This document discusses hemostasis, the process by which bleeding is stopped. It describes the three main stages of hemostasis: vasoconstriction, platelet plug formation, and blood clotting. When a blood vessel is injured, vasoconstriction occurs to reduce blood loss. Then, platelets adhere to the injury site and aggregate to form a temporary platelet plug. Finally, fibrin threads are produced and attach to the platelet plug to completely seal the break in the blood vessel. The coagulation cascade involves multiple clotting factors that activate one another in a chain reaction to ultimately produce a fibrin clot.

1. Human Anatomy & Physiology I
Hemostasis
Presented By: Lovekesh Singh
Assistant Professor
ISF College Of Pharmacy
Moga, Punjab

2. SCOPE
 To learn and understand about the process and mechanism of blood
clotting.

3.  Hemostasis
 Stages of hemostasis
 Vasoconstriction
 Platelet plug formation
 Blood clotting
 Fibrinolysis
CONTENTS

4.  Hemostasis is defined as arrest or stoppage of bleeding. It is
the process of forming clots in the wall of damaged blood
vessels & preventing blood loss while maintaining blood in a
fluid state with in the vascular system.
 Heme = blood - stasis = to halt
 Stages of Hemostasis When a blood vessel is injured, the injury
initiates a series of reactions, resulting in hemostasis.
HEMOSTASIS

5. Mechanism of Haemostasis involves 3 main steps:
 Vasoconstriction
 Platelet plug formation
 Coagulation of blood
STAGES OF HEMOSTASIS

6.  Immediately after injury, the blood vessel constricts and decreases the loss of
blood from the damages portion.
 When the blood vessels are cut, the endothelium is damaged and the collagen is
exposed. Platelets adhere to this collagen and get activated.
 The activated platelets secrete serotonin and other vasoconstrictor substances
which cause constriction of the blood vessels.
 Adherence of the platelets to the collagen is accelerated by Von Willebrand
factor.
 This factor acts as a bridge between a specific glycoprotein present on the
surface of platelet and collagen.
1. VASOCONSTRICTION

8.  Platelets get adhered to the collagen of ruptured blood vessel and
secrete adenosine di phosphate (ADP) and thromboxane – A.
 These two substances attract more and more platelets and activate
them.
 All these platelet aggregate together and form a loose temporary
platelet plug or temporary hemostatic plug, which close the ruptured
vessel and prevent further blood loss.
 Platelet aggregation is accelerated by Platelet- Activating Factor (PAF).
2. PLATELET PLUG
FORMATION

9. CONT….

10.  During this process , the fibrinogen is converted into fibrin.
 Fibrin threads get attached to the loose platelet plug, which plugs
the ruptured part of blood vessels and prevents further blood loss
completely.
 Mechanism of blood coagulation is explained in detail in the coming
slides.
3. COAGULATION OF
BLOOD

11.  Coagulation or clotting is defined as the process in which blood losses its fluid
and becomes a jelly like mass few minutes after it is shed out or collected in a
container.
 The clotting mechanism involves a cascade of reactions in which clotting factors
are activated. Most of them are plasma proteins synthesized by the liver (vitamin
K is needed for the synthesis of factor II, VII, IX and X).
 They are always present in the plasma in an inactive form. When activated they
act as proteolytic enzymes which activate other inactive enzymes.
 Several of these steps require Ca++ and platelet phospholipid.
BLOOD CLOTTING (COAGULATION)

12. FACTORS INVOLVED IN BLOOD
CLOTTING

13. 1. FORMATION OF PROTHROMBIN ACTIVATOR STAGE
2. CONVERSION OF PROTHROMBIN INTO THROMBIN STAGE
3. CONVERSION OF FIBRINOGEN INTO FIBRIN
ENZYME CASCADE SEQUENCE
STAGE

14. • Damaged tissues leak tissue factor (thromboplastin) into bloodstream
• Prothrombinase forms in seconds
• In the presence of Ca+2, clotting factor X combines with V to form
prothrombinase
EXTRINSIC PATHWAY

15.  Activation occurs – endothelium is damaged & platelets come in
contact with collagen of blood vessel wall – platelets damaged &
release phospholipids
 Requires several minutes for reaction to occur
 Substances involved: Ca+2 and clotting factors XII, X and V
INTRINSIC PATHWAY

16.  Prothrombinase and Ca+2 – catalyze the conversion of prothrombin
to thrombin
 Thrombin – in the presence of Ca+2 converts soluble fibrinogen to
insoluble fibrin threads – activates fibrin stabilizing factor XIII –
positive feedback effects of thrombin
 Accelerates formation of prothrombinase
 Activates platelets to release phospholipids
FINAL COMMON PATHWAY

17. MECHANISM OF BLOOD CLOTTING

18. FIBRINOLYSIS
• After the clot has formed, the process of removing it and healing the
damaged blood vessel begins. The breakdown of the clot, or fibrinolysis, is
the first stage.
• Plasminogen, trapped within the clot as it forms, is converted to the
enzyme plasmin by activators released from the damaged endothelial
cells.
• Plasmin breaks down fibrin to soluble products that are treated as waste
material and removed by phagocytosis.
• As the clot is removed, the healing process restores the integrity of the
blood vessel wall.

19. FORMATION OF HAEMOGLOBIN
• Haemoglobin is a complex protein, consisting of globin and an
iron-containing substance called haem, and is synthesized inside
developing erythrocytes in red bone marrow.
• Haemoglobin in mature erythrocytes combines with oxygen to
form oxyhaemoglobin, giving arterial blood its characteristic red
colour. In this way the bulk of oxygen absorbed from the lungs is
transported around the body to maintain a continuous oxygen
supply to all cells.
• Haemoglobin is also involved, to a lesser extent, in the transport
of carbon dioxide from the body cells to the lungs for excretion.

20. Structure of hemoglobin

21.  Hemoglobin is a protein made up of four polypeptide chains (α1, α2, β1, and
β2).
 Each chain is attached to a heme group composed of porphyrin (an organic
ringlike compound) attached to an iron atom. These iron-porphyrin
complexes coordinate oxygen molecules reversibly, an ability directly
related to the role of hemoglobin in oxygen transport in the blood.
 In the oxygenated state, it is called oxyhemoglobin and is bright red; in the
reduced state, it is purplish blue.
 Each haemoglobin molecule contains four atoms of iron. Each iron atom
can carry one molecule of oxygen, therefore one haemoglobin molecule
can carry up to four molecules of oxygen.
 -Haemoglobin is said to be saturated when all its available binding sites for
oxygen are filled. When oxygen levels are low, only partial saturation is
possible.

22. REFERENCES
 Waugh, A., & Grant, A. (2013). Ross and Wilson: Anatomy and Physiology
in Health and Illness (12th edition). Churchill Livinstone
 Principles of Anatomy and Physiology by Tortora Grabowski. Palmetto,
GA, U.S.A.
 Essentials of Medical Physiology by K. Sembulingam and P. Sembulingam.
Jaypee Brothers Medical Publishers, New Delhi.
 Anatomy and Physiology in Health and Illness by Kathleen J.W. Wilson,
Churchill Livingstone, New York.

23. Questions
Q-1. Define hemostasis.
Q-2 Write down a note on stages of hemostasis.
Q-3 Write down the stages of platelet plug formation..
Q-4 What do you mean by blood clotting?
Q-5 Write down the mechanism of blood clotting in detail.

24. THANKS