Hemostasis & Blood Coagulation - Abir Debnath, Batch 17 AGMC.pptx

imabir2001 70 views 18 slides Jun 22, 2024
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HEMOSTASIS & BLOOD COAGULATION Presented by roll 1 – 10 AGARTALA GOVT MEDICAL COLLEGE BATCH 17

OBJECTIVES 03 01 D efinition of hemostasis 02 Clot Retraction 04 S teps of hemostasis and coagulation Clinical Scenarios HEMOSTASIS & BLOOD COAGULATION Presented by roll 1 - 10

H ow to define ? Hemostasis can be defined as the mechanism by which loss of blood from vascular system can prevented by a complex interaction of vessel wall, platelets and plasma protein.

STAGES OF HEMOSTASIS Primary Secondary Limits blood loss from damaged vessel by temporary hemostatic plug Finally stops the bleeding by formation of a stable fibrin clot from clotting factors by enzymatic reaction

PRIMARY HEMOSTASIS Immediate response of blood vessel to Injury It is a local mechanical response (Stretch induced contraction) Occurs due to contraction of vascular smooth muscle. The contraction results from i ) local myogenic spasm ii) local autacoid factors like TXA2 released from injured tissue iii) Nervous reflex i ) Vasoconstriction

PRIMARY HEMOSTASIS contd. ii) Temporary hemostatic plug formation Involves platelet adhesion, aggregation and secretion Platelets achieves so by rapid change in shape and increased surface adhesiveness to the injured vascular endothelium. Platelets then stick to each other and secrete a number of chemicals; which facilitated the aforesaid process. --------Thus, it arrests the bleeding temporarily by formation of a platelet plug ( temporary hemostasis).

SECONDARY HEMOSTASIS i ) Blood Coagulation Immediately following the injury, the clotting mechanism of the blood is initiated. This results in the formation of a blood clot at the site of injury Now , the plug formed is called a definitive hemostatic plug . This whole process is due to activation of clotting factors There are 13 clotting factors. They are activated in cascade amplification process.

Blood Coagulation Mechanism In general, the blood clotting occurs in 3 stages i ) Formation of prothrombin activator ii) Conversion of prothrombin into thrombin iii) Conversion of fibrinogen into fibrin .

Blood Coagulation Mechanism CONTD. The f ormation of prothrombin activator occurs through two pathways:     Stage - 1: Formation of Prothrombin A ctivator It is triggered by When blood is exposed to the collagen fibres underlying the roughened or damaged endothelium in blood vessels. (ii) Change in blood constituents It is triggered by injury to ( i ) Blood vessel wall or (ii) other body tissues Intrinsic Pathway Extrinsic Pathway

Blood Coagulation Mechanism CONTD Prothrombin activator that is formed in intrinsic and extrinsic pathways converts prothrombin into thrombin in the presence of calcium (factor IV) Once formed thrombin initiates the formation of more thrombin molecules. The initially formed thrombin activates factor V. Factor V in turn accelerates formation of both extrinsic and intrinsic prothrombin activator, which converts prothrombin into thrombin. Stage - 2: CONVERSION OF PROTHROMBIN INTO THROMBIN

Blood Coagulation Mechanism CONTD Thrombin converts inactive fibrinogen into activated fibrinogen the activated fibrinogen is called fibrin monomer. Fibrin monomer polymerizes with other monomer molecule and form loosely arranged strands of fibrin. Later these loose strands are modified into dense and tight fibrin threads by fibrin - stabilizing factor (Factor XIII) in the presence of calcium ions.    All the tight fibrin threads are aggregated to form a meshwork of stable clot ( definitive clot ) STAGE - 3: FIBRINOGEN INTO FIBRIN

CLOT RETRACTION After the formation of Fibrin Clot , within 5 to 30 minutes, clot retracts down to about 40% of its original volume . It liberates serum . This process of clot retraction is impaired in low platelet counts.

How is blood prevented from clotting within the circulation? If blood clots within the circulation, there may be severe hemodynamic pathologic manifestation like embolism which may get lodged and cause infarction. It is due to Endothelial factor- Smooth endothelial lining and negatively charged particles Velocity of circulation- decrease may lead to clotting Presence of natural coagulants like heparin and protein C Fibrinolytic system is activated. Liver comes into action and removes the clotting factors from the circulation. ( Factor IX,X,XI,XII)

FIBRINOLYTIC SYSTEM After a clot is formed, it is also dissolved under various instances. Being lysed by plasmin, there is formation of FIBRINOGEN DEGRADATION PRODUCTS

CLINICAL SCENARIOS Common major causes of bleeding disorders can be classified as: A. Defective blood clotting due to: ( i ) Deficiency of clotting factors - Hemophilia A, Hemophilia B, V on W illebrand’s disease (ii) Deficiency of vitamin K (iii) Anticoagulant overdose    B. Defective capillary contractility – Purpura    C. Combined defects YOU THANK

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