Blood A&P II Lecture

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julianne.elizabeth
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167431
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Blood A&P II Lecture
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2012-08-25 23:27:13
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blood hemostasis plasma wbc rbc
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chapter 17 on blood for A&PII
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  1. What is blood?
    A fluid connective tissue composed of:

    • 1. plasma
    • 2. Formed elements
    • -Erythrocytes (RBCs)
    • -Leukocytes (WBCs)
    • -Platelets (cell fragments)
  2. Blood composition and physical characterisitics
    Blood is a sticky, paque fluid tasting metallic and salty with the color scarlet (O2 rich) to dark red (O2 deficient)

    pH--> 7.35-7.45 slightly alkaline

    38 degrees C or 100.4 degrees F

    About 8% of a person's body weight

    • Males: 5-6L
    • Females: 4-5L

    • When spun in a centrifuge:
    • -plasma is the least dese at 55% of the blood
    • -Buffy coat in the middle makes up less than 1% (made of platelets and WBCs)
    • -Hematocrit is the most dense at 45%

    Hematocrit (RBCs) is 47% (plus or minus 5%) in males and 42% (plus or minus 5% in females)
  3. Functions of Blood
    Blood: Distributes, protects, and regulates

    Distributes: O2 and nutrients to body cells, metabolic wastes to the lungs (CO2) and kidneys (nitrogenous waste) for elimination

    Protects Against: Blood loss (plasma protiens and platelets initiate clot formation), and Infection (antibodies, complement protiens, and WBCs defend against foreign invaders)

    Regulates: body temperature by absorbing and distributing heat, normal pH using buffers (also the alkaline reserve in bicarbonate atoms), and adequate fluid volume in the circulatory system
  4. Blood Plasma
    is 90% water, light yellow, and sticky

    • 8% of the plasma is proteins and proteins are mostly produced by the liver
    • *6-% albumin- major contributer to maintaing plasma osmotic pressure that helps keep water in the blood stream
    • *36% globulins- gamma globulins are actually antibodies released by plasma cells
    • *4% fibrinogen (threads to make fibrin for blood clot)
  5. Besides Proteins, Plasma also contains...
    1. Nitrogenous by-products of metabolism- lactic acid, urea, and creatine

    2. Nutrients- glucose, carbohydrates, amino acids

    3. Electrolytes (help to maintain pH and plasma osmotic pressure)- Na+, K+, Ca2, Cl-, HCO3-


    4. Respiratory Gases- O2 and CO2


    5. Hormones
  6. Formed Elements in the blood
    erythrocytes, leukocytes, and platelets

    Only WBCs are complete cells

    RBCs have no nuclei or organelles

    Platelets are cell fragments

    Most formed elements only survive in the blood stream for a few days

    Most blood cells originate from red bone marrow and do not divide
  7. Erythrocytes
    • Their structural characteristics contribute to gas transport
    • -biconcave shape makes a huge surface area relative to volume
    • -Over 97% Hb (not counting water)
    • -No mitochondria; ATP production is anaerobic so none of the O2 it is carrying gets used up!

    Perfect example of how function mirrors structure!
  8. Function of Erythrocytes
    RBCs are dedicated to respiratory gas transport

    Hb binds reversibly with O2

    • Hb structure: Protein globin- two alpha and two beta chains
    • Heme pigmennt bonde to each globin chain contains iron

    Iron atom in each heme can bind to one O2 molecule

    • Each Hb molecule can transport 4 O2
  9. Hemoglobin (Hb) loading and unloading
    O2 loading in the lungs produces oxyhemoglobin (ruby red)

    O2 unloading in the tissues produces deoxyhemoglobin or reduced hemoglobin (dark red)

    CO2 loading in the tissues procuces carbaminohemoglobin (carries 20% CO2 in the blood)
  10. Hemotopoiesis (hemopoiesis)
    Blood cell formation

    Occurs in the red bone marrow of axial skeleton, gircles and proximal epiphyses of hermus and femur

    • Hemocytoblasts (hemopoietic stem cells)-
    • *give rise to all formed elements
    • *hormones and frowth factos push the cell toward a specific pathway of blood cell development

    New blood cells enter sinusoids
  11. Erythropoiesis
    Red blood cell production

    A hemocytoblast (myeloid stem cell) is transformed into a proerythroblast

    proertythroblasts develop into early erythroblasts
  12. Phases of development in erythropoiesis
    15 day process

    • 1.Ribosome sythesis (Early to late erythroblast)
    • 2. Hemoglobin accumulation (late to normoblast)
    • 3. Ejection of the nucleus and formation of reticulocytes (normoblast to reticulocytes)

    • Reticulocytes become mature erythrocytes (reticulocytes help determine the rate of RBC production)
  13. Regulation for Erythropoiesis
    too few RBCs leads to hypoxia (O2 deprivation)

    too many RBCs increases blood viscosity

    • balance between RBC production and desctruction depends on:
    • 1. hormone controls
    • 2. adequate supplies of iron, amino acids, annd B vitamins
  14. Hormonal Control of erythropoesis
    • Erythropoietin (EPO)
    • -direct stimulus for erythropoiesis
    • -released by the kidneys (and a small amount in the liver) in response to hypoxia
    •        *hypoxia causes HIF (hypoxia-inducible factor) and as it accumulates it signals the release of EPO

    • Effects of EPO
    • - more rapid maturation of committed bone marrow cells
    • -Increased curculatin reticulocyte count in 1-2 days

    Testosterone also enhances Epo production, resulting in higher RBC counts in males
  15. What causes Hypoxia?
    Hemorrhage or increased RBC destruction

    Insufficient Hb (iron deficiency)

    Reduced availability of O2 (such as high altitudes)
  16. Mechanism for regulation  of Erythropoiesis
  17. Dietary requirements for Erythropoiesis
    Nutrients: - amino acids, lipids, and carbohydrates

    • Iron
    • *stored in Hb (65%), the liver, spleen, and bone marrow
    • *stored in cells as ferritin and hemosiderin because free iron is toxic
    • *transported loosely bound to the protein transferrin

    Vitamin B12 and folic acid- necessary for DNA synthesis for cell division
  18. Fate and destruction of Erythrocytes
    Life span: 100-120 days

    Old RBCs become fragile and Hb begins to degenerate

    Macrophages engulf dying RBCs in the spleen (called the RBC graveyard)

    • How it happens:
    • 1. Heme and globin are separated
    • 2. Iron is salvaged for reuse
    • 3. Heme is degraded to yellow pigment bilirubin (binds to albumin for transport)
    • 4. Liver secretes bilirubin (in bile) to intestines
    • 5. Degraded pigment leaves body in the feces as tercobilin
    • 6. Globin is metabolized into amino acids

  19. 3 Main Causes of Anemia
    1. Insufficient erythrocytes

    2. Low Hb content

    3. Abnormal Hb
  20. Causes of Anemia
    Insufficient Erythrocytes
    Hemorrhage anemia: acute or chronic loss of blood

    Hemolytic anemia: RBCs rupture prematurely (due to mismatched transfusion, Hb abnonormalities, certain bacterial and parasitic infections)

    Aplastic anemia: destruction or inhibition of red bone marrow (the cause is unknown in most cases
  21. Causes of Anemia
    Low Hb content
    • 1. Iron deficiency anemia
    • - secondary result of hemorrhagic anemia or
    • -inadequate intake of iron-containing foods or
    • - impaired iron absorption (erythrocytes produced are microcytes, small and pale)

    • 2. Pernicious Anemia
    • -Deficiency of vitamin B12
    • -Lack of intrinsic factor in stomache mucosa needed for absoption of B12
    • -treated by intramuscular injection of B12 or application of nascobal (to the nasal lining once a week)
    • *autoimmune and mostly effects the elderly
  22. Causes of Anemia
    Abnormal Hemoglobin
    • 1. Thalassemias (Sea blood)
    • -absent or faulty globin chain
    • -RBCs are thin, delicate, and Hb deficient

    • 2. Sickle cell Anemia
    • -defective gene codes for abnormal hemoglobin (HbS)
    • -causes RBCs to become sickle shaped in low O2 situations
    • *they then rupture easilty and block small blood vessels
    • *strikes mostly african americans from the malaria belt b/c if someone only have one gene of SSA they have a better change against malaria
  23. Erythrocyte disorders
    Polycythemia: excess of RBCs that increase blood viscosity making it thick and sludgy

    • Results from:
    • -Polycythemia vera: bone marrow cancer
    • -Secondary polycythemia- when less O2 is available (high altitudes) or when EPO production increases

    Treated by removing some blood and replacing it with saline

    Blood doping: athletes remove some blood a few days before an event so that new RBCs are created, then the blood is put back in the day of the race.  More RBCs means a high VO2 max
  24. Leukocytes
    make up less than 1% of total blood volume

    can leave capillaries via diapededsis

    move through tissue spaces by ameboid motion and positive chemotoxis (following a train of molecules released by damaged cells)

    • Leukocytosis: when WBC count is over 11,000/mm3
    • -normal response to bacterial or viral invasion
    • -WBC count can double in just a few hours

    • Two main types:
    • granulocytes and agranulocytes
  25. Granulocytes
    Neutrophils, eosinophils, and basophils

    Cytoplasmic granules stain specifically with wright's stain

    larger and shorter-lived than RBCs

    Lobed nuclei

    • Phagocytic- engulf foreign cells
  26. Neutrophils
    most numerous WBCs

    polymorphonuclear leukocytes (PMNs)

    Fine granules take up bot acidic and basic dyes-gives the cytoplasm a lilac color

    granules contain hydrolytic enzymes and defensins

    Very Phagolytic-"bacteria slayers"-promoted by the respiratory burst where they stab bacteria
  27. Eosinophils
    redstaining, bilobed nuclei

    red to crimson (acidophilic) coarse, lysosome-like granules

    digest parasitic worms that are too large to be phagocytized (they gather around a parasite and release enzymes to digest it)

    modulators of the immmune response
  28. Basophils
    rarest WBCs

    • large, purplish-black (basophilic) granules contain histamine
    • -histamine: an inflammatory checmical that acts as a vasodialiator (makes blood vessels dialate) and attracts other WBCs to the inflamed site

    Are functionally similar to mast cells
  29. List the Leukocytes from most common to least common
    Never Let Monkeys Eat Bananas

    • Neutrophils
    • Lymphocytes
    • Monocytes
    • Eosinophils
    • Basophils
  30. Agranulocytes
    Lymphocytes and Monocytes

    Lack visible cytoplasmic granules (they simply don't stain)

    • have spherical or kidney shaped nuclei
  31. Lymphocytes
    Large, dark purple, circular nuclei with a thin rim of blue cytoplasm

    mostly in lymphoid tissue, few circulate in the blood

    crucial to immunity

    • Two types:
    • T Cells- act against virus-infected cells and tumor cells
    • B Cells- give rise to plasma cells, whic produce antibodies (immunoglobulins)
  32. Monocytes
    The largest leukocytes

    Abundant pale blue cytoplasm

    Dark purple staining, U or kidney shaped nucleus, crushed glass looking cytoplasm

    • They can leave circulation and enter tissues where they turn ameboid and differentiate into macrophages
    • -actively phagocytic cells; crucial against viruses, intracellular bacterial parasites, and chronic infections such as TB

    Activate lymphocytes to mount an immune response
  33. Summarize the formed elements in the blood
  34. Leukopoiesis
    Production of WBCs

    • Stimulated by chemical messengers from bone marroe to mature WBCs
    • -Interleukins (eg. IL-1, IL-2)
    • -Colony-stimulation factors (CSFs)- named for the WBC type that they stimulate (ex. CSF granulocytes)

    • All leukicytes originate from hemocytoblasts
  35. Leukocyte disorders
    1.Leukopenia: abnormally low WBC count- drug induced (esp by anti-cancer agents)

    • 2. Leukemias: cancerous conditions involving WBCs
    • -Named according to the abnormal WBC clone involved
    • -Myolocytic leukemia involved myeloblasts while lymphocytic leukemia involved lymphocytes

    Acute leukemia involved blast-type cells and primarily affects children (quickly advancing)

    Chronic leukemia is more prevalent in the elderly and is slow advancing
  36. Leukemia
    bone marrow totally occupied with cancerous leukocytes

    immature nonfunctional WBCs in the bloodstream

    Death caused by internal hemorrhage and overwhelming infections

    treatments include irradiation, antileukemic drugs, and stem cell transplants
  37. Platelets
    Small fragments of Megakaryocytes (anucleate, degenerate quickly)

    formation is regulated by thrombopoietin

    blue staining outer region, purple granules

    Granules contain serotonin, Ca2+, enzyme ADP, and platelet derived growth factor (PDGF)

    They form a termporary platelet plug that helps seal breaks in blood vessels

    Circulating platelets are kept inactive and mobile by Nitric Oxide (NO) and prostacyclin from endothelial cells of blood vessels
  38. Stages of Hemostasis
    The fast series of reactions for stoppage of bleeding

    • 1. Vascular Spasm
    • 2. Platelet Plug Formation
    • 3. Coagulation (blood clotting)
  39. Vascular spasm
    Vasoconstriction of a damaged blood vessel

    • Triggered by:
    • -a direct injury
    • -chemicals that are released by endothelial cells and platelets
    • -pain reflexes
  40. Platelet plug formation
    POSITIVE FEEDBACK MECHANISM

    • at the site of blood vessel injury, platelets:
    • -stick (aggregate) to exposed collagen fibers with the help of von Willebrand factor, a plasma protein
    • -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 more platelet aggregation
  41. Coagulation
    A set of reaction in which lood is transformed from a liquid to a gel using clotting factors and procoagulants

    Reinforces the platelet plug with fibrin threads

    • Three Phases of coagulation
    • 1. Prothrombin activator is formed (both intrinsic and extrinsic pathways)
    • 2. Prothrombin in converted into thrombin
    • 3. Thrombin catalyzes the joing fibrinogen to form fibrin mesh

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