Blood Chapter 10

Blood “river of life” Transports everything through blood vessels Nutrients Wastes Body heat

Components of blood Only fluid tissue having both solid and liquid components It is a complex connective tissue with formed elements (cells) suspended in nonliving matrix (plasma) Erythrocytes (red blood cells) Buffy coat (leukocytes or white blood cells, and platelets) 45% RBC, <1% “buffy coat”, 55% plasma

Physical characteristics Sticky, opaque fluid Metallic taste Ranges from scarlet (oxygen-rich) to dull red (oxygen – poor) Heavier than water (due to RBCs) and more viscous Slightly alkaline, pH 7.35-7.45 Temperature (100.4 F) slightly higher than normal body temp. (98.6 F) 8% of body weight; in adult males is 5-6 liters (6 quarts)

Plasma 90% water with >100 different substances dissolved in it (nutrients, ions (salts), gases, hormones, proteins, wastes) Plasma proteins are most abundant solutes Most made by liver Variety of functions (maintaining blood pressure to immunity) Are NOT used for metabolic fuel

Erythrocytes Red blood cells (RBCs) Primarily carry oxygen to all cells Anucleate (Iack a nucleus when mature) Have few organelles; contain mostly hemoglobin (iron-containing protein Use anaerobic methods to make ATP; so RBCs do NOT consume the oxygen they carry

RBCs

Erythrocytes Biconcave disks; flattened with depressed centers Have large surface area Outnumber WBCs by 1000 to 1 (5 million cells / mm3 of blood) Contribute to blood viscosity The more hemoglobin contained in RBCs, the more oxygen can be carried Normal blood has 12-18 g hemoglobin per 100 mL blood (men 13-18 g; women 12-16 g)

Homeostatic imbalance Anemia – decrease in oxygen carrying capacity, can be caused by (see sickle cell anemia) Lower-than-normal number of RBCs Abnormal or deficient hemoglobin content See table 10.1 on p. 311

Homeostatic imbalance Polycythemia – an excessive or abnormal increase in number of RBCs; can result from Bone marrow cancer Response to living at high altitudes Causes an increase in blood viscosity and impairs circulation

Leukocytes White blood cells (WBCs) Less numerous but crucial to defense against disease Only complete cells in blood (having a nucleus and organelles) 4000-11000 per mm3 Have the ability to move in / out of blood vessels (diapedesis)

Leukocytes Locate areas of damage or infection by chemical signals (positive chemotaxis) Then they “rally” and destroy the foreign substances WBCs mobilized for action will increase in numbers (leukocytosis) Leukopenia is lower than normal WBCs often caused by drugs or anticancer agents

Homeostatic imbalance Leukemia-excessive production of abnormal WBCs Bone marrow becomes cancerous New WBCs are immature and incapable of defending the body Patient is more susceptible to secondary infection

Leukocytes Classified in two categories based on visible granules Granulocytes – granules in cytoplasm Have lobed nuclei 3 forms Agranulocytes No visible granules Normal nuclei (not lobed)

Granulocytes Neutrophils Eosinophils Basophils Multilobed nucleus and fine granules Cytoplasm stains pink Phagocytes to get rid of infection Eosinophils Blue-red nucleus Large red granules Numbers increase with allergies or infections of worms Basophils Histamine-containing granules Stain dark blue

Agranulocytes Lymphocytes Monocytes Large dark purple nucleus (most of cell’s volume) Contained in lymph tissue, part of immune response Monocytes Largest More cytoplasm and indented nucleus Convert to macrophages when entering tissue Fight chronic infections

Platelets Not cells Fragments of multinucleate cells (megakaryocytes) that rupture releasing the “pieces” Required for clotting

Hematopoiesis Blood cell formation Occurs in red marrow (myeloid tissue) In adults: flat bones of skull and pelvis, ribs, sternum, proximal epiphyses of humerus and femur After formation, blood cells are sent into blood

Hematopoiesis All formed elements (solids) come from one type of stem cell, hemocytoblast Forms two types of cells Lymphoid stem cell – produces lymphocytes Myeloid stem cell – forms all other formed elements

Hematopoiesis RBCs are anucleate and cannot synthesize proteins, grow, or divide Become rigid at 100-120 days and begin to fragment Remains are eliminated by spleen and liver Lost cells are repeatedly replaced by division of hemocytoblasts RBCs divide repeatedly then begin to make hemoglobin When enough hemoglobin is produced, organelles and nucleus are ejected and the RBC collapses inward producing the reticulocyte (still has some ER) After 2 days, ER is ejected and they become functional erythrocytes

Hematopoiesis RBC production takes 3-5 days Controlled by hormone erythropoietin, produced mainly by kidneys Normally, RBCs are produced at constant rate When blood oxygen levels drop, more erythropoietin is produced to trigger higher production of erythrocytes

Hematopoiesis Leukocyte and platelet formation controlled by hormones: colony stimulating factors (CSFs) and interleukins These hormones released due to chemical signals, such as inflammatory chemicals, bacteria, toxins, etc. Hormones also enhance the immune response Platelet production is enhanced by thrombopoietin

Hemostasis Stopping blood flow Breakage of a vessel results in reactions to start hemostasis Fast and localized process involving components in blood plasma Also involves platelets 3 major phases Platelet plug formation Vascular spasms Coagulation (clotting)

Hemostasis Platelet plug formation Vascular spasms Platelets will stick to a broken area on a vessel Anchored platelets release signals to attract more platelets Stack of platelets is a white thrombus Vascular spasms Anchored platelets release serotonin which causes the vessel to spasm Spasms narrow the vessel and decrease blood flow and blood loss

Hemostasis Coagulation Injured tissue releases thromboplastin (during platelet plug and spasms) PF3 (phospholipid) coats the platelets and interacts with thromboplastin, blood proteins, Ca ions to cause the clotting cascade Prothrombin activator converts prothrombin to thromibin (enzyme) Thrombin joins soluble fibrinogen proteins into long molecules of insoluble fibrin which traps RBCs to begin the clot Within an hour, clot retracts, squeezing serum from the mass and pulling the edges of the vessel together Clotting normally takes 3-6 minutes, clot triggering factors are quickly inactivated to prevent widespread clotting

Homeostatic imbalance Undesirable clotting Production of thrombus (clot) in an unbroken vessel Can cause fatal heart attacks or stroke Caused by poor circulation, burns, physical blows, or fat accumulation in the vessel Bleeding disorders Thrombocytopenia (platelet deficiency) Caused by suppression of myeloid tissue Bone marrow cancer, radiation, some drugs Hemophilia (lack of clotting factors) Genetic disorder (sex-linked recessive)

Human blood groups: transfusions Plasma membranes of RBCs have proteins (antigens) to identify them An antigen is a substance that a body can recognize as foreign, which stimulates the immune system If the wrong blood type (with different antigens) is transfused into a patient, the patient’s immune system will attack the transfused RBCs causing agglutination (clumping) which will clog small vessels.

Human blood groups: transfusions Transfusion reactions (other than agglutination) Kidney failure Fever Chills Nausea and vomiting Agglutination is the only reaction that is potentially fatal.

ABO blood groups Based (classified) by the 2 antigens that can be found on the RBCs Absence of both antigens = type O blood Presence of both antigens = type AB blood Presence of only A antigens = type A blood Presence of only B antigens = type B blood

ABO blood groups Antibodies are formed in infancy against the ABO antigens NOT present on your RBCs Type O people form antibodies against both A and B antigens Type AB people form no ABO antibodies Type A people form B antibodies Type B people form A antibodies

Rh blood groups Named for one of eight Rh antigens (agglutination D) identified in Rhesus monkeys Most Americans are Rh+ so RBCs carry Rh antigen Anti-Rh antibodies are not automatically formed in infancy (like the ABO groups) The first “wrong” transfusion will trigger the production of the anti-Rh antibodies Subsequent “wrong” transfusions will lead to agglutination

Rh Blood groups and pregnancy Pregnant Rh- women that carry an Rh+ baby First pregnancy results in delivery of a healthy baby Mother becomes sensitized to the Rh+ antigens (and produces anti-Rh+ antibodies) and must be treated with RhoGAM right after birth RhoGAM is an immune serum that prevents the sensitization and the immune response If not treated, and she becomes pregnant with another Rh+ baby, antibodies will cross the placenta and attack the baby’s RBCs Hemolytic disease of the newborn Baby is anemic and hypoxic Brain damage and death may occur unless the fetus receives transfusions before birth

Blood typing Important to be done before transfusions Mix blood with different immune serums, anti-A or anti-B If agglutination occurs, then that will indicate the blood type

Developmental aspects In embryo, development of the circulatory system occurs very early (1st trimester) Blood cell formation starts in the liver and spleen, but by 7th month has moved primarily to the red marrow Embryonic blood cells are circulating in blood vessels by day 28 HbF has a greater ability to pick up oxygen for the fetus After birth, fetal blood cells are replaced by RBCs containing “normal” hemoglobin (HbA)