Hemopoiesis, Formation of Hemoglobin, Anemia and Mechanisms of Coagulation : Pharmaguideline

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Hemopoiesis, Formation of Hemoglobin, Anemia and Mechanisms of Coagulation

Red blood cells, white blood cells, and platelets make up the three types of blood cells. Hematopoiesis or hemopoiesis refers to the formation of BCs.
Red blood cells, white blood cells, and platelets make up the three types of blood cells. Hematopoiesis or hemopoiesis refers to the formation of blood cells. A continuous process serves to replenish the cellular constituents in the blood as they are depleted. It isn't from the bloodstream itself that blood cells are formed, but rather from certain bone marrow cells. Adult humans acquire all of their red blood cells, 60-70 percent of their white cells, and all of their platelets from their bone marrow.

Formation of hemoglobin
Traditionally, hemoglobin is described as being composed of globular protein (globin) and a pigmented iron-containing complex called haem. Hemoglobin molecules contain iron atoms in each of their four chains. One hemoglobin molecule can carry up to four oxygen molecules due to the combination of each iron atom with an oxygen atom. There are roughly 280 million hemoglobin molecules in the average red blood cell, giving each cell the capacity to carry billions of oxygen molecules!

Iron is transported to the liver by a protein called transferrin, which binds it to the bloodstream. To produce red blood cells, iron must be available continuously. Although eating a diet rich in iron is very difficult, absorption of iron by the alimentary canal is very slow, making iron deficiency easily attainable if losses exceed intake.

Amenia is a lack of red blood cells or an insufficient amount of hemoglobin in the red blood cells. Various types of anemia exist. Those with iron deficiency anemia do not have enough iron in their diet to produce sufficient hemoglobin. The hemoglobin level of a person with this type of anemia will be below normal and may appear normal in terms of RBC count and hematocrit.

Pernicious anemia - Anaemia is caused by a lack of vitamin B12, which is found in animal products, and is characterized by large, misshapen, and fragile red blood cells.

Sickle-cell anemia - The genetic disorder that causes sickle-cell anemia reduces hemoglobin levels, clogs capillaries, and causes the blood to rupture.

Aplastic anemia - red bone marrow is suppressed in aplastic anemia, resulting in lower RBC, WBC, and platelet counts. Radiation exposure and certain medications may trigger this condition. Benzene and other chemicals can also cause this condition.

Hemolytic anemia - Blood cells that rupture before they reach the end of their normal lifespan are said to have hemolytic anemia. Examples include sickle-cell anemia and newborn Rh diseases. As another example, malaria causes RBCs to be destroyed by a protozoan parasite. Due to the increased production of bilirubin, hemolytic anemias are often characterized by jaundice.

Mechanisms of coagulation
There are many stages involved in this process, which also involves positive feedback. Factors contributing to the situation include
The factor I fibrinogen,
Factor II prothrombin,
Factor III tissue factor (thromboplastin),
Factor IV calcium,
Factor V labile factor, proaccelerin, Ac- globulin,
Factor VII stable factor, pro-convertin,
Factor VIII antihemophilic globulin (AHG), antihemophilic factor A,
Factor IX Christmas factor, plasma thromboplastin component (PTA), antihemophilic factor B,
Factor X Stuart power factor,
Factor XI plasma thromboplastin antecedent (PTA), antihemophilic factor C,
Factor XII Hageman factor, XIII fibrin stabilizing factor
* Factor VI – there is no such factor

Among several factors, vitamin K plays a vital role in the synthesis of factors II, VII, IX, and X.

It is their order of discovery rather than their order of participation in clotting that determines their number. For these clotting factors to work together, they must activate each other, eventually resulting in a prothrombin activator, the first step in forming the common pathway. Inactive fibrinogen is converted to fibrin threads by the enzyme prothrombin, which is powered by thrombin. A three-dimensional mesh of fibrin is laid down within the platelet plug as clotting progresses, gradually stabilizing its shape. Blood cells are trapped by maturing blood clots, which are stronger than platelets that form rapidly.

Both intrinsic and extrinsic pathways can initiate a common pathway in the final phase of the process. The extrinsic pathway is triggered very quickly (within seconds) by tissue damage. Thromboplastin and tissue factors are released by damaged tissue, which causes coagulation to occur. A damaged endothelium (the lining of blood vessels) can trigger the intrinsic pathway (3–6 minutes). Whenever the clot shrinks (retracts), it is caused by the contracting of the platelets, which squeezes out the clotting factors and leaves behind a sticky fluid called serum. The shrinkage of the blood vessel causes the edges to stick together, sealing the hole and reducing bleeding.
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Ankur Choudhary is India's first professional pharmaceutical blogger, author and founder of pharmaguideline.com, a widely-read pharmaceutical blog since 2008. Sign-up for the free email updates for your daily dose of pharmaceutical tips.
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