Slides mostly © Marieb & Hoehn 9th ed.

Slides mostly © Marieb & Hoehn 9th ed.
Ch. 17 Blood Slides mostly © Marieb & Hoehn 9th ed. Other slides by WCR

Blood Composition Blood Fluid connective tissue
Plasma – non-living fluid matrix Formed elements – living blood "cells" suspended in plasma Erythrocytes (red blood cells, or RBCs) Leukocytes (white blood cells, or WBCs) Platelets © 2013 Pearson Education, Inc.

Spun tube of blood yields three layers
Blood Composition Spun tube of blood yields three layers Plasma on top (~55%) Erythrocytes on bottom (~45%) WBCs and platelets in Buffy coat (< 1%) Hematocrit Percent of blood volume that is RBCs 47% ± 5% for males; 42% ± 5% for females © 2013 Pearson Education, Inc.

Figure 17.1 The major components of whole blood.
Slide 1 Formed elements Plasma • 55% of whole blood • Least dense component Buffy coat • Leukocytes and platelets • <1% of whole blood Erythrocytes Withdraw blood and place in tube. 1 Centrifuge the blood sample. 2 • 45% of whole blood (hematocrit) • Most dense component © 2013 Pearson Education, Inc.

Physical Characteristics and Volume
Sticky, opaque fluid with metallic taste Color varies with O2 content High O2 - scarlet; Low O2 - dark red pH 7.35–7.45 ~8% of body weight Average volume 5–6 L for males; 4–5 L for females © 2013 Pearson Education, Inc.

Functions of Blood Functions include Distributing substances
Regulating blood levels of substances Protection © 2013 Pearson Education, Inc.

Distribution Functions
Delivering O2 and nutrients to body cells Transporting metabolic wastes to lungs and kidneys for elimination Transporting hormones from endocrine organs to target organs © 2013 Pearson Education, Inc.

Maintaining body temperature by absorbing and distributing heat
Regulation Functions Maintaining body temperature by absorbing and distributing heat Maintaining normal pH using buffers; alkaline reserve of bicarbonate ions Maintaining adequate fluid volume in circulatory system © 2013 Pearson Education, Inc.

Protection Functions Preventing infection Antibodies
Complement proteins WBCs © 2013 Pearson Education, Inc.

Over 100 dissolved solutes
Blood Plasma 90% water Over 100 dissolved solutes Nutrients, gases, hormones, wastes, proteins, inorganic ions Electrolytes most abundant solutes by number Plasma proteins most abundant solutes by mass Remain in blood; not taken up by cells Proteins produced mostly by liver 60% albumin; 36% globulins; 4% fibrinogen © 2013 Pearson Education, Inc.

Albumin 60% of plasma protein Functions Substance carrier Blood buffer
Major contributor of plasma osmotic pressure © 2013 Pearson Education, Inc.

Only WBCs are complete cells RBCs have no nuclei or other organelles
Formed Elements Only WBCs are complete cells RBCs have no nuclei or other organelles Platelets are cell fragments Most formed elements survive in bloodstream only few days Most blood cells originate in bone marrow and do not divide © 2013 Pearson Education, Inc.

Platelets Erythrocytes Monocyte Neutrophils Lymphocyte
Figure Photomicrograph of a human blood smear stained with Wright's stain. Platelets Erythrocytes Monocyte Neutrophils Lymphocyte © 2013 Pearson Education, Inc.

Biconcave discs, anucleate, essentially no organelles
Erythrocytes Biconcave discs, anucleate, essentially no organelles Diameters larger than some capillaries Filled with hemoglobin (Hb) for gas transport Contain plasma membrane protein spectrin and other proteins Spectrin provides flexibility to change shape Major factor contributing to blood viscosity © 2013 Pearson Education, Inc.

Figure 17.3 Structure of erythrocytes (red blood cells).
2.5 µm Side view (cut) 7.5 µm Top view © 2013 Pearson Education, Inc.

Structural characteristics contribute to gas transport
Erythrocytes Structural characteristics contribute to gas transport Biconcave shape—huge surface area relative to volume >97% hemoglobin (not counting water) No mitochondria; ATP production anaerobic; do not consume O2 they transport Superb example of complementarity of structure and function © 2013 Pearson Education, Inc.

RBCs dedicated to respiratory gas transport
Erythrocyte Function RBCs dedicated to respiratory gas transport Hemoglobin binds reversibly with oxygen Normal values Males - 13–18g/100ml; Females - 12–16 g/100ml © 2013 Pearson Education, Inc.

Globin composed of 4 polypeptide chains
Hemoglobin Structure Globin composed of 4 polypeptide chains Two alpha and two beta chains Heme pigment bonded to each globin chain Gives blood red color Heme's central iron atom binds one O2 Each Hb molecule can transport four O2 Each RBC contains 250 million Hb molecules © 2013 Pearson Education, Inc.

Figure 17.4 Structure of hemoglobin.
 Globin chains Heme group  Globin chains Hemoglobin consists of globin (two alpha and two beta polypeptide chains) and four heme groups. Iron-containing heme pigment. © 2013 Pearson Education, Inc.

Blood cell formation in red bone marrow
Hematopoiesis Blood cell formation in red bone marrow Composed of reticular connective tissue and blood sinusoids In adult, found in axial skeleton, girdles, and proximal epiphyses of humerus and femur © 2013 Pearson Education, Inc.

Figure 17.5 Erythropoiesis: formation of red blood cells.
Stem cell Committed cell Developmental pathway Phase 1 Ribosome synthesis Phase 2 Hemoglobin accumulation Phase 3 Ejection of nucleus Hematopoietic stem cell (hemocytoblast) Basophilic erythroblast Polychromatic erythroblast Orthochromatic erythroblast Proerythroblast Reticulocyte Erythrocyte © 2013 Pearson Education, Inc.

Regulation of Erythropoiesis
Too few RBCs leads to tissue hypoxia Too many RBCs increases blood viscosity > 2 million RBCs made per second Balance between RBC production and destruction depends on Hormonal controls Adequate supplies of iron, amino acids, and B vitamins © 2013 Pearson Education, Inc.

Hormonal Control of Erythropoiesis
Hormone Erythropoietin (EPO) Direct stimulus for erythropoiesis Always small amount in blood to maintain basal rate High RBC or O2 levels depress production Released by kidneys (some from liver) in response to hypoxia Dialysis patients have low RBC counts © 2013 Pearson Education, Inc.

Figure 17.6 Erythropoietin mechanism for regulating erythropoiesis.
Slide 1 IMBALANCE Homeostasis: Normal blood oxygen levels Stimulus: Hypoxia (inadequate O2 delivery) due to 1 O2-carrying ability of blood rises. 5 IMBALANCE • Decreased RBC count • Decreased amount of hemoglobin • Decreased availability of O2 Enhanced erythropoiesis increases RBC count. 4 Kidney (and liver to a smaller extent) releases erythropoietin. 2 Erythropoietin stimulates red bone marrow. 3 © 2013 Pearson Education, Inc.

Dietary Requirements for Erythropoiesis
Nutrients—amino acids, lipids, and carbohydrates Iron Available from diet 65% in Hb; rest in liver, spleen, and bone marrow Free iron ions toxic Stored in cells as ferritin and hemosiderin Transported in blood bound to protein transferrin Vitamin B12 and folic acid necessary for DNA synthesis for rapidly dividing cells (developing RBCs) © 2013 Pearson Education, Inc.

Fate and Destruction of Erythrocytes
Life span: 100–120 days No protein synthesis, growth, division Old RBCs become fragile; Hb begins to degenerate Get trapped in smaller circulatory channels especially in spleen Macrophages engulf dying RBCs in spleen © 2013 Pearson Education, Inc.

Fate and Destruction of Erythrocytes
Heme and globin are separated Iron salvaged for reuse Heme degraded to yellow pigment bilirubin Liver secretes bilirubin (in bile) into intestines Degraded to pigment urobilinogen Pigment leaves body in feces as stercobilin Globin metabolized into amino acids Released into circulation © 2013 Pearson Education, Inc.

Figure 17.7 Life cycle of red blood cells.
Slide 1 Low O2 levels in blood stimulate kidneys to produce erythropoietin. 1 2 Erythropoietin levels rise in blood. Erythropoietin and necessary raw materials in blood promote erythropoiesis in red bone marrow. 3 New erythrocytes enter bloodstream; function about 120 days. 4 Aged and damaged red blood cells are engulfed by macrophages of spleen, liver, and bone marrow; the hemoglobin is broken down. 5 Hemoglobin Heme Globin Bilirubin is picked up by the liver. Iron is stored as ferritin or hemosiderin. Amino acids Iron is bound to transferrin and released to blood from liver as needed for erythropoiesis. Bilirubin is secreted into intestine in bile where it is metabolized to stercobilin by bacteria. Circulation Raw materials are made available in blood for erythrocyte synthesis. 6 Food nutrients (amino acids, Fe, B12, and folic acid) are absorbed from intestine and enter blood. Stercobilin is excreted in feces. © 2013 Pearson Education, Inc.

Slide 5 Low O2 levels in blood stimulate kidneys to produce erythropoietin. 1 2 Erythropoietin levels rise in blood. Erythropoietin and necessary raw materials in blood promote erythropoiesis in red bone marrow. 3 New erythrocytes enter bloodstream; function about 120 days. 4 © 2013 Pearson Education, Inc.

Slide 7 Aged and damaged red blood cells are engulfed by macrophages of spleen, liver, and bone marrow; the hemoglobin is broken down. 5 Hemoglobin Heme Globin Bilirubin is picked up by the liver. Iron is stored as ferritin or hemosiderin. Amino acids Iron is bound to transferrin and released to blood from liver as needed for erythropoiesis. Bilirubin is secreted into intestine in bile where it is metabolized to stercobilin by bacteria. Circulation Raw materials are made available in blood for erythrocyte synthesis. 6 Food nutrients (amino acids, Fe, B12, and folic acid) are absorbed from intestine and enter blood. Stercobilin is excreted in feces. © 2013 Pearson Education, Inc.

Erythrocyte Disorders
Anemia Blood has abnormally low O2-carrying capacity Sign rather than disease itself Blood O2 levels cannot support normal metabolism Accompanied by fatigue, pallor, shortness of breath, and chills © 2013 Pearson Education, Inc.

Causes of Anemia Three groups Blood loss Low RBC production
High RBC destruction © 2013 Pearson Education, Inc.

Causes of Anemia: Blood Loss
Hemorrhagic anemia Blood loss rapid (e.g., stab wound) Treated by blood replacement Chronic hemorrhagic anemia Slight but persistent blood loss Hemorrhoids, bleeding ulcer Primary problem treated © 2013 Pearson Education, Inc.

Causes of Anemia: Low RBC Production
Iron-deficiency anemia Caused by hemorrhagic anemia, low iron intake, or impaired absorption Microcytic, hypochromic RBCs Iron supplements to treat © 2013 Pearson Education, Inc.

Pernicious anemia Autoimmune disease - destroys stomach mucosa Lack of intrinsic factor needed to absorb B12 Deficiency of vitamin B12 RBCs cannot divide  macrocytes Treated with B12 injections or nasal gel Also caused by low dietary B12 (vegetarians) © 2013 Pearson Education, Inc. 35

Aplastic anemia Destruction or inhibition of red marrow by drugs, chemicals, radiation, viruses Usually cause unknown All cell lines affected Anemia; clotting and immunity defects Treated short-term with transfusions; long-term with transplanted stem cells © 2013 Pearson Education, Inc.

Causes of Anemia: High RBC Destruction
Hemolytic anemias Premature RBC lysis Caused by Hb abnormalities Incompatible transfusions Infections © 2013 Pearson Education, Inc.

Causes of Anemia: High RBC Destruction
Sickle-cell anemia Hemoglobin S One amino acid wrong in a globin beta chain RBCs crescent shaped when unload O2 or blood O2 low RBCs rupture easily and block small vessels Poor O2 delivery; pain © 2013 Pearson Education, Inc.

Figure 17.8 Sickle-cell anemia.
Val His Leu Thr Pro Glu Glu … 1 2 3 4 5 6 7 146 Normal erythrocyte has normal hemoglobin amino acid sequence in the beta chain. Val His Leu Thr Pro Val Glu … 1 2 3 4 5 6 7 146 Sickled erythrocyte results from a single amino acid change in the beta chain of hemoglobin. © 2013 Pearson Education, Inc.

Make up <1% of total blood volume
Leukocytes Make up <1% of total blood volume 4,800 – 10,800 WBCs/μl blood Function in defense against disease Can leave capillaries via diapedesis Move through tissue spaces by ameboid motion and positive chemotaxis Leukocytosis: WBC count over 11,000/mm3 Normal response to infection © 2013 Pearson Education, Inc.

Leukocytes: Two Categories
Granulocytes – Visible cytoplasmic granules Neutrophils, eosinophils, basophils Agranulocytes – No visible cytoplasmic granules Lymphocytes, monocytes Decreasing abundance in blood Never let monkeys eat bananas © 2013 Pearson Education, Inc.

Differential WBC count (All total 4800– 10,800/ µl) Formed elements
Figure Types and relative percentages of leukocytes in normal blood. Differential WBC count (All total 4800– 10,800/ µl) Formed elements (not drawn to scale) Platelets Granulocytes Neutrophils (50–70%) Leukocytes Eosinophils (2–4%) Basophils (0.5–1%) Erythrocytes Agranulocytes Lymphocytes (25–45%) Monocytes (3–8%) © 2013 Pearson Education, Inc.

Granulocytes Granulocytes Larger and shorter-lived than RBCs
Lobed nuclei Cytoplasmic granules stain specifically with Wright's stain All phagocytic to some degree © 2013 Pearson Education, Inc.

Also called Polymorphonuclear leukocytes (PMNs or polys)
Neutrophils Most numerous WBCs Also called Polymorphonuclear leukocytes (PMNs or polys) Granules stain lilac; contain hydrolytic enzymes or defensins 3-6 lobes in nucleus; twice size of RBCs Very phagocytic—"bacteria slayers" © 2013 Pearson Education, Inc.

Red-staining granules Bilobed nucleus Granules lysosome-like
Eosinophils Red-staining granules Bilobed nucleus Granules lysosome-like Release enzymes to digest parasitic worms Role in allergies and asthma Role in modulating immune response © 2013 Pearson Education, Inc.

Nucleus deep purple with 1-2 constrictions
Basophils Rarest WBCs Nucleus deep purple with 1-2 constrictions Large, purplish-black (basophilic) granules contain histamine Histamine: inflammatory chemical that acts as vasodilator to attract WBCs to inflamed sites Are functionally similar to mast cells © 2013 Pearson Education, Inc.

Granulocytes Neutrophil: Multilobed nucleus, pale red and blue
Figure 17.10a Leukocytes. Granulocytes Neutrophil: Multilobed nucleus, pale red and blue cytoplasmic granules © 2013 Pearson Education, Inc.

Granulocytes Eosinophil: Bilobed nucleus, red cytoplasmic granules
Figure 17.10b Leukocytes. Granulocytes Eosinophil: Bilobed nucleus, red cytoplasmic granules © 2013 Pearson Education, Inc.

Granulocytes Basophil: Bilobed nucleus, purplish-black
Figure 17.10c Leukocytes. Granulocytes Basophil: Bilobed nucleus, purplish-black cytoplasmic granules © 2013 Pearson Education, Inc.

Agranulocytes Agranulocytes Lack visible cytoplasmic granules
Have spherical or kidney-shaped nuclei © 2013 Pearson Education, Inc.

Second most numerous WBC
Lymphocytes Second most numerous WBC Large, dark-purple, circular nuclei with thin rim of blue cytoplasm Mostly in lymphoid tissue (e.g., lymph nodes, spleen); few circulate in blood Crucial to immunity © 2013 Pearson Education, Inc.

Abundant pale-blue cytoplasm
Monocytes Largest leukocytes Abundant pale-blue cytoplasm Dark purple-staining, U- or kidney-shaped nuclei © 2013 Pearson Education, Inc.

Leave circulation, enter tissues, and differentiate into macrophages
Monocytes Leave circulation, enter tissues, and differentiate into macrophages Actively phagocytic cells; crucial against viruses, intracellular bacterial parasites, and chronic infections Activate lymphocytes to mount an immune response © 2013 Pearson Education, Inc.

Agranulocytes Lymphocyte (small): Large spherical nucleus, thin rim of
Figure 17.10d Leukocytes. Agranulocytes Lymphocyte (small): Large spherical nucleus, thin rim of pale blue cytoplasm © 2013 Pearson Education, Inc.

Agranulocytes Monocyte: Kidney-shaped nucleus, abundant
Figure 17.10e Leukocytes. Agranulocytes Monocyte: Kidney-shaped nucleus, abundant pale blue cytoplasm © 2013 Pearson Education, Inc.

Leukopoiesis Production of WBCs
Stimulated by 2 types of chemical messengers from red bone marrow and mature WBCs Interleukins (e.g., IL-3, IL-5) Colony-stimulating factors (CSFs) named for WBC type they stimulate (e.g., granulocyte-CSF stimulates granulocytes) © 2013 Pearson Education, Inc.

Figure 17.11 Leukocyte formation.
Stem cells Hematopoietic stem cell (hemocytoblast) Figure Leukocyte formation. Myeloid stem cell Lymphoid stem cell Committed cells Myeloblast Myeloblast Myeloblast Monoblast B lymphocyte precursor T lymphocyte precursor Developmental pathway Promyelocyte Promyelocyte Promyelocyte Promonocyte Eosinophilic myelocyte Basophilic myelocyte Neutrophilic myelocyte Eosinophilic band cells Basophilic band cells Neutrophilic band cells Granular leukocytes Agranular leukocytes Eosinophils Basophils Neutrophils Monocytes B lymphocytes T lymphocytes (a) (b) (c) (d) (e) (f) Some become Some become Some become Macrophages (tissues) Plasma cells Effector T cells © 2013 Pearson Education, Inc.

Cytoplasmic fragments of megakaryocytes
Platelets Cytoplasmic fragments of megakaryocytes Form temporary platelet plug that helps seal breaks in blood vessels Circulating platelets kept inactive and mobile by nitric oxide (NO) and prostacyclin from endothelial cells lining blood vessels Age quickly; degenerate in about 10 days Formation regulated by thrombopoietin © 2013 Pearson Education, Inc.

Figure 17.12 Formation of platelets.
Stem cell Developmental pathway Hematopoietic stem cell (hemocytoblast) Megakaryoblast (stage I megakaryocyte) Megakaryocyte (stage II/III) Megakaryocyte (stage IV) Platelets © 2013 Pearson Education, Inc.

Table 17.2 Summary of Formed Elements of the Blood (1 of 2)
© 2013 Pearson Education, Inc.

Table 17.2 Summary of Formed Elements of the Blood (2 of 2)

Fast series of reactions for stoppage of bleeding
Hemostasis Fast series of reactions for stoppage of bleeding Requires clotting factors, and substances released by platelets and injured tissues Three steps Vascular spasm Platelet plug formation Coagulation (blood clotting) © 2013 Pearson Education, Inc.

Hemostasis: Vascular Spasm
Vasoconstriction of damaged blood vessel Triggers Direct injury to vascular smooth muscle Chemicals released by endothelial cells and platelets Pain reflexes Most effective in smaller blood vessels © 2013 Pearson Education, Inc.

Hemostasis: Platelet Plug Formation
Positive feedback cycle Damaged endothelium exposes collagen fibers Platelets stick to collagen fibers via plasma protein von Willebrand factor Swell, become spiked and sticky, and release chemical messengers ADP causes more platelets to stick and release their contents Serotonin and thromboxane A2 enhance vascular spasm and platelet aggregation © 2013 Pearson Education, Inc.

Hemostasis: Coagulation
Reinforces platelet plug with fibrin threads Blood transformed from liquid to gel Series of reactions using clotting factors (procoagulants) # I – XIII; most plasma proteins Vitamin K needed to synthesize 4 of them © 2013 Pearson Education, Inc.

Figure 17.13 Events of hemostasis.
Slide 5 Step Vascular spasm • Smooth muscle contracts, causing vasoconstriction. Step 2 Platelet plug formation • Injury to lining of vessel exposes collagen fibers; platelets adhere. Collagen fibers • Platelets release chemicals that make nearby platelets sticky; platelet plug forms. Platelets Step 3 Coagulation • Fibrin forms a mesh that traps red blood cells and platelets, forming the clot. Fibrin © 2013 Pearson Education, Inc.

Coagulation: Overview
Three phases of coagulation Prothrombin activator formed in both intrinsic and extrinsic pathways Prothrombin converted to enzyme thrombin Thrombin catalyzes fibrinogen  fibrin © 2013 Pearson Education, Inc.

Coagulation Phase 1: Two Pathways to Prothrombin Activator
Initiated by either intrinsic or extrinsic pathway (usually both) Triggered by tissue-damaging events Involves a series of procoagulants © 2013 Pearson Education, Inc.

Coagulation Phase 1: Two Pathways to Prothrombin Activator
Intrinsic pathway Triggered by negatively charged surfaces (activated platelets, collagen, glass) Uses factors present within blood (intrinsic) Extrinsic pathway Triggered by exposure to tissue factor (TF) or factor III (an extrinsic factor) Bypasses several steps of intrinsic pathway, so faster © 2013 Pearson Education, Inc.

Coagulation Phase 2: Pathway to Thrombin
Prothrombin activator catalyzes transformation of prothrombin to active enzyme thrombin Once prothrombin activator formed, clot forms in 10–15 seconds © 2013 Pearson Education, Inc.

Coagulation Phase 3: Common Pathway to the Fibrin Mesh
Thrombin converts soluble fibrinogen to fibrin Fibrin strands form structural basis of clot Fibrin causes plasma to become a gel-like trap for formed elements Thrombin (with Ca2+) activates factor XIII which: Cross-links fibrin Strengthens and stabilizes clot © 2013 Pearson Education, Inc.

Figure 17.14 The intrinsic and extrinsic pathways of blood clotting (coagulation). (1 of 2)
Phase 1 Intrinsic pathway Extrinsic pathway Vessel endothelium ruptures, exposing underlying tissues (e.g., collagen) Tissue cell trauma exposes blood to Platelets cling and their surfaces provide sites for mobilization of factors Tissue factor (TF) XII Ca2+ XIIa XI VII XIa VIIa IX Ca2+ IXa PF3 released by aggregated platelets VIII VIIIa IXa/VIIIa complex TF/VIIa complex X Xa Ca2+ PF3 Va V Prothrombin activator © 2013 Pearson Education, Inc.

Phase 2 Phase 3 Prothrombin (II) Thrombin (IIa) Fibrinogen (I)
Figure The intrinsic and extrinsic pathways of blood clotting (coagulation). (2 of 2) Phase 2 Prothrombin (II) Thrombin (IIa) Phase 3 Fibrinogen (I) (soluble) Ca2+ Fibrin (insoluble polymer) XIII XIIIa Cross-linked fibrin mesh © 2013 Pearson Education, Inc.

Figure 17.15 Scanning electron micrograph of erythrocytes trapped in a fibrin mesh.

Removes unneeded clots after healing
Fibrinolysis Removes unneeded clots after healing Begins within two days; continues for several Plasminogen in clot is converted to plasmin by tissue plasminogen activator (tPA), factor XII and thrombin Plasmin is a fibrin-digesting enzyme © 2013 Pearson Education, Inc.

Factors Limiting Clot Growth or Formation
Two mechanisms limit clot size Swift removal and dilution of clotting factors Inhibition of activated clotting factors Thrombin bound onto fibrin threads Antithrombin III inactivates unbound thrombin Heparin in basophil and mast cells inhibits thrombin by enhancing antithrombin III © 2013 Pearson Education, Inc.

Disorders of Hemostasis
Thromboembolic disorders: undesirable clot formation Bleeding disorders: abnormalities that prevent normal clot formation Disseminated intravascular coagulation (DIC) Involves both types of disorders © 2013 Pearson Education, Inc.

Thromboembolic Conditions
Thrombus: clot that develops and persists in unbroken blood vessel May block circulation leading to tissue death Embolus: thrombus freely floating in bloodstream Embolism: embolus obstructing a vessel E.g., pulmonary and cerebral emboli Risk factors – atherosclerosis, inflammation, slowly flowing blood or blood stasis from immobility © 2013 Pearson Education, Inc.

Dabigatran directly inhibits thrombin
Anticoagulant Drugs Aspirin Antiprostaglandin that inhibits thromboxane A2 Heparin Anticoagulant used clinically for pre- and postoperative cardiac care Warfarin (Coumadin) Used for those prone to atrial fibrillation Interferes with action of vitamin K Dabigatran directly inhibits thrombin © 2013 Pearson Education, Inc.

Dagatriban and related anticoagulants are based on molecules which leeches create and use to help them suck blood. Medicinal leeches are still used by some physicians, for example to promote blood flow around skin grafts and after reattachment surgery. Buy at

Thrombocytopenia: deficient number of circulating platelets
Bleeding Disorders Thrombocytopenia: deficient number of circulating platelets Petechiae appear due to spontaneous, widespread hemorrhage Due to suppression or destruction of red bone marrow (e.g., malignancy, radiation, drugs) Platelet count <50,000/μl is diagnostic Treated with transfusion of concentrated platelets © 2013 Pearson Education, Inc.

Impaired liver function
Bleeding Disorders Impaired liver function Inability to synthesize procoagulants Causes include vitamin K deficiency, hepatitis, and cirrhosis Impaired fat absorption and liver disease can also prevent liver from producing bile, impairing fat and vitamin K absorption © 2013 Pearson Education, Inc.

Bleeding Disorders Hemophilia includes several similar hereditary bleeding disorders Hemophilia A: most common type (77% of all cases); factor VIII deficiency Hemophilia B: factor IX deficiency Hemophilia C: mild type; factor XI deficiency Symptoms include prolonged bleeding, especially into joint cavities Treated with plasma transfusions and injection of missing factors Increased hepatitis and HIV risk © 2013 Pearson Education, Inc.

Whole-blood transfusions used when blood loss rapid and substantial
Packed red cells (plasma and WBCs removed) transfused to restore oxygen-carrying capacity Transfusion of incompatible blood can be fatal © 2013 Pearson Education, Inc.

Human Blood Groups RBC membranes bear 30 types of glycoprotein antigens Anything perceived as foreign; generates an immune response Promoters of agglutination; called agglutinogens Mismatched transfused blood perceived as foreign May be agglutinated and destroyed; can be fatal Presence or absence of each antigen is used to classify blood cells into different groups © 2013 Pearson Education, Inc.

Blood may contain preformed anti-A or anti-B antibodies (agglutinins)
ABO Blood Groups Types A, B, AB, and O Based on presence or absence of two agglutinogens (A and B) on surface of RBCs Blood may contain preformed anti-A or anti-B antibodies (agglutinins) Act against transfused RBCs with ABO antigens not present on recipient's RBCs Anti-A or anti-B form in blood at about 2 months of age; adult levels by 8-10 © 2013 Pearson Education, Inc.

52 named Rh agglutinogens (Rh factors) C, D, and E are most common
Rh Blood Groups 52 named Rh agglutinogens (Rh factors) C, D, and E are most common Rh+ indicates presence of D antigen 85% Americans Rh+ © 2013 Pearson Education, Inc.

Anti-Rh antibodies not spontaneously formed in Rh– individuals
Rh Blood Groups Anti-Rh antibodies not spontaneously formed in Rh– individuals Anti-Rh antibodies form if Rh– individual receives Rh+ blood, or Rh– mom carrying Rh+ fetus Second exposure to Rh+ blood will result in typical transfusion reaction © 2013 Pearson Education, Inc.

Transfusion Reactions
Occur if mismatched blood infused Donor's cells Attacked by recipient's plasma agglutinins Agglutinate and clog small vessels Rupture and release hemoglobin into bloodstream Result in Diminished oxygen-carrying capacity Diminished blood flow beyond blocked vessels Hemoglobin in kidney tubules  renal failure © 2013 Pearson Education, Inc.

Type AB universal recipient
Transfusions Type O universal donor No A or B antigens Type AB universal recipient No anti-A or anti-B antibodies Misleading - other agglutinogens cause transfusion reactions Autologous transfusions Patient predonates © 2013 Pearson Education, Inc.

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