Blood Physiology Lecture Notes PDF

BLOOD PHYSIOLOGY DR. THERESE RUANE-O’HORA PL1400 & PL1001 1 LEARNING OUTCOMES 5A List the cellular components of blood List the components of plasma Outline the structure of a RBC/Erythrocytes Outline the phases of red cell production in the bone marrow Outline the rol...

BLOOD PHYSIOLOGY DR. THERESE RUANE-O’HORA PL1400 & PL1001 1 LEARNING OUTCOMES 5A List the cellular components of blood List the components of plasma Outline the structure of a RBC/Erythrocytes Outline the phases of red cell production in the bone marrow Outline the role of Erythropoietin in RBC production 2 TOTAL BODY WATER Total Body Water = approx. 60%c body weight , so 40-45 Litres in 70Kg male Divided between Extracellular Fluid (ECF) and Intracellular Fluid (ICF) ECF = (Interstitial Fluid (ISF) + plasma 3 COMPOSITION OF BLOOD > PLASMA Remember plasma is a component of the ECF compartment 4 CELLULAR CONTENT OF BLOOD 3. 2. 1. 5 RED BLOOD CELLS Mature cells are non-nucleated Note the size and unusual shape,> biconcave, why this shape? 6 RBC/ERYTHROCYTE PRODUCTION REQUIREMENTS Begins in utero Adequate nutrition 6-7 months the bone Protein marrow takes over Vitamins e.g. B12 folic acid Children all bone marrow Hormone > Erythropoietin involved released by the kidney Later life only sternum Lack of RBC and/or Hb > vertebrae ribs and pelvis anaemia = Reduced O2 carrying capacity of the blood 7 SEQUENCE OF EVENTS IN RBC PRODUCTION 8  ROLE OF ERYTHROPOIETIN IN PRODUCTION OF ERYTHROCYTES In absence of any disease, accent to high altitude will initiate a physiological increase in RBC production to combat the lack of O2 in the air Synthetic EPO available e.g patients with Chronic Renal failure Use of EPO for blood doping in sport. Potentially v Dangerous > Polycytaemia > increased viscosity > Heart failure and /or stroke 9 LEARNING OUTCOMES List the functions of RBC Outline the normal structure of haemoglobin Describe the process of RBC breakdown Define the term anaemia 10 FUNCTION OF RBC Contain HAEMOGLOBIN (Hb) Oxygen transport Carbon dioxide transport Blood buffer > to maintain normal blood pH of 7.4 11 STRUCTURE OF HAEMOGLOBIN - 4 polypeptide chains ( 2  / 2  adult Hb A, 2 2γ in foetus > HbF Foetal Hb binds O2 much more easily than Hb A – very useful in utero. Change to HbA around 6 months Each linked to one Haem molecule - Each haem contains one iron atom to which O2 associates - Haemoglobinopathies > Abnormal Hb? e.g HbS Sickle Cell Disease, Thalassaemias 12 ANAEMIA > MANY CAUSES Sickle Cell Disease > genetic disorder > Symptoms in children > Sickle Cell Haemolytic Anaemia > Sickled cells are fragile. Need for blood transfusions ++. Cells become trapped in microcirculation > obstruct blood flow > ischaemia & pain 13 which can be severe, also stroke, jaundice, resp symptoms RED BLOOD CELL BREAKDOWN Lifespan around 120 days > cells become very fragile Trapped in spleen ( Red Cell Graveyard!!) Heme seperated from globin > globin recycled as amino acids Heme breakdown yields iron > recycled Other heme breakdown products yield > Biliverdin > Bilirubin Bilirubin > yellow pigment which is taken to the liver and ultimately secreted in bile Jaundice > Results from high level of bilirubin in blood, can also occur in liver disease where diseased liver is unable to handle even normal levels of bilirubin 14 KNOW THE HAEMATOCRIT, RBC AND HAEMOGLOBIN CONCENTRATION 15 BLOOD GROUPS HAEMOSTASIS 5C PL1400 & PL1001 LEARNING OUTCOMES 1C Explain the basis for the major blood group systems Outline the applied physiology of blood transfusions Explain the role of platelets in haemostasis Outline the sequence of events that lead to formation of the clotting protein fibrin BLOOD GROUPS Blood group is determined by the antigen present on the Red cell Membrane Also, each blood group is either Rhesus + or Rhesus - Blood group O Rhesus negative termed “Universal Donor” > no antigens to react with whatever antibodies may be present in the patient’s plasma 18 BLOOD TRANSFUSION Patients blood is typed and then crossmatch is performed between donor cells and patients serum If the antigen on the donor’s cells comes in contact with corresponding antibody e.g. Patient Blood group “B” receives a transfusion of group “A” blood Result: A antigens on donors red cells contact A antibodies in patients blood causing Antigen-Antibody reaction Agglutination of patients RBC with haemolysis and release of Hb and K+ into circ Kidney damage and Liver damage RIP! 19 HAEMOSTASIS/COAGULATION 20 21  Fibrin Formation Note the blue and yellow pathway Fibrin polymer is merge at the Common pathway is the clot! Clot dissolution is also essential > where Plasminogen is converted to > Plasmin 22