blood and blood vessels. module 17.3: red blood cell production and recycling rbc production and...

Download Blood and Blood Vessels. Module 17.3: Red blood cell production and recycling RBC production and recycling Events occurring in red bone marrow Blood cell

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Blood and Blood Vessels Slide 2 Module 17.3: Red blood cell production and recycling RBC production and recycling Events occurring in red bone marrow Blood cell formation (erythropoiesis) occurs only in red bone marrow (myeloid tissue) Located in vertebrae, ribs, sternum, skull, scapulae, pelvis, and proximal limb bones Fatty yellow bone marrow can convert to red bone marrow in cases of severe, sustained blood loss Developing RBCs absorb amino acids and iron from bloodstream and synthesize Hb Slide 3 Module 17.3: Red blood cell production and recycling Stages Proerythroblasts Erythroblasts Actively producing Hb After four days becomes normoblast Reticulocyte (80% of mature cell Hb) Ejects organelles including nucleus Enters bloodstream after two days After 24 hours in circulation, is mature RBC Slide 4 Module 17.3: Red blood cell production and recycling Events occurring at macrophages Engulf old RBCs before they rupture (hemolyze) Hemoglobin recycling Iron Stored in phagocyte Released into bloodstream attached to plasma protein (transferrin) Globular proteins disassembled into amino acids for other uses Heme biliverdin bilirubin bloodstream Hemoglobin not phagocytized breaks down into protein chains and eliminated in urine (hemoglobinuria) Slide 5 Module 17.3: Red blood cell production and recycling Events occurring at liver Bilirubin excreted into bile Accumulating bile due to diseases or disorders can lead to yellowish discoloration of eyes and skin (jaundice) Events occurring at the large intestine Bacteria convert bilirubin to urobilins and stercobilins which become part of feces Give feces yellow-brown or brown coloration Slide 6 Module 17.3: Red blood cell production and recycling Events occurring at kidneys Excrete some hemoglobin and urobilins Give urine its yellow color Presence of intact RBCs in urine (hematuria) Only after urinary tract damage Slide 7 Figure 17.3 Events in the life cycle of RBCs Events Occurring in Macrophages Macrophages in liver, spleen, and bone marrow Fe 2+ 90% 10% Fe 2+ transported in circulation by transferrin Average life span of RBC is 120 days Old and damaged RBCs In the bloodstream, the rupture of RBCs is called hemolysis. Heme Biliverdin Bilirubin Amino acids Bilirubin bound to albumin in bloodstream Bilirubin Hemoglobin that is not phagocytized breaks down, and the alpha and beta chains are eliminated in urine. When abnormally large numbers of RBCs break down in the bloodstream, urine may turn red or brown. This condition is called hemoglobobinuria. Liver Excreted in bile Bilirubin Events Occurring in the Liver Events Occurring in the Large Intestine Urobilins, sterconilins Eliminated in feces Absorbed into the circulation Eliminated in urine Urobilins Hb Events Occurring in the Kidney New RBCs released into circulation RBC formation Ejection of nucleus Events Occurring in the Red Bone Marrow Developing RBCs absorb amino acids and Fe2+ from the bloodstream and synthesize new Hb molecules. Cells destines to become RBCs first differentiate into proerythroblasts. Proerythroblasts then differentiate into various stages of cells called erythroblasts, which actively synthesize hemoglobin. Erythroblasts are named according to total size, amount of hemoglobin present, and size and appearance of the nucleus. After roughly four days of differentiation, the erythroblast, now called a normoblast, sheds its nucleus and becomes a reticulocyte (re-TIK--l-st), which contains 80 percent of the Hb of mature RBC. After two days in the bone marrow, reticulocytes enter the bloodstream. After 24 hours in circulation, the reticulocytes complete their maturation and become indistinguishable from other mature RBCs. Start Slide 8 Module 17.3 Review a. Define hemolysis. b. Identify the products formed during the breakdown of heme. c. In what way would a liver disease affect the level of bilirubin in the blood? Slide 9 Module 17.4: Blood types Blood types Determined by presence or absence of cell surface markers (antigens) Are genetically determined glycoproteins or glycolipids Can trigger a protective defense mechanism (immune response) Identify blood cells as self or foreign to immune system More than 50 blood cell surface antigens exist Three particularly important A, B, Rh (or D) Slide 10 Module 17.4: Blood types Four blood types (AB antigens) 1.Type A (A surface antigens) Anti-B antibodies in plasma 2.Type B (B surface antigens) Anti-A antibodies in plasma 3.Type AB (Both A and B surface antigens) No anti-A or anti-B antibodies in plasma 4.Type O (no A or B surface antigens) Both anti-A and anti-B antibodies in plasma Slide 11 Figure 17.4 1 The characteristics of blood for each of the four blood types Type A Type AB Type O Type O blood has RBCs lacking both A and B surface antigens. Type A blood has RBCs with surface antigen A only. Type B blood has RBCs with surface antigen B only. Type AB blood has RBCs with both A and B surface antigens. Type B Surface antigen A Surface antigen B If you have Type A blood, your plasma contains anti-B antibodies, which will attack Type B surface antigens. If you have Type B blood, your plasma contains anti-A antibodies. If you have Type AB blood, your plasma has neither anti-A nor anti-B antibodies. If you have Type O blood, your plasma contains both anti-A and anti-B antibodies. Slide 12 Module 17.4: Blood types Rh surface antigens Separate antigen from A or B Presence or absence on RBC determines positive or negative blood type respectively Examples: AB+, O Slide 13 Figure 17.4 3 Slide 14 Module 17.4 Review a. What is the function of surface antigens on RBCs? b. Which blood type(s) can be safely transfused into a person with Type O blood? Slide 15 CLINICAL MODULE 17.5: Newborn hemolytic disease Newborn hemolytic disease Genetically determined antigens mean that a child can have a blood type different from either parent During pregnancy, the placenta restricts direct transport between maternal and infant blood Anti-A and anti-B antibodies are too large to cross Anti-Rh antibodies can cross Can lead to mothers antibodies attacking fetal RBCs Slide 16 CLINICAL MODULE 17.5: Newborn hemolytic disease First pregnancy with Rh mother and Rh + infant During pregnancy, few issues occur because no anti-Rh antibodies exist in maternal circulation During birth, hemorraging may expose maternal blood to fetal Rh + cells Leads to sensitization or activation of mothers immune system to produce anti-Rh antibodies Slide 17 Figure 17.5 First Pregnancy of an Rh Mother with an Rh + infant The most common form of hemolytic disease of the newborn develops after an Rh women has carried an Rh + fetus. Problems seldom develop during a first pregnancy, because very few fetal cells enter the maternal circulation then, and thus the mothers immune system is not stimulated to produce anti-Rh antibodies. Exposure to fetal red blood cell antigens generally occurs during delivery, when bleeding takes place at the placenta and uterus. Such mixing of fetal and maternal blood can stimulate the mothers immune system to produce anti-Rh antibodies, leading to sensitization. Roughly 20 percent of Rh mothers who carried Rh + children become sensitized within 6 months of delivery. Because the anti-Rh antibodies are not produced in significant amounts until after delivery, a womans first infant is not affected. During First Pregnancy Hemorrhaging at Delivery Maternal Antibody Production Rh antigen on fetal red blood cells Maternal antibodies to Rh antigen Maternal blood supply and tissue Fetal blood supply and tissue Maternal blood supply and tissue Fetal blood supply and tissue Maternal blood supply and tissue Placenta Rh + fetus Rh mother Slide 18 CLINICAL MODULE 17.5: Newborn hemolytic disease Second pregnancy with Rh mother and Rh + infant Subsequent pregnancy with Rh + infant can allow maternal anti-Rh antibodies to cross placental barrier Attack fetal RBCs and cause hemolysis and anemia = Erythroblastosis fetalis Full transfusion of fetal blood may be necessary to remove maternal anti-Rh antibodies Prevention RhoGAM antibodies can be administered to maternal circulation at 2628 weeks and before/after birth Destroys any fetal RBCs that cross placenta Prevents maternal sensitization Slide 19 Figure 17.5 During Second Pregnancy Rh mother Rh + fetus Maternal blood supply and tissue Fetal blood supply and tissue Maternal anti-Rh antibodies Hemolysis of fetal RBCs Second Pregnancy of an Rh Mother with an Rh + Infant If a subsequent pregnancy involves an Rh+ fetus, maternal anti-Rh antibodies produced after the first delivery cross the placenta and enter the fetal bloodstream. These antibodies destroy fetal RBCs, producing a dangerous anemia. The fetal demand for blood cells increases, and they begin leaving the bone marrow and entering the bloodstream before completing their development. Because these immature RBCs are erythroblasts, HDN is also known as erythroblastosis fetalis. Fortunately, the mothers anti-Rh antibody production can be prevented if such antibodies (available under the name RhoGAM) are administered to the mother in weeks 2628 of pregnancy and during and after delivery. These antibodies destroy any fetal RBCs that cross the placenta before they can stimulate a maternal immune response. Because maternal sensitization does not occur, no anti-Rh antibodies are produced. Slide 20 CLINICAL MODULE 17.5 Review a. Define hemolytic disease of the newborn (HDN). b. Why is RhoGAM administered to Rh mothers? Slide 21 Module 17.6: White blood cells White blood cells (leukocytes) Spend only a short time in circulation Mostly located in loose and dense connective tissues where infections often occur Can migrate out of bloodstream Contact and adhere to vessel walls near infection site Squeeze between adjacent endothelial cells = Emigration Are attracted to chemicals from pathogens, damaged tissues, or other WBCs = Positive chemotaxis Sl