BIOH 113 1st Edition Lecture 8Outline of Last Lecture I. BloodII. Blood CirculationIII. Characteristics of BloodIV. Blood PlasmaV. Formed ElementsVI. ErythrocytesVII. HematopoiesisVIII. ErythropoiesisIX. LeukocytesOutline of Current Lecture I. LeukopoiesisII. Leukocyte DisordersIII. PlateletsIV. Hemostatic DisordersV. Blood TransfusionVI. Transfusion ReactionsCurrent LectureI. Leukopoiesisa. Stem cells differentiate into myeloid stem cells and lymphoid stem cellsb. Myeloid stem cells become myeloblasts or monoblastsc. Lymphoid stem cells become lymphoblastsd. Myeloblasts develop into eosinophils, neutrophils, and basophilse. Monoblasts develop into monocytesf. Lymphoblasts develop into lymphocytesII. Leukocyte Disordersa. Leukemia: i. Leukemia refers to cancerous conditions involving white blood cellsThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.ii. Leukemias are named according to the abnormal white blood cells involved1. Myelocytic leukemia: involved myoblasts2. Lymphocytic leukemia: involves lymphocytesiii. Acute leukemia involves blast-type cells and primarily effects childreniv. Chronic leukemia is more prevalent in older people v. Immature white blood cells are found in the bloodstream in all leukemiasvi. Bone marrow becomes totally occupied with cancerous leukocytesvii. The white blood cells are not functionalviii. Death is caused by internal hemorrhage and overwhelming infectionsix. Treatments include irradiation, antileukemic drugs, and bone marrow transplantsIII. Platelets (thrombocytes)a. Platelets are fragments of megakaryocytes with a blue-staining outer region and a purple granular centerb. Their granules contain chemicals necessary for clotting to occurc. Platelets function in the clotting mechanism by forming a temporary plug that helps seal breaks in blood vesselsd. Platelets not involved in clotting re kept inactive by other chemicals including nitric oxidee. Hemostasis: a series of reactions designed for stoppage of bleedingi. during hemostasis, three stages occur in rapid sequencing1. Vascular spasms: immediate vasoconstriction in response to injury2. Platelet plug formation3. Coagulation (blood clotting)f. Platelet plug formation:i. Platelets do not stick to each other or to the endothelial lining of blood vesselsii. Upon damage to blood vessel endothelium platelets:1. Adhere to collagen2. Become activated and release their chemicals which helps to sustain the vascular spasm3. Release more chemicals which attract still more platelets and helps to form platelet plugg. Coagulation: set of reactions in which blood is transformed from a liquid to a geli. Follows intrinsic and extrinsic pathways which use clotting factorsii. The final 3 steps of this series of reactions are:1. Prothrombinase is formed2. Prothrombin is converted into thrombin3. Thrombin catalyzes the joining of fibrinogen into a fibrin meshh. Clot retraction and repair:i. Clot retraction: stabilization of the clot by squeezing serum from the fibrinstrandsii. Repair:1. Fibroblasts form a connective tissue patch2. Endothelial cells multiply and restore the endothelial liningi. Factors limiting clot growth or formationi. Two homeostatic mechanisms prevent clots from becoming too large1. Swift removal of clotting factors2. Inhibition of activated clotting factorsIV. Hemostatic Disordersa. Thromboembolytic Conditions:i. Thrombus: a cloth that develops and persists in an unbroken blood vessel1. Thrombi can block circulation, resulting in tissue death2. Coronary thrombosis: thrombus in blood vessels of the heartii. Embolus: thrombus freely floating in the blood stream1. Pulmonary emboli can impair the ability of the body to obtain oxygen2. Cerebral emboli can cause strokesiii. Prevention of undesirable clots:1. Substance used to prevent undesirable clots include:a. Aspirin-inhibits chemical that is needed during platelet plug formationb. Heparin: an anticoagulant used clinically for pre and postoperative cardiac carec. Warfarin: used for those prone to atrial fibrillationV. Blood Transfusionsa. Whole blood transfusions are used:i. When blood loss is significantii. In treating thrombocytopeniab. Packed red cells are used to treat anemiac. Human blood groups: RBC membranes have glycoprotein antigens on their external surfacesi. These antigens are:1. Unique to the individual2. Recognized as foreign if transfused into another individual3. Promoters of agglutination and are referred to as agglutinogensii. Presence or absence of these antigens are used to classify blood groupsd. Humans have 30 varieties of naturally occurring RBC antigense. The antigens of the ABO and Rh blood groups cause vigorous transfusion reactions when they are improperly transfusedf. ABO blood groups consist of:i. Two antigens (A and B) on the surface of the RBCsii. Two antibodies in the plasma (anti-A or anti-B)g. An individual with ABO blood may have various types of antigens and spontaneously preformed antibodiesh. Agglutinogens and their corresponding antibodies cannot be mixed without serious hemolytic reactionsi. Rh blood groups:i. Presence of Rh agglutinogens on RBCs is indicated as Rh +ii. Anti-Rh antibodies are not spontaneously formed in Rh – individualsiii. However, if an Rh- individual receives Rh+ blood; anti=Rh antibodies formiv. A second exposure to Rh+ blood will result in a typical transfusion reactionVI. Transfusion Reactionsa. Transfusion reactions occur when mismatched blood is infusedb. Donor’s cells are attacked by the recipient’s plasma agglutinins causing:i. Diminished oxygen-carrying capacityii. Clumped cells that impede blood flowiii. Ruptured RBCs that release free hemoglobin into the bloodstreamc. Circulating hemoglobin precipitates in the kidneys and causes renal