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DEFINATION
Prevention of blood loss from a traumatized blood vessel
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Mechanism of Hemostasis Vascular constriction Formation of platelet plug Formation of blood clot Growth of fibrous tissue
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Vascular constriction
Traumatized blood vessels causes smooth muscle of blood vessels to contract by
1. Local myogenic spasm
2. Local autacoids factors
3. Nervous reflexes
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PLATELETS
Thrombocytes formed from Megakarocytes
Normal concentration 150,000 to 300,000
Half life of 8 to 12 days Its membrane contains phospholipids
and it is coated by Glycoprotein Don't have nuclei
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Cytoplasm contains
1. Actin, myosin and thrombosthenin
2. Residual of endoplasmic reticulum and golgi apparatus
3. Mitochondrial enzyme system
4. Fibrin-stabilizing factor
5. Growth factor
6. Prostaglandins synthesizing enzymes
7. Thromboxane A2 ( Vasoconstrictor)
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Formation of platelet plug Minute ruptures from small blood vessels1. Contact of platelet with damaged vascular
collagen fibers2. Platelet swell, protruding pseudopods,
contractile protein causes release of granules3. Becomes sticky with collagen and to a
protein called Von Willebrand factor
4. Secretes ADP and Thromboxane A2 which activates other platelets and formed platelet plug
5. fibrin threads makes unyielding plug
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Formation of blood clot CLOTTING
FACTORS
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INTIATION OF COAGULATION
EXTRINSIC PATHWAY
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INTRINSIC PATHWAY
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FORMATION OF BLOOD CLOT
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Composition of blood clot1. Meshwork of fibrin fibers2. Blood cells3. Platelets4. Plasma Clot Retraction With in 20 to 60 minutes clot retracts and
expresses fluid devoid of fibrinogen and other clotting factors called SERUM
PlateletsThrombinCa++
Vicious circle of clot formation
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Growth of fibrous tissue After clot is formed it can
1. Invaded by fibroblast which form connective tissue
2. It can dissolve
When a clot is formed it entrapped a plasma protein named as PLASMINOGEN that is activated by TISSUE PLASMINOGEN ACTIVATOR (t-PA) to PLASMIN after few days. That digest fibrin fibers, factor I,11,V,VIII,XII
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INTRAVASCULAR ANTICOAGULANT ENDOTHELIAL SURFACE FACTOR
1. Smoothness (intrinsic pathway)
2. Layer of Glycocalyx
3. Thrombomodulin
Binds Thrombin
Activates protein C (V and VIII)
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FIBRIN FIBERS
Prevents spread of thrombin ANTITHROMBIN III
Inactivates thrombin HEPARIN
Binds with antithrombin III
Factor XII, XI, X, IX
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ANTICOAGULANT FOR CLINCAL USE HEPARIN I.V 0.5 to 1 mg/kg of body weight Increases clotting time to 30 minutes Action lasts for 1.5 to 4 hours Destroyed by enzyme known as Heparinase COUMARINS Warfarin Factor II, VII, IX and X levels decreases Inhibits VKOR c1
Vitamin K not in active reduced form
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OUTSIDE THE BODY1. SILICONIZED GLASS CONTAINERS
Prevents contact activation of platelets and factor XII
2. HEPARIN
3. DECREASES Ca ion CONCENTRATION
Oxalate compounds
Citrate compounds
Citrate are better than oxalate, removed from liver
But in large quantities and liver failure can lead to TETANY and CONVULSIVE DEATH
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FACTORS RESPONSIBLE FOR INCREASE BLEEDING TENDENCY VITAMIN K DEFICIENCY1. Fat soluble
2. Bacterial intestinal flora
3. Cause -: decreased absorption of vitamin k from intestine as seen in obstruction of bile
4. II, VII,IX, X and protein C (V, VIII)
5. Liver carboxylase that add a carboxyl group to glutamic acid residues
6. Role of VKOR c1
7. Treatment is IV vitamin K
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HEMOPHILIA Genetically transferred through female
chromosome and occurred more exclusively in males. Bleeding occurs from larger vessels
Hemophilia A or Classic hemophilia1. Smaller component of factor VIII2. Responsible for intrinsic pathway of
coagulation Von Willebrand’s disease1. Larger component of factor VIII
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Hemophilia B
1. Due to deficiency of factor IX Treatment
Injectable purified factor VIII
Recombinant factor VIII
Fresh frozen plasma
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THROMBOCYTOPENIA Very low number of platelets Bleeding occurs from small blood vessels Small punctate hemorrhages through out the
tissues Purplish blotches on skin (Thrombocytopenia
Purpura) Frequent bleeding occurs when platelet count
decreases to 50,000/µL IDIOPATHIC THROMBOCYTOPENIA Fresh whole blood transfusion Splenectomy
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THROMBOSIS AND EMBOLISM THROMBUS
Abnormal clot formed in blood vessels
Types of thrombus
1. Arterial thrombus
2. Venous thrombus EMBOLI
The floating clot in blood
Massive pulmonary embolism
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Causes
1. Any roughened endothelial surface of vessels
2. Stasis of blood Treatment
T-PA genetically engineered
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DISSEMINATED INTRAVASCULAR COAGULATION (DIC) Widespread of clotting mechanism in the
circulation CAUSES
1. Large amount of traumatized or dying tissues causes release of tissue factor
2. Widespread septicemia (endotoxin) EFFECTS
1. Septicemic shock
2. Bleeding
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Blood Coagulation Tests
Bleeding Time
1 to 6 minutes Clotting time
6 to 10 minutes
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Prothrombin Time
1. Removal of blood
2. Addition of oxalate
3. Addition of large quantities of Ca and tissue factor
4. Activation of extrinsic pathway
5. Normal prothrombin time is 10 to 12 sec
6. factors I, II, V, VII, and X
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International Normalized Ratio Different individuals have different tissue
factor activity INR is advised
INR= (PT test )ISI
(PT normal) International sensitivity index 1.0 to
2.0 Normal INR= 0.9 TO 1.3
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Partial Thromboplastin Time (PTT) OR Activated Partial Thromboplastin Time (aPTT or APTT) Performance indicator measuring the
efficacy of both the Intrinsic and the common coagulation pathways.
1. Removal of blood2. Addition of oxalate3. Addition of large quantities of Ca and
Phospholipids4. Activation of intrinsic pathway5. Normal PTT time is 25sec to 32 sec6. factors: I, II, V, VIII, IX, X, XI, & XII.