BLOOD

COAGULATION
&
HEMOSTASIS
HEMOSTASIS
“Prevention of blood loss”
MECHANISMS OF HEMOSTASIS

 Vascular constriction
 Formation of platelet plug
 Blood clot formation
 Fibrous tissue organization to close the hole
of veins.
VASCULAR CONSTRICTION

 Smooth muscle contraction to reduce blood

flow after an injury or cut.
 3 factors responsible for contraction.
 Nerve reflexes
 Autocoids from platelets or traumatized tissue
 Myogenic spasm
PLATELETS

 Thrombocytes
 Formed from megakaryocytes
 Anucleated
 1,50000 – 300,000 / µl
 Actin myosin molecules & thrombosthenin
 Residual ER & golgi apparatus
 Enzyme system to synthesize ATP from ADP
 Enzyme system to synthesize PGs.
 Fibrin stabilizing factor – form stable
fibrin threads
 Growth factor
 Glycoprotein on surface
 Phospholipids
 Adenyl cyclase  cAMP for further
activation of platelets
FORMATION OF PLATELET PLUG

 Platelets in contact with collagen in damaged

vessels
 Stick to collagen fibres
 Secretion of ADP & thromboxane A2
 Increased number of activated platelets
gathered to form platelet plug.
 Close small dents in vessel wall
 Fibrin threads
BLOOD COAGULATION IN RUPTURED
BLOOD VESSEL
 Clot – when blood looses its fluidity.
 Clot forms – 15 – 20 sec
 Activator substances – adheres to
traumatized vessel
 Clot formed
MECHANISM OF HEMOSTASIS
 CLOTTING FACTORS
CLOTTING FACTOR SYNONYMS
Fibrinogen Factor I
Prothrombin Factor II
Tissue factor Factor III
Calcium Factor IV
Labile factor Factor V
Accelerin Factor VII
Antihemophillic factor Factor VIII
Christmas factor Factor IX
Stuart factor Factor X
Plasma thromboplastin antecedent Factor XI
Hageman factor Factor XII
Fibrin stabilizing factor Factor XIII
Prekallikrien Fletcher factor
Kininogen HMWK
FIBROUS ORGANIZTION /
DISSOLUTION OF CLOT
 Clot Follows 2 ways.
 Invaded by fibroblasts
 Can be dissolved
MECHANISM OF COAGULATION

 Procoagulants
 Anticoagulants
 Formation of prothrombin activator
 Conversion of prothrombin to thrombin
 Conversion of fibrinogen to fibrin
CONVERSION OF PROTHROMBIN TO
THROMBIN
 Rate limiting step - formation of prothrombin
activator.
 Calcium and prothrombin activator – convert
prothrombin to thrombin
 Prothrombin – unstable protein
 Produced by liver
 Vitamin K – formation of prothrombin.
FIBRINOGEN TO FIBRIN

 HMW high molecular weight

 Formed in liver
 Small leakage from capillary to interstitial fluid
 Pathological increase in permeability –
abnormal coagulation.
 Thrombin form fibrin monomer.
 Thrombin – activation of fibrin stabilizing factor
 Covalent bond formation
 Formation of fibrin fibers
PROTHROMBIN ACTIVATOR
FORMATION
 Extrinsic pathway
 Intrinsic pathway
EXTRINSIC PATHWAY

 Traumatized vessel release tissue factor .

 Factor III with factor VII  act on factor X 
Factor Xa
 Factor Xa complexes with phospholipids &
factor V .
 Prothrombin activator formed.
INTRINSIC PATHWAY
 Trauma to blood or damage s platelets due to
adherence to collagen.
 Activates factor XII.
 XIIa in presence of HMW kinogens &
prekallikrien  XI
 XIa  IXa
 IXa + VIII  Xa
 Xa + phospholipids + V  prothrombin activator
CLOT RETRACTION

 Extraction of fluid after coagulation i.e.

serum
ALTERED PHYSIOLOGY

 Disseminated intravascular coagulation (DIC)

 Hemophilia
 Thrombocytopenia
 Purpura
 Thrombo embolic condition
HEMOPHILIA

 Hemophilia A
(VIII small component def.)
 Von willebrands disease
(VIII large component def.)
 Hemophilia B
(IX def)
 Hemophilia C
(XI def.)
 THANK
YOU!!!!!!!