to the transition of the process to the vascular wall from the surrounding ones. Systemic vasculitis, which can be the basis of independent diseases (primary vasculitis) or a manifestation of some other disease (secondary vasculitis), is characterized by widespread vascular damage.

The etiology has not been clarified, but there is a connection with various infectious diseases. Occupational hazards also play a role.

Classification 1. By etiology - Infectious - Non-infectious - antineurophilic, antiendothelial, medicinal - Combined 2. Morphologically - Alterative - fibrinoid necrosis of the walls - Exudative - infiltration - Proliferative - lymphohistiocytic infiltration, including granulomatous - Mixed

A. Primary vasculitis:

I. With predominant damage to the aorta and its large branches and giant-cell granulomatous reaction

II. With predominant damage to medium- and small-caliber arteries and a destructive and productive reaction

III. With a predominant lesion of small-caliber arteries, vessels of the microcirculatory bed and veins

IV. With lesions of arteries of various calibers — a mixed (unclassifiable) form.

B. Secondary vasculitis:

V. In infectious diseases

VI. In case of systemic connective tissue diseases

VII. Vasculitis of "hypersensitivity"

Pathological anatomy. Most often, the lesion is localized in the area of the aortic arch. The vessels have a characteristic appearance: their walls are thickened, rigid, and represented by whitish tissue. Intima may have thickenings that narrow the lumen, in which parietal or obstructing blood clots are found. Sclerosis phenomena are expressed in adventitia and perivascular tissue, and aneurysmal protrusions of the wall occur. The lesion may be segmental or diffuse.

135. Atherosclerosis: definition, etiology, pathogenesis. Macro- and microscopic changes in arteries, complications, outcomes, clinical significance .

Atherosclerosis is a chronic disease based on a violation of fat and protein metabolism, characterized by damage to elastic and muscle – elastic arteries, deposition of lipids and proteins in the intima with a reactive proliferation of CT.

Etiology

1) metabolic (exo- and endogenous);

2) hormonal;

3) hemodynamic;

4) nervous;

5) vascular;

6) hereditary and ethnic.

Pathogenesis – increased permeability against the background of the predominance of atherogenic lipoproteins leads to damage to the endothelium and accumulation of cholesterol in the cell. An excess of HC in cells leads to the formation of "foam cells", the appearance of which anticipates the appearance of morphological changes.

Morphology

The pre–lipid stage is changes in the blood (hyperlipidemia, hypercholesterolemia), in the vessels (fly swell, fibrinosis, parietal thrombi), in connective tissue (accumulation of acidic GAG matrix for lipoprotein attachment).

Lipoidosis is the accumulation of droplets or bands of lipids in the intima that do not rise above the surface of the intima. Microscopically, the appearance of foamy cells, which are macrophages that absorb excess HC. The elastic membrane of the vessels is destroyed.

Liposclerosis is the appearance of pale yellow lipid plaques towering over the intima. They are reactive overgrown connective tissue. Microscopically, it is a young connective tissue with many vessels.

Atheromatosis – begins with the breakdown of fat protein mass with the formation of detritus. Collagen and elastic fibers are destroyed. The vessels of the young CT are exposed and bleed into the thickness of the plaque (under the plaque cap).

Ulceration – begins with a ruptured tire and hemorrhage. The edges of the ulcer are covered with blood clots.

Atherocalcinosis is the deposition of calcium salts in detritus, fragments of elastic fibers. Dense brittle plates are formed.

Complications

1. Tendency to thrombosis and embolism;

2. Organ ischemia:

in the heart - coronary heart disease, fibrosis, myocardial infarction;

in the kidneys - chronic renal ischemia, chronic fibrosis, kidney failure; in the intestine - chronic intestinal ischemia; in the lower extremities - chronic ischemia with the formation of intermittent lameness and the development of gangrene;

3. Aortic aneurysm.

Outcomes: Atherosclerosis of the branches of the aortic arch leads to insufficient blood supply to the brain, which can lead to a stroke. And atherosclerosis of the coronary (coronary) arteries of the heart leads to the development of coronary heart disease.