Ch 15 - Lecture notes 13 PDF

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CH 15: Cardiovascular system: Blood

15.1 Overview of the composition of blood: the hematocrit -

15.2 -

Hematocrit: the fractional contribution of erythrocytes to the blood o Determined by centrifuging a sample of blood  presented in percentage Normal hematocrit range for men: 42 – 52% Normal hematocrit range for women: 37 – 47% Polycythemia: a higher than normal concentration of erythrocytes in bood; normal adaptive response in low oxygen environments o Adaptive response within two weeks Plasma Plasma: aqueous solution containing variety of solutes (90% water) o Small nutrients, metabolic wastes, gases o Electrolytes  Relatively high concentration of Na+ and Cl Relatively low concentrations of H+, HCO3-, K+, and Ca^2+  o 6-8% plasma proteins  Most abundant solute in plasma by weight  Smaller solutes are present in higher concentration  Albumins: synthesized by liver  most abundant plasma protein  makes large contribution to osmotic pressure of plasma  affects movement of fluid across capillaries  Globulins: transports lipids, steroid hormones, and other substances in blood  critical role in formation of blood clots and defending  Fibrinogen: synthesized by liver  key substance in formation of blood clots

o Serum: Plasma without the fibrinogen and other clotting proteins o Plasma is similar to ISF  Capillary walls  highly permeable to small solutes  solutes move freely between plasma and ISF  Differs due to higher concentration of protein in plasma  capillary walls = low permeability to protein 15.3 Erythrocytes -

Most abundant: 5 million/mm3 No nuclei, mitochondria, and ribosomes (cannot manufacture proteins) Biconcave disks o Shape due to cytosolic protein: spectrin  fibrous proteins that forms a network to the plasma membrane called the spectrin net

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Spectrin net is flexible  allows erythrocytes to bend and flex to move through capillaries that are smaller

Oxygen and carbon dioxide transport 1. Hemoglobin’s reversible binding of O2 and CO2 - Greatly increases O2 transport o 98.5% of transported O2 is bound to hemoglobin o 1.5% of transported O2 is dissolved in plasma o Also binds to CO2, H+, and CO - Iron containing ring structure  heme group (Fe2+) - Transports considerably less CO2 than O2 **Carbonic anhydrase transports ONLY CO2** Life cycle of erythrocytes - Erythrocytes only live for 120 days - Bone marrow produces erythrocytes by process called erythropoiesis 1. Erythrocyte production a. All blood cells develop from precursor cells called hematopoietic stem cells (blood forming) b. Development of a particular type of blood cell depend on cytokines called hematopoietic growth factors (HGFs) i. HGF for erythrocyte = erythropoietin ii. Erythropoietin is released from certain cells in kidney  response to low oxygen levels iii. Erythropoietin travels from bloodstream to bone marrow  triggers differentiation of erythrocytes iv. Reticulocytes are red blood cells with ribosomes  under rapid erythrocyte synthesis  may be released to blood stream

c. Dietary supplements i. Iron  Component of hemoglobin (heme)  Normal hemoglobin content o Men: 13 – 18g/dL o Women: 12 – 16g/dL  Iron – deficiency anemia o Characteristically smaller  due to decrease in hemoglobin/ erythrocyte ii. Folic acid and vitamin B12  Necessary for synthesis of DNA  Deficiencies affect cell division of cells

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Effects on erythropoiesis are most notable  due to rapid production of erythrocytes Pernicious anemia o Characterized by larger than normal erythrocytes o Decrease in number of total erythrocyte count o Usually an overall increase in hematocrit

**anemia can be resulted from hemorrhage and or hemolysis** 2. Filtering and destruction of erythrocytes by the spleen a. Hemolysis: destruction of red blood cells b. Spleen = lymphoid organ  stores blood cells and removes old erythrocytes c. Some erythrocytes hemolyze in bloodstream d. most engulfed by macrophages in spleen, and a bit in the liver i. Hemoglobin = catabolized ii. After iron is removed, resulting heme converts to bilirubin (yellow compound)  Bilirubin is released to bloodstream, gives plasma yellow tinge  Some travels to liver to be catabolized further  secreted as bile to small intestine  pooped out (reason why feces is brown)  Some bilirubin travel to kidneys  eliminated through urine (reason why urine is yellow) e. Iron is recycled i. Transferrin picks up iron from GI tract or spleen  transports to bone marrow  transports to liver, where it can be stored, bound to ferritin (ferritin also exists in spleen and cells in lining of the small intestine)

15.4 Leukocytes -

nucleated and possess cellular machinery found in blood stream and tissue Most develop to full maturity in bone marrow HGF: colony – stimulating factors and interleukins total white blood cells and differential white blood cell count

1. Neutrophils (50 – 80%) o Phagocytosis of foreign material o Elevated neutrophils during infection (neutrophilia) 2. Eosinophils (1 – 4%)

o Defend against parasites o Granules contain toxic molecules 3. Basophils (Less than 1%) o May defend against large parasites  releases toxic substances o Allergic reaction  histamine & heparin 4. Monocyte (5%) o Phagocytosis o New monocytes circulate in blood then migrate to tissue  macrophages  Wandering macrophages  Fixed macrophages 5. Lymphocytes (30%) o B cells  plasma cells  secretes antibodies o T cells  cytotoxic T cells  secretes cytokines – direct damage  T lymphocytes migrate to thymus gland to fully mature o Null cells  mainly NK cells 15.5 Platelets and hemostasis -

Platelets: colourless cell fragments  from portions of large bone marrow cells called megakaryocytes that break off Smaller than erythrocytes, but contain mitochondria, smooth ER and cytoplasmic granules No nucleus Hemostasis: mechanism to stop bleeding 1. Vascular spasm a. Blood vessel damage  vascular spasm (constriction)  increases b. Blood loss minimized 2. Formation of platelet plug a. Platelets = thrombocytes  possesses granules containing variety of substances, can be released into plasma (ADP, serotonin, epinephrine, and other chemicals that aid in clotting b. Platelets can be sticky when bound to vWf c. Key protein: von Willebrand factor (vWf)  secreted by megakaryocytes, platelets, and endothelial cells lining the blood vessels d. Platelet adhesion  occurs when subendothelial tissue is exposed e. vWf binds to collagen fibers in subendothelium  triggers binding of platelets to vWf  anchors platelets f. Platelets release serotonin and epinephrine  vasoconstriction  constricts blood  blood loss minimized g. Platelets release ADP  morphological changes of platelet to allow them to adhere to one another and platelet aggregation (positive feedback loop) h. ADP stimulates the release of thromboxane A2 (TXA2) (formed by arachidonic acid) aids platelet aggregation

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i. Healthy cells release prostacyclin and nitric oxide  inhibits platelet aggregation j. Healthy cells convert arachnidonic acid to prostacyclin k. Platelets contain high concentrations actin and myosin  they contract to increase “tightness” of plug 3. Thrombus (formation of a blood clot) a. Fibrin is needed for coagulation  traps erythrocytes b. Blood clots = fibrin clots c. Secondary hemostasis d. Formation of fibrin clots require a coagulation cascade e. Coagulation factors undergo a series of proteolytic activation  due to hydrolysis of certain peptide bonds  Fibrinogen  catalyzed by thrombin  fibrin  fibrin stabilizing factor (XIII) links loose meshwork of fibrin stands covalently f. Prothrombin  Factor Xa forms prothrombin activating complex with factor V , Ca2+, and PF3  thrombin Intrinsic: involves coagulation factors and other chemicals already present in the plasma Extrinsic: involves some coagulation factors present in damaged tissue adjacent to site of vessel damage Both occur simultaneously

Factors limiting clot formation -

Anticoagulant: chemicals that inhibit coagulation Healthy endothelial cells  tissue factor pathway inhibitor  inhibits extrinsic pathway Healthy endothelial cells  thrombomodulin  binds to thrombin, forms a complex to activate protein C (inhibits intrinsic and extrinsic pathways) Fibrin clots are dissolved by plasmin protein (enzyme) o Derived from plasma protein plasminogen by plasminogen activators

Role of coagulation factors in clot formation disorders -

Hemophilia: genetic disorder that does not allow blood clot formation due to deficiency of gene  coagulation factor VIII Von Willebrand’s disease: reduced levels of vWf, results to decreased platelet plug formation Vitamin K deficiencies: decrease synthesis of clotting factors - Aspirin (anticoagulant) o In low doses: acts as anticoagulant  Inhibits formation of thromboxane A2  Decreases aggregation and platelet plug formation o High doses: increases likelihood of clot formation  Inhibits formation of prostacyclin...