Homeostasis,HEMOSTASIS, BLOOD GROUPING.pptx

HEMOSTASIS
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Hemostasis:
Hemostasis is the mechanism that leads to cessation (stopping) of bleeding from a blood vessel.
Steps/stages:
vascular spasm
(2) platelet plug formation
(3) blood clotting (coagulation)



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.


2- Platelet Plug Formation:
Platelets store a of chemicals including clotting factors, ADP, ATP, Ca2, and serotonin.
Also present are enzymes that produce thromboxane A2, fibrin-stabilizing factor (which helps to strengthen a blood clot).
Also within platelets is platelet-derived growth factor (PDGF), a hormone that help repair damaged blood vessel walls.
Steps of Platelet Plug Formation:
i) Initially, platelets contact and stick to parts of a damaged blood vessel. This process is called platelet adhesion.

ii) Platelets now extend many projections that enable them to contact with one another, and they begin to liberate the contents of their vesicles. This phase is called the platelet release reaction.
Liberated ADP and thromboxane A2 activate nearby platelets.
Serotonin and thromboxane A2 function as vasoconstrictors, causing contraction of vascular smooth muscle, which decreases blood flow through the injured vessel.
iii) The release of ADP makes other platelets in the area sticky and so they adhere to the originally activated platelets. This gathering of platelets is called platelet aggregation. Eventually, the attachment of large numbers of platelets form a mass called a platelet plug that can stop blood loss completely if the hole in a blood vessel is not too large.

3- Blood Clotting:
If blood is drawn from the body, it thickens and forms a gel that separates from the straw-colored liquid, called serum (blood plasma minus the clotting proteins).
The gel is called a clot. It consists of a network of fibrin (insoluble protein fibers) in which the formed elements of blood are trapped. The process of gel formation, called clotting or coagulation.
Clotting involves several substances known as clotting factors; including calcium ions (Ca2), several inactive enzymes that are synthesized by hepatocytes (liver cells), and various molecules associated with platelets or released by damaged tissues.


3 Stages of clotting:
Two pathways, called the extrinsic pathway and the intrinsic pathway, lead to the formation of prothrombinase. Once prothrombinase is formed, the steps involved in the next two stages of clotting are the same for both the extrinsic and intrinsic pathways, and together these two stages are referred to as the common pathway.
Prothrombinase converts prothrombin (a plasma protein formed by the liver) into the enzyme thrombin.
Thrombin converts soluble fibrinogen (another plasma protein formed by the liver) into insoluble

1. HEMOSTASIS .

2. Hemostasis: Hemostasis is  the mechanism that leads to cessation (stopping) of bleeding from a blood vessel. Steps/stages: vascular spasm (2) platelet plug formation (3) blood clotting (coagulation)

3. 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.

4. 2- Platelet Plug Formation: Platelets store a of chemicals including clotting factors, ADP, ATP, Ca2, and serotonin. Also present are enzymes that produce thromboxane A2, fibrin-stabilizing factor (which helps to strengthen a blood clot). Also within platelets is platelet-derived growth factor (PDGF), a hormone that help repair damaged blood vessel walls. Steps of Platelet Plug Formation: i ) Initially, platelets contact and stick to parts of a damaged blood vessel. This process is called platelet adhesion .

5. ii) Platelets now extend many projections that enable them to contact with one another, and they begin to liberate the contents of their vesicles. This phase is called the platelet release reaction . Liberated ADP and thromboxane A2 activate nearby platelets. Serotonin and thromboxane A2 function as vasoconstrictors, causing contraction of vascular smooth muscle, which decreases blood flow through the injured vessel. iii) The release of ADP makes other platelets in the area sticky and so they adhere to the originally activated platelets. This gathering of platelets is called platelet aggregation . Eventually, the attachment of large numbers of platelets form a mass called a platelet plug that can stop blood loss completely if the hole in a blood vessel is not too large.

6. 3- Blood Clotting: If blood is drawn from the body, it thickens and forms a gel that separates from the straw-colored liquid, called serum (blood plasma minus the clotting proteins). The gel is called a clot . It consists of a network of fibrin (insoluble protein fibers) in which the formed elements of blood are trapped. The process of gel formation, called clotting or coagulation . Clotting involves several substances known as clotting factors ; including calcium ions (Ca2 ), several inactive enzymes that are synthesized by hepatocytes (liver cells), and various molecules associated with platelets or released by damaged tissues.

7. 3 Stages of clotting: Two pathways, called the extrinsic pathway and the intrinsic pathway , lead to the formation of prothrombinase. Once prothrombinase is formed, the steps involved in the next two stages of clotting are the same for both the extrinsic and intrinsic pathways, and together these two stages are referred to as the common pathway. Prothrombinase converts prothrombin (a plasma protein formed by the liver) into the enzyme thrombin . Thrombin converts soluble fibrinogen (another plasma protein formed by the liver) into insoluble fibrin . Fibrin forms the threads of the clot.

8. The Extrinsic Pathway: Has fewer steps than the intrinsic pathway and occurs rapidly (within seconds). It is so named because a tissue protein (lipoproteins and phospholipids) called tissue factor (TF), also known as thromboplastin , leaks into the blood from damaged cells outside (extrinsic to) blood vessels and initiates the formation of prothrombinase. In the presence of Ca2, TF begins a sequence of reactions that activates clotting factor X that combines with factor V in the presence of Ca2 to form the active enzyme prothrombinase , completing the extrinsic pathway.

9. The Intrinsic Pathway: More complex and slower (require several minutes) than the extrinsic pathway. Named so because its activators are either in direct contact with blood or contained within (intrinsic to) the blood; outside tissue damage is not needed. If endothelial cells of blood vessels become roughened/damaged, blood can come in contact with collagen fibers around the endothelium of the blood vessel. Contact with collagen fibers (or with the glass sides of a blood collection tube) activates clotting factor XII that eventually activates clotting factor X. Also damage to endothelial cells of blood vessels causes damage to platelets, resulting in the release of phospholipids by the platelets . Platelet phospholipids and Ca2 can also participate in the activation of factor X . Activated factor X then combines with factor V to form the active enzyme prothrombinase (just as occurs in the extrinsic pathway), completing the intrinsic pathway.

10. The Common Pathway: In the second stage of blood clotting, prothrombinase and Ca2 catalyze the conversion of prothrombin to thrombin . In the third stage, thrombin, in the presence of Ca2, converts fibrinogen (soluble) to loose fibrin threads (insoluble). Thrombin also activates factor XIII (fibrin stabilizing factor ), which strengthens and stabilizes the fibrin threads into a sturdy clot.

11. Some definitions/ terminologies/ important points: Clot retraction is the tightening of the fibrin clot. As the clot retracts, it pulls the edges of the damaged vessel closer together, decreasing the risk of further damage. Vitamin K is not involved in actual clot formation, it is required for the synthesis of some clotting factors. Clotting in an unbroken blood vessel is called thrombosis. Such a clot itself is called a thrombus. A blood clot, bubble of air, fat from broken bones, or a piece of debris transported by the bloodstream is called an embolus . When an embolus lodges in the lungs, the condition is called pulmonary embolism .

12. :BLOOD GROUPS AND BLOOD TYPES: The surfaces of erythrocytes contain antigens called agglutinogens composed of glycoproteins and glycolipids. Based on the presence or absence of various antigens, blood is categorized into different blood groups. Within a given blood group, there may be two or more different blood types. There are at least 24 blood groups and more than 100 antigens that can be detected on the surface of red blood cells. Two major blood groups— ABO and Rh

13. ABO BLOOD GROUP: The ABO blood group is based on two glycolipid antigens called A and B. People whose RBCs display only antigen A have type A blood. Those who have only antigen B are type B. Individuals who have both A and B antigens are type AB. Those who have neither antigen A nor B are type O.

14. Blood plasma usually contains antibodies called agglutinins that react with the A or B antigens if the two are mixed. These are the anti-A antibody , which reacts with antigen A, and the anti-B antibody , which reacts with antigen B. You do not have antibodies that react with the antigens of your own RBCs, but you do have antibodies for any antigens that your RBCs lack. ………For example, if your blood type is B, you have B antigens on your red blood cells, and you have anti-A antibodies in your blood plasma.

15. TRANSFUSIONS: In an incompatible blood transfusion , antibodies in the recipient’s plasma bind to the antigens on the donated RBCs, which causes agglutination or clumping , of the RBCs . Agglutination is an antigen–antibody response in which RBCs become crosslinked to one another. When these antigen–antibody complexes form, they activate plasma proteins of the complement family that make the plasma membrane of the donated RBCs leaky, causing hemolysis (rupture) of the RBCs and the release of hemoglobin into the blood plasma that may cause kidney damage.

16. Rh BLOOD GROUP: The Rh blood group is so named because the antigen was discovered in the blood of the Rhesus monkey . People whose RBCs have Rh antigens are designated Rh (Rh positive ); those who lack Rh antigens are designated Rh (Rh negative ). Normally, blood plasma does not contain anti-Rh antibodies. If an Rh negative person receives an Rh positive blood transfusion, however, the immune system starts to make anti-Rh antibodies that will remain in the blood. If a second transfusion of Rh positive blood is given later, the previously formed anti-Rh antibodies will cause agglutination and hemolysis of the RBCs in the donated blood, and a severe reaction may occur.

17. Hemolytic disease of the newborn: The most common problem with Rh incompatibility , hemolytic disease of the newborn (HDN), may arise during pregnancy. If a small amount of Rh positive blood leaks from the fetus through the placenta into the bloodstream of an Rh negative mother (during delivery), the mother will start to make anti-Rh antibodies. The firstborn baby usually is not affected. If the mother becomes pregnant again, however, her anti-Rh antibodies can cross the placenta and enter the bloodstream of the fetus. If the fetus is Rh negative, there is no problem, because Rh negative blood does not have the Rh antigen. If the fetus is Rh positive, however, agglutination and hemolysis brought on by fetal–maternal incompatibility may occur in the fetal blood.

18. During pregnancy, if women is Rh negative , she will have blood tests to check for antibodies. If no antibodies are found, she will have an injection of Rh immune globulin at about 28 weeks. Rh immune globulin stops her body from making the antibodies that could harm the baby.