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The Blood

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Title: The Blood Author: bmusolf Last modified by: Dr. Annette M. Parrott Created Date: 9/21/2006 12:19:14 AM Document presentation format: On-screen Show (4:3) – PowerPoint PPT presentation

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Title: The Blood


1
The Blood
2
Functions of Blood
  • Transportation
  • O2, nutrients, waste, hormones, heat
  • Regulationmaintain homeostasis of body fluids
  • Regulate pH, body temperature, maintain fluid
    volume
  • Protection
  • Clotting prevents loss of fluids
  • White blood cells protect against disease
  • Blood proteins protect against disease

3
Physical characteristics and volume
  • Salty and metallic tasting
  • More dense than water
  • Slightly alkaline, pH between 7.35 and 7.45
  • Temperature 38o C or 100.4o F
  • Makes up 8 of body weight
  • Volume in adult males is 5-6 L and in females 4-5
    L
  • Only fluid tissue in the body

4
Blood components
  • Blood plasma 55
  • Formed elements 45
  • RBCsmeasurement is hematocrit 14 5
  • Leukocytes and platelets

5
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6
Blood plasma
  • Includes over 100 different dissolved solutes

7
Formed Elements
8
Hematopoiesis
  • Occurs in the red bone marrow from hemocytoblast/
    hematopoietic stem cell
  • Specialization based on receptors that respond to
    hormones

9
Erythrocyte structure
  • Flexible structure, large surface area
  • Lack a nucleus and other organelles.
  • 33 of weight is hemoglobin molecules.
  • Other proteins include antioxidants and those to
    maintain RBC shape (spectrin)

10
Erythrocyte function
  • Dedicated to carry respiratory gas

11
Regulation of RBCs
Erythropoietin (EOP)? glycoprotein hormone
produced by kidneys to liver
12
Dietary needs to produce RBCs
  • Iron, AAs, lipids, and carbohydrates.
  • Iron is absorbed from the diet
  • 65 found in hemoglobin
  • The rest stored in liver, spleen and bone marrow
  • Iron is toxic and requires transferrin as a
    transporter
  • Some iron is lost in feces and menstrual blood
  • Vitamin B12 and folic acid are necessary for DNA
    synthesis

13
Fate and death of RBCs
  • RBCs have a lifespan of 100 to 120 days
  • Age makes them less flexible and the hemoglobin
    begins to degenerate.
  • Old RBCs get trapped in the small capillaries of
    the spleen
  • Macrophages destroy and digest RBCs
  • Heme and globin are separated
  • Globin broken down into a.a.s
  • Heme? bilirubin?urobilinogen?stercobilin
  • Blood?liver?intestine?anus

14
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15
Erythrocyte Imbalances
  • Anemia ? reduced O2 carrying capacity of the
    blood
  • Insufficient number of RBCs
  • Hemorrhagic - due to blood loss associated with
    an injury, undiagnosed bleeding ulcer, etc.
  • Hemolytic - due to blood loss due to transfusion
    reactions certain bacterial and parasite
    infections
  • Aplastic - due to destruction or inhibition of
    red marrow by drugs, ionizing radiation or
    certain bacterial toxins.

16
Erythrocyte Imbalances
  • Anemia ? reduced O2 carrying capacity of the
    blood
  • Low hemoglobin content
  • Iron Deficiency - inadequate intake or absorption
    of iron, forms microcytes.
  • Pernicious - dietary deficiency of Vitamin B12 or
    inadequate production of intrinsic factor for
    absorption of Vitamin B12 , forms macrocytes

17
Erythrocyte Imbalances
  • Anemia ? reduced O2 carrying capacity of the
    blood
  • Abnormal Hemoglobin in RBCs
  • Thalassemias- one globin chain is absent/faulty
  • Polycythemia-excess of erythrocytes increasing
    blood viscosity

18
Erythrocyte Imbalances
  • Polycythemia - abnormally high number of RBCs (8
    - 11 million/mm3). Increases blood viscosity
    blood pressure.
  • most often the result of bone marrow cancer.
  • Lecuopenia - abnormally low number of WBCs
    (less than 5,000/mm3).
  • drugs, steroids anti-cancer agents.

19
Leukocytes Structure
  • WBCs have a nucleus and other organelles.
  • WBCs can undergo diapedesis using amoeboid motion
    when in the tissues
  • Use chemical chemotaxis to follow trail to
    infection or damaged tissue.

20
Granular leukocytes
  • Neutrophils
  • multilobed nucleus, inconspicuous granules
  • Phagocytize bacteria some fungi
  • Produced in bone marrow by myeloblasts
  • Eosinophils
  • bilobed nucleus, red granules
  • Destroy parasitic worms immune complexes
  • Produced in bone marrow by myeloblasts
  • Basophils
  • lobed nucleus, purple-black granules
  • Cause vasodilation by release of histamines
  • Produced in bone marrow by myeloblasts

21
Agranular leukocytes
  • Lymphocyte
  • B lymphocytes - Humoral Immunity (antibodies)
  • T lymphocytes - Cellular Immunity
  • Produced in lymphatic tissues
  • Monocytes
  • Differentiate into macrophages in tissues.
  • Provide defense against viruses intracellular
    bacteria in chronic infections.
  • Produced by monoblasts in lymphatic tissues.

22
Production of leukocytes
  • Leukopoiesis is stimulated by interleukins and
    colony-stimulating factors (CSFs)
  • Pluripotent stem cells have the capacity to
    differentiate into several types of cells.
  • Myeloid stem cells
  • Lymphoid stem cell

23
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24
Leukocyte Imbalances
  • Leukopenialow WBC count
  • Leukemiaunchecked growth of a single
    unspecialized clone. Abnormally high numbers of
    immature WBCs that are mitotic unspecialized
  • Acute leukemia occurs if it derives from
    blast-type cells
  • Chronic leukemia occurs if it derives from later
    stages
  • Bone marrow is compromised and defense system
    becomes nonfunctional
  • Infectious mononucleosis derives from excessive
    numbers of agranulocytes (Epstein-Barr virus)

25
Platelets
  • Under the influence of thrombopoietin, myeloid
    stem cells develop into megakaryocytes (huge
    cells).
  • These cells fragment into 2-3K particles.
  • They have a very short life of 5- 9 days.

26
Hemostasis
  • Damaged blood vessels require a rapid, localized
    and controlled hemostatic response to reduce
    blood loss.
  • Vascular spasm/constriction
  • Platelet plug formation
  • Blood clotting/ coagulation

27
Platelet plug formation platelet adhesion
28
Platelet plug formation platelet release action
29
Platelet plug formation platelet aggregation
30
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31
Stages of clotting
  • Extrinsic (s) and intrinsic (min) pthwys make
    prothrombinase.
  • Prothrombinase Ca2 Catalyze prothrombin ?
    thrombin
  • Thrombin Ca2 converts soluble fibrinogen
    ?insoluble fibrin (thread of the clot)
  • Thrombin activates factor XIII which stabilizes
    strengthens threads

32
Hemostasis Animation
33
Thromboemolitic Disorders
  • Thrombus? clot in an unbroken vessel
  • Ebolus? an abnormal object moving through a blood
    vessel, Clot, air bubble, lipid droplet,
    thrombus, etc.
  • Disorders
  • Embolisms (pulmonary, cerebral, cardiac)
  • Artherosclerosis
  • Inflammation
  • Treatment
  • Aspirin
  • Heparin
  • Warfarin

34
Bleeding disorders
  • Thrombocytopenialow platelet levels
  • Impaired liver function
  • Vitamin K
  • Hemophilia
  • Deficiency of factor VIII (antihemophilic factor)
  • Deficiency of factor IX
  • Lack of factor XI

35
ABO blood typing
  • Based on two glycolipid antigens, A and B.
  • Blood has agglutinogens (antibodies) that react
    to A or B antigens.

36
Blood groups and blood types
37
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38
Rh blood groups
Hemolytic disease of newborn (HDN)
39
Transfusion reactions
  • Agglutination clogs blood capillaries
  • Clumped cells will rupture and be phagocytized by
    macrophages
  • Hemoglobin is released into the blood
  • Oxygen carrying is disrupted
  • Blood flow is impaired
  • Hemoglobin passing into kidney tubules causes
    cell death and renal shutdown

40
Diagnostic blood tests
  • Lipidemia is characteristic of those with heart
    disease
  • Erythrocyte morphology can detect anemias
  • Differential white blood cell count
  • High eosinophil indicates allergies or parasitic
    infection
  • Platelet count (thrombocytopenia)
  • SMAC is blood chemistry profile
  • CBC provides information on the formed elements

41
Resources
  • Heart Anatomy Tutorial
  • Hematopoiesis Overview
  • BodySmart Blood Bloodcells
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