Blood PDF

BLOOD FACTS ABOUT BLOOD Has a sticky, opaque fluid with a characteristic metallic taste Salty The color of blood varies from scarlet (oxygen-rich) to dull red (oxygen-poor) Heavier than water and about five times thicker With a pH between 7.35 and 7.45 Tem...

BLOOD FACTS ABOUT BLOOD Has a sticky, opaque fluid with a characteristic metallic taste Salty The color of blood varies from scarlet (oxygen-rich) to dull red (oxygen-poor) Heavier than water and about five times thicker With a pH between 7.35 and 7.45 Temperature is slightly higher than body temp (38 °C) Accounts 8% of the body weight Humans have approximately 5-6 liters of blood FUNCTIONS OF BLOOD Transport of gases, nutrients, and waste products Transport of processed molecules Transport of regulatory molecules Regulation of pH and osmosis Maintenance of body temperature Protection against foreign substances Clot formation COMPONENTS OF BLOOD Plasma Non-living fluid matrix 55% of total blood pale, yellow liquid that surrounds cells 91% water, 7% proteins, and 2% other With proteins namely: albumin, globulins, fibrinogen Formed Elements Living blood cells RBCs, WBCs, platelets 45% of total blood a. Erythrocyte Disk-shaped with thick edges Anucleate cell Cannot divide Red blood cells live for about 120 days in males and 110 days in females. Has spectrin: Enables RBCs to squeeze through the smallest of capillaries. Function: Transport oxygen Hemoglobin Main component of erythrocytes Transports O2 Each globin protein is attached to a heme molecule Each heme contains one iron atom O2 binds to iron Oxyhemoglobin: hemoglobin with an O2 attached Although oxygen is the primary molecule that binds to hemoglobin, other molecules can also bind to hemoglobin. b. Platelets Mediates the process of blood clotting, or coagulation, to prevent excessive blood loss. c. Leukocytes Mnemonics: Never Let Monkeys Eat Banana HEMATOPOIESIS The process that produces formed elements. Continuous throughout our lives. In the fetus, hematopoiesis occurs in several tissues, including the liver, thymus, spleen, lymph nodes, and red bone marrow. After birth, hematopoiesis is confined primarily to red bone marrow, but some white blood cells are produced in lymphatic tissues. In children, hematopoiesis occurs in the long bones, like the thighbone (femur). In adults, it's mostly in the spine (vertebrae) and hips, ribs, skull, and breastbone (sternum). RED BLOOD CELL (RBC) Red blood cell production depends on: o Level of blood oxygen: Typical causes of low blood oxygen ▪ decreased numbers of red blood cells ▪ decreased or defective hemoglobin ▪ diseases of the lungs and high-altitude ▪ inability of the cardiovascular system to deliver blood to tissues ▪ increased tissue demand for oxygen, as occurs during endurance exercises. o the presence of several vitamins as well as sufficient iron. The process of cell division that produces new red blood cells requires the B vitamins folate and B12, which are necessary for the synthesis of DNA. Iron is required for the production of hemoglobin. The developing RBCs divide many times and then begin synthesizing huge amounts of hemoglobin. Suddenly, when enough hemoglobin has been accumulated, the nucleus and most organelles are ejected, and the cell collapses inward. What happens to the components of RBC as they age? The developing RBCs divide many times and then begin synthesizing huge amounts of hemoglobin. Suddenly, when enough hemoglobin has been accumulated, the nucleus and most organelles are ejected, and the cell collapses inward. The remains are eliminated by phagocytes in the spleen, liver, and other body tissues. Iron is bound to protein as ferritin Heme group is degraded to bilirubin, which is then secreted into the intestine by liver cells. There it becomes a brown pigment called stercobilin that leaves the body in feces. Globin is broken down into amino acids, which are released into the circulation. WHITE BLOOD CELL (WBC) Colony stimulating factors (CSFs) and interleukins Stimulates the production of WBC They are released in response to specific chemical signals in the environment, such as inflammatory chemicals and certain bacteria or their toxins. PLATELET The stem cell (megakaryocyte) undergoes mitosis many times, forming a large multinucleate cell, which then fragments into platelets. The primary regulator of platelet production is thrombopoietin, an acidic glycoprotein produced primarily in the liver, kidney, and BM. BLOOD DOPING Blood doping is an intentional process that increases the number of circulating red blood cells. Having more red blood cells increases the blood’s ability to transport oxygen. HEMOSTASIS/BLOOD CLOT FORMATION Stoppage of bleeding Fast and localized Involves 3 major phases: (a) vascular spasm, (b) platelet plug formation, (3) blood clotting. Vasoconstriction occurs (smooth muscle within the wall of the vessel contracts). Spasms narrow the blood vessel at that point, decreasing blood loss until clotting can occur. Vasoconstriction is also stimulated by the chemicals released by the damaged blood vessel wall and of the platelets. platelets release thromboxanes (derived from prostaglandins)  Endothelial cells – release endothelin A platelet plug is an accumulation of platelets that can seal up a small break in a blood vessel. People who lack the normal number of platelets tend to develop numerous small hemorrhages in their skin and internal organs. the platelets become “sticky” and cling to the damaged site. Anchored platelets release chemicals that enhance the vascular spasms and attract more platelets to the site. Platelet plug or white thrombus forms 1. Platelet adhesion: platelets stick to the collagen exposed by blood vessel damage; von Willebrand factor (produced by blood vessel endothelial cells). Von Willebrand factor forms a bridge between collagen and platelets by binding to platelet surface receptors and collagen. After platelets adhere to collagen, they become activated, change shape, and release chemicals. 2. Platelets release chemicals like ADP and thromboxane which bind to their respective receptors on the surfaces of other platelets, activating the platelets. a cascade of chemical release activates many platelets. As platelets become activated, they express surface receptors called fibrinogen receptors, which can bind to fibrinogen, a plasma protein. 3. Fibrinogen forms bridges between the fibrinogen receptors of numerous platelets, resulting in a platelet plug. A clot is a network of threadlike structures called FIBRIN that traps blood cells, platelets, and fluid. The formation of a blood clot depends on a number of proteins found within plasma, called clotting factors. ✓ Activation of clotting factors. A series of reactions results in which each clotting factor activates the next until the clotting factor prothrombinase, or prothrombin activator, is formed. ✓ Prothrombinase converts an inactive clotting factor called prothrombin into an active form of thrombin. ✓ Thrombin converts the plasma protein fibrinogen to fibrin.  ✓ Most clotting factors are activated in the liver, and many of them require vitamin K for their synthesis. ✓ Formation of blood clots requires Ca2+ and the chemicals released from platelets. ✓ Including low levels of vitamin K, low levels of Ca2+, low numbers of platelets, or liver dysfunction that reduces clotting factor production. Anticoagulants - they make sure that clot formation does not spread to other areas. 1) Antithrombin 2) Heparin ABO BLOOD GROUPING o Antibodies (Ab) bind to antigens. o Antibodies are very specific. o When Ab binds with Ag, they form molecular bridges that connect the red blood cells. o This results in AGGLUTINATION The combination of the antibodies with the antigens can also initiate reactions that cause hemolysis The antigens on the surface of red blood cells have been categorized into blood groups. These are also genetically determined. Types of Antigen: ▪ Type A antigen ▪ Type B antigen TRANSFUSION REACTIONS: characterized by clumping or rupture of blood cells and clotting within blood vessels. This is because plasma from type A blood contains anti-B antibodies, which act against type B antigens; plasma from type B blood contains anti-A antibodies, which act against type A antigens. Type AB blood plasma has neither type of antibody, and type O blood plasma has both anti-A and anti-B antibodies. Historically, people with type O blood have been called universal donors. (same thing with AB as universal recipient) Transfusion reactions can still occur. Mismatch of blood groups other than ABO. (can be confirmed through Type and Crossmatch) Antibodies in the donor’s blood can react with antigens in the recipient’s red blood cells. For example, type O blood has anti-A and anti-B antibodies. If type O blood is transfused into a person with type A blood, the anti-A antibodies (in the type O donor blood) react against the A antigens (on the red blood cells in the type A recipient blood). Usually, such reactions are not serious because the antibodies in the donor’s blood are diluted in the large volume of the recipient’s blood. Even though such transfusion reactions seldom occur, type O blood is given to a person with another blood type only in life-or-death situations. RH BLOOD GROUP First studied in the Rhesus Monkey Rh positive – have Rh antigens in RBC Rh negative – does not have Rh antigens ABO blood type and the Rh blood type are usually expressed together. Example: A+ or A- Antibodies against the Rh antigens do not develop unless an Rh-negative person is exposed to Rh-positive red blood cells. When an Rh-negative person receives a transfusion of Rh-positive blood, the recipient becomes sensitized to the Rh antigens and produces anti-Rh antibodies. If the Rh-negative person is unfortunate enough to receive a second transfusion of Rh-positive blood after becoming sensitized, a transfusion reaction results. How Rh factor affect a pregnancy? If an Rh-negative woman is pregnant and carrying an Rh-positive fetus, the mother might obtain some RBCs from the fetus during the birth process or during miscarriage. As a result, the Rh-negative mother would begin producing anti-D antibodies, creating complications for future pregnancies. This condition is known as hemolytic disease of the fetus and newborn (erythroblastosis fetalis). This condition can be prevented with the proper administration of RhoGAM, which prevents the mother from producing anti-D antibodies. Hemolytic disease of the newborn (HDN) Rh incompatibility The mother is Rh-negative and the fetus is Rh-positive. The mother produces anti-Rh antibodies that cross the placenta and cause agglutination and hemolysis of fetal red blood cells.  If fetal blood leaks through the placenta and mixes with the mother’s blood, the mother becomes sensitized to the Rh antigen. The mother produces anti-Rh antibodies that cross the placenta and cause agglutination and hemolysis of fetal red blood cells. Because HDN can be fatal to the fetus, the levels of anti-Rh antibodies in the mother’s blood should be monitored. If they increase to unacceptable levels, the fetus should be tested to determine the severity of the HDN. In severe cases, a transfusion to replace lost red blood cells can be performed through the umbilical cord, or the baby can be delivered if mature enough.