circulatory disturbances: part ii - БГМУ · thrombosis morphology i. according to the structure...
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CIRCULATORY
DISTURBANCES:
Part II
Thrombosis, embolism,
disseminated intravascular
coagulation (DIC), infarct
THROMBOSIS
Definition - vital coagulation of blood in lumen of
blood vessels or heart cavities with formation of
a thrombus.
Postmortem blood coagulation – postmorten blood
clot.
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ETIOLOGY AND PATHOGENESIS OF
THROMBOSIS
Local factors:
1. The main factor – damage of the vascular wall (endothelium):
– vasculitis, endocarditis, atherosclerosis, angioneurotic disorders (spasms of arteries and arterioles))
2. Abnormal blood flow:
turbulance or stasis: Local widening of the vessel (such as an aneurysm);
Impaired passage (such as calcified venous valves);
Vascular bifurcations
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ETIOLOGY AND PATHOGENESIS OF
THROMBOSIS
General Factors:
1. abnormality in the regulation between coagulation
and anticoagulation systems;
2. changes in composition of blood:
• disorders of blood rheological properties
– increase of viscosity, number of platelets and proteins:
• atherosclerosis,
• autoimmune diseases
• leukemia
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STAGES of THROMBOGENESIS
I. Vascular-platelet stage:
1. Damage of endothelium
2. Adhesion and aggregation of platelets
3. Formation of platelet thrombus.
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II. Coagulation stage :
1.Thrombokinase formation;
2.Thrombin formation;
3.Fibrin formation: fibrinogen – fibrin monomers - the aggregation of fibrin monomers (unstabilized fibrin) – fibrin monomers polymerization (stabilized fibrin);
4.Blood clot retraction.
STAGES of THROMBOGENESIS
Postmortem blood coagulation is
formed mainly from unstabilized
fibrin and there is no retraction
As a consequence :
Postmortem blood clot is jelly-
like and flexible located freely, with
a smooth and shiny surface;
Thrombus attached to the vessel
wall, dense, with a corrugated
surface, micro – Lines of Zahn.
POSTMORTEM BLOOD CLOT
THROMBOSIS MORPHOLOGY
I. According to the structure –
1. white thrombus (fibrin + Tr and Le) is formed slowly with
rapid blood flow (usually in the arteries);
2. red thrombus (fibrin + Er) formed rapidly at slow blood flow
(usually in the veins);
3. mixed thrombus: combination of white and red (layered
thrombus) – consists of attached to the vessel wall head
(white thrombus), body (mixed thrombus) and tail (red
thrombus) – usually in veins and aneurysms.
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THROMBOSIS MORPHOLOGY
II. In relation to the vessel lumen –
1. mural thrombus
2. occlusive thrombus formed during growth of mural thrombus;
Special forms:
– progressive thrombus, growing throughout blood flow;
– ball-like(left atrium)
– dilatation (aneurysms) thrombus
– microthrombus (see DIC)
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THROMBOSIS OUTCOMES
Favourable
1. aseptic autolysis,
2. organization with sewage and vascularization,
3. petrification (phlebolit/veinstone)
Unfavorable
1. septic autolysis
2. thrombobacterial embolism (sepsis),
3. thromboembolism.
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EMBOLISM
Definition - circulation in the blood (or lymph)
foreign particles (embolus), followed by
blockage of blood vessels
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EMBOLISM TYPES
I. Orthograde (direct) – with blood flow:
1. From venous system of the systemic circulation and right heart into vessels of the pulmonary circulation
2. From left heart cavities, aorta and large arteries, rarely from the pulmonary veins and arteries of internal organs into smaller vessels
3. From branches of the portal system into the portal vein of the liver
II. Retrograde – against blood flow (in case of heavy embolus)
III. Paradoxical – moving of embolus from arteries to the veins, bypassing the microcirculation (through the defects of heart septum, or arterio-venous anastomoses).
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EMBOLUS TYPES ACCORDING TO
THE AGGREGATE STATE
1. Solid:
1. thromboembolism,
2. tissue
3. microbial embolus
4. foreign bodies
2. Liquid: fatty embolus;
3. Gaseous: air and gas embolus;
4. Mixed: the amniotic fluid. 19
THROMBOEMBOLISM
Types: arterial and venous
Arterial thromboembolism Sources: the left cavity of the heart, the aorta and other
arteries. Effects: infarcts of various organs and tissues (including
gangrene, ischemic stroke). Venous thromboembolism Sources: veins of systemic circulation (more often veins of
lower limbs, pelvis).
Thromboembolism of the pulmonary artery
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Thrombosis of the main tube of pulmonary artery with sudden death
Reflexogenic
zone in area
of bifurcation
pulmonary artery
tube
EMBOLISM’S
SOURCES AND OUTCOMES
Tissue (cell) embolism
Sources: tissue damage or malignant tumor.
Effects : infarctions and metastasis - embolism with subsequent growth embolus elements.
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EMBOLISM’S
SOURCES AND OUTCOMES
Microbial embolism
Sources: bacteria, fungus, animals, parasites, protozoa
Effects: metastatic abscesses (pyelophlebetical
abscesses)
Embolism by foreign bodies
fragments of shells and mines, bullets etc., cholesterol
crystals of atherosclerotic plaques
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EMBOLISM’S
SOURCES AND OUTCOMES
Fatty embolism
Sources: long bone fractures or massive subcutaneous
tissue and
Effects: acute lung failure and cardiac arrest at blockade
2/3 of pulmonary capillaries
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EMBOLISM’S
SOURCES AND OUTCOMES
Aeroembolism:
Sources: neck veins with injuries, uterus veins after childbirth
Effects: sudden death
Gas embolism
Sources: rapid decompression (divers), gas gangrene.
Effects : centers of necrosis and hemorrhages mainly in the brain
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EMBOLISM’S
SOURCES AND OUTCOMES
Amniotic fluid embolism
Sources: rupture of the cervix and uterus during childbirth.
Composition: liquid part, including tissue thromboplastin; solid fetus elements - meconium, the scales of epidermis, fat, lanugo.
Effects : DIC-syndrom
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DIC
Disseminated intravascular coagulation
(syn.: thrombohemorrhagic syndrome, consumption
coagulopathy) is an acquired nonspecific process of
hemostatic disorders developed as a result of
excessive activation of coagulation and anti-
coagulation systems.
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DIC is NOT a primary disease
The main symptoms of DIC
• phase changes of haemostasis in a hypercoagulable state replaced by incoagulability
• blockade of microcirculatory by aggregates of blood cells and microthrombus
• bleeding and hemorrhage (apoplexy)
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DIC etiology
1. Infections, especially generalized (sepsis) - 30-50%;
2. All types of shock;
3. Acute intravascular hemolysis;
4. Obstetrical pathology– premature detachment of the placenta, amniotic fluid embolism, intrauterine fetal death, and others;
5. Tumors, especially leukemia;
6. Thermal and chemical burns, etc.
7. Extreme trauma
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DIC pathogenesis
1. activation of hemostatic system by various factors;
2. diffuse intravascular coagulation and aggregation of blood cells mainly in the microcirculatory
3. consumption coagulopathy– spending a part of clotting factors and platelets;
4. spread of hemorrhage;
5. alterative changes in various organs and tissues.
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DIC stages
• Stage I– hypercoagulation and aggregation of blood (lab. – ↓ blood clotting time);
• Stage II– transitional (lab. – normal blood clotting time; ↓ fibrinogen content, thrombocytopenia);
• Stage III– hypocoagulation (lab. – ↑ blood clotting time; ↓ fibrinogen content, thrombocytopenia);
• Stage IV– regenerative or outcomes and complications.
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DIC types according to the course
– peracute (hypercoagulation phase lasts up to a few
minutes, followed by hypocoagulation) – ex.:shock;
– acute (develops in 24 hours) – ex.: septicemia;
– subacute (develops in a few days with recurrence) –
pyosepticemia;
– chronic = subacute relapsing
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Pathology of DIC
DIRECT SIGNS – aggregation of blood elements (RBC and platelets) and fibrin structures:
1. individual fibers and bundles of fibrin in subthrombus;
2. covering by fibrin layer vessel walls;
3. microthrombi: fibrin, hyaline, globular, platelet, leukocyte, erythrocyte and mixed.
INDIRECT SIGNS : hemorrhage, necrosis.
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DIC pathology IV stage
– «shock lung» (ARDS/DAD): edema, hemorrhage, aggregation of red blood cells, microthrombosis, hyaline membranes: ex.: shock
– symmetrical cortical necrosis of the kidneys: microthrombosis of glomerular capillaries with necrotizing nephrosis: ex.: bacterial shock;
– hemorrhage and necrosis of the adrenal glands (syndrome Waterhouse-Friderichsen): ex.: meningococcemia;
– Multiple small focal necrosis and hemorrhage of brain, hypophysis, myocardium, liver, pancreas;
– hemorrhages, erosions and ulcers of gastrointestinal tract: ex.: thermal burns and bacterial shock
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INFARCTION
Is a vascular necrosis (syn.: ischemic, angiogenic
necrosis)
CAUSES :
1. thrombosis
2. embolism
3. arteries spasm
4. functional hyperload with expressed artery stenosis
Types of infarcts
Depending on the form – conical: spleen, kidneys, lungs;
– irregular shape: heart, brain, intestines
Depending on the appearance (color) – white (ischemic): spleen, kidney;
– white with haemorrhagic corolla: myocardium;
– red (haemorrhagic): lungs, intestine
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Types of myocardial infarction
Depending on the size: – microfocal (subendocardial, subepicardial, intramural);
– macrofocal
– transmural
Depending on the location: apex, front and side wall of the left ventricle, interventricular
septum, etc.
Depending on time of occurrence : – primary (acute) myocardial infarction
– relapsing myocardial infarction (up to 8 weeks from primary);
– recurrent myocardial infarction (after 8 weeks from primary).
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Transmural myocardial
infarction, left ventricular
and interventricular septum
of the heart
Myocardial infarction.
15 hours after the beginning of
ischemia. Cariolysis.
Types of cerebral infarctions
Cerebral infarction– ischemic stroke.
– white infarct (center of gray softening of the
brain);
– red infarct (center of red softening of the brain);
– mixed infarct (combination of white and red).
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Infarcts types
In kidneys : as a rule, cone-shaped white or with hemorrhagic corolla
infarct of cortical or the entire parenchyma. When closing the main
arterial trunk – total or subtotal renal infarct. While DIC with
thrombosis of glomerular capillaries - symmetrical cortical necrosis
of the kidneys.
In the spleen: conical white infarcts with fibrinous inflammation of the
capsule and the formation of adhesions
In the intestine: hemorrhagic infarction with transition to gangrene
with wall perforation and peritonitis.
Infarctions occur rarely in retina, liver, muscles, bones.
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