This document discusses the process of blood clot formation and prevention of blood loss. It describes that vascular constriction, platelet plug formation, and blood clotting close holes in veins. Platelets are formed from megakaryocytes, contain enzymes and glycoproteins, and adhere to collagen in damaged blood vessels to form platelet plugs. The clotting cascade involves the extrinsic and intrinsic pathways activating coagulation factors and converting prothrombin to thrombin and fibrinogen to fibrin to form a clot. Deficiencies in coagulation factors can cause bleeding disorders like hemophilia A, B, and C.

2. “Prevention of blood loss”

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

4.  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

5.  Thrombocytes
 Formed from megakaryocytes
 Anucleated
 1,50000 – 300,000 / µl
 Actin myosin molecules & thrombosthenin
 Residual ER & golgi apparatus
 Enzyme system to synthesizeATP from ADP

6.  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

7.  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

8.  Clot – when blood looses its fluidity.
 Clot forms – 15 – 20 sec
 Activator substances – adheres to
traumatized vessel
 Clot formed

11. CLOTTING FACTOR SYNONYMS
Fibrinogen Factor I
Prothrombin Factor II
Tissue factor Factor III
Calcium Factor IV
Labile factor FactorV
Accelerin FactorVII
Antihemophillic factor FactorVIII
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

12.  Clot Follows 2 ways.
 Invaded by fibroblasts
 Can be dissolved

13.  Procoagulants
 Anticoagulants
 Formation of prothrombin activator
 Conversion of prothrombin to thrombin
 Conversion of fibrinogen to fibrin

14.  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.

15.  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

17.  Extrinsic pathway
 Intrinsic pathway

18.  Traumatized vessel release tissue factor .
 Factor III with factorVII  act on factor X 
Factor Xa
 Factor Xa complexes with phospholipids &
factorV .
 Prothrombin activator formed.

19.  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

21.  Extraction of fluid after coagulation i.e.
serum

22.  Disseminated intravascular coagulation (DIC)
 Hemophilia
 Thrombocytopenia
 Purpura
 Thrombo embolic condition

23.  HemophiliaA
(VIII small component def.)
 Von willebrands disease
(VIII large component def.)
 Hemophilia B
(IX def)
 Hemophilia C
(XI def.)