SUBMITTED BY: GUIDED BY:

Maryum Siddiqui Dr. Shail Jain

BHM Ist Proff. Dr. Vikrant Garg
Dr. Naveen Jaggi
Hemostasis is a physiological mechanism which causes
spontaneous arrest of hemorrhage, when a blood vessel is
injured. It is a process of forming clot in the walls of
damaged blood vessels and preventing blood loss, while
maintaining blood in a f luid state within the vascular
system.
Hemostasis involves 3 main steps:

a)VASCULAR SPASM
b)PLATELET PLUG FORMATION
c)BLOOD COAGULATION
Because of injury, wall of the blood vessel gets damaged and
highly thrombogenic sub-endothelial tissue gets exposed.
Endothelial area around the affected area secrete signals and
smooth muscles contract, enhancing vaso-constriction.
Normal reflexes are also released which further enhance
vaso-constriction.

Chemically, Serotonin and Thromboxane A2 are also

released from platelets, which act as important vaso-
constrictors.
Platelets form a temporary plug to reduce blood
flow from the body. It takes place in four following
steps :

1.Platelet adhesion : Von williebrand factors assist

the thrombocytes to attach to injured cells of injured
site. Platelets bind easily to exposed collagen.
2.Platelet release reaction: platelets release specific
chemicals to release more platelets and increase
vaso-constriction. These chemicals are: ATP,
serotonin, thromboxane A2.
3.Platelet aggregation: platelets start aggregating
together like a seal and leads to plug formation.

4.Platelet plug formation: platelets do not adhere to

healthy cells due to the secretion of Prostaglandins
and Nitric acid.

STEP 3: BLOOD COAGULATION

This process involves clotting factors which enhances
and strengthens the plug formed by platelets by
creating a meshwork of fibrin.
It is a process in which blood looses its
fluidity and becomes jelly like and shed out.
The clotting mechanism involves a cascade of
reactions in which clotting factors are
activated.
I. Fibrinogen
II. Prothrombin
III. Thromboplastin
IV. Calcium
V. Proaccelarin
VI. Accelarin
VII. Proconvertin
VIII. Anti-haemophilic factor
IX. Christmas factor
X. Stuart-prower factor
XI. Plasma-thromboplastin antecedent
XII. Hageman factor
XIII. Fibrin stabilizing factor
Clotting factors are present in the form of enzymes.
Normally, all factors are present in the form of
Inactive proenzymes which must be activated into
enzymes, to enforce clot formation.
It is done by series of Proenzyme-enzyme conversion
reactions.
This theory explains how various reactions takes
place in form of a cascade.
 It occurs in 3 main steps :

1.Formation of Prothrombin activator

2.Conversion of Prothrombin into Thrombin
3.Conversion of Thrombin into Fibrin
Blood clotting commences the formation of a substance
called Prothrombin Activator, which converts the
prothrombin into thrombin.
Its formation is initiated by substances produced either
within or outside the blood.

It occurs in two pathways-

i)Intrinsic pathway
ii)Extrinsic pathway
Prothrombin activator is initiated by Platelets.
During the injury, blood vessel rupture ,endothelium
is damaged and collagen is exposed.
When factor XII comes in contact with collagen, it is
converted into XII a in presence of Kalikrein and
Kinogen.
XIIa converts Factor XI into Factor XIa in presence of
HMW Kinogen.
XIa activates Factor IX into Factor IXa in presence of
Calcium (Factor IV).
Factor IXa activates Factor X into Factor Xa in presence
of Factor VIII and calcium (Factor IV).
 When Platelets come in contact with collagen, it
gets activated and releases Phospholipids.
 Factor Xa reacts withPhospholipids and Factor V to
form Prothrombin Activator.
 Factor V is also activated by Positive feedback effect
of thrombin.
 Prothrombin activator is initiated by Tissue
thromboplastin.
 Damaged tissues release tissue Thromboplastin
(Factor III) which contains Phospholipids, Proteins
and Proteolytic enzymes.
 Glycoprotein and Phospholipid converts Factor X into
Factor Xa in presence of Factor VII.
 Factor Xa reacts with Factor V and Phospholipid to
form Prothrombin acivator. This process requires
Ca++ ions.
 Prothrombin activator converts Prothrombin into
Thrombin in presence of Calcium(Factor IV).
 Thus,Thrombin initiates formation of more
Thrombin molecules and activates Factor V
whichincreases formation ofIntrisic and Extrinsic
Prothrombin activator, which converts it into
Thrombin. This is known as Positive Feedback.
 Thrombin converts inactive Fibrinogen into activated
Fibrinogen, due to loss of 2 pairs of Polypeptides from
each Fibrinogen molecule. The activated fibrinogen is
called Fibrinogen monomer.
 Fibrin monomer polymerises with other monomers to
form loosely arranged strands of fibrin.
 Later, these strands are modified into dense and tight
fibrin threads by Fibrin-stabilising factor in presence
of Ca++ ions.all threads aggregate then, to form a
meshwork of Stable clot.
 Mass of coagulated blood which contains RBCs,
WBCs, and platelets entrapped in fibrin
meshwork.
 When clot is formed, these cells are trapped in
along with platelets. THE trapped RBCs, are
responsible for the red color of clot.
 external blood is also called Scab. It adheres to the
opening of damaged blood vessel and prevents
blood loss.
 After its formation, blood clot starts contracting.
 After 30-45 minutes, straw-colored serum oozes out of
the clot; because of contractile proteins in cytoplasm
namely, Actin, Myosin and Thromboplastin.
Haemostatic substances which accelerate process of blood
coagulation.

 THROMBIN
SNAKE VENOM
SODIUM AND CALCIUM ALGINATE
OXIDATED CELLULOSE
 Reducing the temperature to about 5oC
 Collecting blood in a container with smooth surface
like silicone-coated container.
 BLEEDING TIME
 CLOTTING TIME
 PROTHROMBIN TIME
 THROMBIN TIME
 Time interval of oozing off blood after a cut or injury
till the arrest of bleeding.
 3-6 minutes
 Duke’s Method
 Prolonged in PURPURA
 Time interval from oozing of blood till the formation
of clot.
 3-8 minutes
 Capillary method
 Prolonged in HAEMOPHILIA
 Time taken by blood to clot after adding tissue
thromboplastin to clot.
 10-12 seconds
 Prolonged in deficiency of factor I, V, VII and IX.
 Normal in haemophilia
 Time taken for blood to clot after adding thrombin to
it.
 12-20 seconds
 Prolonged in Heparin therapy during
DYSFIBRINOGENIMIA
 HAEMOPHILIA
 PURPURA
 VON WILLIEBRAND DISEASE
 It is sex linked inherited blood disorder featured by
prolonged clotting time
 It occurs due to lack of Prothrombin activator.
 Depending upon the deficiency involved, it is of three
types:
1.Haemophilia A
2.Haemophilia B
3.Haemophilia C
 It is a disorder characterized by prolonged bleeding
time.
 There is spontaneous bleeding under the skin from
ruptured capillaries. Small, tiny hemorrhagic clots are
formed in various areas of the body.
 It is of three types, based on the causes:
1.Thrombocytopenic purpura
2.Idiopathic thrombocytopenic purpura
3.Thrombasthenic purpura
 Intravascular blood clotting.
 It refers to coagulation of blood inside the blood
vessels.
 It is caused due to:
 1.blood vessel injury
 2.roughened endothelial lining
 3.agglutination of RBCs
 4.toxications
 5.cogenital absence of protein C