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					Hematopoiesis
              Hematopoiesis

   the process of blood cell
       proliferation
       differentiation
       maturation
        Hematopoietic Tissue

   Definition: Tissue in which blood
    cells are formed


   Sites of hematopoeisis
     bone marrow in adults
       –also spleen and liver of fetus
         Hematopoietic Tissue
   Bones:
        containing hematopoietic marrow
        (red marrow)
        –flat bones of pelvis
        –vertebra
        –skull
        –ribs and sternum
        Process of Hematopoiesis

   process begins with the stem cell
    (precursor cells)
     totopotential stem cell
       –primitive cell
       –potential to turn into any blood
        cell
        Process of Hematopoiesis

   Differentiation follows along 2 cell
    lines (pathways)
      see Figure 19-9
   myeloid and lymphoid
Myeloid Cell Line
          Myeloid Cell Line

   granulocytes (4,000 - 6,000/µl)
     50 - 70% neutrophils
       –segments = mature cells
       –bands = immature cells
          Myeloid Cell Line

   1 - 4% eosinophils
     increase during parasitic
      infections
   < 1 % basophils
     involved in allergic reactions
         Myeloid Cell Line

   monocytes/macorphages
    2-8% monocytes of WBCs in blood
          Myeloid Cell Line

   Platelets: 150,0000 - 400,000/µl

   red blood cells (RBC) erythrocytes:
     4.2-6.2 million/µl
Lymphoid Cell Line
         Lymphoid Cells
   Lymphocytes (25-35% of WBCs)

   T-cells: cell mediated immunity
     70% of lymphocytes
   B-cells: humoral immunity
     20-25% of lymphocytes
Figure 19-9
Colony Stimulating
     Factors
    Colony Stimulating Factors

   factors that direct proliferation and
    differentiation of stem cells into
    mature blood cells
     RBCs
       –erythropoietin
     Platelets
       –thrombopoietin
    Colony Stimulating Factors
   Monocytes
    GM-CSF: granulocyte-
     macrophage colony-stimulating
     factor
    M-CSF: monocyte colony
     stimulating factor
    Colony Stimulating Factors

   Granulocytes
    G-CSF: Granulocyte colony-
     stimulating factor
    GM-CSF
    Colony Stimulating Factors
   Neutrophils
     GM-CSF
   Lymphocytes
     GM-CSF
     M-CSF
     IL-2
     IL-4
Disorders of White Blood
  Cells and Lymphoid
         Tissues
           Diagnostic tests

   CBC: complete blood count
    quantitative analysis of blood cells
    Measure:
      –WBC
      –Hgb
      –Hct
      –Platelets
           Leukocytosis

   abnormally high WBC count
     above 10,000/mm3 (µl)
     normal protective response to
      inflammation
             Leukopenia

   Below normal WBC count
    below 4,500/mm3
    never considered a normal
     response
    risk of infection great if WBCs <
     1000 mm3
             Differential

   Table 19-8
     Percent of total WBC count of
      each type of WBC
              Differential

   Provides indication of infection or
    disease processes
     Neutrophils:  with infection
     Monocytes:  late acute infection/
      chronic
     Lymphocytes:
       – viral and chronic infections
       – high stress or corticosteroid use
        Bone Marrow Biopsy

   site of hematopoiesis
     bone marrow
      aspiration/biopsy
       –posterior iliac crest
       –need “red” marrow
Normal Bone Marrow
Disorders of
   WBCs
Problems with
 Neutrophils
                Neutropenia

   Definition:
    decreased neutrophils, below 2000
     per microliter (L)

       Based on absolute neutrophil count
        (ANC)
       Calculating ANC
            Total WBC x (% segs + % bands)
          Calculating ANC

   WBC 4000/ uL
    Segments        20%
    Bands           10%

    4000 x (.20 +.10) = 1200
         Interpreting ANC

   Normal: > 2000 (others >1500)

   Safe: 1000-2000

   Concern: <1000

   Institute precautions: < 500
            Neutropenia

   Causes
    decreased production due to:
      –chemotherapy, irradiation,
       genetic disorder
      –drugs (chloramphenicol,
       Dilantin, Bactrim)
             Neutropenia

   removal from circulation
     infection
       –used up plus short life span
     appearance of bands
       –Segments: mature
       –Bands: immature neutrophils
          normally < 5%
          > 5% indicates infection
              Agranulocytosis

   Severe neutropenia:
     <500 neutrophils/ µl
     usually due to blockage of
      hematopoiesis or cell destruction

   Manifestations:
       signs of infection
           Agranulocytosis

   Treatment:
     antibiotics
     life threatening
     death 3-6 days if become septic
Neoplastic Disorders of
Hematopoietic Origin
  Cancers of the Blood Cells
            Leukemias
   Def: malignancy of hematopoietic
    stem cells
     uncontrolled proliferation of
      leukocytes
     dysfunctional cells
            Leukemias
   Can be
     acute or chronic
     myelocytic or lymphocytic
     depends on cell type and level of
      cell maturation
   Figure 20-7
            Leukemias
   Replacement of normal bone
    marrow cells with immature (blasts)
    neoplastic cells
     cells don’t respond to normal
      regulatory mechanisms
             Leukemias
   Cells travel from bone marrow to
    blood to spleen to lymphatic
   Increased proliferation of blasts
     interfere with development of
      normal bone marrow cells
       –RBCs, WBCs, Platelets
               Causes

   unknown, but may be due to:
     high doses of
      radiation/chemotherapy
       –e.g., Hodgkins disease
     viruses
       –e.g., EBV
               Causes

   chromosomal defect
     may need environmental factor to
      trigger expression
   environmental factors
            Leukemias
   Leading cancer in children
     most common cancer in children
   Leading cause of death, ages 3-14
Acute Leukemias
         Acute Leukemias

   Sudden onset
    usually less than three months
    results in massive number of
     immature lymphocytes
Acute Lymphoblastic
  Leukemia (ALL)
                  ALL
   affect T-cells, B-cells, and NK cells
   majority are B-cells
                  ALL
   children and young adults
     but also increases in adults after
      age 50
               ALL
   good prognosis, especially in
    the young
    – if receive chemotherapy early
Acute Myelocytic
   Leukemia
        AML
  nonlymphoblastic
               AML

   affects monocytes, PMN, RBCs,
    & platelets
     in adults
       –only 15% of childhood
        leukemias
           Manifestations
   fatigue, infection, weight loss,
    bruising, bleeding, fever

   why?
Diagnosis

   bone marrow
   biopsy
     look at cells
               Diagnosis

   blood studies:
      increased number of blasts
     lower red blood cell, white blood
      cell, and platelet counts
Normal with PMNs
Normal with PMNs & lymphocyte
Normal with lymphocyte (note platelets)
ALL (note decreased RBCs)
AML (note size)
            Treatment

   aggressive chemotherapy
     soon as possible after onset
   bone marrow transplant
     during first remission
Chronic Leukemia
 Life expectancy longer
        Chronic Leukemia

   Slower course, insidious
     cells more mature
     some with normal function
Chronic Lymphocytic
  Leukemia (CLL)
               CLL
   increased lymphocytes
     mostly from B-cell line
     cells are well differentiated
     but don’t mature into plasma
      cells
Chronic Myelocytic
    Leukemia
       CML
                CML

   increased leukocytes from
    myeloid line
     RBCs, PMNs, platelets

   Primarily seen in adults
            Manifestations

   nonspecific symptoms
     fatigue, anorexia, weight loss,
      fever
     others relate to cell line affected

   Diagnosis: same as acute
            Treatment
   oral chemotherapy
     –does not necessarily improve
      survival
   IV chemotherapy if blast crisis
     –life threatening
   bone marrow transplant
     –improves survival with chemo
Normal with PMNs
CLL   (note number and smaller sized cells)
CML (note large immature cells, some normal)
Lymphomas
           Lymphomas

   Definition: malignancy of the
    lymph system proliferation of
    lymphoid tissue
               Lymphomas

   Two most common types

       Hodgkin’s disease
       Non-Hodgkin’s lymphoma: a
        family of lymphomas with variable
        outcomes
             Lymphomas

   Cause remains unknown
    ? inflammatory reaction to
     infection, viral, exposure to
     pesticides
      –occurs in higher SES
       Hodgkin’s Disease

   Manifestations: painless enlarged
    node (usually above diaphragm),
    fever, night sweats, weight loss
Hodgkin’s Lymphadenopathy
              Diagnosis
   Staging and biopsy to determine
    site and numbering of nodes
     e.g. Stage 1 = 1 node
         Stage 2 = 2 or more closely
                        related nodes
     Table 26-7
               Diagnosis

   Presence of Reed-Sternberg cells
     believed to be the cell that is
      malignant
Reed-Sternberg Cell
               Treatment

   considered curable
     Radiation in early stages
       –Stages 1 & 2
       Add chemotherapy in later stages
        –Stages 3 & 4
           with high dose chemo, still

            curable
          Hodgkin’s Disease

        –bone marrow transplant

   60-90% cure if localized
     look at figure 26-10
Non-Hodgkin’s
 Lymphoma
    Non-Hodgkin’s Lymphoma

   Tumor of lymph nodes

       spreads easily to the liver,
        spleen, and bone marrow
    Non-Hodgkin’s Lymphoma

   May originate from B lymphocytes
    (resident in lymph nodes)
       B cell abnormality most common
   Cause: virus? (Epstein-Barr,
    retrovirus, HIV)
       immunosuppressed more
        vulnerable
    Non-Hodgkin’s Lymphoma

   Manifestations: similar to Hodgkin’s
    symptoms are more systemic

   Diagnosis: lymph node biopsy
    Non-Hodgkin’s Lymphoma

   Treatment:
    chemotherapy/radiation
     not considered curable,
      survival up to 15 yrs
       –worse if systemic
       –better if remains nodular
Multiple Myeloma
           Multiple Myeloma

   Malignant proliferation of the
    plasma (B cells) in the bone
    marrow
       may originate from immature B
        cell
         Multiple Myeloma

   Seen in adults over 40 years old
     incidence increases with age

   Invades bony structures
     moves out of marrow into
      structure
Multiple Myeloma of Skull
Multiple Myeloma Skull
         Multiple Myeloma

   Destroys bone
    see Fig. 26-5

   Plasma cells produce Bence-Jones
    protein, which is excreted in urine,
    part of antibody
          Manifestations

   fractures
     pathologic
   hypercalcemia
     causes increased release and
      impaired uptake
         Manifestations

   bone pain in the back
     –vertebra common site of
      infiltration

   renal failure
     –Bence-Jones toxic to the
      kidneys
               Diagnosis

   Bence-Jones protein in the urine
   bone X-rays/scans
    CT and Bone Scans


              Treatment

   chemotherapy/radiation therapy
   plasmapheresis
     plasma exchange
   bone marrow transplant
              Prognosis

   6 - 12 months if untreated
   median survival 2-2½ years
   3% up to 10 yrs
Problems with B
 Lymphocytes
 Infectious
Mononucleosis
        Infectious Mononucleosis

   Lymphoproliferative disorder of B
    lymphocytes
     that reside in lymphoid tissue
   Caused by Epstein-Barr virus
    (Herpes virus)
     also others such as CMV
        Infectious Mononucleosis

   Virus attacks B lymphocytes
     binds to a B cells receptor
       –EBV receptor
     causes atypical B cells
Infectious mononucleosis
        Infectious Mononucleosis

   “Kissing disease”
       transmitted in saliva
         –young adults 15-30 yrs old
       can persist for 18 months in
        oropharynx
        Infectious Mononucleosis

   disease is self-limiting
     (2 - 3 weeks)
   ~ 100% adults have antibodies
        Infectious Mononucleosis

   Manifestations: fever,
    lymphadenopathy/ tenderness,
    pharyngitis
     mild for first 3 - 5 days
     most severe 7 - 20 days after
      infection
     lethargy can last months
             Diagnosis

   Paul-Bunnel antibody
     specific for EBV
              Diagnosis

   increased lymphocytes (12,000-
    18,000 per microliter
     atypical
     can persist for up to 8 weeks

				
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