DEFINATION

Prevention of blood loss from a traumatized blood vessel

Mechanism of Hemostasis Vascular constriction Formation of platelet plug Formation of blood clot Growth of fibrous tissue

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

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

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)

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

Formation of blood clot CLOTTING

FACTORS

INTIATION OF COAGULATION

EXTRINSIC PATHWAY

INTRINSIC PATHWAY

FORMATION OF BLOOD CLOT

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

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

INTRAVASCULAR ANTICOAGULANT ENDOTHELIAL SURFACE FACTOR

1. Smoothness (intrinsic pathway)

2. Layer of Glycocalyx

3. Thrombomodulin

Binds Thrombin

Activates protein C (V and VIII)

FIBRIN FIBERS

Prevents spread of thrombin ANTITHROMBIN III

Inactivates thrombin HEPARIN

Binds with antithrombin III

Factor XII, XI, X, IX

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

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

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

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

Hemophilia B

1. Due to deficiency of factor IX Treatment

Injectable purified factor VIII

Recombinant factor VIII

Fresh frozen plasma

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

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

Causes

1. Any roughened endothelial surface of vessels

2. Stasis of blood Treatment

T-PA genetically engineered

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

Blood Coagulation Tests

Bleeding Time

1 to 6 minutes Clotting time

6 to 10 minutes

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

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

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.