Hematology Rotation

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  1. Low Power Bone Marrow examination
    • @20x examine marrow to fat ratio
    • normal= 1:1
    • Hyper= >4:1, hypo = <1:4
  2. High power BM evaluation
    • @100x examine myeloid to erythroid ratio
    • normal= 4:1 will also see macrophages, osteoblasts and osteoclasts
  3. Why so many more WBC precursors in BM?
    WBC dont live as long, so you need to be making more to keep up
  4. Top 3 cells seen in BM
    Neutrophils, erythroblasts, lymphocytes
  5. Hyperplasia
    increase in tissue due to cell proliferation, gross enlargement
  6. Types of hyperplasia
    • Infection, M:E 5:1 unless a chronic hemolytic process
    • Dysplasia, increased number of precursors getting stuck somewhere in development
    • Leukemia, >20% blasts
    • Lymphoma, increased lymphocytes
  7. Dysplasia
    abnormality of cell development, increases number of blasts
  8. Hypoplasia
    underdevelopment of tissue
  9. Reasons for hypoplasia
    • old age, fewer precursor stem cells left
    • improper BM collection
    • aplastic anemia, stem cell autoimmunity
    • reticular fibrosis, fiber cells replacing BM
  10. What does it mean when you see a nucleolus
    cell is more transcriptionally active, less mature cell
  11. What does it mean when you see increased cytoplasm?
    More proteins have been made, more mature cell
  12. Whats a give away for myeloid precursors?
    primary and secondary granules
  13. What is a give away for promonocytes?
    folding within the nucleus
  14. How do monocytes differ from lymphocytes?
    cytoplasm is more grey, nucleus is folded, cytoplasm doesnt usually bend around RBCs
  15. What cells look like ginger snap cookies?
    prolymphocytes
  16. What does a T cell do
    present antigen
  17. What does a B cell do
    bind antigen for specific antibody response
  18. How does a lymph morphology change from non-reactive to reactive?
    Non reactive lymphs are very round with course clumped chromatin, reactive lymphs spread out to attack cells
  19. What is the clearing you see in plasma cells?
    Golgi apparatus, making proteins
  20. Acid Phosphatase stain
    for llymphocytes (T cells)
  21. TRAP stain
    + in hairy cell leukemia
  22. Alkaline phosphatase stain
    For neutrophils
  23. LAP score
    • differentiates btwn leukemoid reaction (high) and leukemia (low)
    • stains certain cytoplasmic components that are not present in abnormal cells
  24. Chloroacetate stain
    neutrophils and mast cells
  25. Non-specific esterase stain
    Monocytes, megakaryocytes and plasma cells
  26. Peroxidase stain
    varies based on maturity of cell, differentiates btwn myelocytes
  27. Sudan Black B stain
    + in granulocytes and monocytes, - in lymphocytes
  28. Iron Stain
    stains iron stores, ringed sideroblasts
  29. PAS
    • carbohydrate stain
    • differentiates btwn Guahcer's and Nieman Pick
  30. Why is flow cytommetry better than staining?
    it can identify cells by their surface markers which are more specific than staining
  31. What are megaloblsatic changes
    • Changes in cell morphology that occur due to issues with DNA replication
    • hypersegmentation, discontinuity of development, etc.
  32. What causes toxic granulation?
    infection or activation of neutrophils
  33. What are Dohle Bodies?
    • Rough ER remnants
    • Associated with stress, infection, exposre to cytotoxic agents, etc.
  34. Pelger Huet
    • look for bilobed neutrophils
    • Cells act normally, but can be pre-leukemic
  35. Alder- Reilly
    • Lipids in the cytoplasm of cells, looks a lot like toxic granulation
    • cell function is normal but can point to Hurler's or Hunter's disease
  36. Chediak-Higashi
    • Giant fused granules in neuts and lymphs
    • Cell can engulf but dont kill bacteria causing pyrogenic
  37. May-Hegglin
    • Autosomal dominant, blue Dohle-like inclusions and giant platelets
    • cells function normalls but can have thrombocytopenia due to size of platelets
  38. Chronic Granulomatous
    • Normal wright's stain
    • Cells cant kill bacteria, lacking oxidative burst.
  39. Gaucher's Disease
    • accumulation of glucocerebroside in macrophages (tissue paper cytoplasm)
    • Casues enlarged spleen and liver to try to process out the bad macrophages
  40. Niemann-Pick
    • Foamy macrophage cytoplasm due to accumulation of sphingomyelinase, complete ensyme knock out
    • Fatal before childhood
  41. HTLV
    • sibling disease to HIV, also a retrovirus
    • infects T cells diagnosed with antibody assay
    • long incubation period
  42. HIV
    • attacks CD4+ T cells, kills the cells that perform the everyday immune responses
    • Diagnosed with nucleic acid based tests
    • now treated like a chronic disease, not a death sentence
  43. Epstein-Barr Virus
    • infectious mononucleosis, infects B cells
    • diagnosed with monospot (heterophile Ab), although not 100% accurate
  44. Myeloproliferative disorder
    The overproduction of one or more of the myeloid cells, the brakes are off!
  45. CML
    • extreme elevation of myeloid cells in PB and BM
    • Chronic phase: way too many cells, normal function
    • accelerated phase: non-funtional mature cells
    • Blast crisis: so many blasts, starting to make their way into circulation
  46. In what disorder will you find the Philadelphia (Ph) chromosome? What does it do?
    • CML
    • Translocation is stuck in on, errors in cells accumulation due to such high production
  47. How is CML most often found?
    Usually incidentally, lab sees high WBCs
  48. Signs of CML
    • Can present with petechiae
    • bone marrow ME ratio 10:1-50:1
    • <20% blasts
  49. What is Gleevec?
    • Medication for CML based on understanding of molecular basis of the disease
    • doesn't work in juvenile CML
  50. How to distinguish Leukemoid reaction from CML
    • CML: low LAP, blasts present, Ph chromosome,
    • Leukemoid: dohle bodies, toxic granulation, vacuoles, high LAP
  51. Chronic Idiopathic Myelofibrosis
    fibroblast proliferation in BM replaces normal hematopoetic tissue
  52. What to look for in Chronic Idiopathic myelofibrosis?
    • Extramedullary hematopoesis due to fibrosis, BM will go wherever it an. 
    • Tear drop cells (dacrocytes), elevated LAP
  53. Polycythemia Vera
    Increased cells, especially RBCs (due to long lifespan).  Stem cells extra sensitive to EPO
  54. What are you looking for in Polycythemia vera
    • a combination of things that say I have a lot of everything
    • Increased RBC, splenomegaly, Thrombocytosis, etc.
  55. Essential Thrombocythemia
    Increased megakaryoctes, normal RBCs but decreased HgB
  56. What is a myelodysplastic syndrome
    • AKA BM failure, not enough healthy RBCs, brakes are on!
    • decreased or ineffective cell cycling
  57. What to look for in myelodysplastic disorders
    • signs the DNA replication isnt working right
    • oval macrocytes, siderocytes, howell-jolly bodies, etc.
    • abnormal precursors
  58. What is refractory anemia?
    • anemia unresponsive to iron therapy
    • reticulocytopenia, oval macrocytes
  59. What is RARS
    Refractory anemia with ringed sideroblasts, >15% of BM cells are ringed sideroblasts
  60. What is RAEB?
    • Refractory anemia with excess blasts
    • up to 19% blasts, hypogranular neutrophils, pseudo pelger huet cells
  61. 5q syndrome
    Deletion of the q arm of chromosome s
  62. What to look for in 5q syndrome
    • mostly older women, refractory macrocytic anemia, thrombocytosis, erythroid hypoplasia
    • Responds to lenalidomide
  63. What is chronic myelomonocytic leukemia?
    • Technically MDS/MPD
    • peripheral blood looks like RA with high WBC count
    • BM 5-20% blasts
  64. What is the key thing to look for in AML?
    >20% blasts in PB or BM
  65. What is AML M3
    Acute promyelocytic leukemia
  66. What to look for in acute promyelocytic leukemia
    • promyelocytes predominate in PB, folded nucleus, often auer rods
    • Can by hyper or hypogranular
  67. Stain results in acute promyelocytic leukemia
    • Myeloperoxidase +
    • chloroacetate +
    • non specific esterase -
  68. How do you treat acute promyelocytic leukemia? Why?
    • High dose of vitamin A to push along maturation process
    • Disease has a vitamin A receptor defect that prevents maturation
  69. What is AML M0? What are its stain results?
    • AML, minimally differentiatied, myeloblasts without granules
    • Myeloperoxidase -
    • chloroacetate -
    • Non specific -
    • all stains are negative because the cells are very immature, really can't be identified yet
  70. What is AML M1? What are the stain results?
    • AML without maturation, <10% myeloid cells show maturation, auer rods often seen
    • Myeloperoxidase + (light)
    • chloroacetate + (strongt)
    • Non specific  -
  71. What is AML M2? What are the stain results?
    • AML with maturation, 50% of the time leukocytosis, thrombocytopenia, myeloblasts in PB and BM
    • Myeloperoxidase +
    • chloroacetate +
    • Non specific  -
  72. What is AML M4? What are the stain results?
    • Acute myelomonocytic leukemia, myeloid and monocytic cells in PB and BM. >30% blasts in BM, increased serum muramidase (monocytic component)
    • Myeloperoxidase +
    • chloroacetate +
    • Non specific +
    • Lysozyme 3x normal
  73. What is AML M5? What are the stain results?
    • Acute monoblastic leukemia, most common in young 2 subtypes
    • a= less mature cells, b= more mature cells
    • Myeloperoxidase -
    • chloroacetate -
    • Non specific +
  74. What is AML M6?
    • Acute Erythroid leukemia, only seen in adults, erythroblast is predominant BM cell, can evolve into M1 or M2
    • 2 subtypes
    • erythroleukemia= significant myeloblastic component
    • pure erythroid leukemia= no significant myeloblastic component
  75. What is AML M7?
    Acute megakaryoblastic leukemia, dry tap due to fibrosis  from increase in megakaryocytes, ID'd by immunophenotyping and cytochemistry
  76. What is the cell specific to Hodgkin's lymphoma?
    Reed Sternberg cells
  77. What are non-hodgkin's lymphomas?
    • B-cell neoplasms
    • small cell lymphocytic lymphoma- nodes
    • chronic lymphocytic leukemia- PB and BM
  78. What does CD tell you about the lymphocytes effected?
    • <10 (excluding 5)= T cell
    • >10 (plus 5)= B cell
  79. If you see a smudge cell in a case study you think...
    CLL
  80. What cells predominate in Waldenstrom Macroglobulinemia?
    Plasma cells (B cells)
  81. What is Multiple Myeloma
    malignant proliferation of plasma cells, lytic bone lesions, elevated serum calcium, bence jones proteins
  82. What is MGUS?
    Monoclonal ab present in the absence of plasma cell dyscrasia, can progress to multiple myeloma
  83. What is sezary cell syndrome?
    mycosis fungoides, T cell derived tumors of the skin, only bad prognosis if it progresses beyond the skin
  84. What is ALL?
    Most common in young children, typical findings are neutropenia, thrombocytopenia, anemia
  85. What are the different types of ALL?
    • Immature B cell (most common)
    • Pre B cell
    • T cell
    • B cell
  86. When is the TdT stain positive?
    early B cell ALL
  87. Hemostasis
    balancing of clotting and bleeding
  88. Cardiovascular system
    deliver O2 and nutrients, take away waste
  89. lymphatic system
    transport lymph fluid, water and cells
  90. Thromboresistant
    inert to platelets and coag factors, (i.e. blood vessels)
  91. Primary hemostasis
    • formation of the primary platelet plug
    • adhere via vWF
  92. Secondary hemostasis
    • stabilize and strengthen via XIII
    • activate the coag cascade via VIIa after exposure to TF
  93. Platelet production
    in the BM by megakaryocytes
  94. pseudothrombocytopenia
    • in-vitro sampling, anticoag clumps
    • remedy by using sodium citrate (blue top) tubes
  95. Platelets shape change
    disk-->spiky-->pancake
  96. 3 stages of clot formation
    adhersion, aggregation, secretion
  97. Adhesion
    • platelets roll and cling to non platelet surfaces to seal endothelial gaps
    • vWF required
    • Reversible
  98. Aggregation
    • platelets adhere to each other
    • requires fibrinogen
    • irreversible
  99. Secretion
    • Platelets secrete granular contents, essential for coagulation
    • \irreversible
  100. Types of platelet granules
    • Alpha- larger, factor V, factor XI, fibrinogen, vWF, etc.
    • Delta- smaller, Ca, Mg, serotonin, etc.
  101. Dense bodies
    AKA delta granules
  102. Gray platelet deficiency
    alpha granule deficiency
  103. GP Ib/IX/V
    vWF receptor, facilitates adhesion to exposed collagen
  104. GP IIb/IIIa
    Fibrinogen receptor, allows platelets to bind to each other.
  105. Where are most coag factors made
    Liver
  106. Von willebrand Disease
    • most common bleeding disorder in the US
    • quantitative or qualitative vWF defect
  107. Types of vWFD
    • 1: you just don't have as much (most common)
    • 2A: chopped up faster
    • 2B: cleared out quicker
    • 2M: less GP Ib, no primary plug
    • 2N: factor VIII deficiency
    • 3: absence of all multimers
  108. Pseudo vWFD
    platelet type, mutation in GP Ib gene instead of vWF gene
  109. Bernard Soulier Syndrome
    • deficiency/dysfunction of GP Ib (vWF receptor)
    • Qualitative PLT disorder--> giant platelets
  110. Glanzmann's Thrombasthemia
    • deficiency/dysfunction of GP IIB/IIIA
    • aggregation cannot occur unless treated with ristocetin
  111. PFA 100
    assessment of PLTs for adequate function via exposure to collagen and ADP or epi
  112. Thrombin
    • induces full aggregation and secretion of granular components
    • conversion of fibrinogen to fibrin
  113. ADP
    binds PLT membrane to stimulate dense granule release and shape change
  114. ITP
    • Immune Thrombocytopenia Purpura
    • PLT destruction due to autoantibodies
    • labeled PLTs are removed quickly from the system leaving the patient with thrombocytopenia
  115. TTP
    • Thrombic Thrombocytopenia Purpura
    • single acute episode in which clots form in the small vessels of the body
    • leaves body with fewer clotting resources, PLT and vWF thrombi w/o fibrin
    • clotting cannot occur without ristocetin
  116. HUS
    • Hemolytic Uremic Syndrome
    • resembles TTP but in children
  117. T/F Coag specimens should be kept refridgerated
    • False
    • coag factors precipitate in the cold
  118. If you see a fibrinogen level of <25..
    be suspicious of a clot!
  119. Instrinci pathway
    XII-->XI-->IX(+VIII)-->X(+V)-->II-->I
  120. Extrinsic pathway
    III(TF)-->VII-->X(+V)-->II-->I
  121. Stago
    type of coag analyzer, if iron ball stops moving signifies a clot
  122. Sysmex
    scattered light detection to look for clots
  123. Lupus anticoagulant
    • prothrombotic agent
    • causes clotting in vivo, prolongs clotting in vitro
    • anti-phospholipid protein complexes
  124. TT
    • Thrombin Time
    • Time to clot with thrombin added
    • qualitative measurement of fibrinogen
    • heparin interference
  125. Reptilase time
    Like thrombin time but with reptilase

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Author:
luvleigh
ID:
336474
Filename:
Hematology Rotation
Updated:
2017-12-12 20:56:54
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cls hematology
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CLS Hematology Rotation
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