Theformationofaclotinabloodvesselsmaybecalled

thrombophlebitis

Abloodclotthatblocksanarterytothebraincancausea
stroke

Athrombus, or colloquially ablood clot, is the final

product of theblood coagulationstep inhemostasis

Blood coagulation or Hemostasis is the cessation of bleeding

from a cut or several vessels.

Blood Clotting Factors

Factor I: Fibrinogen
Fibrinogen is globulin in nature but has much bigger
molecule than serum globulin. The molecular weight is
about 3, 30,000. It is coagulated at around 560C. It is
distinguished from other plasma proteins by its property of
clotting.

Factor II: Prothrombin

Prothrombin is a protein found in nature and present in
normal plasma. It has molecule weight of about 62,700. It is
very labile in aqueous solution and is inactivated by acids
atpH4.8. In oxalated plasma two form of prothrombin are
found A and B. In normal plasma the two forms remain
united as calcium compound.

Factor III: Thromboplastin

Thromboplastin is derived from two sources. First source is
Intrinsic Thromboplastin which is formed in the plasma due
to interaction between different Plasma factors. Second
source is Extrinsic Thromboplastin which is formed from
different tissue (extract of brain, lungs etc) is also called
Tissue Thromboplastin.

Factor IV: Calcium

Ionic calcium greatly helps in blood clotting by acting as a
co-factor in the coagulation process. It is essential for the
formation of both intrinsic and extrinsic thromboplastin and
in conversion of prothrombin into thrombin.

Factor V: Labile factor or Accelerator globulin

Labile factor is necessary for the complete conversion of
prothrombin into thrombin by the extrinsic or intrinsic
thromboplastin. It is a protein, heat labile and is inactivated
within half an hour at 560C or by increasingpHto 10.5. It is
present in plasma but is used up during clotting.

Factor VI: Accelerin

Accelerin is the hypothetical activation product of
proaccelerin i.e. factor V.

Factor VII: Stable factor or Proconvertin

Proconvertin is present in plasma and is not used up during
clotting. It is protein remains associated with prothrombin. It
accelerates tissue thromboplastin or extrinsic factor. During
blood clotting Proconvertin converted into Convertin.

Factor IX: Christmas factor

Christmas factor is necessary for intrinsic factor or intrinsic
thromboplastin formation. Haemophilia C was first found in
a patient named Christmas and hence named Christmas
factor

Factor X: Stuart factor

In 1959 the international nomenclature has been given to
this factor. It is stable at room temperature.

Factor XI: Plasma Thromboplastin antecedent (PTA)

This factor is activated by active Hageman factor and
ultimately leads to formation of thrombin.

Factor XII: Hagemen or surface factor

Hagemen or surface factor is protein in nature. Inactive form
is activated on surface contact. This is turn activates the
protein splitting enzyme kallikrein to produce plasma Kinins.
The resulting effects are increased vascular permeability
and dilatation of blood vessels.

Factor XIII: Fibrin Stabilizing or Laki Lorand factor

This form is active along with Ca2+ion convert soft fibrin clot
to a solid, fibrous one. Its action also decreases the solubility
of the clot in urea solution.

Factors preventing Coagulation

There are following factors which prevent coagulation.

By lowering temperature, Coagulation can be prevented.
By avoiding contact with water weltable surface and injured
tissues. This prevents Thrombokinase action.
Removal of calcium ion.
Precipitation of fibrinogen.
By adding the substances of biological origin. These are
Protamines simple protein found in fish.
Peptone When it is injected in vein
Heparin Mucoitin Polysulphuric acid produced by mast cells.
Hirudin Leech extract and venom of certain snakes.
Heparin, Hirudin and venom of certain snakes prevent blood
clotting by inhibiting action of prothrombin and thrombin
fibrinogen reaction.

Factors hastening Coagulation Process

Coagulation process can pace up with following factors:

Warmth.
Contact with water wettable surface and rough surfaces.
Additions of foreign bodies into a sample of blood.
Addition of thrombin.

Addition of thromboplastin.

The most immediate biochemical change that occurred post-mortem is a fall in the
concentration of oxygen due to absence of circulation, resulting in a switch to
anaerobic metabolism with the absence of the citric acid cycle. Anaerobic
glycolysis resulted in the accumulation of lactic acid and an increase in the
concentration of NADH. Formic acid also increased post-mortem but because the
production of this metabolite requires enzymes that function at physiological pH as
well as NAD+as a co-factor, the increase in formic acid is most probably attributed
to bacterial putrefaction rather than anaerobic metabolism. It is unclear why the
pigs and the rats had such large differences in the concentration of formic acid
post-mortem. It may be because they possibly have different bacterial microflora.
The accumulation of lactic acid and formic acid initiates the fall in pH postmortem. Furthermore, because the circulatory system is stasis, the blood buffer
systems fail resulting in a rapid pH decline as more acidic metabolites are
produced. The speed of the plasma pH decrease was illustrated inFigure 1Awhere
post-mortem blood pH fell from 7.45 to 6.0 within the first 24 hours after death.
The plasma pH decrease is significant because it is thought to activate fibrinolysin
enzymes which prevent blood clotting resulting in an increase in fluidity (noncoagulation) of the blood [28-31]. Although fibrinolysis was not examined in this
study, the post-mortem blood remained fluid inside the rat and pig corpses over
the 96 hour examination period, consistent with fibrinolysin enzymes being active.

The time interval may be short or extended depending upon

the degree of clotting, source and quantity of blood, and
environmental conditions existing at the time.

An average time of 3 to 15 minutes for blood to commence

clotting outside the body may be used as a guideline for a
minimal interval

Red blood cells are delivering oxygen to tissues, but

they cannot do this anymore in the lack of blood flow.
White blood cells degenerate and after about 84 hours
are no longer existing as cells (Babapulle CJ,
Jayasundera NP, 1993). Neutrophiles degenerate first
and lymphocytes last.
Platelets follow an apparent increase in number due to
hypostatic phenomena (Thomsen H et al, 1999). Then
thrombolytic activity is increased and platelet-platelet
aggregates form. Some also adhere to fibrinogen and
erythrocytes.
Overall, due to increase of acidic metabolites
concentration, the pH of the blood decreases. It takes
about 20 hours to reach a blood pH of 5.5