Haemodynamic Disorders Flashcards by Ipek Tuzcu

Thrombosis and Embolism both causes

Infarction

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Normal Hemostasis depends on

Vascular wall
Platelets
Blood clotting system

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What is hemorrhage

Injury without blood clotting which results with blood escape from the vessels

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4 steps of Blood clotting

1- Vasoconstriction
2-Primary Hemostasis
3-Secondary Hemostasis
4-Thrombus and Antithrombotic events

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What happens first step of blood clotting

Vasoconstriction
Endothelin release causes vasoconstriction
Maintained by endothelial cells
Inhibit the escaping from BV
Injury to vessel wall
Shrinkage of BV

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What happens and which molecules take place in the second step of Blood clotting

Primary Hemostasis
Normal functioning epi cells and platelets take role
1-Platelet adhesion
2-Shape of platelets change
3-Granule release (ADP,TXA2)
4-Increase in the number of platelets bc of TXA2
5- Hemostatic plug formation

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What happens and which molecules take place in the third stage of blood clotting?

Platelets, clotting factors,epi cells,fibrin
1- Tissue factor secretion and stimulates clotting cascades
2-Phospholipd complex expression
3-Thrombin activation
4-Fibrin polymerization
At the end solid plaque

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Function of Fibrin

Adhere platelets to each other while forming the solid plaque

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What happens and which molecules take place at the last stage of blood clotting

Clotting factors,platelets
Release of t-PA (fibrinolysis)
Release of Thrombomodulin — blocks coagulation cascade —secreted from platelets
Degradation of the solid plaque

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2 mechanisms of Endothelium and Subendothelium

1-Passive mechanism
2-Active mechanism

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Passive Mechanism

Covers the subendo which is thrombogenic — plug formation
Fibriller collagen
Fibronectin

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Role of Fibriller collagen in Passive mechanism

Platelet adhesion
Platelet activation
Contact activation of clotting factor

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Role of Fibronectin in Passive mechanism

Stabilize cell to cell, cell to substrate attachments in the endothelial lining
*Cross-linked to fibrin

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Active mechanism of Endothelium and Subendothelium

Antithrombotic factors
Prothrombotic factors

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What happens at the Thrombotic stage of Blood clotting

Platelet stimulation—vWF and collagen binding
Platelet adhesion— held together by fibrinogen
Procoagulant—Coagulation stimulation—membrane bound tissue factor, coagulation sequence
Antifibrinolytic

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What happens at the Antithrombotic stage of Blood clotting

Anticoagulant— Thrombin inactivation—Thrombomodulin and thrombin direct binding, Heparin-like molecule and Antithrombin 3 binding.

Antiplatelet— PGI2,NO,Adenosine Diphosphate releasing from endo cells— inhibits platelet aggregation.

Fibrinolytic— t-PA

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Control of PGI2,NO and Adenosine Diphosphate is belong to

Thrombin— anti-coagulant

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Types of platelets receptors

Gp1b
Gp2b-3a

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Role of Gp1b receptor

Binding of platelets to vWF
**Adherence

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Role of Gp2b-3a

Binding 2 platelets together by binding the same fibrinogen
Fibrinogen binds first after than the second platelet comes and binds
**Platelet aggregation

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Role of vWF

Binds to platelets by Gp1b receptor

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Secretion of vWF by

Endothelial cells

Deficiency of Gp2b-3a causes

Glanzmann thrombasthenia

Deficiency of Gp1b causes

Bernard-Soulier syndrome

Deficiency of vWF causes

Von Willebrand disease— rapid hemorrhage

Platelet activation maintained by (*)

Collagen

In order to activate platelets which events should occur

Adhesion and shape change Secretion Aggregation

Platelets synthesize_?

TXA2 for aggregation/vasoconstriction

2 groups of platelet secretions

1-Alpha granules = Fibrinogen,TGF-beta,Platelet factor 3,vWF 2-Dense bodies= ADP,ATP,Ca,histamine,serotonin, epinephrine

Role of ADP in blood clotting

Formation of primary and secondary hemostotic plague

Fibrinogen converted to fibrin how

By activated thrombin(active coagulant factor 2) and Ca

Which of the platelet factor limites the excess blood clotting in the are of injury

Unmasking platelet factor 3

Gp2b-3a activated by?

Thromboxane

Gp1b inhibited by

Heparin

What are the secretions of endothelium when stimulated by Thrombin

T-PA NO PGI2 All of them inhibit aggregation of platelets

Two coagulant effects of Thrombin

Pro-coagulant Anti-coagulant

Anticoagulant mechanisms

Depletion of clotting factors Clearance of activated clotting factors Inhibition of activated proteases Fibrinolysis—main anti-coagulant mechanism

How is Fibrinolysis occur?

Fibrin+Fibrinogen—> Split products Enzyme= Plasmin protease Plasmin is formed from Plasminogen(Zymogen)

Plasminogen activators

Urokinase-like PA—>fluid phase, plasma Tissue type PA —>fibrin,endo cells

Thrombosis

Clotted mass of blood in a specific area Limits the blood flow Attached to the vessel wall Endothelial injury,Hypercoagulability, Abnormal blood flow causes Thrombosis

Alterations in normal blood flow

Turbulence= Countercurrents,local pockets of stasis Stasis= sluggish venous thrombosis, varicose veins

Hypercoagulability seen in

Deficiency of antithrombin 3/protein C Kidney diseases Severe trauma or burns Disseminated cancer Late pregnancy

Hazards of thrombosis

Race Age Smoking Obesity

Types of thrombi

Venous Thrombi= occlusive. Occurs in superficial varicose veins, deep leg veins. Attached to the underlying vessel wall.emboli in lung. Venous infarction Arterial Thrombi=occlusive, coronary,cerebra,femoral. Due to atherosclerosis,vasculitis,traumatic injury. Infraction in myocardial,cerebral. Emboli in cardiac chambers and aorta

Mural thrombi

Non-occlusive At heart chambers of aorta

Vegetations thrombi

Thrombotic masses on the heart valves

What is Lines of Zahn

Alternating layers of platelets+ fibrin(pale) and RBC (darker) Characteristic for thrombus In autopsy *

Types of Embolism

Pulmonary= thrombi of large veins of the lower leg Systemic = thrombi from the heart

Critical determinants for Embolism

Site of lodgement Size of the emboli

Amniotic fluid embolism

Result of tear in placental membranes+rupture of uterine veins—>Amniotic fluid enters in circulation HUMORAL FACTOR (PGF2)—> Pulmonary vasoconstriction +impaired cardiac contractility—> cardiac shock+ pulmonary edema

Fat embolism

Fractures of large bones Affects lung,brain,kidney Embolism of fat globules Emulsion instability Chemical injury to microvessels Activation of the coagulant system

Air or Gas Embolism Barotrauma

Caused by delivery or abortion

Decompression sickness

Sudden change in atmospheric pressure Acute= effects small blood vessels Chronic= causes Caisson disease —> Platelet activation and Intravascular coagulation

Infarction

Localized areas of ischemic necrosis Red infarct White infarct Septic infarct Bland infarct