Blood

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Seeley's Essentials of Anatomy & Physiology Chapter 11 abridged Fundamental Human Form and Function (University at Buffalo)

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Ch. 11: Blood ● Functions of Blood ○ Transport of Gases, Nutrients, and Waste ○ Transport of Processed Molecules ■ i.e. vitamin D transport during synthesis ○ Transport of Regulatory Molecules ■ i.e. hormones, enzymes ○ Regulation of pH and Osmosis ■ Buffers are found in blood ○ Maintenance of Body Temperature ○ Protection against Foreign Substances ○ Clot Formation ● Composition of Blood ○ Sticky, heavier than water, higher temp than rest of body, more in males ○ Connective tissue consisting of liquid matrix that contains cells and cell fragments ■ Plasma: fluid portion of blood ■ Formsd ElsmsFts: cell and/or cell fragments in blood ● i.e. red blood cell (cell), white blood cell (cell), platelet (cell fragment) ● Plasma (55% of total blood) ○ Pale, yellow fluid that surrounds cells ○ 91% water, 7% proteins, 2% other (ions, nutrients, gases, waste, etc.) ○ Contains dissolved proteins: ■ AlbumiF (58%) ● Maintains water balance ● Transportation ■ GlobuliFs (38%) ● Help w/ immune system ● Transportation ■ FibriFogsF (4%) ● Clotting ○ Converted into fibrin to form blood clots ○ Ssrum: plasma without clotting factors

● Formed Elements (45% of total blood) → cells and cell fragments ○ Red blood cells (erythrocytes) constitute 95% of volume of formed elements ○ White blood cells (leukocytes) → mostly Neutrophils; and platelets (thrombocytes) constitute 5% of volume of formed elements

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● Production of Formed Elements ○ Hsmatopoissis: process of blood cell production ■ Occurs in liver, thymus, spleen, lymph nodes, and red bone marrow within the fetus ● After birth, hematopoiesis confined to red bone marrow (in adults) and white blood cells are made in lymphatic tissue ○ All formed elements of blood derive from stsm cslls (hsmocytoblasts) ■ Differentiate to give rise to formed elements ● Regulated by specific growth factors ○ Growth factors determine the types of formed elements derived from the stem cells and how many formed elements are produced ● Red Blood Cells ○ Biconcave shape → increases surface area ○ During development, RBCs lose their nuclei and organelles ■ Unable to divide ■ Live for 120 days ○ ⅓ of a RBC’s volume is from hsmoglobiF (maiF compoFsFt) ■ Hemoglobin is responsible for RBC’s red color ○ Transport oxygen from lungs to various tissues of the body ○ Transport carbon dioxide from the tissues to the lungs ○ Oxygen transport is accomplished by hemoglobin (4 protein chains, 4 heme groups) → 98.5% of oxygen transport is due to hemoglobin ■ 1 globin (protein) is bound to 1 heme (red pigmented molecule) ■ 1 heme contains 1 iroF atom for function ● Each iron can reversibly bind to an oxygen molecule ■ Hemoglobin picks up oxygen in lungs and releases oxygen in other tissues ● Bright red hemoglobin is bound to oxygen (OxyhsmoglobiF) ● Darker red, blueish hemoglobin is not bound to oxygen (DsoxyhsmoglobiF) ○ 1.5% of oxygen transport is done by being dissolved in plasma ○ Carbon monoxide can also bind to hemoglobin (VERY EASY) ■ Tends to not unbind ● Hemoglobin bound to carbon monoxide no longer transports oxygen → nausea, headache, unconsciousness, death! ○ Carbon dioxide is produced in tissues, transported in blood to lungs, then removed from blood ■ CO2 transport involves bicarbonate ions, hemoglobin, and plasma ● 70% of CO2 is transported in form of bicarbonate ions ○ CarboFic AFhydrass (inside RBCs) catalyzes the rxn that converts CO2 and H2O into H+ and HCO3● CO2 can reversibly bind to globin part of hemoglobin, making up about 23% of CO2 transport

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○ Remaining 7% of CO2 is transported by being dissolved in plasma ○ Life History of Red Blood Cells ■ ~2.5 million RBCs destroyed each second; produced just as rapidly ■ Stem cells form prosrythroblasts → give rise to red blood cell line ■ Involves series of cell divisions ● Newly formed RBCs manufacture large amounts of hemoglobin ● After final division, RBCs lose nuclei and become completely mature RBCs ■ Cell division requires: ● Folats aFd B12 ○ DNA synthesis ● IroF ○ Production of hemoglobin ■ RBC production is sparked by low blood oxygen levels ● Results from lower number of RBCs, defective hemoglobin, lung disease, high altitude, endurance exercise, etc. ■ Low blood oxygen levels spark RBC production by increasing release of a glycoprotein via kidneys, ErythropoistiF (EPO) ● EPO stimulates red bone marrow to make more RBCs ● Negative-feedback system → EPO release can be increased or decreased depending on blood oxygen levels ○ When RBCs become old/damaged, they’re removed by macrophagss located in spleen and liver ■ Within macrophage, globin part of hemoglobin is broken down into amino acids to be reused for new proteins ● Iron is released from heme, transported back to red bone marrow to make new hemoglobin → recycled ○ Heme is converted into Bilirubin (yellow molecule) ■ BilirubiF is taken up by liver and released into small intestine as bile ● If liver or bile flow is disrupted, Bilirubin can build up in circulation → JauFdics ■ After entering intestine, Bilirubin is converted into other pigments by bacteria ● Pigments give brown color to feces and yellow color to urine ● White Blood Cells (Leukocytes) ○ Spherical cells, no hemoglobin ○ Larger than RBCs

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○ Each WBC has a nucleus (unlike erythrocytes) ○ WBCs and platelets make up Buffy Coat when blood is separated into components ○ WBCs can travel throughout the body via Ameboid Movement → aren’t limited to blood for movement ■ Cell projects cytoplasmic extension to attach to object ○ WBCs protect body against invaders and remove dead cells/debris from tissues via phagocytosis ○ Granulocytes (large cytoplasmic granules) vs. Agranulocytes (small cytoplasmic granules) ○ Granulocytes (3 types): ■ Nsutrophils: most common; phagocytic WBCs (remove foreign substances) ■ Basophils: least common; release histamine to generate inflammation; release heparin to prevent blood clots ■ EosiFophils: reduce inflammation ○ Agranulocytes (2 types): ■ Lymphocytss: smallest; immune response, regulate immune system (T cells and B cells) ■ MoFocytss: largest; produce macrophages ● Platelets ○ Blood-clotting cells ○ Produced in red bone marrow by Megakaryocytes ● Preventing Blood Loss ○ Vascular Spasm ■ Immediate, but temporary constriction of blood vessel ○ Platslst Plug FormatioF ■ Accumulation of platelets that can seal up small break in blood vessel ■ Positivs-Fssdback mechanism → cascade of chemical release to activate many platelets ○ Blood ClottiFg (CoagulatioF) ■ Occurs when damage is severe! ■ Blood transformed from liquid to a gel ■ Clot: network of threadlike protein fibers (fibriF) that traps blood cells and fluid ■ Formation of blood clot depends on clotting factors (proteins in plasma) ● Only activated following surgery ■ Steps: ● Chemical reaction can be started 2 ways: ○ Inactive clotting factors come into contact w/ exposed connective tissue which causes activation of clotting factors

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○ Chemicals like ThromboplastiF are released from injured tissues, causing activation of clotting factors ● Clotting factors activate other clotting factors until ProthrombiFass (clottiFg factor) is formed ● ProthrombiFass converts prothrombiF (inactive clotting factor) into thrombiF (active form) ● ThrombiF converts fibriFogsF (plasma protein) to fibriF

■ At each step of process, each clotting factor activates many additional clotting factors → formation of clot ■ Clotting factors are made in the livsr ○ Require vitamiF K for production of clotting factors ■ Chemical rxns of clot formation require calcium and other chemicals released from platslsts ○ Clotting process can be stalled due to low levels of vitamin K, low levels of calcium, low number of platelets, reduced production of clotting factors due to dysfunctional liver ■ Control of Clot Formation ○ Clots need to be controlled so they don’t spread throughout the body ○ AFticoagulaFts: chemical that prevents blood clotting ■ i.e. AFtithrombiF & HistamiFs inactivate ThrombiF ○ Injury causes enough clotting factors to be activated that anticoagulants can’t work in that particular area of the body ■ Clot Retraction and Fibrinolysis ○ After a clot forms, begins to form into more compact structure → clot rstractioF ■ Platelets contain actin and myosin (contractile proteins) ● Form small extensions that attach to fibrin through surface receptors ● Contraction of extension pulls on fibrin and leads to clot retraction ■ During clot retraction, ssrum (plasma without clotting factors) is squeezed out of clot ■ Retraction of clot pulls edges closer together, repaired by fibroblasts ○ Clots are dissolved by fibriFolysis ■ PlasmiFogsF (inactive plasma protein) is converted into plasmiF (active form) ● Stimulated by thrombin, tissue plasminogen activator (t-PA) and other clotting factors being released from surrounding tissues

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■ Plasmin then slowly breaks down the fibrin, dissolves clot ■ A heart attack occurs when clot blocks blood vessels that supply the heart ● Plasmin activators quickly dissolve the clot and restore blood flow ○ StrsptokiFass & t-Pa can be used to dissolve clots ● Blood Grouping ○ TraFsfusioF: transfer of blood or blood components from one individual to another ■ Early attempts were unsuccessful due to transfusion reactions ● Caused by interactions between antigens and antibodies ● AFtigsFs: molecules on surface of RBCs ○ Can force body to produce antibodies when exposed to foreign antigens → vaccinations ● AFtibodiss: proteins in plasma; very specific ○ IFfusioF: introduction of fluid other than blood, such as saline or glucose, into the blood ○ When antibodies in plasma bind to antigens on surface of RBCs, they form molecular bridges that connect RBCs together ■ AgglutiFatioF: clumping of blood cells (bad) ■ Hsmolysis: rupturing of RBCs due to an improper of antibodies w/ antigens ● Debris from rupturing can cause severe tissue damage, especially in the kidneys ○ ABO Blood Groups ■ Type A Antigen is in Type A blood ● Plasma of Type A blood has anti-B antibodies that act against Type B antigens ■ Type B Antigen is in Type B blood ● Plasma of Type B blood has anti-A antibodies that act against Type A antigens ■ Type O blood has neither antigen → UNIVERSAL DONOR ● Plasma of Type O has both anti-A and anti-B antibodies ■ Type AB blood plasma has neither antibody → UNIVERSAL ACCEPTOR ■ Anti-A and anti-B antibodies are not found in blood until 2 months after birth ■ Antibodies can be produced if type A or B antigens on bacteria/food are ingested ■ Type O blood is universal → can give blood without causing an ABO reaction (no ABO surface antigens)

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● Can only receive from other Type O however ● Rh Blood Group ○ Rh-positive individuals have Rh antigens on surface of RBCs, Rh-negative individuals do not ■ Most people are Rh-positive ■ Rarest combination in the US is AB-negative blood ○ Antibodies against Rh antigens do not develop unless Rh-negative person is exposed to Rh-positive RBCs multiple times ○ Hsmolytic Dissass of ths NswborF (HDN) (Erythroblastosis fstalis): destruction of RBCs in fetus caused by antibodies produced in the Rhnegative mother acting on the Rh-positive blood of the fetus ■ Won’t occur until 2nd baby ○ HDN can be prevented ■ Rh-negative mother injected w/ Rho(D) immune globulin (RhoGAM) ● Contains antibodies against Rh antigens ● Bind to Rh antigens of any fetal RBCs that enter the mother’s blood ● Inactivates fetal Rh antigens and prevents sensitization of the mother ● Diagnostic Blood Tests ○ Typs & Crossmatch ■ To prevent transfusion reactions, blood must be typed ■ Blood typing determines ABO and Rh blood groups of a sample ■ Cells are separated from serum then tested with known antibodies to determine type of antigen on cell surface ■ Crossmatch: donor’s blood cells are mixed w/ recipient’s serum and donor’s serum is mixed w/ recipient’s blood cells ● Donor’s blood is considered safe if no agglutination occurs in either match

○ Complsts Blood CouFt (CBC) ■ RBC count, hemoglobin and hematocrit measurements, and WBC count ■ RBC Count ● Performed electronically or microscopically ● About 4.6-6.2 million RBCs/microliter for males ● About 4.2-5.4 million RBCs/microliter for females ● Erythrocytosis: overabundance of RBCs ■ Hemoglobin Measurement ● About 14-18 g/100mL of blood for males ● About 12-16 g/100mL of blood for females ● AFsmia: low number of RBCs or low number of hemoglobin in each RBC

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■ Hematocrit Measurement ● Hsmatocrit: percentage of total blood volume that is composed of RBCs ● Centrifuge used ○ White Blood Count (WBC) ○ Measures total number of WBCs in blood ○ 5000-9000 WBC/microliter ○ LsukopsFia: low WBC count due to destruction of red marrow ■ Caused by radiation, drugs, tumors, folate/B12 deficiency ○ Lsukocytosis: high WBC count ■ Caused by bacterial infections that increase neutrophil number ■ Can lead to anemia/bleeding ○ Lsuksmia: abnormal production of WBC types; red marrow cancer ■ WBC do not function normally → susceptible to infection ○ DiffsrsFtial Whits Blood CouFt ■ Percentage of each of the 5 kinds of WBCs ○ Clotting ○ Can be assesed by platelet count and prothrombin time measurement ○ Platslst CouFt ■ 250,000-400,000 platelets/microliter ■ Thrombocytopenia: low platelet count ● Due to lack of B12 → bleeding ○ Prothrombin Time Measurement ■ Measures how long it takes blood to start clotting ● Thromboplastin is added to whole plasma ■ Normally, 9-12 seconds ● Can be slowed by vitamin K deficiency, liver disease, etc. ○ Blood Chemistry ○ Composition of materials dissolved in plasma can be used to assess functioning of many of the body’s systems

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