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Blood

The only fluid tissue

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Figure 17.10

Blood Composition

Blood: a fluid connective tissue composed of

Plasma

Formed elements

Erythrocytes (red blood cells, or RBCs)

Leukocytes (white blood cells, or WBCs)

Platelets

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Blood Composition

Hematocrit

Percent of blood volume that is RBCs

47% ± 5% for males

42% ± 5% for females

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Inc. maybe not volume Copyright © 2006 Pearson Education. publishing as Benjamin Cummings Figure 17.Components of Whole Blood Plasma expanders restore blood volume.1 .. not O2 Packed cells restore O2.

45  Temperature is 38C  Blood accounts for approximately 8% of body weight  Average volume: 5–6 L for males.Physical Characteristics and Volume  Blood is a sticky. Inc.35–7. publishing as Benjamin Cummings .. and 4–5 L for females Copyright © 2006 Pearson Education. opaque fluid with a metallic taste  Color varies from scarlet (> O2) to dark red (<O2)  The pH of blood is 7.

publishing as Benjamin Cummings .Functions of Blood  Delivers Oxygen to tissues..to lungs  Distribution  Regulation  Protection Copyright © 2006 Pearson Education. Inc.from lungs  Picks up Carbon dioxide from the tissues.

publishing as Benjamin Cummings . Distribution of :  O2 and nutrients to body cells  Metabolic wastes to the lungs and kidneys for elimination  Hormones from endocrine organs to target organs Copyright © 2006 Pearson Education.. Inc.Functions of Blood 1.

 Body temperature by absorbing and distributing heat  Normal pH using buffers  Adequate fluid volume in the circulatory system Copyright © 2006 Pearson Education.Functions of Blood Regulation of 2. Inc.. publishing as Benjamin Cummings .

Tcells Copyright © 2006 Pearson Education. publishing as Benjamin Cummings .. Inc.Protection   Hemostasis  Activating plasma proteins & platelets  Clot formation when a vessel is broken Immune functions  Antibodies.B cells  Activating complement proteins  Activating WBCs to defend the body against foreign invaders .

Ca2+. amino acids  Electrolytes—Na+. creatinine  Nutrients—glucose. Cl–. publishing as Benjamin Cummings .. HCO3–  Respiratory gases—O2 and CO2  Hormones Copyright © 2006 Pearson Education. Inc.Blood Plasma  Nitrogenous by-products of metabolism—lactic acid. K+. carbohydrates. urea.

Blood Plasma  90% water  Proteins are mostly produced by the liver  60% albumin  36% globulins  4% fibrinogen Copyright © 2006 Pearson Education. publishing as Benjamin Cummings . Inc..

few organelles. leukocytes. “thrombocytes” Copyright © 2006 Pearson Education.. Inc.no nuclei.Formed Elements  Erythrocytes. and platelets make up the formed elements  WBCs .cells  RBCs . publishing as Benjamin Cummings . “a sack of hgb”  platelets .cell fragments.

Megakaryocyte Copyright © 2006 Pearson Education. publishing as Benjamin Cummings . Inc..

Components of Whole Blood Copyright © 2006 Pearson Education. publishing as Benjamin Cummings Figure 17.2 .. Inc.

Erythrocytes (RBCs) No nucleus Copyright © 2006 Pearson Education. Inc..3 . publishing as Benjamin Cummings Figure 17.

ATP production is anaerobic. Inc.. no O2 is used in generation of ATP A superb example of complementarity of structure and function! Copyright © 2006 Pearson Education.Erythrocytes   Structural characteristics contribute to gas transport  Biconcave shape—huge surface area relative to volume  > 97% hemoglobin (not counting water)  No mitochondria. publishing as Benjamin Cummings .

publishing as Benjamin Cummings Figure 17..Structure of Hemoglobin Copyright © 2006 Pearson Education.4 . Inc.

pages 3–13 Copyright © 2006 Pearson Education. Inc.. publishing as Benjamin Cummings .Hemoglobin (Hb)  Oxyhemoglobin – oxygen bound to Hgb (or Hb)  Deoxyhemoglobin .oxygen dissociates from hgb & diffuses into tissues (reduced Hgb)  Carbaminohemoglobin – carbon dioxide bound Hgb PLAY InterActive Physiology ®: Respiratory System: Gas Transport.

Erythrocyte Function  RBCs are dedicated to respiratory gas transport  Hemoglobin binds reversibly with oxygen Copyright © 2006 Pearson Education. publishing as Benjamin Cummings .. Inc.

Hematopoiesis  Hematopoiesis   Red bone marrow of the:  Axial skeleton (sternum) and girdles (iliac crest)  Epiphyses of the humerus and femur Hemocytoblasts give rise to all formed elements  “Pluripotent cell” or stem cell Copyright © 2006 Pearson Education.. publishing as Benjamin Cummings . Inc.

Production of Erythrocytes: Erythropoiesis Peripheral Circulation Bone marrow Copyright © 2006 Pearson Education. publishing as Benjamin Cummings Figure 17..5 . Inc.

1 x 106/ ul whole blood  < RBCs = tissue hypoxia  > RBCs = > blood viscosity Erythropoietin (kidneys) – stimulates RBC production RBC production Requires:  iron  amino acids  B vitamins Copyright © 2006 Pearson Education.Regulation of Erythropoiesis   Normal RBC: 4..2-6. publishing as Benjamin Cummings . Inc.

Inc. or decreased availability of O2 Increases O2-carrying ability of blood Reduces O2 levels in blood Enhanced erythropoiesis increases RBC count Erythropoietin stimulates red bone marrow Copyright © 2006 Pearson Education. decreased amount of hemoglobin.6 ..Erythropoietin Mechanism Im b ala n ce Start Homeostasis: Normal blood oxygen levels Im b ala n ce Stimulus: Hypoxia due to decreased RBC count. publishing as Benjamin Cummings Kidney (and liver to a smaller extent) releases erythropoietin Figure 17.

including amino acids. Fe. 4 New erythrocytes enter bloodstream.. Copyright © 2006 Pearson Education.7 . function about 120 days. hemosiderin Iron is bound to transferrin and released to blood from liver as needed for erythropoiesis Bilirubin is picked up from blood by liver.1 Low O2 levels in blood stimulate kidneys to produce erythropoietin. 2 Erythropoietin levels rise in blood. and folic acid are absorbed from intestine and enter blood 6 Raw materials are made available in blood for erythrocyte synthesis. spleen. secreted into intestine in bile. metabolized to stercobilin by bacteria and excreted in feces Circulation Food nutrients. 5 Aged and damaged red blood cells are engulfed by macrophages of liver. Hemoglobin Heme Globin Bilirubin Amino acids Iron stored as ferritin. and bone marrow. publishing as Benjamin Cummings Figure 17. the hemoglobin is broken down. B12. Inc. RBC life cycle(recycle 80-120 days) 3 Erythropoietin and necessary raw materials in blood promote erythropoiesis in red bone marrow.

and chills Copyright © 2006 Pearson Education. Inc. paleness. shortness of breath.< RBC (normocytic)  Hemorrhagic anemia  Hemolytic anemia  Aplastic anemia Signs/symptoms include fatigue. publishing as Benjamin Cummings ..Erythrocyte Disorders – Types of Anemia   Anemias .

publishing as Benjamin Cummings .. Inc.Types of Anemia : Decreased Hemoglobin Content   Iron-deficiency anemia : (microcytic)  (from hemorrhagic anemia)  < dietary iron  Impaired iron absorption Pernicious anemia : (macrocytic)  Deficiency of vitamin B12  Lack of intrinsic factor needed for absorption of B12  Treatment is intramuscular injection of B12. application of Nascobal Copyright © 2006 Pearson Education.

publishing as Benjamin Cummings .. Inc.Types of Anemia: Abnormal Hemoglobin   Thalassemias –  defective globin chain gene(s)  Many forms  Mediterranean decent Sickle-cell anemia  defective globin chain gene with a single aa substitution  This defect causes RBCs to become sickle-shaped in < oxygen & > oxygen demand situations Copyright © 2006 Pearson Education.

1 2 3 4 5 6 7 146 (b) Sickled erythrocyte results from a single amino acid change in the beta chain of hemoglobin.(a) Normal erythrocyte has normal hemoglobin amino acid sequence in the beta chain. Inc.8 . 1 2 3 4 5 6 7 146 Copyright © 2006 Pearson Education.. publishing as Benjamin Cummings Figure 17.

Inc. publishing as Benjamin Cummings ..Polycythemia  Polycythemia – excess RBCs that increase blood viscosity  Three main polycythemias are:   Polycythemia vera  Secondary polycythemia – test pilots  Blood doping – atheletes RX: phlebotomies Copyright © 2006 Pearson Education.

> 11.leaks from blood into tissues Copyright © 2006 Pearson Education. publishing as Benjamin Cummings . Inc.leukopenia  from bone marrow suppression  leads to infection  never normal > WBC – leukocytosis.Leukocytes (WBCs)  Normal WBC: 5-10..000/ ul whole blood   < WBC . exercise. leukemia Diapedesis. stress.000/ul   From: infection.

Inc.. publishing as Benjamin Cummings Figure 17.Percentages of Leukocytes Copyright © 2006 Pearson Education.9 .

publishing as Benjamin Cummings .. Inc. segmented nuclei. and are phagocytic  Neutrophils – “segs”. first ones to site of inflammation  Eosinophils  Basophils Copyright © 2006 Pearson Education.Granulocytes  All have granules.

(a) Neutrophil. red cytoplasmic granules Copyright © 2006 Pearson Education. multilobed nucleus (b) Eosinophil. bilobed nucleus.10 (a-c) .. Inc. bilobed nucleus. purplish-black cytoplasmic granules Figure 17. publishing as Benjamin Cummings (c) Basophil.

Neutrophils

50-70% total WBC

> Neutrophils – bacterial infections

Very active in inflammation

diapedesis

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Eosinophils

1–4% of WBCs

Red-orange granules (acidophilic)

> : allergies, parasitic infections

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Basophils

0.5% of WBCs

purplish-black (basophilic) granules;

Histamine

Called mast cells in tissues

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Inc. publishing as Benjamin Cummings (e) Monocyte. large spherical nucleus Copyright © 2006 Pearson Education.. e . kidney-shaped nucleus Figure 17.10d.(d) Small lymphocyte.

publishing as Benjamin Cummings . circular nuclei with a thin rim of blue cytoplasm   Are found mostly enmeshed in lymphoid tissue (some circulate in the blood) T cells and B cells  T cells function in cell mediated immune response  B cells produce antibodies in humoral immune response Copyright © 2006 Pearson Education. Inc.Lymphocytes  25-45% WBCs  > in viral infections  Large. dark-purple..

publishing as Benjamin Cummings .. antigen processing or presentation.Monocytes  4–8% WBC  largest leukocytes  Macrophages in tissue  Phagocytosis. Inc. inflammation Copyright © 2006 Pearson Education.

Inc. publishing as Benjamin Cummings Figure 17.Leukocytes Copyright © 2006 Pearson Education.10 ..

IL-2).interleukins & (CSFs)  Interleukins are numbered (e.Production of Leukocytes  Leukopoiesis. granulocyte-CSF stimulates granulocytes)  Macrophages and T cells are the most important sources of cytokines – cytotoxic factors  Many hematopoietic hormones are used clinically to stimulate bone marrow Copyright © 2006 Pearson Education..g. publishing as Benjamin Cummings .. whereas CSFs are named for the WBCs they stimulate (e. Inc.g.. IL-1.

Stem cells Hemocytoblast Myeloid stem cell Committed Myeloblast cells Myeloblast Lymphoid stem cell Myeloblast DevelopPromyelocyte Promyelocyte Promyelocyte mental pathway Eosinophilic myelocyte Basophilic myelocyte Neutrophilic myelocyte Eosinophilic band cells Basophilic band cells Neutrophilic band cells Eosinophils Basophils Neutrophils (a) (b) (c) Lymphoblast Promonocyte Prolymphocyte Monocytes Lymphocytes (e) (d) Agranular leukocytes Granular leukocytes Copyright © 2006 Pearson Education.. Inc.11 . publishing as Benjamin Cummings Some become Macrophages (tissues) Some become Plasma cells Figure 17.

blast-type cells. Inc.WBC cancers  Myelocytic leukemia – myeloblasts  Lymphocytic leukemia – lymphocytes  Acute leukemia.Leukocytes Disorders: Leukemias   Leukemias. publishing as Benjamin Cummings . children  Chronic leukemia – more mature cells. adults Childhood leukemia has high cure rate Copyright © 2006 Pearson Education..

Inc.. publishing as Benjamin Cummings .Megakaryocyte Copyright © 2006 Pearson Education.

Inc. Bone marrow Stem cell Hemocytoblast Developmental pathway Megakaryoblast Promegakaryocyte Copyright © 2006 Pearson Education.. publishing as Benjamin Cummings Megakaryocyte Platelets Figure 17.12 .Genesis of Platelets  The stem cell for platelets is the hemocytoblast  The sequential developmental pathway is as shown.

. Vascular spasms – immediate vasoconstriction in response to injury 2. Platelet plug formation 3. Coagulation – cascade of rxns ending in fibrin clot Copyright © 2006 Pearson Education.Hemostasis  “blood stop” – 3 Phases Involved 1. publishing as Benjamin Cummings . Inc.

.Platelet Plug Formation  Platelets do not stick to each other or to blood vessels  Upon damage to blood vessel endothelium platelets:   With the help of von Willebrand factor (VWF) adhere to collagen  Are stimulated by thromboxane A2  Stick to exposed collagen fibers and form a platelet plug  Release serotonin and ADP. which attract still more platelets The platelet plug is limited to the immediate area of injury by prostacyclin Copyright © 2006 Pearson Education. Inc. publishing as Benjamin Cummings .

Coagulation  A set of reactions in which blood is transformed from a liquid to a gel  Coagulation follows intrinsic and extrinsic pathways  The final three steps of this series of reactions are:  Prothrombin activator is formed  Prothrombin is converted into thrombin  Thrombin catalyzes the joining of fibrinogen into a fibrin mesh Copyright © 2006 Pearson Education. publishing as Benjamin Cummings .. Inc.

Coagulation Copyright © 2006 Pearson Education.. publishing as Benjamin Cummings Figure 17. Inc.13a .

Detailed Events of Coagulation Copyright © 2006 Pearson Education.13b . publishing as Benjamin Cummings Figure 17. Inc..

15 .. publishing as Benjamin Cummings Figure 17. Inc.Copyright © 2006 Pearson Education.

Inc.Clot Retraction and Repair  Clot retracts within 30-60’   Proteins in platelets squeeze serum from clot Repair  Platelet-derived growth factor (PDGF) – repairs vessel wall  Fibroblasts form a connective tissue patch  Stimulated by vascular endothelial growth factor (VEGF). endothelial cells multiply and restore the endothelial lining Copyright © 2006 Pearson Education.. publishing as Benjamin Cummings .

to break down the clot (within 2 days)  tPA.tissue plasminogen activator = clot buster  Two mechanisms prevent clot growth  Swift removal of clotting factors  Inhibition of activated clotting factors Hemostasis vs Fibrinolysis Copyright © 2006 Pearson Education.. inhibit growth of clot 2.Fibrinolysis & Control of Clot Formation As soon as clot is formed. a fibrinolytic process begins to: 1. publishing as Benjamin Cummings . Inc.

Inc. rough spots  Heparin and PGI2 secreted by endothelial cells  Vitamin E quinone. publishing as Benjamin Cummings .Factors Preventing Undesirable Clotting  Unnecessary clotting is prevented by endothelial lining the blood vessels  Platelet adhesion is prevented by:   The smooth endothelial lining of blood vessels. a potent anticoagulant INFLAMMATION may lead to > clots Copyright © 2006 Pearson Education.no plaques..

publishing as Benjamin Cummings . resulting in tissue death  Coronary thrombosis – thrombus in blood vessel of the heart Copyright © 2006 Pearson Education.Hemostasis Disorders: Thromboembolytic Conditions  Thrombus – a clot that develops and persists in an unbroken blood vessel  Thrombi can block circulation. Inc..

 Thromboembolus. etc. cancer cells. Inc.blood clot on the move  Pulmonary emboli can impair the ability of the body to obtain oxygen  Cerebral emboli can cause strokes Copyright © 2006 Pearson Education.. publishing as Benjamin Cummings .Hemostasis Disorders: Thromboembolytic Conditions  Embolus – a clot on the move (in blood)  Can be fat.

. Inc. publishing as Benjamin Cummings .thromboxane A2  Heparin – an anticoagulant used clinically for preand postoperative cardiac care  Warfarin – used for those prone to atrial fibrillation Copyright © 2006 Pearson Education.Prevention of Undesirable Clots  Substances used to prevent undesirable clots:  Aspirin – inhibits prostaglandin .

Hemostasis Disorders  Disseminated Intravascular Coagulation (DIC): widespread clotting in intact blood vessels  Poor prognosis  Residual blood cannot clot..thrombin tied up in clot  Blockage of blood flow and severe bleeding follows  Most common in:  Septic shock  A complication of pregnancy  Incompatible blood transfusions Copyright © 2006 Pearson Education. publishing as Benjamin Cummings . Inc.

malignancy. Inc.g.. radiation)  Treated with whole blood transfusions. publishing as Benjamin Cummings . plasma exchanges Copyright © 2006 Pearson Education.Hemostasis Disorders: Bleeding Disorders  Thrombocytopenia – platelets < 50..000/ul  Petechiae  Caused by suppression or destruction of bone marrow (e.

publishing as Benjamin Cummings . Inc.Hemostasis Disorders: Bleeding Disorders   Liver disease Can’t make procoagulants  Can’t make vitamin K Gene defects in genes for clotting factors:  Hemophilia A ..factor VIII  Hemophilia B – factor IX  Hemophilia C – factor XI (mild) Copyright © 2006 Pearson Education.

Blood Transfusions   Whole blood transfusions are used:  When blood loss is substantial  In treating thrombocytopenia Packed red cells (cells with plasma removed) are used to treat anemia Copyright © 2006 Pearson Education. Inc.. publishing as Benjamin Cummings .

publishing as Benjamin Cummings .Human Blood Groups  RBC membranes have glycoprotein antigens on their external surfaces  These antigens are:   Unique to the individual  Recognized as foreign if transfused into another individual  Promoters of agglutination and are referred to as agglutinogens Presence or absence of these antigens is used to classify blood groups Copyright © 2006 Pearson Education.. Inc.

Kell.Blood Groups  Humans have 30 varieties of naturally occurring RBC antigens  ABO and Rh antigens are Landsteiner group  Other blood groups (M. and Lewis) Copyright © 2006 Pearson Education.. Dufy. publishing as Benjamin Cummings . Inc. N.

4 . publishing as Benjamin Cummings Table 17..ABO Blood Groups Copyright © 2006 Pearson Education. Inc.

anti-Rh antibodies form  A second exposure to Rh+ blood will result in a typical transfusion reaction Copyright © 2006 Pearson Education. if an Rh– individual receives Rh+ blood. three of which (C.Rh Blood Groups  There are eight different Rh agglutinogens. D. publishing as Benjamin Cummings . and E) are common  Presence of the Rh agglutinogens on RBCs is indicated as Rh+  Anti-Rh antibodies are not spontaneously formed in Rh– individuals  However.. Inc.

publishing as Benjamin Cummings .Hemolytic Disease of the Newborn  Erythroblastosis fetalis or HDN: Rh+ antibodies of a sensitized Rh– mother cross the placenta and attack and destroy the RBCs of an Rh+ baby  Usually first birth ok  RhoGAM – blocks antibodies against Rh+ fetus  RX.pre-birth transfusions. Inc.. exchange transfusions after birth  Copyright © 2006 Pearson Education.

Transfusion Reactions  Life threatening.mismatched blood is infused  Antigens (cells) & antibodies (plasma) agglutinate:  Diminished oxygen-carrying capacity  Clumped cells that impede blood flow  Ruptured RBCs.renal failure Copyright © 2006 Pearson Education.. publishing as Benjamin Cummings . Inc.release hgb  Hgb ppts in kidneys.

Blood Typing Unknown cells Blood type being tested Known antisera RBC agglutinogens Serum Reaction Anti-A Anti-B AB A and B + + B B – + A A + – O None – – Copyright © 2006 Pearson Education. Inc.. publishing as Benjamin Cummings .

Inc. publishing as Benjamin Cummings Figure 17..Blood being tested Anti-A Type AB (contains agglutinogens A and B. agglutinates with anti-A) Type B (contains agglutinogen B. agglutinates with both sera) Serum Anti-B RBCs Type A (contains agglutinogen A. agglutinates with anti-B) Type O (contains no agglutinogens. does not agglutinate with either serum) Copyright © 2006 Pearson Education.16 .

plasminate. Inc.Restoring Fluid Volume  Hypovolemic shock  Restore fluid volume-Plasma. human serum albumin OR the following may be better  Normal saline  Electrolyte solution – Ringer’s Copyright © 2006 Pearson Education. publishing as Benjamin Cummings . plasma expanders  Dextran..

Inc. MCV. publishing as Benjamin Cummings .Diagnostic Blood Tests  CBC  # RBCs. WBCs.e. indications of anemias  Hct  Serum chemistry analysis can provide a comprehensive picture of one’s general health status in relation to normal values. MCHC  Differential  Microscopic examination reveals variations in size and shape of RBCs.. Hct. blood glucose Copyright © 2006 Pearson Education. i. Hgb.

Inc.. publishing as Benjamin Cummings .Diagnostic Blood Tests  Differential WBC count  Prothrombin time and platelet counts assess hemostasis  SMAC. a blood chemistry profile  Complete blood count (CBC) Copyright © 2006 Pearson Education.

liver.Hematopoiesis  Fetal blood cells – formed in yolk sac.Developmental Aspects. > affinity for oxygen than adult hemoglobin Copyright © 2006 Pearson Education.. Inc. spleen  By 7th month. publishing as Benjamin Cummings .in red bone marrow  Fetus – HbF.

and the immune system  Increased leukemias are thought to be due to the waning deficiency of the immune system  Abnormal thrombus and embolus formation reflects the progress of atherosclerosis Copyright © 2006 Pearson Education. Inc. blood vessels. publishing as Benjamin Cummings ..Developmental Aspects  Age-related blood problems result from disorders of the heart.