Haemodynamic Disorders Flashcards
Thrombosis and Embolism both causes
Infarction
Normal Hemostasis depends on
Vascular wall
Platelets
Blood clotting system
What is hemorrhage
Injury without blood clotting which results with blood escape from the vessels
4 steps of Blood clotting
1- Vasoconstriction
2-Primary Hemostasis
3-Secondary Hemostasis
4-Thrombus and Antithrombotic events
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
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
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
Function of Fibrin
Adhere platelets to each other while forming the solid plaque
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
2 mechanisms of Endothelium and Subendothelium
1-Passive mechanism
2-Active mechanism
Passive Mechanism
Covers the subendo which is thrombogenic — plug formation
Fibriller collagen
Fibronectin
Role of Fibriller collagen in Passive mechanism
Platelet adhesion
Platelet activation
Contact activation of clotting factor
Role of Fibronectin in Passive mechanism
Stabilize cell to cell, cell to substrate attachments in the endothelial lining
*Cross-linked to fibrin
Active mechanism of Endothelium and Subendothelium
Antithrombotic factors
Prothrombotic factors
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
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
Control of PGI2,NO and Adenosine Diphosphate is belong to
Thrombin— anti-coagulant
Types of platelets receptors
Gp1b
Gp2b-3a
Role of Gp1b receptor
Binding of platelets to vWF
**Adherence
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
Role of vWF
Binds to platelets by Gp1b receptor
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
