33. Reperfusion syndrome

It is a complex of reactions directed to blood supply restoration after ishemia or thrombosis. Main substrate is collateral circulation development. It depends greatly on organ type (see above), ishemia gravity and developmental speed. Also fibrinolysis system state is very important. Experiments are hold under surgical operations conditions.

34. Stasis.

Stasis – blood retardation and stoppage in capillaries, shine arteries and veins.

Variants:

1. ishemic;

2. venous;

3. real (capillary).

Ishemic and venous stasis are developed as a result of ishemia and venous hyperemia and that is why they have the same reasons like ishemia and stasis correspondingly.

Real stasis reasons:

1. physical factors (warmth, coldness);

2. chemical factors (toxins, NaCl hypertonic solution, strong solutions of other salts et al., kerosene );

3. biological (miroorganismic toxins).

Real stasis pathogenetic factors:

1. intracapillary erythrocytes aggregation;

2. blood stream retardation due to blood hyperviscosity (result of vascular wall permeability increasing in the area of stasis).

35. Thrombosis and embolism. Thrombosis characteristics.

Thrombosis is a process of blood clots (thrombi or thrombs) formation on endothelium during life when thrombi consist of vascular wall elements.

Thrombi types:

1. a) wall-near (vessel lumen is decreased particularly);

b) obstructive;

2. a) white – with platelets, leucocytes and plasma proteins little amount;

b) red – erythrocytes binded with fibrin fibers one with another;

c) mixed – consist of alternating red and white layers.

3 Main factors encouraging thrombi formation (Wirhow’s triad):

1. vascular wall injury – it can occur under action of physical (mechanic trauma, electrical current), chemical, biological (microorganisms endotoxins) factors as well as in a result of vascular wall dystrophy and dysmetabolism;

2. hyperactivity of coagulation and hypoactivity of anticoagulation system;

3. blood stream retardation –in veins thrombi formation speed is higher than in veins, in lower extremities veins it is higher than in upper ones; it is the explanation of thrombi increased rate at circulation decompensation as well as being at prolonged bed regimen.

Thrombosis phases:

1. cellular – platelets adhesion, aggregation and agglutination;

2. plasmatic – blood coagulation.

Embolism –see below.

36. Embolism.

Embolism – vessels occlusion with the bodies carried with blood or lymph flow. These bodies are called emboli (embols).

Embolism types:

1. Dependently on emboli character and their origin:

a) exogenous (embols come from outside);

b) endogenous;

2. by localization:

   1. of small circulation circle;

   2. of large circulation circle;

   3. of portal vein;

3. a) retrograde – embol movement is determined by embol gravity force but not haemodynamic laws;

b) paradoxal – due to foramen in interatrial and interventricular septum – embols from large circulation circle and heart right half transfer to left one pass small circle.

Exogenous embolism (dependently on embol nature and character):

1. air;

2. gas (at kessonic disease or at rapid rising up in the mountains);

3. bacterial;

4. parasite;

5. with solid side bodies.

Endogenous embolism:

1. thromboembolism;

2. fatty (due to bone marrow, subcutaneous or pelvic cellula injury);

3. tissular (particularly at tumors metastazing);

4. with embryo-near water (waters come in tomb injured vessels in locus of separated placenta during labours).