hamostasis and blood coagulation
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Hemostasis And Blood Coagulation
Prof. M.C. Bansal MBBS ., MS., MICOG . , FICOG.
Fonder principal & Control, Jhalwar Medical College & Hospital Jhalawar
Ex principal & Controller MGMC & Hospital Sitapura ., Jaipur.
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Normal Blood Coagulation
intra vascular coagulation is linked with three different interrelated systems.
1. Coagulation System .
2. Coagulation Inhibitory System .
3. Fibrinolytic System .
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Events in Hemostasis Hemostasis means prevention of blood
loss after blood vessel is severed or ruptured.
It is achieved by a complex mechanism . 1, Vascular constriction. 2, Formation of Platelet plug . 3, Clot formation by coagulation
process switched on by trauma, 4, Eventual fibrosis in clot closed to the
hole in blood vessel.
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Vascular constriction
It is brought about by -- a. Local auto acid factor released from
traumatized tissue ., b. spontaneous and its own Spasm of
myofibrils of blood vessel. c . Nervous reflex ---traumatized
sensory nerve endings convey to higher center and efferent nerves carry action orders to myofibrils .
d. Thromboxane A produced by Platelets .
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Formation Of Platelet Plug Small holes are immediately closed by platelet plugs. Platelet Cytoplasm has many active factors like Actin,
myocine molecules , thromboplastin , Adenoplasmin Reticulum , Golgi apparatus ( synthesize Various enzymes and store Ca ++ ), Mitochondria and enzyme system capable to produce ATP, ADP , Prostgandins , fibrin stabilizing factor and growth factor.
Growth factor growth of and repair of vascular endothelium myofibrils and fibroblasts needed for blood vessel repair.
Platelet membrane is coated with glycoprotein which prevent their adherence to healthy endothelium .but once endothelium is damaged the platelets quickly and abundantly adhere to damaged endothelium and exposed collegen fibers in the vessel wall there by plugging the hole / defect.
Platelet membrane also contain phospholipids.
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3rd mechanism of hemostasis---clot formation
It starts to develop with in 15-20 seconds of injury to blood vessel .
clotting process activating substances are released from traumatized tissue , vascular endothelium, platelets and plasma proteins.
If vascular hole is small , it is plugged with in 2-3 minutes but in case of large defect it may take 20 minutes to 1 hour .
The clot formed in damaged followed by repaired site retracts and further closes the vessel.
Platelets also play an important role in clot retraction .
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Fibrous Organization / dissolution of clot
Once the clot is formed , blood vessel defect is repaired the clot is invaded by fibroblasts ( promoted by Growth factor produced by platelets ) . This continues till complete organization of clot in to fibrous tissue is completed with in 1-2 weeks .
Extra vagated blood is also clotted similarly and is dissolved by fibrinolysis activity.
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Prevention of blood clotting in normal blood vessels – mechanism of Intra vascular anti coagulation
The smoothness of vascular endothelium prevents platelet adhesion and contact activation of intrinsic clotting cascade.
A layer of Glycocalyx on endothelium repels platelets and intrinsic factor to contact .
Protein bound to endothelium called Trombomodulin binds with Thrombin and slows the process of clotting and their complex molecule “ Thrombomodulin-thrombin “ activates protein C ., inhibits factor V and VIII.
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Prevention of blood clotting in normal blood vessels – mechanism of Intra vascular anti coagulation-----
In damaged / rough endothelium –Glycocalyx and Thrombomodulin is lost hence both factor XII, platelet adhesion and intrinsic factor initiate the clotting cascade .
Anti Coagulants are also present in blood itself ----They remove thrombin from the blood.
1 Fibrin fibers . 2 Alpha globulin also called antithrombin III or
antithrombin Co factor. This prevents excessive clot formation .
3 free Thrombin combines with fibrin fibers and anti thrombin III , so free thrombin is no more available to fibrinogen to form fibrin clot
.Heparin –secreted by mast cells , its physiological role is limited and insignificant , but pharmacological use is very common in clotting disorders in clinical practice.
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Lyses of Blood clot Plasma proteins contain euglobin called
Plasminogen when activated changes into Plasmin ( Fibrinlysin ) . It is proteolytic like trypsin enzyme .
It digests fibrin fibers , fibrinogen , factor V , VIII , IX and prothrombin , causing dissolution of clot .
After few days of trauma when bleeding is stopped , repair work / healing process starts Endothelium librates a powerful activator called tissue plasminogen activator (t-PA ) , which converts plasminogen in to plasmin to remove the undesired clot to facilited neo vascularisation and patency of blood vessel necessary for tissue perfusion .
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Normal Values Of Blood Coagulation Profile
Test Value
Bleeding Time – Duke’s Method Ivy’s Method
1-3 Mins1-9 Mins
Coagulation Time- Wright’s Tube Method
Lee & White’s Methods
3-7 Mins4-9 Mins
Clot Observation Test (Weiner’s) 6-12 Mins
Clot Retraction Time 30 Mins
Fibrindex Or Thrombin Test Formation Of A Clot In 1 Min
Prothrombin Time 11-17 Mins
Thrombin Time 10-15 Secs
Platelet Count 1.5-4 Lacs/Cumm
Fibrin Degeneration Products 0-5 Micro G/Ml
Euglobin Clot Lysis Time 2-4 Hours
Fibrinogren 300-600 Mg%
D-dimer 0-200 Mg/Ml
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Collection Of Blood Samples For Lab Tests
Test Method Of Collection Of Blood In Test Tube / Vial
Amount Of Blood
Hb% Or PCV EDTA Vial 2 Ml
ABO & Rh Group Plain (Clotted) And 3.8% Sodium
Citrate Solution
2 Ml & Few Drops
Vdrl Plain (Clotted) 2ml
Direct / Indirect Coomb’s Test
Plain (Clotted) 2ml
Prothrombin Time 0.5 Ml Of 3.8 % Sodium Citrate
Solution
4.5 Ml
Fibrinogen EDTA Vial 2ml
Platelet EDTA Vial 2ml
Edp Special Tubes Supplied With Kits
Eclt Citrate Solution 4.5 Ml
D-dimer EDTA Vial 2 Ml
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Conditions causing excessive Bleeding
Deficiency of one / more blood clotting factors .
Vit. K . Deficiency . Hemophillia . Thrombocytopenia. Liver disease ==not able to produce
clotting factors . DIC
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Thrombo –Embolic Conditions Abnormal that develops in blood
vessel being loosely attached may get detached and flow in circulation –get lodged at distance is called Embolus ( in pulmonary or aortic circulation ---chocks the end arteries).the affected area / organ does not get O2 resulting in Acute Ischemia and infarction .
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Causes Of Thrombi-Embolism Roughened breeched endothelium in blood
vessels ---arteriosclerosis , atheroscerosis , infection , traumatic .
Blood flow is very slow or stagnant . Intra venous therapy cannulatios left in situ for a
longer time , trombophlebitis . Intravenous thrombosis ----Central sinus vein ,
deep veins of calf and pelvis . Intramural thrombus in heart chambers . Its incidences increases in pregnancy ,
puerperium LSCS ( hyper coagulability state of pregnancy , tissue trauma, inflammation , dehydration , prolong bed rest ) , pelvic surgery
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