It explains blood clotting pathways. It is very simple form student point of view. The language is very easy to understand and retrieval is easy.

1. HEMOSTASIS
Mrs. Mayuri Padhye, Assistant professor,
Department of Pharmacology,
Saraswathi Vidya Bhavan’s College of Pharmacy

2. HEMOSTASIS
 Hemostasis (he¯-mo¯-STA¯ -sis), not to be
confused with the very similar term
homeostasis, is a sequence of responses that
stops bleeding.
 When blood vessels are damaged or ruptured,
the hemostatic response must be quick, localized
to the region of damage, and carefully controlled
in order to be effective.

3. HEMOSTASIS
 Three mechanisms reduce blood loss: (1)
vascular spasm, (2) platelet plug formation, and
(3) blood clotting (coagulation).
 When successful, hemostasis prevents
hemorrhage (HEM-o-rij; -rhage burst forth),
the loss of a large amount of blood from the
vessels.

4. HEMOSTASIS
 Hemostatic mechanisms can prevent hemorrhage
from smaller blood vessels, but extensive
hemorrhage from larger vessels usually requires
medical intervention.

5. 1. VASCULAR SPASM
 When arteries or arterioles are damaged, the
circularly arranged smooth muscle in their walls
contracts immediately, a reaction called vascular
spasm
 This reduces blood loss for several minutes
to several hours, during which time the other
hemostatic mechanisms go into operation

6. 1. VASCULAR SPASM
 The spasm is probably caused by damage to the
smooth muscle, by substances released from
activated platelets, and by reflexes initiated by
pain receptors

7. 2. PLATELET PLUG FORMATION
 Considering their small size, platelets store an
impressive array of chemicals.
 Within many vesicles are clotting factors, ADP,
ATP, Ca+2
and serotonin.

8. 2. PLATELET PLUG FORMATION
 Also present are enzymes that produce
thromboxane A2, a prostaglandin; fibrin-stabilizing
factor, which helps to strengthen a blood clot;
lysosomes; some mitochondria; membrane
systems that take up and store calcium and
provide channels for release of the contents of
granules; and glycogen.

9. 2. PLATELET PLUG FORMATION
 Also within platelets is platelet-derived
growth factor (PDGF), a hormone that can
cause proliferation of vascular endothelial
cells, vascular smooth muscle fibers, and
fibroblasts to help repair damaged blood vessel
walls.

10. 2. PLATELET PLUG FORMATION
1. Platelet Adhesion
 Initially, platelets contact and stick to parts of a
damaged blood vessel, such as collagen fibers of
the connective tissue underlying the damaged
endothelial cells.
 This process is called platelet adhesion.

11. 2. PLATELET PLUG FORMATION
2. Platelet Release Reaction
 Due to adhesion, the platelets become
activated, and their characteristics change
dramatically. They extend many projections that
enable them to contact and interact with one
another, and they begin to liberate the contents
of their vesicles.
 This phase is called the platelet release
reaction.

12. 2. PLATELET PLUG FORMATION
2. Platelet release reaction
 Liberated ADP and thromboxane A2 play a
major role by activating nearby platelets.
 Serotonin and thromboxane A2 function as
vasoconstrictors, causing and sustaining
contraction of vascular smooth muscle, which
decreases blood flow through the injured
vessel.

13. 2. PLATELET PLUG FORMATION
3. Platelet Aggregation
 The release of ADP makes other platelets in the
area sticky, and the stickiness of the newly
recruited and activated platelets causes them to
adhere to the originally activated platelets
 This gathering of platelets is called platelet
aggregation.

14. 2. PLATELET PLUG FORMATION
3. Platelet Aggregation
 Eventually, the accumulation and
attachment of large numbers of platelets form
a mass called a platelet plug.

16. 3. BLOOD COTTING
 If blood is drawn from the body, however, it
thickens & forms a gel, gel separates from liquid
 Serum is a straw colored liquid
Serum = Blood plasma – Clotting proteins
 The gel is called as clot which consists of a
network of insoluble protein fibers called fibrin
in which the formed elements of blood are
trapped

17. COTTING PATHWAYS
1. Two pathways, called the extrinsic pathway &
the intrinsic pathway which lead to the
formation of prothrombinase.
After this, the steps involved in the next two
stages of clotting are same in both the
pathways; common pathway

18. COTTING PATHWAYS
Prothrombinase
2. Prothrombin Thrombin
[plasma protein [Enzyme]
formed by liver]
Thrombin
3. Fibrinogen Loose fibrin threads
[Soluble] Ca+2
[Insoluble]

19. EXTRINSIC PATHWAY
1. It has fewer steps, occurs rapidly
2. A tissue protein called Tissue Factor [TF] or
Thromboplastin, leaks into the blood from cells
outside [extrinsic] blood vessels & intiates the
formation of Prothrombinase
3. TF is a complex mixture of lipoproteins &
Phospholipids released from the surfaces of
damaged cells

20. EXTRINSIC PATHWAY [EP]
4. In the presence of Ca+2
, TF begins a sequence of
reactions that ultimately activates factor X
Ca+2
5. Factor X + Factor V
Prothrombinase
End of EP

21. INTRINSIC PATHWAY
1. More complex than extrinsic pathway; occurs
more slowly
2. The activators are either in direct contact with
blood or contained [within] [intrinsic] the blood

22. INTRINSIC PATHWAY
3. Endothelial cells
when roughened or damaged blood comes in
contact with collagen fibres in the connective
tissue
around the endothelium of blood vessels
trauma to the endothelial cells leads to platelet
damage.
Then release of phospholipids by platelets

23. INTRINSIC PATHWAY
4. Contact with the Ca+
Activation of clotting
collagen fibers factor X
& Factor XII
Phospholipids
5. Factor X + Factor V
Prothrombinase
Ca+2
End of IP

24. COMMON PATHWAY
1. Formation of Prothrombinase is the beginning
of common pathway
Prothrombinase
2. Prothrombin Thrombin
Ca+2
Thrombin
3. Fibrinogen Loose fibrin threads
[Soluble] Ca+2
[Insoluble]

25. COMMON PATHWAY
4. Thrombin activates Factor XIII [Fibrin Stabilizing
Factor] which strengthens & stabilizes fibrin
threads into a sturdy clot
5. Factor XIII in plasma is released by platelets & is
trapped in a clot

26. COMMON PATHWAY
6. Two positive feedback mechanisms
 Factor V accelerates formation of
Prothrombinase & Thrombin
 Thrombin activates platelets and due to platelet
aggregation platelet phospholipids are released

28. ROLE OF VITAMIN K
 Clotting requires adequate levels of Vitamin K
 It is required in the synthesis of clotting factors
 It is a fat soluble vitamins which is absorbed
through the lining of intestine & then into the
blood; if the absorption of lipid is normal
 Due slow absorption of lipids, the person may
have Vitamin K deficiency & may have
Uncontrolled bleeding

29. INTRAVASCULAR CLOTTING
 It refers to clot formation within the
cardiovascular system
 This clot may be initiated by roughened
endothelial surfaces of a blood vessel resulting
from trauma, infection due to which adhesion of
platelets occurs

30. INTRAVASCULAR CLOTTING
Thrombosis Clotting in an unbroken blood
vessels
Thrombus Clot itself
Embolus A blood clot, bubble of air, fat ,
debris
Embolus in
lungs
Pulmonary embolism