Hematology and Oncology Physiology

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jknell
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211276
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Hematology and Oncology Physiology
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2013-04-03 20:21:32
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  1. Erythrocyte
    -function
    -structure
    -energy source
    • Function:
    • -carries O2 to tissue and CO2 to lungs
    • -membrane contains Cl-/HCO3- antiporter (allows RBCs to sequester HCO3- and transport CO2 from periphery to lungs for  elimination)

    • Structure:
    • -anucleate
    • -biconcave
    • -large surface to volume ratio for gas exchange
    • -life span = 120 days

    • Source of energy:
    • -glucose
    • -90% used in glycolysis
    • -10% used in HMP shunt
  2. Erythrocytosis
    • -polycythemia
    • -increased hematocrit
  3. Anisocytosis
    Varying sizes
  4. Poikilocytosis
    Varying shapes

  5. Reticulocyte
    • -Immature erythrocyte
    • -marker of erythroid proliferation

  6. Platelet (thrombocyte)
    -structure
    -function
    -sign of dysfunction
    • Function:
    • -primary hemostasis
    • -activated by endothelial injury
    • -aggregates with other platelets and interacts with fibrin to form platelet plug

    • Structure:
    • -small cytoplasmic fragment derived from megakarycytes
    • -Dense granules (ADP, calcium)
    • -α granules (vWF, fibrinogen)

    *approximately 1/2 of platelets stored the spleen

    *thrombocytopenia and and platelet dysfunction result in petechiae
  7. Leukocyte
    -types
    -function
    -normal count
    • Granulocytes:
    • -neutrophils
    • -eosinophils
    • -basophils

    • Mononuclear Cells:
    • -monocytes
    • -lymphocytes

    • Function:
    • -defense against infection

    Normal count = 4000-10,000 cells/mm3
  8. WBC Differential Normal Counts
    • Neutrophils (54-62%)
    • Lymphocytes (25-33%)
    • Monocytes (3-7%)
    • Eosinophils (1-3%)
    • Basophils (0-0.75%)

    Neutrophils Like Making Everything Better

  9. Neutrophil
    -function

    -structure
    -granule contents
    • Function:
    • -acute inflammatory cell
    • -increased in bacterial infections
    • -phagocytic

    • Structure:
    • -multilobed nucleus

    • Small, numerous granules:
    • -alk phos
    • -collagenase
    • -lysozyme
    • -lactoferrin

    • Lysosomes:
    • -Large, less numerous
    • -azurophilic granules
    • -acid phosphatase
    • -peroxidase
    • -β-glucuronidase
  10. Hypersegmented Neutrophils
    • ->5 lobes
    • -seen in vitamin B12/folate deficiencies
  11. Band cells
    • -immature neutrophils
    • -reflect states of increased myeloid proliferation (bacterial infection, CML)

  12. Monocyte
    -function
    -structure
    • Function:
    • -differentiates into macrophages in tissues

    • Structure:
    • -large, kidney shaped nucleus
    • -Extensive "frosted glass" cytoplasm

  13. Macrophage
    -function
    -structure
    • Function:
    • -phagocytoses bacteria, cell debris and senescent RBCs
    • -scavenges damaged cells and tissues
    • -long life in tissues
    • -activated by IFNg
    • -can act as APC via MHC II

    • Structure:
    • -differentiate from circulating monocytes
    • -marker: CD14

  14. Eosinophil
    -function
    -structure
    • Function:
    • -defends against helminthic infections (MBP)
    • -highly phagocytic for antigen-antibody complexes
    • -produces histaminase and arylsulfatase (helps limit reaction following mast cell degranulation)

    • Structure:
    • -bilobate nucleus
    • -large eosinophilic granules of uniform size
  15. Causes of Eosinophilia
    • "NAACP"
    • Neoplastic
    • Asthma
    • Allergic process
    • Collagen vascular diseases
    • Parasites

  16. Basophil
    -function
    -structure
    • Function:
    • -mediates allergic reaction

    • Granules:
    • -densely basophilic
    • -heparin (anticoagulant)
    • -histamine (vasodilator)
    • -leukotrienes (LTD4)

  17. Mast Cell
    -function
    -structure
    • Function:
    • -mediates allergic reaction in local tissues
    • -involved in Type I hypersensitivity
    • -can bind Fc portion of IgE to membrane
    • -IgE cross-links upon antigen binding causing degranulation

    • Structure:
    • -resemble basophils structurally and functionally

    • Granules:
    • -histamine
    • -heparin
    • -eosinophil chemotactic factors

  18. Dendritic Cell
    -function
    -structure
    • Function:
    • -highly phagocytic APCs
    • -link between innate and adaptive immune system

    • Structure:
    • -express MHCII and Fc R on surface
    • -called Langerhans cells in skin

  19. Lymphocyte
    -function
    -structure
    • Function:
    • -mediates adaptive immunity
    • -B cells and T cells

    • Structure:
    • -round, densely staining nucleus
    • -small amount of pale cytoplasm

  20. B Lymphocyte
    -function
    -development
    -structure
    • Function:
    • -part of humoral immune response
    • -can act as APC via MHC II

    • Development:
    • -arises from stem cells in bone marrow
    • -matures in marrow
    • -migrates to peripheral lymphoid tissue (follicles of LN, white pulp of spleen, unencapsulated lymphoid tissue)
    • -differentiate in plasma cells when encounter antigen

  21. Plasma Cell
    -function
    -structure
    • Function:
    • -produces large amounts of antibody specific to a particular antigen

    • Structure:
    • -off center nucleus
    • -clock-face chromatin distribution
    • -abundant RER
    • -well-developed golgi

    **neoplasm = multiple myeloma

  22. T lymphocyte:
    -function
    -development
    • Function:
    • -mediates cellular immune response
    • -majority of circulating lymphocytes (80%)

    • Development:
    • -originates from stem cell in the BM
    • -matures in the thymus
    • -T cells differentiate into cytotoxic cells, helper cells and regulatory T cells
    • -CD28 costimulation is necessary for T cell activation
  23. Blood Groups:
    • A
    • B
    • AB
    • O
    • Rh
  24. Blood Group: A
    • Antigen on RBC: A
    • Antibody in plasma: anti-B (IgM)
  25. Blood Group: B
    • Antigen on RBC: B
    • Antibody in plasma: anti-A (IgM)
  26. Blood Group: AB
    • Antigen on RBCs: A and B
    • Antibody in plasma: None

    • -Universal recipient of RBCs
    • -Universal donor of plasma
  27. Blood Group: O
    • Antigen on RBCs: Neither A or B
    • Antigen in plasma: anti-A and anti-B

    • -universal donor of RBCs
    • -universal recipient of plasma
  28. Blood Group: Rh
    Antigen on RBCs: Rh antigen

    RH- mothers exposed to fetal Rh+ blood (often during delivery) may make anti-Rh IgG

    In subsequent pregnancy anti-Rh IgG cross the placenta causing hemolytic disease of the new born (erythroblastosis fetalis) if the next fetus is Rh+

    • Treatment:
    • -Rho(D) Ig form mother at first delivery to prevent initial sensitization of Rh- mother to Rh antigen
  29. Coagulation Pathway
  30. Extrinsic Pathway


    • -"lucky pathway" (only have to remember two)
    • Factors:
    • -Tissue Factor (TF)
    • -VII

    • Test:
    • -PT (less numbers, less letters)
  31. Intrinsic Pathway


    -"unlucky pathway"

    • Factors:
    • -XII
    • -XI
    • -IX
    • -VII

    • Test:
    • -PTT (more numbers, more letters)
  32. Common Pathway
    • Fibrin monomer Aggregation:
    • -requires Ca2+ and XIIIa

    "Small dollar bills"

    • Factors:
    • -I
    • -II
    • -V
    • -X

    • Tests:
    • -PT and PTT
  33. Fibrinolytic System


    • Plasminogen:
    • -plasmin breaks down fibrin
    • -activated by t-PA, U-PA

    • Inhibition of Fibrinolytic system:
    • -TAFIa (shields fibrin from degradation, activated by thrombin/TM)
    • -PAI-1 (inhibits t-PA)
  34. Procoagulation Components
    -Vitamin K dependent factors
    • Vitamin K dependent factors:
    • -II
    • -VII
    • -IX
    • -X
    • -Protein C
    • -Protein S

    • **VIII is not produced in liver and is protected by vWF
    • Deficiency:
    • -Warfarin inhibits epoxide reductase
    • -neonates lack enteric bacteria that produce vitamin K
  35. Anticoagulation Components
    • Protein C
    • -activated by thrombomodulin
    • -works with Protein S to inactivate Va, VIIIa

    • Antithrombin
    • -inhibits activated forms of II, VII, IX, X, XI, XII
    • -inactivated by heparin
  36. Primary Hemostasis
    = platelet plug formation
  37. Platelet Plug Formation
    **Transient vasoconstriction

    • 1. Injury
    • -vWF binds exposed collagen upon endothelial damage

    • 2. Platelet Adhesion
    • -platelets bind vWF via GpIb receptor at site of injury
    • -platelets release ADP and Ca2+ (necessary for coagulation cascade)
    • -ADP helps platelets adhere to endothelium

    • 3. Platelet Activation:
    • -ADP binding induces GpIIb/IIIa expression on platelet surface

    • 4. Platelet Aggregation
    • -Fibrinogen binds GpIIb/IIa and links platelets
    • -temporary plug stops bleeding
  38. Pro Platelet Aggregation Factors
    • -TXA2 (released by platelets)
    • -decreased blood flow
  39. Anti Platelet Aggregation Factors
    • -PGI2 and NO (released by endothelial cells)
    • -increased blood flow
  40. Thrombogenesis (Image)
  41. Disease and Drugs of Thrombogenesis
    • Diseases:
    • vWF deficiency: von Willebrand's disease
    • GpIb deficiency: Bernard Soulier syndrome
    • GpIIb/IIIa deficiency: Glanzmann's thrombasthenia

    • Drugs:
    • ADP receptor blocked by (inhibit GpIIb/IIIa expression): clopidogrel and ticlopidine
    • GpIIb/IIIa blocked by: abciximab
    • COX inhibited by (decreased TXA2 synthesis): ASA
  42. Erythrocyte Sedimentation Rate
    -elevated ESR
    -decreased ESR
    Acute phase reactants in plasma (eg: fibrinogen) can cause RBC aggregation and increase ESR

    • Elevated ESR:
    • -infections
    • -autoimmine diseases (SLE, RA, temporal arteritis)
    • -malignancy
    • -GI disease (UC)
    • -pregnancy

    • Decreased ESR:
    • -polycythemia
    • -SCA
    • -CHF
    • -microcytosis
    • -hypofibrinogenemia

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