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

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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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Virchow’s triad in thrombosis

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

Postmortem blood clot in

the pulmonary artery

Thrombus of the aorta

(atherosclerosis)

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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Occlusive Arterial Thrombus

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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Metastasis of breast cancer into lung

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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Embolic

suppurative nephritis

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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Fatty pulmonary embolism.

Stained with Sudan III.

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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Amniotic fluid embolism. Fetal scales on skin epidermis of mother’s pulmonary vessels

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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Acute respiratory distress syndrome/ diffuse alveolar damage

INFARCTION

Is a vascular necrosis (syn.: ischemic, angiogenic

necrosis)

CAUSES :

1. thrombosis

2. embolism

3. arteries spasm

4. functional hyperload with expressed artery stenosis

Occlusive thrombosis in coronary artery

Myocardium Infarction

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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Cerebral

infarction

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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Outcomes of infarcts

• Autolysis with complete recovery;

• Organization;

• Encapsulation;

• Petrification (ossification);

• Haemosiderosis;

• Formation of the cysts;

• Suppuration

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