This document provides an overview of hemostasis (blood clotting). It discusses:
- The mechanisms of primary hemostasis mediated by platelets, including platelet adhesion, activation, release of granule contents, and aggregation.
- The process of secondary hemostasis (blood coagulation) mediated by coagulation proteins generating thrombin which converts fibrinogen to fibrin.
- Methods of achieving hemostasis including mechanical methods, electrosurgery, pharmacological agents, and topical hemostatic products.
3. Blood is considered as fluid of life as it carries oxygen
and carbondioxide.
Fluid of growth as it carries nutritive substance.
Fluid of health as it protects body against disease.
4. 1. Color- red , arterial blood is scarlet in color and venous
blood is purple red
2. Volume- adult (5L), new born (450ml), female(4.5l)
3. Reaction and ph – 7.4
4. Viscosity – 5 times more viscous than water.
5. Three types of cells are present in blood-
1. Red blood cells or erythrocytes
2. White blood cells or leukocytes
3. Platelets or thrombocytes
6. Ranges- 4-5.5 millon per cu mm of blood
Male – 5 millions/cu mm
Female – 4.5 millions/ cu mm
Lifespan – 120 days
It plays vital role in transport of respiratory gases.
Red color is due to presence of hemoglobin.
7. Transport of oxygen from lungs to the tissue
Transport carbondioxide from the tissue to the lungs
Buffering action in blood
In blood group determination
8. Total wbc count- 4,000 – 11,000/cu mm of blood
Colorless
Plays vital role in defense mechanism of body and protects
the body from invading organism by acting like soldiers
9. Based on presence or absence of granules
Granulocytes
1. Neutrophilis
2. Eosinophilis
3. Basophilis
Agranulocytes
1. Monocytes
2. lymphocytes
10. Lifespan
Neutrophilis – 2-5 days
Eosinophilis – 7-12 days
Basophilis – 12-15 days
Monocytes – 2-5 days
Lymphocyte – half to 1 day
11. Neutrophilis plays an important role in defense mechanism .
First line of defense is against the invading microorganism.
Eosinophilis mainly against parasite.
Basophilis plays important role in healing
Lymphocyte in immunity
12. It is also known as thrombocytes.
Total count- 150000 – 450000 cc mm of blood
Life span- 8-9 days.
It helps in formation of blood clot and prevent from
bleeding.
13. It is a normal physiological process for the prevention and
stopping of bleeding/heomorrahge whenever a vessel is
ruptured.
14. To maintain the blood in fluid state while it remains
circulating within vascular system.
To maintain the integrity of the vessels wall.
To arrest bleeding at the site of injury or blood loss by the
formation of haemostatic plug.
Eventual removal of plug when healing is complete.
15.
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18. Endothelial cells produce vasoconstrictors such as
angiotensin II and serotonin which help in vasoconstriction.
Activated platelets produce thromboxane A2 (TXA2) which is
a potent vasoconstrictor
19. With in 1-2 sec after injury to blood vessel, hemostatic
process begins & proceed as
1. platelet adhesion
2. platelets activation
3. platelets release reaction
4. platelets aggregation
20. Platelets attach to non-platelet surfaces, such as collagen
fibers in the subendothelium.
Platelets move from the blood vessels and into the tissues.
Exposure to surfaces in the tissues causes them to bind to
collagen with the presence of von Willebrand factor ( vWF) and
Glycoprotein IbIX, making a bridge formation.
Binding via GpI b initiates activation of platelet.
21. The adhesion of platelets to the vessel wall activates them.
Platelets undergo a shape change from disc to tiny sphere
with projecting pseudopodes.
Activation required for hemostatic plug formation.
Activators released or synthesized at the site of injury
22. Immediately after adhesion & activation process of release
reaction or secretion begins.
In this process content of platelets organelles are released to
the exterior.
23. Secretion of α granules
a) Fibrinogen
b) Factor V
c) Fibronectin
d) PDGF
24. Secretion of dense granules:
ADP, GTP, GDP
Calcium, serotonin
Histamin, epinephrin
25. Process by which platelets interact with one another to form a
hemostatic plug.
Chemical changes cause platelets to aggregate and stick to
one another
GPIIb-IIIa complex binds vWF, undergoes Ca++dependent
structural change, then acts as receptor for fibrinogen
Fibrinogen activated platelets serve as a bridge between two
platelets .
26. Clot develops in 15 -20s if trauma is severe.
1-2 mints if trauma has been minor.
If vessel opening is not too large it fills within 3-6 mints.
27. Once blood clot is formed it follows two courses
1. It can become invaded by fibroblast, which forms
connective tissue all through the clot.
2. It can dissolve
3. The usual course for clot that forms in a small hole of a
vessel wall is invasion by fibroblast, within few hours after
the clot is formed. This continues to complete organization
of the clot into fibrous tissue within about 1-2 weeks.
28. Procoagulant that promote coagulation, anticoagulant that
inhibit coagulation
Blood coagulation depends upon these two group
Clotting takes place in three steps
1. In response to rupture of the vessel or damage to the blood
itself
2. Prothrombin activator catalyse the conversion of prothrombin
into thrombin.
3. Thrombin acts as a enzyme to convert fibrinogen into fibrin
fibers that enmesh the platelets, blood cell and plasma to form
clot.
29.
30. First physiological response to vascular injury, which is
mediated by platelets, in order to arrest bleeding
Mechanism:
Activation of platelets via stimulators such as thrombin
Adhesion of platelets to subendothelium via interaction
between GPIb and von Willebrand Factor (VWF)
Release of platelet granule products in order to recruit
more platelets to the injured site
Aggregation of platelets via interaction between GPIIb/IIIa
(aIIb3) and fibrinogen to form the initial plug.
Triggers secondary hemostasis (coagulation proteins)
31. Process of blood coagulation
Mechanism:
Coagulation proteins work in concern to generate thrombin
Thrombin converts fibrinogen to fibrin
Fibrin consolidates the platelet plug made in primary
hemostasis such that a thrombus (secondary hemostatic plug)
is formed
Prevents further blood loss from the injury site
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33.
34. Calcium ions are required for promotion or acceleration of all
the blood clotting reactions.
Therefore in the absence of calcium ions, blood clotting by
either pathway does not occur
When blood is removed from a person, it can be prevented
from clotting by reducing the calcium ion concentration
below the threshold level for clotting.
35. Fibrinolysis is due to action of proteolytic enzyme fibrinolysis
or plasmin.
It is present in inactive plasminogen which gets converted to
plasmin by action of thrombin and tissue plasminogen
activator.
Plasmin lyses fibrin and fibrinogen with the production of
fibrinogen degradation product that inhibit thrombin
36. Procedural Factors
Type of procedure
Patient position
Surgical incisions
Exposed bone (eg, spinal reconstructive procedures)
Large surfaces of exposed capillaries
Unseen sources of bleeding •
Tissues that cannot be sutured or low-pressure suture lines
Adhesions stripped during surgery
37. Patient Factors
Specific anatomical considerations
Medications (eg, anticoagulants) Coagulopathies
Platelet dysfunction or deficiency Fibrinolytic activity
Coagulation factor deficiencies
Medical conditions
Nutritional status
42. 2. Active agents
Thrombin products
3. Flowables
4. Sealants
Fibrin sealants
Polyethylene glycol (PEG)
polymers Albumin and glutaraldehyde Cyanoacrylate
43. 1. Bleeding time
Time from onset of bleeding to stoppage of bleeding (1-5 min)
2. Clotting time
Time from the onset of bleeding till the clot formation (2-8
min)
3. Prothrombin time
Time required for coagulation to take place (12-16 s)
45. 1. Haemophilia
It is also known as haemophilia A
Sex linked inherited disorder
Males
It involves total lack of factor 8 activity. The level of
coagulation factor 8 in blood may be less than 1% of normal
individual.
cryoprecipitate
Fresh blood or fresh frozen plasma
46. 2. Christmas disease
It is also known as haemophilia B
Deficiency of factor 9
Cryoprecipitate
Fresh frozen plasma
47. 3. Von willebrands disease
Low plasma level of factor 8
Platelet abnormlities
Bizarre episodic bleeding
Bleeding more from mucous membrane than from the
mucoskeletal system