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Fluids of the Body
Cells of the body are serviced by 2 fluids ± blood composed of plasma and a variety of cells transports nutrients and wastes ± interstitial fluid bathes the cells of the body Nutrients and oxygen diffuse from the blood into the interstitial fluid & then into the cells Wastes move in the reverse direction
Functions of Blood
Transportation ± O2, CO2, metabolic wastes, nutrients, heat & hormones Regulation ± helps regulate pH through buffers ± helps regulate body temperature coolant properties of water vasodilatation of surface vessels dump heat ± helps regulate water content of cells by interactions with dissolved ions and proteins Protection from disease & loss of blood
Physical Characteristics of Blood Thicker (more viscous) than water and flows more slowly than water Temperature of 100.4 (7.45) 8 % of total body weight Blood volume ± 5 to 6 liters in average male ± 4 to 5 liters in average female ± hormonal negative feedback systems maintain constant blood volume and osmotic pressure 4 .35-7.4 degrees F pH 7.
COMPONENTS OF BLOOD Blood consists of 55% plasma and 45% formed elements Blood plasma consists of 91. enzymes. 5 . globulins. fibrinogen). Principal solutes include proteins (albumins.5% water and 8. hormones.5% solutes. and waste products. respiratory gases. electrolytes. nutrients.
Components of Blood Hematocrit ± 55% plasma ± 45% cells 99% RBCs < 1% WBCs and platelets 6 .
gases.Blood Plasma 0ver 90% water 7% plasma proteins created in liver confined to bloodstream ± albumin maintain blood osmotic pressure ± globulins (immunoglobulins) antibodies bind to foreign substances called antigens form antigen-antibody complexes ± fibrinogen for clotting 2% other substances ± electrolytes. waste products 7 . nutrients. hormones.
eosinophils. B cells. and natural killer cells monocytes Platelets (special cell fragments) 8 .Formed Elements of Blood Red blood cells ( erythrocytes ) White blood cells ( leukocytes ) ± granular leukocytes neutrophils. basophils ± agranular leukocytes lymphocytes = T cells.
tissue hypoxia.54% (average of 46%) testosterone Anemia ± not enough RBCs or not enough hemoglobin Polycythemia ± too many RBCs (over 65%) ± dehydration. blood doping in athletes 9 .Hematocrit Percentage of blood occupied by cells ± female normal range 38 .46% (average of 42%) ± male normal range 40 .
Formation of Blood Cells Most blood cells types need to be continually replaced ± die within hours. lymph nodes & red bone marrow In adult ± occurs only in red marrow of flat bones like sternum. spleen. ribs. liver. skull & pelvis and ends of long bones 10 . days or weeks ± process of blood cells formation is hematopoiesis or hemopoiesis In the embryo ± occurs in yolk sac. thymus.
Hematopoiesis 11 .
1% of red marrow cells ± replenish themselves as they differentiate into either myeloid or lymphoid stem cells Myeloid stem cell line of development continues: ± progenitor cells(colony-forming units) no longer can divide and are specialized to form specific cell types example: CFU-E develops eventually into only red blood cells ± next generation is blast cells have recognizable histological characteristics develop within several divisions into mature cell types Lymphoid stem cell line of development ± pre-B cells & prothymocytes finish their develop into B & T lymphocytes in the lymphatic tissue after leaving the red marrow 12 .Stages of Blood Cell Formation Pluripotent stem cells ± .
This process of hemopoiesis (or hematopoiesis) is stimulated by several hematopoietic growth factors. platelets. 13 . These hematopoietic growth factors stimulate differentiation and proliferation of the various blood cells. Lymphoid stem cells give rise to lymphocytes.Blood Cells Myeloid stem cells give rise to RBCs. and all WBCs except for lymphocytes.
8 million/drop ± new RBCs enter circulation at 2 million/second Principles of Human Anatomy and Physiology.4 million/drop ---.female 4. 11e 14 .Red Blood Cells or Erythrocytes Contain oxygen-carrying protein hemoglobin that gives blood its red color ± 1/3 of cell¶s weight is hemoglobin Biconcave disk 8 microns in diameter ± increased surface area/volume ratio ± flexible shape for narrow passages ± no nucleus or other organelles no cell division or mitochondrial ATP formation Normal RBC count ± male 5.
hold great potential for use in patients who cannot normally form the blood cells. available through recombinant DNA technology. 11e 15 . Growth factors. Thrombopoietin increases the number of platelet precursors. Principles of Human Anatomy and Physiology.(Hormones)Hemopoietic Growth Factors Erythropoietin increases the number of RBC precursors. Cytokins (colony-stimulating factors and interleukins) increase the number of WBC precursors.
11e 16 .Hemoglobin Globin protein consisting of 4 polypeptide chains One heme pigment attached to each polypeptide chain ± each heme contains an iron ion (Fe+2) that can combine reversibly with one oxygen molecule Principles of Human Anatomy and Physiology.
RBC Life Cycle RBCs live only 120 days ± wear out from bending to fit through capillaries ± no repair possible due to lack of organelles Worn out cells removed by fixed macrophages in spleen & liver Breakdown products are recycled Principles of Human Anatomy and Physiology. 11e 17 .
Recycling of Hemoglobin Components In macrophages of liver or spleen ± globin portion broken down into amino acids & recycled ± heme portion split into iron (Fe+3) and biliverdin (green pigment) Principles of Human Anatomy and Physiology. 11e 18 .
Fate of Components of Heme Iron(Fe+3) ± transported in blood attached to transferrin protein ± stored in liver. muscle or spleen attached to ferritin or hemosiderin protein ± in bone marrow being used for hemoglobin synthesis Biliverdin (green) converted to bilirubin (yellow) ± bilirubin secreted by liver into bile converted to urobilinogen then stercobilin (brown pigment in feces) by bacteria of large intestine if reabsorbed from intestines into blood is converted to a yellow pigment. urobilin and excreted in urine 19 .
Erythropoiesis: Production of RBCs Erythrocyte formation. they eject the remaining organelles to become a mature RBC 20 . occurs in adult red bone marrow of certain bones The main stimulus for erythropoiesis is hypoxia Reticulocytes escape from bone marrow into the blood In 1-2 days. called erythropoiesis.
Feedback Control of RBC Production Tissue hypoxia (cells not getting enough O2) ± high altitude since air has less O2 ± anemia RBC production falls below RBC destruction ± circulatory problems Kidney response to hypoxia ± release erythropoietin ± speeds up development of proerythroblasts into reticulocytes 21 .
and neutrophils based on the straining of the granules. Leukocytes have surface proteins. as do erythrocytes. eosinophils. basophils. Two principal types are granular (neutrophils. 22 . basophils) and agranular (lymphocytes and monocytes) Granular leukocytes include eosinophils. which differentiate into macrophages (fixed and wandering). are unique for each person (except for identical siblings). ± Agranular leukocytes do not have cytoplasmic granules and include the lymphocytes and monocytes.WHITE BLOOD CELLS Leukocytes (white blood cells or WBCs) are nucleated cells and do not contain hemoglobin. and can be used to identify a tissue. They are called major histocompatibility antigens (MHC).
000 cells per drop of blood ± 1 WBC for every 700 RBC Leukocytosis is a high white blood cell count ± microbes. skin.WBC Physiology Less numerous than RBCs ± 5000 to 10. strenuous exercise. lymph nodes & spleen 23 . lungs. anesthesia or surgery Leukopenia is low white blood cell count ± radiation. shock or chemotherapy Only 2% of total WBC population is in circulating blood at any given time ± rest is in lymphatic fluid.
differentiate into tissue plasma cells that produce antibodies. phagocytize antigen-antibody complexes. ± Basophils develop into mast cells that liberate heparin.Function of WBCs Different WBCs combat inflammation and infection in different ways. 24 . ± B lymphocytes. ± T lymphocytes destroy foreign invaders directly. in response to the presence of foreign substances called antigens. ± Neutrophils and wandering or fixed macrophages (which develop from monocytes) do so through phagocytosis. and serotonin in allergic reactions that intensify the inflammatory response. histamine. and combat parasitic worms. ± Eosinophils combat the effects of histamine in allergic reactions.
particularly neutrophils and macrophages. 25 . The chemical attraction of WBCs to a disease or injury site is termed chemotaxis. are active in phagocytosis.Function of WBCs WBCs leave the blood stream by emigration Some WBCs.
eosinophils or basophils ± agranulocytes are monocyes or lymphocytes 26 .WBC Anatomy and Types All WBCs (leukocytes) have a nucleus and no hemoglobin Granular or agranular classification based on presence of cytoplasmic granules made visible by staining ± granulocytes are neutrophils.
Neutrophils (Granulocyte) Polymorphonuclear Leukocytes or Polys Nuclei = 2 to 5 lobes connected by thin strands ± older cells have more lobes ± young cells called band cells because of horseshoe shaped nucleus (band) Fine. pale lilac practically invisible granules Diameter is 10-12 microns 60 to 70% of circulating WBCs 27 .
Eosinophils (Granulocyte) Nucleus with 2 or 3 lobes connected by a thin strand Large. uniform-sized granules stain orange-red with acidic dyes ± do not obscure the nucleus Diameter is 10 to 12 microns 2 to 4% of circulating WBCs 28 .
dark purple. s-shaped.Basophils (Granulocyte) Large. bilobed nuclei Diameter is 8 to 10 microns Less than 1% of circulating WBCs 29 . variable-sized granules stain with basic dyes ± obscure the nucleus Irregular.
14 microns in diameter ± increase in number during viral infections 20 to 25% of circulating WBCs 30 . oval to round nucleus Cytoplasm sky blue in color ± amount varies from rim of blue to normal amount Small cells 6 .9 microns in diameter Large cells 10 .Lymphocyte (Agranulocyte) Dark.
20 microns Cytoplasm is a foamy blue-gray 3 to 8% o circulating WBCs 31 .Monocyte (Agranulocyte) Nucleus is kidney or horse-shoe shaped Largest WBC in circulating blood ± does not remain in blood long before migrating to the tissues ± differentiate into macrophages fixed group found in specific tissues ± alveolar macrophages in lungs ± kupffer cells in liver wandering group gathers at sites of infection Diameter is 12 .
± adhesion molecules (selectins) help WBCs stick to endothelium displayed near site of injury ± molecules (integrins) found on neutrophils assist in movement through wall Neutrophils & macrophages phagocytize bacteria & debris ± chemotaxis of both kinins from injury site & toxins 32 . stick to it & squeeze between cells.Emigration & Phagocytosis in WBCs WBCs roll along endothelium.
Neutrophil Function Fastest response of all WBC to bacteria Direct actions against bacteria ± release lysozymes which destroy/digest bacteria ± release defensin proteins that act like antibiotics & poke holes in bacterial cell walls destroying them ± release strong oxidants (bleach-like. strong chemicals ) that destroy bacteria 33 .
but arrive in larger numbers Become wandering macrophages.Monocyte Function Take longer to get to site of infection. once they leave the capillaries Destroy microbes and clean up dead tissue following an infection 34 .
histamine & serotonin ± heighten the inflammatory response and account for hypersensitivity (allergic) reaction 35 .Basophil Function Involved in inflammatory and allergy reactions Leave capillaries & enter connective tissue as mast cells Release heparin.
Eosinophil Function Leave capillaries to enter tissue fluid Release histaminase ± slows down inflammation caused by basophils Attack parasitic worms Phagocytize antibody-antigen complexes 36 .
B cells ± destroy bacteria and their toxins ± turn into plasma cells that produces antibodies T cells ± attack viruses, fungi, transplanted organs, cancer cells & some bacteria Natural killer cells ± attack many different microbes & some tumor cells ± destroy foreign invaders by direct attack
Complete Blood Count
Screens for anemia and infection Total RBC, WBC & platelet counts; differential WBC; hematocrit and hemoglobin measurements Normal hemoglobin range ± infants have 14 to 20 g/100mL of blood ± adult females have 12 to 16 g/100mL of blood ± adult males have 13.5 to 18g/100mL of blood
Differential WBC Count
Detection of changes in numbers of circulating WBCs (percentages of each type) ± indicates infection, poisoning, leukemia, chemotherapy, parasites or allergy reaction Normal WBC counts ± neutrophils 60-70% (up if bacterial infection) ± lymphocyte 20-25% (up if viral infection) ± monocytes 3 -- 8 % (up if fungal/viral infection) ± eosinophil 2 -- 4 % (up if parasite or allergy reaction) ± basophil <1% (up if allergy reaction or hypothyroid)
PLATELETS Platelets help stop blood loss from damaged vessels by forming a platelet plug. Thrombopoietin stimulates myeloid stem cells to produce platelets 40 . Their granules also contain chemicals that promote blood clotting.
Platelet (Thrombocyte) Anatomy Disc-shaped.000400.000 white blood cells 41 .000/drop of blood Other blood cell counts ± 5 million red & 5-10. 2 .4 micron cell fragment with no nucleus Normal platelet count is 150.
Platelets--Life History Platelets form in bone marrow by following steps: ± myeloid stem cells to megakaryocyte-colony forming cells to megakaryoblast to megakaryocytes whose cell fragments form platelets Short life span (5 to 9 days in bloodstream) ± formed in bone marrow ± few days in circulating blood ± aged ones removed by fixed macrophages in liver and spleen 42 .
and conversion of soluble fibrinogen into insoluble fibrin 43 . most are in blood plasma. and one is released from damaged tissue cells Blood clotting involves a cascade of reactions that may be divided into three stages: formation of prothrombinase (prothrombin activator).HEMOSTASIS A clot is a gel consisting of a network of insoluble protein fibers (fibrin) in which formed elements of blood are trapped The chemicals involved in clotting are known as coagulation (clotting) factors. some are released by platelets. conversion of prothrombin into thrombin.
and factors V. Normal coagulation requires vitamin K and also involves clot retraction (tightening of the clot) and fibrinolysis (dissolution of the clot). The fibrinolytic system dissolves small. 44 . prothrombin. inappropriate clots and clots at a site of damage once the damage is repaired. and XII.HEMOSTASIS The clotting cascade can be initiated by either the extrinsic pathway or the intrinsic pathway. Plasmin (fibrinolysin) can dissolve a clot by digesting fibrin threads and inactivating substances such as fibrinogen. VIII.
Hemostasis Stoppage of bleeding in a quick & localized fashion when blood vessels are damaged Prevents hemorrhage (loss of a large amount of blood) Methods utilized ± vascular spasm ± platelet plug formation ± blood clotting (coagulation = formation of fibrin threads) 45 .
Vascular Spasm Damage to blood vessel produces stimulates pain receptors Reflex contraction of smooth muscle of small blood vessels Can reduce blood loss for several hours until other mechanisms can take over Only for small blood vessel or arteriole 46 .
Platelet Plug Formation Steps in the process ± (1) platelet adhesion (2) platelet release reaction (3) platelet aggregation 47 .
11e 48 .Platelet Adhesion Platelets stick to exposed collagen underlying damaged endothelial cells in vessel wall Principles of Human Anatomy and Physiology.
11e 49 .Platelet Release Reaction Platelets activated by adhesion Extend projections to make contact with each other Release thromboxane A2 & ADP activating other platelets Serotonin & thromboxane A2 are vasoconstrictors decreasing blood flow through the injured vessel Principles of Human Anatomy and Physiology.
Platelet Aggregation Activated platelets stick together and activate new platelets to form a mass called a platelet plug Plug reinforced by fibrin threads formed during clotting process Principles of Human Anatomy and Physiology. 11e 50 .
Overview of the Clotting Cascade Prothrombinase is formed by either the intrinsic or extrinsic pathway Final common pathway produces fibrin threads 51 .
clotting factor X combines with V to form prothrombinase 52 .Extrinsic Pathway Damaged tissues leak tissue factor (thromboplastin) into bloodstream Prothrombinase forms in seconds In the presence of Ca+2.
X and V 53 .Intrinsic Pathway Activation occurs ± endothelium is damaged & platelets come in contact with collagen of blood vessel wall ± platelets damaged & release phospholipids Requires several minutes for reaction to occur Substances involved: Ca+2 and clotting factors XII.
Final Common Pathway Prothrombinase and Ca+2 ± catalyze the conversion of prothrombin to thrombin Thrombin ± in the presence of Ca+2 converts soluble fibrinogen to insoluble fibrin threads ± activates fibrin stabilizing factor XIII ± positive feedback effects of thrombin accelerates formation of prothrombinase activates platelets to release phospholipids 54 .
Clot Retraction & Blood Vessel Repair Clot plugs ruptured area of blood vessel Platelets pull on fibrin threads causing clot retraction ± trapped platelets release factor XIII stabilizing the fibrin threads Edges of damaged vessel are pulled together Fibroblasts & endothelial cells repair the blood vessel 55 .
VII. IX and X Produced by bacteria in large intestine 56 .Role of Vitamin K in Clotting Normal clotting requires adequate vitamin K ± fat soluble vitamin absorbed if lipids are present ± absorption slowed if bile release is insufficient Required for synthesis of 4 clotting factors by hepatocytes ± factors II (prothrombin).
Hemostatic Control Mechanisms Fibrinolytic system dissolves small. inappropriate clots & clots at a site of a completed repair ± fibrinolysis is dissolution of a clot Inactive plasminogen is incorporated into the clot ± activation occurs because of factor XII and thrombin ± plasminogen becomes plasmin (fibrinolysin) which digests fibrin threads Clot formation remains localized ± fibrin absorbs thrombin ± blood disperses clotting factors ± endothelial cells & WBC produce prostacyclin that opposes thromboxane A2 (platelet adhesion & release) Anticoagulants present in blood & produced by mast cells ± 57 .
TIAs and myocardial infarctions 58 .Intravascular Clotting Thrombosis ± clot (thrombus) forming in an unbroken blood vessel forms on rough inner lining of BV if blood flows too slowly (stasis) allowing clotting factors to build up locally & cause coagulation ± may dissolve spontaneously or dislodge & travel Embolus ± clot. air bubble or fat from broken bone in the blood pulmonary embolus is found in lungs Low dose aspirin blocks synthesis of thromboxane A2 & reduces inappropriate clot formation ± strokes.
Anticoagulants and Thrombolytic Agents Anticoagulants suppress or prevent blood clotting ± heparin administered during hemodialysis and surgery ± warfarin (Coumadin) antagonist to vitamin K so blocks synthesis of clotting factors slower than heparin ± stored blood in blood banks treated with citrate phosphate dextrose (CPD) that removes Ca+2 Thrombolytic agents are injected to dissolve clots ± directly or indirectly activate plasminogen ± streptokinase or tissue plasminogen activator (t-PA) 59 .
An example is heparin. blood clots sometimes form within the cardiovascular system. Substances that inhibit coagulation. Patients who are at increased risk of forming blood clots may receive an anticoagulant drug such as heparin or warfarin.Hemostatic Control Mechanisms Clots are generally localized due to fibrin absorbing thrombin into the clot. clotting factors diffusing through blood. a substance that removes Ca+2 such as EDTA or CPD may be added to the blood. 60 . Despite the anticoagulating and fibrinolytic mechanisms. and the production of prostacyclin. called anticoagulants. To prevent clots in donated blood. are also present in blood. a powerful inhibitor of platelet adhesion and release.
At low doses aspirin inhibits vasoconstriction and platelet aggregation thereby reducing the chance of thrombus formation. or piece of debris transported by the bloodstream that moves from its site of origin is called an embolus.HEMOSTASIS Clotting in an unbroken blood vessel is called thrombosis. 61 . bubble of air. A thrombus (clot). fat from broken bones. Thrombolytic agents are injected into the body to dissolve clots that have already formed. Streptokinase or tissue plasminogen activator (TPS) are thrombolytic agents.
62 . designated as a and b. agglutinogens (antigens) A and B determine blood types Plasma contains agglutinins (antibodies). that react with agglutinogens that are foreign to the individual.ABO Group In the ABO system.
Blood Groups and Blood Types RBC surfaces are marked by genetically determined glycoproteins & glycolipids ± agglutinogens or isoantigens ± distinguishes at least 24 different blood groups ABO. Rh. Kidd and Duffy systems 63 . Lewis. Kell.
blood type A ± display only antigen B -.blood type B ± display both antigens A & B -.ABO Blood Groups Based on 2 glycolipid isoantigens called A and B found on the surface of RBCs ± display only antigen A -.blood type AB ± display neither antigen -.blood type O Plasma contains isoantibodies or agglutinins to the A or B antigens not found in your blood ± anti-A antibody reacts with antigen A ± anti-B antibody reacts with antigen B 64 .
blood type & only with exposure to the antigen ± transfusion of positive blood ± during a pregnancy with a positive blood type fetus Transfusion reaction upon 2nd exposure to the antigen results in hemolysis of the RBCs in the donated blood 65 .RH blood groups Antigen was discovered in blood of Rhesus monkey People with Rh agglutinogens on RBC surface are Rh+. Normal plasma contains no anti-Rh antibodies Antibodies develop only in Rh.
hemolytic disease of the newborn may develop causing hemolysis of the fetal RBCs 66 . miscarriage or abortion ± RhoGam binds to loose fetal blood and removes it from body before she reacts In 2nd child.Hemolytic Disease of Newborn Rh negative mom and Rh+ fetus will have mixing of blood at birth Mom's body creates Rh antibodies unless she receives a RhoGam shot soon after first delivery.
cells or plasma into the bloodstream of recipient ± used to treat anemia or severe blood loss Incompatible blood transfusions ± antigen-antibody complexes form between plasma antibodies & ³foreign proteins´ on donated RBC's (agglutination) ± donated RBCs become leaky (complement proteins) & burst ± loose hemoglobin causes kidney damage Problems caused by incompatibility between donor¶s cells and recipient¶s plasma Donor plasma is too diluted to cause problems 67 .Transfusion and Transfusion Reactions Transfer of whole blood.
Universal Donors and Recipients People with type AB blood called ³universal recipients´ since have no antibodies in plasma ± only true if cross match the blood for other antigens People with type O blood cell called ³universal donors´ since have no antigens on their cells ± theoretically can be given to anyone 68 .
and Rh) Typing is the determination of blood types. 69 . in which a sample of blood is mixed with serum containing agglutinins to each of the major agglutinogens (AB.Typing and Cross-Matching Blood for Transfusion The Rh and ABO blood groups may be detected by a simple medical test. whereas crossmatching is the mixing of donor and recipient blood for compatibility. blood typing. B.
DISORDERS: HOMEOSTATIC IMBALANCES Anemia Sickle-cell Hemophilia Disseminated intravascular clotting Acute leukemia chronic leukemia 70 .
Anemia = Not Enough RBCs Symptoms ± oxygen-carrying capacity of blood is reduced ± fatigue. cold intolerance & paleness lack of O2 for ATP & heat production Types of anemia ± iron-deficiency =lack of absorption or loss of iron ± pernicious = lack of intrinsic factor for B12 absorption ± hemorrhagic = loss of RBCs due to bleeding (ulcer) ± hemolytic = defects in cell membranes cause rupture ± thalassemia = hereditary deficiency of hemoglobin ± aplastic = destruction of bone marrow (radiation/toxins) 71 .
RBC is deformed by changes in hemoglobin molecule within the RBC sickle-shaped cells rupture easily = causing anemia & clots Found among populations in malaria belt ± Mediterranean Europe. sub-Saharan Africa & Asia Person with only one sickle cell gene ± increased resistance to malaria because RBC membranes leak K+ & lowered levels of K+ kill the parasite infecting the red blood cells 72 .Sickle-cell Anemia (SCA) Genetic defect in hemoglobin molecule (Hb-S) that changes 2 amino acids ± at low very O2 levels.
Hemophilia Inherited deficiency of clotting factors ± bleeding spontaneously or after minor trauma ± subcutaneous & intramuscular hemorrhaging ± nosebleeds. articular bleeding & pain Hemophilia A lacks factor VIII (males only) ± most common Hemophilia B lacks factor IX (males only) Hemophilia C (males & females) ± less severe because alternate clotting activator exists Treatment is transfusions of fresh plasma or concentrates of the missing clotting factor 73 . blood in urine.
trauma. hypotension & hemolysis Clots cause ischemia and necrosis leading to multisystem organ failure 74 . hypoxia. low blood flow rates.Disseminated Intravascular Clotting Life threatening paradoxical presence of blood clotting and bleeding at the same time throughout the whole body ± so many clotting factors are removed by widespread clotting that too few remain to permit normal clotting Associated with infections.
75 . lymphocytic.Leukemia Acute leukemia ± uncontrolled production of immature leukocytes ± crowding out of normal red bone marrow cells by production of immature WBC ± prevents production of RBC & platelets Chronic leukemia ± accumulation of mature WBC in bloodstream because they do not die ± classified by type of WBC that is predominant--monocytic.
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