Human Anatomy & Physiology - Chapter 19: Blood - PDF

Human Anatomy & Physiology Second Edition Chapter 19 Blood Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved OVERVIEW OF BLOOD Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Blood Ov...

Human Anatomy & Physiology Second Edition Chapter 19 Blood Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved OVERVIEW OF BLOOD Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Blood Overview About 5 liters of blood (fluid connective tissue) makes up about 8% of total body weight; circulates through blood vessels at all times Figure 19.1a The three visible layers of blood. Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Blood Overview Plasma—one of two major components of blood; liquid extracellular matrix of blood Formed elements—include cells and cell fragments found suspended in plasma – Erythrocytes—red blood cells (RBCs) – Leukocytes—white blood cells (WBCs) – Platelets—small cellular fragments Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Blood Overview Three distinct layers are formed when blood sample is centrifuged: – Top layer—plasma; about 55% of total volume – Middle layer—leukocytes and platelets; called buffy coat; makes up only 1% of total blood volume – Bottom layer—remaining 44% of total volume; erythrocytes; percentage of blood (by volume) composed of erythrocytes is called hematocrit Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Overview of Blood Functions Blood functions: – Exchanging gases—both oxygen and carbon dioxide are transported in blood – Distributing solutes—plasma transports ions, nutrients, hormones, and wastes, and plays role in regulating ion concentrations in tissues – Performing immune functions—both leukocytes and immune system proteins are transported throughout body in blood – Maintaining body temperature—blood carries away heat generated as by- product of many chemical reactions in body – Functioning in blood clotting—platelets and certain proteins form blood clot; seals damaged blood vessels to prevent blood loss – Preserving acid-base homeostasis—pH of blood is maintained between 7.35 and 7.45; remains relatively constant as blood contains several important buffering systems – Stabilizing blood pressure: blood volume is major factor in determining blood pressure Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Plasma Plasma – Pale yellow liquid whose volume is 90% water; factor in determining viscosity (thickness) of blood – Less water leads to greater viscosity and sluggish blood flow Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Plasma Plasma proteins form colloid; makes up about 9% of plasma volume Albumin—large protein synthesized in liver; responsible for blood’s colloid osmotic pressure; draws water into blood by osmosis; example of Gradients Core Principle – Immune proteins (gammaglobulins); also known as antibodies; made by leukocytes; components of immune system – Transport proteins—bind to lipid-based molecules otherwise incompatible with mostly water-based plasma; allows transportation of these molecules in blood – Clotting proteins—stop bleeding from injured blood vessels by forming blood clot with assistance from platelets Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Plasma Last 1% of plasma volume consists of several small molecules mostly dissolved in water portion of plasma, forming solution These molecules can be readily exchanged between blood and interstitial fluid in most capillary beds Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved ERYTHROCYTES AND OXYGEN TRANSPORT Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Erythrocyte Structure Shape and components of erythrocytes facilitate their transport of oxygen and carbon dioxide through blood Typical erythrocyte, or red blood cell (RBC)—biconcave disc; flattened, donut-shaped cell; concave on both sides Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Erythrocyte Structure RBC shape increases surface area of cell; vital to role in gas exchange; example of Structure-Function Core Principle – Mature RBCs are anucleate; lost nucleus during maturation; also lack most other cellular organelles – Creates room in cytosol for enzymes and nearly 1 billion oxygen-binding hemoglobin (Hb) proteins Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Erythrocyte Structure Hemoglobin—large protein that consists of four polypeptide subunits: two alpha () chains and two beta () chains (Figure 19.3) – Each polypeptide is bound to iron-containing compound called heme group – An iron ion in each heme group is oxidized when it binds to oxygen in regions of high oxygen concentration (such as lungs); forms red molecule called oxyhemoglobin (HbO2) Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Erythrocyte Structure Hemoglobin (continued): – Releases oxygen into regions (tissues surrounding systemic capillary beds) where oxygen concentration is low – Also binds to carbon dioxide (CO2) forming carbaminohemoglobin where oxygen levels are low; accounts for about 23% of CO2transported in blood – Hemoglobin also binds to carbon monoxide (CO) to form carboxyhemoglobin; binds more strongly to iron ion than oxygen – Changes shape of Hb making it unable to unload oxygen into oxygen-deprived tissues; can lead to death Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Erythrocyte Life Span Erythrocyte life span is relatively short, ranging from 100–120 days – Due to damage incurred by harsh environment in which they exist – Lack means for repair; lost majority of organelles by replacing them with hemoglobin during maturation – Body must continuously make new erythrocytes Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Erythropoiesis Hematopoiesis—takes place in red bone marrow; formed elements in blood are produced by hematopoietic stem cells (HSCs) Erythropoiesis—specific hematopoietic process that produces erythrocytes from HSCs – takes approximately 5–7 days to complete  Begins when HSCs differentiate into progenitor cells called erythrocyte colony-forming units (CFUs); committed to forming only one cell type  Erythrocyte CFUs differentiate into proerythroblasts when hormone erythropoietin (EPO) (secreted by kidneys) is present Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Erythropoiesis Erythropoiesis (continued): – Proerythroblasts develop into erythroblasts; rapidly synthesize Hb and other proteins – Nucleus in erythroblast shrinks as it matures; eventually ejected resulting in reticulocyte – Reticulocytes enter bloodstream (after ejecting remaining organelles) by exiting through pores in sinusoidal capillaries of bone marrow Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Erythropoiesis Regulation of Erythropoiesis—erythropoietin triggers negative feedback loop; maintains hematocrit within normal range; demonstrates Feedback Loops Core Principle (Figure 19.5): – Stimulus: Blood levels of oxygen fall below normal – Receptor: Kidney cells detect falling oxygen levels – Control center: Kidneys produce more erythropoietin and release hormone into bloodstream – Effector/Response: Production of erythrocytes increases; example of Cell-Cell Communication Core Principle – Homeostasis: Blood levels of oxygen rise to normal Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Erythropoiesis Figure 19.5 Regulation of erythropoiesis. Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Erythrocyte Death Erythrocyte destruction takes place in following steps (Figure 19.6): – Erythrocytes become trapped in sinusoids of spleen (organ in upper left abdominal cavity) – Spleen macrophages digest erythrocytes – Hemoglobin is broken down into amino acids, iron ions, and heme – Heme is first converted to waste product biliverdin (greenish pigment); can then be converted further to yellowish waste product called bilirubin – Iron ions and amino acids are recycled; used to make new hemoglobin in red bone marrow  Iron ions are transported back to red bone marrow in bloodstream by protein called transferrin  Bilirubin is sent to liver for excretion Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Anemia Anemia – Common condition defined as decreased oxygen-carrying capacity of blood – Three primary causes: decreased hemoglobin, decreased hematocrit, and abnormal hemoglobin – Variety of events or conditions are associated with anemia, many of which have similar symptoms; reflects decreased oxygen delivery to tissues Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Anemia Anemia (continued): – General symptoms include: pallor (pale skin), fatigue, weakness, and shortness of breath – Many types of anemia cause elevated numbers of circulating reticulocytes; body boosts EPO production in response to diminished oxygen-carrying capacity – Severe anemia can elevate heart rate; body attempts to increase cardiac output to match demand for oxygen from oxygen-deprived tissues Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Anemia Decreased hemoglobin: – Most common form of anemia is iron deficiency anemia; caused by inadequate dietary iron intake, reduced intestinal absorption of iron, or slow blood loss – Without functional heme groups, erythroblasts are unable to synthesize oxyhemoglobin – Anemia of chronic disease, also common, develops as result of another underlying disease state, such as cancer; interferes with iron transportation from liver to red bone marrow – Vitamin B6 deficiency, malnutrition, poisoning with certain drugs or heavy metals (like lead), and pregnancy can all decrease hemoglobin levels Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Anemia Decreased hematocrit—factors can reduce number of erythrocytes in blood; lowers hematocrit – Blood loss—due to number of causes from acute injury to stomach ulcers can lead to significant loss of circulating erythrocytes – Pernicious anemia—results from vitamin B12 deficiency; interferes with DNA synthesis of rapidly dividing cells, including hematopoietic cells in bone marrow – Erythrocyte destruction can be caused by bacterial infections, diseases of immune system or liver, and lead poisoning; can result in hemolytic anemia – Certain medications or exposure to ionizing radiation can inhibit or stop production of erythrocytes in red bone marrow; condition called aplastic anemia; cause is often unknown Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Anemia Abnormal hemoglobin—most common example of abnormal hemoglobin is sickle-cell disease – Individuals with single copy of defective gene have sickle-cell trait; generally asymptomatic – Individuals with two defective copies of gene have sickle-cell disease; produce abnormal hemoglobin called hemoglobin S (HbS) Figure 19.7a Erythrocytes in sickle-cell disease. Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Anemia Abnormal hemoglobin (continued): – When oxygen levels are low, RBCs containing HbS change into sickle shape; leads to erythrocyte destruction in small blood vessels and reduction in circulating erythrocytes Figure 19.7b Erythrocytes in sickle-cell disease. Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved  LEUKOCYTES AND IMMUNE FUNCTION Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Leukocytes Leukocytes or white blood cells (WBCs)—larger than erythrocytes with prominent nucleus; use blood-stream as transportation; generally don’t perform their functions within blood – Adhere to walls of blood vessels, then squeeze between endothelial cells to enter surrounding tissue – Leukocytes are divided into two basic categories:  Granulocytes readily distinguished by their unusual nuclei; single nucleus composed of multiple connected lobes; contain cytoplasmic granules that are released when activated – lysosomal granules as well as granules unique to each type of granulocyte  Agranulocytes lack visible cytoplasmic granules; do contain lysosomes (like granulocytes) Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Leukocytes List of WBCs, from most to least abundant – Neutrophils – Lymphocytes – Monocytes – Eosinophils – Basophils Easy way to remember this list – Never – Let – Monkeys – Eat – Bananas Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Granulocytes Neutrophils—most common leukocyte -- 3000-7000 neutrophils/mm3 of blood (40-70% of WBC) – Active phagocytes that ingest and destroy bacterial cells – Also called polymorphonucleocytes (polys or PMNs); uniquely shaped nucleus composed of three to five lobes – Injured cells release chemicals that attract neutrophils (chemotaxis); neutrophils exit bloodstream and release granules in damaged tissue – Granule contents directly kill bacterial cells, attract more neutrophils and leukocytes to region, and enhance inflammation Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Granulocytes Eosinophils—have bilobed nucleus – 100-400 eosinophil's per mm3 of blood (1-4% of WBCs) – Phagocytes that ingest foreign molecules – Respond to infections with parasitic worms and allergic reactions – Granules contain enzymes and toxins specific to parasites; also chemicals that mediate inflammation Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Granulocytes Basophils—least common leukocyte; S-shaped nucleus – Rarest of the WBCs – 20-50 basophils per mm3 of blood (0-1% of WBCs) – Chemicals in granules mediate inflammation – histamine-containing granules – Contain heparin (anticoagulant) Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Agranulocytes Lymphocytes  Second most common leukocyte in blood, contain large – 1,500-3,000 lymphocytes per mm of blood (25-40% of WBCs)  Two basic types; similar appearances but different functions; both types are activated by cellular markers found on all cells called antigens  Play a role in immune response Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Agranulocytes Agranulocytes (continued): – B lymphocytes (B cells)  When activated, produce antibodies which bind to and remove antigens from tissues  Each population of B lymphocytes secretes antibodies that bind only to specific unique antigen  Become immunocompetent at Bone marrow Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Agranulocytes Agranulocytes (continued): – T lymphocytes (T cells)  Also activated by specific antigens; do not produce antibodies; have membrane-bound receptors for individual antigens  T lymphocytes activate other immune system components and directly destroy abnormal body cells, such as cancer cells or virally infected cells  Become immunocompetent at Thymus Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Agranulocytes Monocytes—largest leukocyte; have large U-shaped nuclei – 100-700 monocytes per mm of blood (4-8% of WBCs) – Only circulate in blood briefly before exiting capillaries to enter tissues where some mature into macrophages – Macrophages—phagocytic cells that ingest dead and dying cells, bacteria, antigens, and other cellular debris – Activate other components of immune system by displaying phagocytosed antigens to other leukocytes Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Complete Blood Count Complete Blood Count (CBC)—important test for anemia and other conditions Blood sample is drawn and examined under the microscope and by an automated analyzer to evaluate number and characteristics of blood cells: – RBC count in cells per milliliter; used to calculate hematocrit – Hemoglobin concentration – RBC characteristics—size, volume, and concentration of hemoglobin in cytosol – Platelet count and volume – Numbers and types of leukocytes Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Leukemia Leukemias—cancers of blood cells or bone marrow; classified as acute or chronic based on speed of disease progression: – Acute—rapid increase in immature, nonfunctional, or poorly functional blood cells – Chronic—slow accumulation of abnormal mature leukocytes Also classified by cell line from which abnormal cells derive: – Lymphocytic—from lymphoid cell line; generally abnormal B lymphocytes – Myelogenous—from myeloid cell line; can involve any of myeloid cells Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Leukemia Acute lymphocytic leukemia—most common leukemia in children Abnormal cells crowd marrow; reduce ability to manufacture healthy cells; cancerous cells enter bloodstream; spread (metastasize) to other tissues Treatment and prognosis vary with type of leukemia; generally acute forms metastasize earlier and require more aggressive management Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved PLATELETS Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Platelets Platelets—small cell fragments surrounded by plasma membrane; following characteristics (Figure 19.10a): – Smallest of formed elements; involved in hemostasis; process that stops blood loss from injured blood vessel – Platelets don’t have nuclei or organelles found in most whole cells – Platelets contain several types of granules; contain clotting factors, enzymes, some mitochondria, and glycogen deposits; enable them to carry out oxidative catabolism – Also contain cytoskeletal elements; include microtubules associated with actin and myosin filaments Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Thrombopoiesis Platelet formation (thrombopoiesis) begins as HSCs differentiate into committed precursor cells called megakaryoblasts from myeloid cell line – Megakaryoblasts develop into megakaryocytes; go through repeated cycles of mitosis without cytokinesis; cell itself never divides; results in massive cell with multiple copies of DNA within single nucleus – Mature megakaryocytes, when stimulated by hormones (thrombopoietin), send cytoplasmic extensions through clefts in bone marrow sinusoids into bloodstream; break off into thousands of platelets – Platelets have limited lifespan of about 7–10 days; after which removed from circulation by liver and spleen Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Putting It All Together: The Big Picture of Formed Elements Figure 19.11 The Big Picture of Formed Elements. Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved HEMOSTASIS Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Hemostasis Hemostasis involves series of five distinct events; form gelatinous blood clot that plugs broken vessel; primary function is to limit significant blood loss – Part 1: Vascular Spasm – Part 2: Platelet Plug Formation – Part 3: Coagulation (Intrinsic and Extrinsic Pathway) – Part 4: Clot Retraction – Part 5: Thrombolysis Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Hemostasis—Vascular Spasm Hemostasis Part 1: Vascular Spasm begins immediately when blood vessel is injured and blood leaks into extracellular fluid with following two responses: – Vasoconstriction and increased tissue pressure both act to decrease blood vessel diameter – Blood loss is minimized as both blood pressure and blood flow are reduced locally by these responses Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Hemostasis—Platelet Plug Hemostasis Part 2: Platelet plug formation—patch, consisting mostly of platelets, adheres only to injury site, further reducing blood loss – Injured endothelial cells release von Willebrand factor (vWF); glycoprotein that binds to receptors on surface of platelets’ plasma membranes – Exposed collagen plus vWF (continued):  Granule contents attract and activate nearby platelets causing them to clump together or aggregate  Platelet aggregation forms platelet plug and seals injured vessel temporarily Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Hemostasis—Coagulation Hemostasis Part 3: Coagulation—process that forms molecular glue; binds platelets, endothelial cells, and other formed elements together – Cascade of events proceeds down two pathways:  Intrinsic (Contact Activation pathway) – Exposed collagen fibers activate clotting factors  Extrinsic (Tissue Factor pathway) – Damaged tissue activates clotting factors – Both converge at common pathway; leads to activation of fibrin Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Hemostasis—Coagulation Hemostasis Part 3 (continued): – Fibrin—threadlike protein that converts soft, liquid platelet plug into more substantial solid mass  Fibrin is found circulating in plasma and in platelets in inactive form called fibrinogen  Fibrinogen is converted into fibrin by series of reactions (coagulation cascade) that occur at surface of platelets and/or damaged endothelial cells Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Hemostasis—Coagulation Hemostasis Part 3 (continued): – Fibrin (continued):  Cascade depends on clotting factors; mostly enzymes synthesized in liver; circulate in blood in inactive form  Clotting factors are labeled with Roman numeral in order they were discovered  II, VII, IX, and X depend on vitamin K for their synthesis Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Hemostasis—Clot Retraction Hemostasis Part 4: Clot Retraction—occurs as coagulation cascade nears its completion – Actin and myosin fibers in involved platelets contract; bring edges of wounded vessel closer together – Serum—fluid consisting of plasma without clotting proteins; forced out of clot during clot retraction Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Hemostasis—Thrombolysis Hemostasis, Part 5: Thrombolysis—process that begins after injury has healed and blood clotting is no longer necessary – Fibrinolysis—process that breaks down fibrin glue Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Regulation of Clotting Blood clotting is produced by a positive feedback mechanism; example of Feedback Loops Core Principle; must be tightly regulated to prevent mishaps – Endothelial cells produce and secrete two chemicals that regulate first and second stages of clot formation  Prostacyclin—prostaglandin; inhibits platelet aggregation  Nitric oxide—causes vasodilation – Endothelial cells and hepatocytes produce anticoagulants; inhibit coagulation:  Antithrombin III (AT-III)—protein that binds and inhibits activity of both factor Xa and thrombin; also prevents activation of new thrombin  Heparin sulfate—polysaccharide that enhances antithrombin activity  Protein C—when activated by protein S, catalyzes reactions that degrade clotting factors Va and VIIIa Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Disorders of Clotting Clotting disorder—condition in which clotting is not regulated properly; can create drastic consequences for maintaining homeostasis; two types of clotting disorders: – Bleeding disorders – Hypercoagulable conditions Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Disorders of Clotting Clotting disorders (continued): – Bleeding disorders can increase blood loss from even minor injuries because blood is unable to clot; usually due to clotting protein deficiency such as following:  Hemophilia A—caused by a shortage of factor VIII  Hemophilia B—caused by a shortage of factor IX Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Disorders of Clotting Clotting disorders (continued): – Hypercoagulable conditions  Result in formation of inappropriate clots (thrombosis)  Clots (thrombus) are dangerous; can obstruct blood flow through vessel  Thromboembolism may break off of thrombus and occlude smaller vessels downstream  Thrombi commonly form in deep veins of legs causing condition called deep vein thrombosis (DVT)  Pulmonary embolism—dangerous complication of DVTs; emboli break off thrombi in legs and lodge in small blood vessels in lungs Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Anticlot Medications Patients with thrombi or emboli are treated with drugs that prevent clotting process Anticoagulants—widely used group of medications; manage and prevent emboli; include: – Heparin (and derivatives)—used in hospitals; action is nearly immediate but must be injected – Warfarin (Coumadin)—used for outpatients; can be given by mouth; inhibits production of vitamin K-dependent clotting factors by liver (II, VII, IX, and XII); does not affect factors already in plasma; takes 2–3 days for noticeable effect Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Anticlot Medications Antiplatelet drugs: – Aspirin—inhibits enzymes that contribute to aggregation – Clopidogrel—blocks platelet receptors and inhibits platelet activation (glycoprotein IIb/IIIa inhibitors used in heart attack patients work similarly) Thrombolytic agents (tPA or urokinase) used to restore blood flow rapidly to prevent tissue damage; when thrombi or emboli have caused stroke or heart attack Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved BLOOD TYPING AND MATCHING Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Blood Transfusions Blood transfusions—blood taken from donor is given to recipient; commonly used treatment modality in today’s medicine, but was not always case – Discovery of surface markers or antigens found on most biological molecules and all cells, including erythrocytes; lead to development of safer transfusion practices  Immune system recognizes foreign antigens; responds by trying to remove them  Response was responsible for many fatalities in early-era transfusion patients – Antigens on erythrocytes (genetically determined carbohydrate chains) give rise to different blood groups – Two groups of 30 different antigens found on erythrocytes are particularly useful for clinical use: ABO blood group and Rh blood group Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Blood Typing ABO blood group features two antigens, A and B antigens; gives rise to four ABO types: Type A—only A antigen is present on erythrocytes Type B—only B antigen is present on erythrocytes Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Blood Typing ABO blood groups (continued): Type AB—both A and B antigens are present on erythrocytes Type O—neither A nor B antigens are present on erythrocytes; there is no O antigen; O denotes absence of A and B antigens only Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Blood Typing Rh blood group features Rh antigen first discovered in rhesus monkeys; individuals with Rh antigen (D antigen) on their erythrocytes are Rh-positive (Rh+) and those without D antigen are Rh-negative (Rh−) ABO and Rh blood groups combined give rise to eight common blood types Type O+ is most common blood type in US populations, while AB− is least common Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Blood Typing Blood typing in laboratory uses antibodies that bind to individual antigens on erythrocytes – Antibodies (called agglutinins) bind to surface-bound antigens; cause them to clump together or agglutinate – Ultimately, agglutination promotes erythrocyte destruction; called hemolysis Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Blood Typing Blood sample is treated with three different antibodies; agglutination indicates that antigen is present on erythrocytes; no agglutination indicates that specific antigen is absent; antibodies used: – Anti-A antibodies bind and agglutinate A antigens – Anti-B antibodies bind and agglutinate B antigens – Anti-Rh (Anti-D) antibodies bind and agglutinate Rh antigens Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Blood Typing Blood samples from four patients are combined with antibodies. Agglutination indicates that a specific antigen is present on that patient’s erythrocytes. Figure 19.19 Blood type testing. Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Blood Transfusions Immune system recognizes antigens on erythrocytes as “self ” antigens; does not produce antibodies to self antigens, because if it did, antibodies would bind own antigens Immune system does produce antibodies to foreign antigens; means that antibodies are present in plasma only if antigens are absent from erythrocytes Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Blood Transfusions Note that anti-A and anti-B antibodies are pre-formed; they are present in plasma even if individual has never been exposed to those antigens Anti-Rh antibodies, however, are produced only if person has been exposed to blood containing Rh antigens Therefore, an Rh− individual generally has no anti-Rh antibodies unless he or she has been exposed (sensitized) to Rh+ erythrocytes Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Blood Transfusions Antigens and antibodies are basis for blood matching; blood taken from donor is screened for compatibility prior to its administration to recipient – Patients cannot receive any blood containing antigens that his/her immune system would recognize as foreign – Match occurs if donor blood type is compatible with recipient blood type – Transfusion reaction—recipient antibodies bind to donor antigens; causes agglutination that destroys donor erythrocytes, possibly leading to kidney failure and death Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Blood Transfusions Figure 19.20 Matching blood types for blood transfusions. Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Blood Transfusions Universal donor—Blood type O− – Erythrocytes do not have A, B, nor Rh surface antigens – Can be given to any other blood type in emergency when blood matching is not option Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Blood Transfusions Universal recipient—blood type AB+ – These individuals do not make antibodies to A, B, or Rh antigens – Individuals with AB+ blood type can generally receive blood from any blood type donors – Matching is still safest practice Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Blood Transfusions Table 19.4 The Eight Major Blood Types. Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Concept Boost: What about the Donor’s Antibodies? Donor antibodies can bind to recipient’s antigens, and unless blood types are exactly matched, some donor antibodies might destroy few recipient’s erythrocytes – Key word is few—only a few of recipient’s erythrocytes are likely to be harmed – Take a closer look at example in Figure 19.20a Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved Hemolytic Disease of the Newborn Also known as erythroblastosis fetalis; occurs when Rh− mother gives birth to Rh+ fetus During birth fetal RBCs enter mother’s blood; stimulates her immune system to produce anti-Rh antibodies First pregnancy is not typically at risk; in subsequent pregnancies maternal anti-Rh antibodies can cross placenta and hemolyze Rh+ fetal RBCs Effectively prevented with blood type screening; if woman is Rh−, can be given Rho (D) immune globulin; contains anti-Rh antibodies that bind fetal cells in maternal circulation; prevents maternal production of anti-Rh antibodies Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved