46. Arterial hyperemia: definition, types. Types of pathological arterial hyperemia, significance for the body.

Arterial fullness or arterial hyperemia is an increased blood supply to an organ or tissue due to increased arterial blood flow.

AP classification:

1. general (increase in BCC or number of erythrocytes)

2. local; a) physiological b) pathological

Types of physiological arterial hyperemia:

a) reflex - the effect of adequate doses of physico-chemical factors, feelings of shame

b) working - strengthening the function of organs

Types of pathological arterial hyperemia and their morphology:

a) Angioedema (neuroparalytic) - with paralysis of the vasoconstrictive nerves, lesion of the nodes of the SNC infection: skin, mucous membranes are red, slightly swollen, warm or hot to the touch

b) Collateral - obstruction of blood flow along the trunk and its aspiration along reflexively expanding collaterals

c) Postanemic - the factor that previously squeezed the artery and created anemia is quickly eliminated (tourniquet, fluid in the cavity) - a sharp vasodilation of previously exsanguinated tissue, their overflow with blood, possible rupture, vascular hemorrhage, anemia of other organs (g/m)

d) Vacant - as a result of a decrease in barometric pressure: general - in divers with rapid ascent from an area of high pressure, combined with gas embolism, vascular thrombosis, hemorrhages and local - on the skin under the action of medical cans

e) Inflammatory - one of the main properties and signs of inflammation

f) Hyperemia on the background of an arteriovenous fistula - with the formation of a junction between an artery and a vein and the rush of arterial blood into a vein (with a bullet wound)

The value is determined by the type of AP: collateral hyperemia is a compensatory reaction, inflammatory is an obligatory component of inflammation, vacant is a component of caesarean disease.

47. Venous hyperemia: definition, classification. Pathological and anatomical characteristics of general venous plethora, causes, mechanisms of development.

Venous fullness (GDP) is an increased blood supply to an organ or tissue due to a decrease (difficulty) in blood outflow; blood flow is not changed or decreased.

Classification of VF:

1. general VP: acute and chronic

b) local VP.

General venous fullness develops in heart disease leading to acute or chronic cardiac (cardiovascular) insufficiency.

The pathophysiological and pathomorphological essence of general venous fullness consists in the redistribution of blood volume in the general circulation with its accumulation in the venous part of the large circulation (hollow veins, and sometimes in the vessels of the lungs) and a decrease in the arterial part.

48. Acute general venous plethora: definition, causes, pathogenesis. Pathological changes in organs, outcomes, clinical significance.

Acute general venous plethora is a manifestation of acute heart failure syndrome (insufficiency of myocardial contractility, for example, in myocardial infarction, acute myocarditis).

The cause of acute general VP is acute HF syndrome in MI, acute myocarditis. Hypoxia → damage to histohematic barriers → sharp increase in capillary permeability:

a) plasma impregnation (plasmorrhagia) and edema in tissues

b) stasis in capillaries and multiple diapedesis hemorrhages

c) dystrophic and necrotic changes in parenchymal organs: lungs - edema and hemorrhages, kidneys - dystrophy and necrosis of the tubular epithelium, liver - centrolobular hemorrhages and necrosis.

Micro: As a result of hypoxic damage to histohematic barriers and increased capillary permeability in tissues, plasma impregnation, edema, blood arrest in capillaries and multiple small-point hemorrhages are observed, dystrophic and necrotic changes appear in parenchymal organs.

Macro-: Structural and functional features of the organ in acute venous stasis determine the predominance of edematous plasmorrhagic, hemorrhagic or dystrophic and necrotic changes. A combination of them is also possible.

Issue:In the lungs, the histophysiological features of the aerogematic barrier explain the development of edema and hemorrhage in acute venous congestion. In the kidneys, due to the peculiarities of the structure of the nephron and blood circulation, mainly dystrophy and necrosis occur, especially the epithelium of the tubules. In the liver, due to the peculiarities of the architectonics of the hepatic lobule and its circulation in acute fullness, centrolobular hemorrhages and necrosis appear.