Blood physiology 2024.pptx

Blood Mrs. Quratulain Lecturer Mphil (Physiology) Identify the pH of human blood? Options: a. 7.15-7.35 b. 7.25-7.45 c. 7.35-7.45 d. 7.45-7.55 e. 7.55-7.45 Which of the following component is/are present in the buffy coat in greater amount after whole blood centrifug...

Blood Mrs. Quratulain Lecturer Mphil (Physiology) Identify the pH of human blood? Options: a. 7.15-7.35 b. 7.25-7.45 c. 7.35-7.45 d. 7.45-7.55 e. 7.55-7.45 Which of the following component is/are present in the buffy coat in greater amount after whole blood centrifuge? Options: a. Blood cells b. Plasma, platelets c. Platelets, blood cells d. RBCs, platelets e. WBCs Which of the following statement is true for plasma? Options: a. Composed of serum and clotting factors b. Contains clotting factors c. Obtain as a precipitate after blood centrifuge d. Synthesis begin in bone marrow e. Used for diagnosis RBC Life Cycle cont…. Ferritin is an intracellular protein that stores iron and releases it in a controlled fashion Transferrin is a blood-plasma glycoprotein, which plays a central role in iron metabolism and is responsible for ferric-ion delivery. Transferrin functions as the most critical ferric pool in the body. It transports iron through the blood to various tissues such as the liver, spleen, and bone marrow. Erythropoiesi s Production of RBCs, starts in the red bone marrow with a precursor cell called a proerythroblast Proerythroblast divides several times, producing cells that begin to synthesize hemoglobin Ultimately, a cell near the end of the development sequence ejects its nucleus and becomes a reticulocyte Loss of the nucleus; red blood cell attains distinctive biconcave shape Reticulocytes retain some mitochondria, ribosomes, and endoplasmic reticulum Erythropoiesis cont……… Normally, erythropoiesis and red blood cell destruction proceed at roughly the same pace In case of decreased Oxygen carrying capacity, a negative feedback system steps up RBC production Hypoxia; cellular oxygen deficiency  Hematocrit The percentage of total blood volume occupied by RBCs The normal range of hematocrit for, Adult females is 38–46% Adult males, it is 40–54% Testosterone, present in much higher concentration in males than in females, stimulates synthesis of erythropoietin (EPO) REASON Impact of menstruation in females Anaemia deficiency of hemoglobin in the blood Cause: either too few RBCs or too little hemoglobin in the cells  Polycythemia Abnormally high number of RBCs Hematocrit may be 65% or higher Raises Blood viscocity Increase PVR (peripheral vascular resistance) More difficult for the heart to pump High blood pressure and increased risk of stroke Causes of polycythemia include, Abnormal increases in RBC production Tissue hypoxia Dehydration PLATELETS / Thrombocytes  Liver +kidney+ bone marrow Platelets: thrombopoie small, colorless cell fragments tin form clots and stop or prevent bleeding Platelets are made in bone marrow, Under the influence of thrombopoietin, myeloid stem cells develop into megakaryocyte colony-forming cells that in turn develop into precursor cells called megakaryoblasts Megakaryoblasts transform into megakaryocytes Megakaryocytes, splinter into 2000 to 3000 fragments (platelets) 150,000 and 400,000/ microliter of blood Platelets disc-shaped, 2–4 µm in diameter has many vesicles but no nucleus Granules contain chemicals that promote blood clotting Short life span, normally just 5 to 9 days Aged and dead platelets are removed by fixed macrophages in the spleen and liver Hemostasis “Sequence of responses that stops bleeding” Vascular Contraction Probably caused by, Damage to the smooth muscle Platelet Plug Formation Blood Clotting growth of fibrous tissue into the blood clot to close the hole in the vessel permanently. Steps of Hemostasis Hemostasis cont…… cut/ ruptured blood vessel VASCULAR CONSTRICTION (lasts for minutes –hours local myogenic spasm reduces the flow of blood from the ruptured vessel local autacoid factors from nervous the traumatized reflexes. tissues and blood platelets  Hemostasis cont…… Platelet plug -aggregation of platelets formed during the earlier stage of hemostasis in response to blood vessel wall injury. REMEMBER!!!! platelet plug is successful in stopping blood loss if the damaged endothelium vessel opening is small. for large hole, a blood clot is required. Platelets become sticky and develop finger-like platelet plug formation processes platelet adhesion platelet aggregation platelet activation ADP, thromboxane A2, and serotonin  Hemostasis cont…… od Clot formation-coagulation begins to develop within few seconds of injury initiated by Activator substances from: traumatized vascular wall Platelets blood proteins adhering to the traumatized vascular wall Requires Ca-ion to begin when blood comes in contact when blood comes into with tissue factors (from contact with damaged tissues) rough surface extrinsic pathway intrinsic pathway extrinsic pathway is activated by external trauma that causes blood to escape from the vascular system. This pathway is quicker than the intrinsic pathway intrinsic pathway is activated by trauma inside the vascular system, and is activated by platelets, exposed endothelium, chemicals, or collagen. Coagulation Cascade Similarities Between Intrinsic and Extrinsic Pathways in Blood Clotting Intrinsic and extrinsic pathways are two processes of blood coagulation. Both pathways proceed towards the formation of prothrombin activator or the factor X. Both pathways end up in a common pathway. Intravascular Anticoagulants Prevent Blood Clotting in the Normal Vascular System Endothelial Surface Factors (1) the smoothness of the endothelial cell surface, which prevents contact activation of the intrinsic clotting system (2) a layer of glycocalyx on the which repels clotting factors and platelets, thereby preventing activation of clotting (3) thrombomodulin-a protein bound with the endothelial membrane slow the clotting process (4) Heparin-anti coagulant BLOOD GROUPS AND BLOOD TYPES  Agglutinogens/antigens Assortment of antigens composed of glycoproteins and glycolipids, present on the RBC surface There are at least 24 blood groups and more than 100 antigens that can be detected We shall discuss two major blood groups—ABO and Rh Other blood groups include the Lewis, Kell, Kidd, and Duffy systems ABO Blood Group They are produced in response to similar environmental carbohydrate structures, such as those found in plants and bacteria. These antibodies are produced after birth, reaching a peak level at 5– 10 years of age Rh Blood Group The Rh blood group is so named because the Rh antigen, called Rh factor, was first found in the blood of the Rhesus monkey Rh positive Rh negative Typing and Cross-Matching Blood for Transfusion The blood will agglutinate if: antigens in the patient's blood match the antibodies in the test tube A antibodies attach to A antigens they match like a lock and key form a clump of red blood cells Erythroblastosis Fetalis hemolytic anemia in the fetus caused by transplacental transmission of maternal antibodies leading to the destruction of neonatal red blood cells (often Rho(D) antigens) by maternal immunoglobulin G (IgG) antibodies. The formation of maternal antibodies in response to a fetal antigen is called isoimmunization.  generally occurs when mother's blood is Rh–ve hese antibodies usually don't cause problems during a first pregnancy But Rh incompatibility may cause problems in later pregnancies if the baby is Rh-positive the antibodies stay in your body once they have formed. The antibodies cross the placenta and attack the fetual red blood Coombs test can be used to determine whether there are antibodies to the Rhcells. factor in the mother's blood. Read and interpret! Consider what happens if a person with type A blood receives a transfusion of type B blood. The recipient’s blood (type A) contains A antigens on the red blood cells and anti-B antibodies in the plasma. The donor’s blood (type B) contains B antigens and anti-A In this situation, two things can happen. First, the anti-B antibodies in the recipient’s plasma can bind to the B antigens on the donor’s erythrocytes, causing agglutination and hemolysis of the red blood cells. Second, the anti-A antibodies in the donor’s plasma can bind to the A antigens on the recipient’s red blood cells, a less serious reaction because the donor’s anti-A antibodies become so diluted in the recipient’s plasma that they do not cause significant agglutination and hemolysis of the recipient’s RBCs.