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Blood clot formation and fibrinolysis processes explained
1. Prepared By : Muhammad Halmii (016-3626470)
TEAM GENESIS
2. DEFINE
CAUSE (-)
DISEASE PROCESS (PATHOGENESIS) (X)
TYPES (X)
EFFECT (- )
CLINICAL MENIFESTATIONS (SIGNS & SYMPTOMS)
TEAM GENESIS
3. Blood Clot:
A thickened mass in the blood formed by tiny substances
called platelets. Clots form to stop bleeding preventing
excessive blood loss
Fibronolysis: (Lysis Of Fibrin)
Fibrinolysis is a process that prevents blood clots from
growing and becoming pathologic
BOTH PROCESS ARE STEPS OF WOUND HEALING &
PHYSIOLOGICAL TEAM GENESIS
9. Made In Bone Marrow From The Megakaryocytes’ Cytoplasm
Not A Cell
Below Normal Count = Thrombocytopenia
High Normal Count = Thrombisis
F(x) = Hemostatic Plug etc.
Binding Site = Between Platelets , VWFTEAM GENESIS
11. Platelet adhesion: First event in hemostasis is the adhesion of platelets to exposed subendothelium. mediated
by von Willebrand factor (vWf), which binds to glycoprotein Ib.
Platelet activation:The adhesion of platelets to the vessel wall activates them, causing the platelets to change
shape & activates the receptor glycoprotein IIb/IIIa. Upon activation, platelets synthesize and release
thromboxane A2 (TXA2) and platelet activating factor (PAF), which are potent platelet aggregating agonists and
vasoconstrictors. {POSITIVE FEEDBACK}
PRIMARY HEMOSTASIS
TEAM GENESIS
12. Synthesized At Gene No. 12
F(x) = Grips Platelets At Glycoprotein Ib To Stabilize
Clot
TEAM GENESIS
13. Converts Fibrinogen To Fibrin
Activates Factor 13 (Hardening Of )
Generates Procoagulant Activity
Activates (Protein C) Fibrinolysis After A While
TEAM GENESIS
14. Involves Both Intrinsic (Inside BV) & Extrinsic (Outside BV) Activity To Generate Thrombin Which Ultimately
Generates Fibrin
Happens After Primary Hemostasis
Extrinsic Initiate But Produces Little Fibrin While Intrinsic Amplifies Action
INtrinsic
Twelve
Eleven
Nina
Eight
Ten
12
11
9
8
10
5
7
TEAM GENESIS
15. Initiation of coagulation: The coagulation cascade is initiated by the extrinsic pathway with the
generation/exposure of tissue factor. Tissue factor then binds to factor VII and this complex activates factor X.
Factor X, in the presence of factor V, calcium and platelet phospholipid ("prothrombinase complex") then
activate prothrombin to thrombin. This pathway is rapidly inhibited by a lipoprotein-associated molecule,
called tissue factor pathway inhibitor. However, the small amount of thrombin generated by this pathway
(before inhibition) activates factor XI of the intrinsic pathway, which amplifies the coagulation cascade.
Amplification of coagulation: The coagulation cascade is amplified by the small amounts of thrombin
generated by the extrinsic pathway. This thrombin activates the intrinsic pathway by activation of factors TENET.
generating large amounts of thrombin. Thrombin, in turn, then cleaves fibrinogen to form soluble fibrin
monomers, which then spontaneously polymerize to form the soluble fibrin polymer. Thrombin also activates
factor XIII, which, together with calcium, serves to crosslink and stabilize the soluble fibrin polymer, forming
cross linked (insoluble) fibrin.
TEAM GENESIS
17. Clot Would Be Dangerous If It Were To Expand
Beyond Boundary
Thus They Are Inhibited By:
Clotting Factors Are Rapidly Inhibited At Other Places
(Enzymes In Blood Inactivate Clotting Factors)
End Product Inhibition Of Fibrin (The Higher Fibrin,
The Higher The Intensity Of Thrombin Inhibition)
TEAM GENESIS
18. Activated Protein C & Protein S
Tissue Factor Inhibitor
Anti-Thrombin
Heparin Cofactor II
GO AND READ YRSELF
In Short, They Prevent Unnecessary Clotting At
Unwounded Areas
PREVENTS CLOT FORMATION BUT DOES NOT
DESTROYS THE CLOT !!!!! TAKE NOTE
TEAM GENESIS
19. The Clot Stimulates Tissue Plasmin Activator
TPA Converts Plasminogen To Plasmin
Plasminogen Is Found In Blood
Clot Removal Happens At A Slow Pace To Enable
Endothelial To Divide For Healing
TEAM GENESIS
21. Reaction Time Is Delayed
Prolonged Clotting Time
Increase Blood Loss
TEAM GENESIS
22. Vascular Disorder
Scurvy (Scurvy is a disease resulting from a deficiency of vitamin C,
which is required for the synthesis of collagen in humans.)
Bruising Vulneribility (Lack Of Endothelial Integrity)
Platelets Disorder
Thrombocytopenia (Platelet count below 50,000 per microlitre.)
Platelets Dysfunction (Platelets Lacking Of Receptors)
Coagulation Disorder
Hemophilia (Lacking Of Intrinsic Factors)
TEAM GENESIS
23. Blood Count
Bleeding Time (Diagnose Thrombocytopenia)
Prothrombin Time (Measure Extrinsic Factor)
PT Excellent
Activated Partial Thromboplastin Time (Intrinsic &
Common)
Thrombin Time (Tome For Fibrinogen To Fibrin Formation)
Mixing Test (Detect Factor Dificiency)
TEAM GENESIS