Circulatory disturbances.Arterial and venous hyperemia. Edema. Bleeding and hemorrhage.

Adequacy of bloodstream is provided with:

Adequate function of heart;

Continuity of vascular wall;

Balance between coagulative and anticoagulative blood systems.

Types of circulatory disturbances:Vascularity disturbances (hyperemia, ischemia);Vascular wall permeability disturbance (hemorrhage, bleeding);Disturbance of rheological blood properties (stasis, thrombosis, embolism, sludge-phenomenon, DIC-syndrome [disseminated intravascular coagulation]).

HyperemiaArterial;Venous.

Arterial hyperemiaIncrease of hyperemia through increase of arterial blood flow.

But blood outflow is not changed.

Arterial hyperemiaBy localization:general;local.

General arterial hyperemiaIt is specified by 2 factors:

Increase of erythrocyte quantity erythremia;Increase of blood volume plethora.

Local arterial hyperemiaPhysiological:Reflex or emotional;Working?

2) Pathological: Angioneurotic is developed at overstimulation of vasodilator nerve or paralysis of vasoconstrictive nerve (as a result of trauma, neuritis);Vacatnaya? occurs under the conditions of low barometric pressure;

At arteriovenous abnormality/commumication: is developed under anastomosis/fistula between artery and vein, at vascular malformation in pia;Collateral occurs at the obstruction of the basic arterial trunk by thrombus or embolus. It is a kind of compensatory and adaptive process.Inflammatory at any inflammation. It is also a kind of compensatory and adaptive process.Hyperemia after anemia

All types of arterial local hyperemia are developed briefly and that is why structural changed do not occur in organs and tissues.

Anatomical manifestationsRedness of skin, mucous, and organs;Increase of arterial blood pressure;Increase of body temperature.

Value of arterial hyperemiaIt has often compensatory and adaptive character.Structural change does not occur in the organs.

Venous hyperemiaIt is an increased vascularity/blood filling of organ or tissue as a result of venous blood outflow disturbanceBlood inflow is not changed.

By distribution:General;Local.

By course:Acute;Chronic.

Causes:of general venous hyperemia: Cardiac insufficiency;

of local:Thromboses in veins;Compression of veins (adhesion, cicatrix/scar, tumor, fluid)

Anatomical manifestationsOrgan is enlarged; is sclerosed;of dark-red or dark-blue (cyanotic) colour.

Morphological changes in the tissuesVascular permeability is increased under the development of hypoxia; as a result the edema and diapedesis of erythrocytes are developed. There is primarily fatty dystrophy in parenchymatous cells So, microscopically: plethoric (full-blooded) veins, edema of stroma, diapedetic hemorrhage, dystrophic changes of parenchymatous cells.

Chronic course: - at the place of hemorrhage hemosiderin is formed; - in stroma the connective tissue is developed;- in parenchymatous cells atrophy is developed along with dystrophy.

Effects/consequences: At acute course the process is reversible;At chronic course atrophy of parenchyma and sclerosis of stroma with outcome into cirrhosis.

Organopathology:Nutmeg liver;Brown [pigment] induration of lungs;The kidneys, spleen, skin - cyanotic induration.

Brown induration of lungsPrimarily the edema is developed in the lungs; the fluid is stored/accumulated in the lumen of alveoli. Subsequently the diapedesis of erythrocytes occurs in the lumen of alveoli; the erythrocytes are caught with macrophages; and hemosiderin is formed.The connective tissue is developed in alveolar septum because of hypoxia and the septum becomes thicken. The lungs obtain dense consistency.

Nutmeg liverAt disturbance of venous blood outflow the central vein is dilated and plethoric/full-blooded. Hyperemia comes to sinusoids which become enlarged and constrict hepatocytes (as a result they are atrophied). All centre of lobule/clove has red colour. On the lobule periphery the hepatocytes are subjected to fatty dystrophy, and the liver in these department has yellow-brown colour. Alternation of red and yellow-brown colors makes a parti/multicolored view of liver and looks like the nutmeg. Outcome nutmeg cirrhosis.

Dark spots (plethoric/full-blooded centers of lobules) on yellow background (dystrophy) of general venous hyperemia manifestation

Cyanotic indurationAt the beginning the edema is developed, then enlargement of connective tissue occurs. Under these process the organs obtain dense consistency, and under the dilated plethric veins cyanotic edema.Outcome cyanotic induration.

Bleeding blood issue from heart cavity or vascular lumen into environment or tissues and body cavities.

Internal;External.

Mechanisms of bleedingRupture of vascular wall:Medianecrosis of aorta;Syphilitic meseorthite?;Rupture of enlarged organs (liver, spleen);Aneurysm of heart, aorta, cerebral artery;Traumatic rupture.

Mechanisms of bleeding2. Erosion of wall:In inflammation focuses;At ulceration;At fallopian pregnancy;In zone of necrosis.

Mechanisms of bleeding3. Diapedesis through/across the uninjured vascular wall with higher permeabilityAt hypertonic disease;At vasculitis/angiitis;At infections (typhus, scarlatina/scarlet fever, sepsis/septicemia);At diseases of hemopoietic [blood-forming] organs;DIC-syndrome (disseminated intravascular coagulation);In hypoxic states.

Hemorrhage blood accumulation in the tissues.

Types of hemorrhagePetechia or petechial [punctate] hemorrhage fine/small dot hemorrhage on mucous and skin. Mechanism diapedesis.Bruise (fruise) flat-bed hemorrhage.Hemorrhagic infiltration blood impregnates muscles and fatty tissue.Hematoma haemorrhage following the tissue destruction.

Outcomes of hemorrhageResorption / resolution;Organization (encapsulation) displacement of blood with connective tissue;Formation of cyst (in the brain);Suppuration / purulence.

Effects / consequences of bleeding and hemorrhage:

depend on: Rate of blood loss;Volume of blood loss and hemorrhage;Localization.

Disturbance of interstitial [tissue] contentTranssudate hydropic fluid (transparent, contains less 2% proteins).Edema fluid is accumulated in the tissues.Hydrops/dropsy transsudate is stored in the cavities.Anasarca / hydrosarca fluid accumulation in the tissues, organs, and cavities (hydrothorax, hydropericardium).

Mechanisms of edema developmentIncrease of hydrostatic pressure (congestive edema);Decrease of colloid-osmotic pressure (oncotic edema);Membranogenic edema (disturbance of Na balance);Lymphogenous edema at disturbance of lymph outflow.