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

4. Anticoagulant Coagulant
Eg: Heparin, Antithrombin Eg: Fibrin
Thrombin
Excessive:Hemophilia Excessive:Thrombosis
TEAM GENESIS

5. Haemostasis
Inflammation
GranulationRemodelling
/ Maturation
Proliferative
Angiogenesis
Overlaps
Blood Clot
Fibrinolysis
TEAM GENESIS

6. TEAM GENESIS

7. Local Response : Release Thromboxane
Systemic Response : Adrenal Medulla Regulates Hormones (i.e epinephrine & norepinephrine)
Stimulates Cross Bridge Of Smooth Muscle Cell {i.e. contraction}
Exposes Large area of collagen surface to BV & Limits Blood Loss
Initiates Platelet Activation TEAM GENESIS

8. Primary Secondary
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

10.  Immediate Initiation (20 sec) & Immediate Completion
(Few Minutes)
 Platelets Undergo Conformational Shape Change To Enhance
Clot
 Main Components : Platelets 100%
 Moderately Stable
TEAM 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

16. 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

20.  Destroys Fibrinogen & Fibrin
 Produces D-Dimer
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