Minarcik robbins 2013_ch13-rbc


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  • RBC 7.4 microns in diameter
  • Topics
  • Classical RBC’s and platelets, as in in the lab or your office with WRIGHT’s stain.
  • Classical features of peripheral white cells
  • Erythroblasts (normoblasts) seen in the marrow and/or the peripheral smear.
  • HGB X 3 = HCT, a rough rule of thumb
  • Bone marrow biopsy stained with H&E (left), and smear stained with Giemsa (right). BOTH have special advantages!
  • This is a very intense slide, you may have to write a lot of stuff down and listen well!
    This is the basis on which I was trained, and have been reading bone marrows all my life.
  • SCF = Stem Cell Factor
    CFU = Colony Forming Unit
    FLT3L = Fms-related tyrosine kinase 3 ligand, another stem cell stimulating cytokine
  • This is also a very INTENSE slide!
  • One logical (blood loss), two functional (↑ dest, ↓prod) concepts.
    Platelet analogy also
    Losses occur when the rate of destruction is greater then the rate of production, i.e., the rate of production can’t keep up with the rate of destruction!
  • MCV = 80-95
    MCHC = 33-37
  • To understand why there is an erythroid HYPER-plasia in marrows, with patients having HEMOLYTIC anemias, is CRITICAL!
    Would you say all the above levels mean that these are good tests for hemolysis? YES
    How about hemoglobinuria too? YES
  • Which one would be more likely to produce hemoglobinuria? ANS: INTRA-
  • The most common reason for a DECREASED M:E ratio with a NORMAL marrow cellularity might be a hemolytic anemia, although a DECREASE in the M cells (myeloid) would also cause this, especially if the cellularity was DE-creased. Please understand this!
  • Note lack of a central pallor and a microcytosis, i.e., low MCV
    If most of the RBCs are chewed up in the spleen, do you think splenectomy is often helpful in the management of this disease? YES
  • G6PD converts glucose-6-phosphate into 6-phosphoglucono-δ-lactone and is the rate-limiting enzyme of the pentose phosphate pathway.
    What are Heinz bodies? (denatured Hgb) Does G6PD deficiency put RBCs at more risk to oxidative DAMAGE? Ans: YES Is that why it is a hemolytic anemia? YES
  • Heinz bodies, precipitated hemoglobin are seen quite well on a methylene blue stain.
    Heinz bodies are seen with alpha-thalasemia, NADPH deficiency, and liver disease too.
  • Is sickling more likely in oxygenated blood or NON-oxygenated blood? NON (i.e., REDUCED HGB)
    Is sickle cell anemia the mother of all hemoglobinopathies? YES
  • What is the normal weight of a spleen? 150 gms
  • At first the spleen may be enlarged (left) because of HYPERPLENISM due to hemolysis, later it may infarct itself due to small vessel occlussive disease and be quite small (right), perhaps only 1/10 its normal size. What is a NORMAL spleen weight? 150 gm, same as kidney, 1/10th liver.
  • Note the “spiculated” or “spiked” appearance of the outer table of the skull due to extreme erythroid hyperplasia! How is this different from a myeloma skull?
  • H= High affinity
    Why is HIGH AFFINITY bad? Sucks in the O2 very readily, but won’t give it up to the tissues!
  • NOT all hydrops fetalis is RH antigen related, is it?
  • Phosphatidylinositol N-acetylglucosaminyltransferase subunit A is an enzyme that in humans is encoded by the PIGA gene.
    PIGA makes GPI, defective PIGA makes defective or inadequate GPI. Why does the term hemoglobinuria imply hemolysis? What does “paroxysmal” mean” Ans: Sudden, UN-controllable, like a seizure
  • IHA was often called AHA, but AHA is a bad term because not all are autoimmune, but caused by drugs.
  • What is the difference between an “agglutinin” and a “hemolysin”? Ans: “-lysis” implies complement fixation.
    The most common drugs to cause warm agglutinins are anti-microbials (e.g., cefotetan, ceftriaxone and piperacillin).
  • The Coombs is a routine test used in the workup of just about ALL kinds of hemolytic anemias
  • HUS often follows an E. Coli enteric infection in kids, and is a associated with a wide variety of disorders in adults, most closely linked to TTP.
  • Anemias of diminished erythropoesis.
    Fe def
  • Megaloblasts on top, macrocytes on bottom. What is the difference between a megaloblast and a macrocyte? What is the difference between a megaloblast and an erythroblast? Do the arrows point to macrocytes, i.e., RBCs with a high MCV. Why is it silly to say a single RBC has a high MCV?
  • This is the HARD way to remember megaloblastic anemias
  • This is the EASY way!
    Now lets go back to the previous slide and it will all make sense!
  • But are all macrocytic anemias megaloblastic? Hell NO!
    Liver diseases, hypothyroidism, hemolytic anemias can frequently show HIGH MCV, but NO megaloblasts in the marrow!
  • Why do neurologists carry tuning forks in their bags?
    Why jaundice if PA is an anemia of impaired production rather than increased destruction? ANS: I don’t know!
    What senses do the dorsolateral tracts carry? Pain, Temperature, Pressure, VIBRATION
  • Is iron deficiency anemia the mother of all anemias? YES
  • A great diagram of the iron cycle. Know what heme, transferrin, ferritin, and hemosiderin are in the iron cycle.
    Is serum FE a horrible test of iron deficiency anemia? YES
    Is a serum FERRITIN a GREAT test for iron deficiency anemia? YES!
  • Relate hypochromia, microcytosis, anisocytosis to the Wintrobe indices: Ans: MCHC, MCV, RDW, respectively
  • Golden brown refractile pigment on H&E is HEMOSIDERIN when it stains BLUE by the Prussian Blue method!
    Any marrow that has stuff staining with Prussian Blue, is NOT an iron deficiency!
  • Most are hypochromic (low MCHC), and microcytic (low MCV) like Fe deficiency anemias but have NORMAL iron stores (i.e., hemosiderin).
  • Fanconi syndrome and Fanconi anemia are two completely different disorders, but named after the same guy, even though the “syndrome” was NOT described by him. Fanconi’s anemia is characterized by short stature, skeletal anomalies, increased incidence of solid tumors and leukemias, bone marrow failure (aplastic anemia), and cellular sensitivity to DNA damaging agents such as mitomycin C.
    If you understand the cell differentiation concept, why would an aplastic anemia be less likely to involve lymphocytes?
  • The NORMAL adult RED bone marrow in the axial skeleton should be about 50% cells and 50% fat. What is this?
    Perhaps around 10:90?
    What would you think if the few cells you see here were primarily lymphocytes?
  • Does this sound like the usual suspects again?
    How about radiation? Sure, if enough axial skeleton is zapped!
  • What are “dacryo-”cytes?
    Wouldn’t marrow crowding by tumor cells or leukemia cells ALSO be considered DECREASED RBC production?
  • What do you think the most serious consequence might be for a person with increased RBCs and platelets?
  • Doesn’t this really boil down to TWO things? 1) Reduced platelet function/numbers, and, 2) everything else?
  • Normal platelets, but DAMAGED vessel walls, the so-called “angiopathic” thrombocytopenias.
  • At what platelet count level does SPONTANEOUS bleeding generally occur? Ans: ~20K Platelets normally 150K-300K. This is one “normal range” you should memorize.
  • Note the last three items are ALL in the same category. Are platelets low in a “consumption” coagulopathy? Answer: Yes!
    What are the “consumable” clotting factors, classically? Answer: Platelets, fibrinogen, V, VIII
  • At what platelet count level does SPONTANEOUS bleeding generally occur? Ans: 20K Platelets normally 150K-300K
  • Any thrombocytopenia of increased destruction should have INCREASED megakaryocytes in the marrow! JUST LIKE a hemolytic anemia has an erythroid HYPER-plasia, same principle! Does this follow the pattern of a classic “autoimmune” disease? Yes!
  • Remember MANY autoimmune diseases are triggered off by previous infections!
  • Platelet numbers may be normal but do not function well.
  • Hypercoagulability is anything which accelerates the cascade (common), or inhibits its inhibitors (rare).
  • By the way, von Willebrand patients are ALWAYS on the step-1 exam.
  • Because von Willebrand is so closely linked to Factor VIII, it has also been called “pseudo”-hemophilia, but so have many other clotting disorders, so avoid using this term.
  • Hypercoagulability is anything which accelerates the cascade (common), or inhibits its inhibitors (rare).
  • For all practical purposes, the same as Hemophilia A. How to differentiate? Factor assays! Note the AMAZING similarities between Hemophilia A and B
  • What is a “consumptive” coagulopathy? Ans: the platelets and many clotting factors are “consumed”, i.e., used up!
  • Would you feel confident taking a patient to surgery if all these tests were normal, especially the first four? Answer: YES
  • Lets familiarize ourselves with all these abnormal RBC critters.
  • Minarcik robbins 2013_ch13-rbc

    2. 2. RBC and Bleeding Disorders • NORMAL – Anatomy, histology – Development – Physiology • ANEMIAS – Blood loss: acute, chronic – Hemolytic – Diminished erythropoesis • POLYCYTHEMIA • BLEEDING DISORDERS
    3. 3. TABLE 13-2 -- Adult Reference Ranges for Red Blood Cells Measurement (units) Hemoglobin (gm/dL) Men 13.6–17.2 39–49 Hematocrit (%) Red cell count (10 /µL) 6 Women 12.0–15.0 33–43 4.3–5.9 3.5–5.0 Reticulocyte count (%) 0.5–1.5 Mean cell volume (µm ) MCV 82–96 Mean corpuscular hemoglobin (pg) MCH 27–33 Mean corpuscular hemoglobin concentration (gm/dL) MCHC 33–37 3 RBC distribution width 11.5–14.5
    5. 5. MARROW FEATURES • • • • • • • • CELLULARITY 50% MEGAKARYOCYTES at least 1-2/hpf M:E RATIO  3:1 MYELOID MATURATION  1/3 bands or more ERYTHROID MATURATION  nucleus/cytoplasm LYMPHS, PLASMA CELLS  small percentage STORAGE IRON, i.e., HEMOSIDERIN present “FOREIGN CELLS”
    7. 7. ANEMIAS* • BLOOD LOSS – ACUTE – CHRONIC • IN-creased destruction (HEMOLYTIC) • DE-creased production * A good definition would be a decrease in OXYGEN CARRYING CAPACITY, rather than just a decrease in red blood cells, because you need to have enough blood cells THAT FUNCTION, and not just enough blood cells.
    8. 8. Features of ALL anemias • Pallor, where? • Tiredness • Weakness • Dyspnea, why? • Palpitations • Heart Failure (high output), why?
    9. 9. Blood Loss Acute: trauma Chronic: lesions of gastrointestinal tract, gynecologic disturbances. The features of chronic blood loss anemia are the same as iron deficiency anemia, and is defined as a situation in which the production cannot keep up with the loss.
    10. 10. HEMOLYTIC • HEREDITARY – MEMBRANE disorders: e.g., spherocytosis – ENZYME disorders: e.g., G6PD deficciency – HGB disorders (hemoglobinopathies) • ACQUIRED – MEMBRANE disorders (PNH) – ANTIBODY MEDIATED, transfusion or autoantibodies – MECHANICAL TRAUMA (vascular or mechanic) – INFECTIONS – DRUGS, TOXINS – HYPERSPLENISM
    11. 11. IMPAIRED PRODUCTION • Disturbance of proliferation and differentiation of stem cells: aplastic anemias, pure RBC aplasia, renal failure • Disturbance of proliferation and maturation of erythroblasts • Defective DNA synthesis: (Megaloblastic) • Defective heme synthesis: (Fe) • Deficient globin synthesis: (Thalassemias)
    12. 12. MODIFIERS • MCV, microcytosis, macrocytosis • MCH • MCHC, hypochromic • RDW, anisocytosis
    13. 13. HEMOLYTIC ANEMIAS • Life span LESS than 120 days • Marrow hyperplasia (M:E), EPO+ • Increased catabolic products, e.g., bilirubin, serum HGB, hemosiderin, haptoglobin-HGB
    14. 14. HEMOLYSIS • INTRA-vascular (vessels) • EXTRA-vascular (spleen)
    15. 15. M:E Ratio normally 3:1
    16. 16. HEREDITARY SPHEROCYTOSIS Genetic defects affecting ankyrin, spectrin, usually autosomal dominant Children, adults Anemia, hemolysis, jaundice, splenomegaly, gallstones (what kind?)
    17. 17. Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency • A- and Mediterranean are most significant types
    18. 18. FEATURES of G6PD Defic. • Genetic: X-linked • Can be triggered by foods (fava beans), oxidant substances drugs (primaquine, chloroquine), or infections • HGB can precipitate as HEINZ bodies • Acute intravascular hemolysis can occur: – Hemoglobinuria – Hemoglobinemia – Anemia
    19. 19. Sickle Cell Disease • Classic hemoglobinopathy • Normal HGB is α2 β2: β-chain defects (Val>Glu) • Reduced hemoglobin “sickles” in homozygous • 8% of American blacks are heterozygous
    20. 20. Clinical features of HGB-S disease • • • • Severe anemia Jaundice PAIN (pain CRISIS) Vaso-occlusive disease: EVERYWHERE, but clinically significant bone, spleen (autosplenectomy) • Infections: Pneumococcus, Hem. Influ., Salmonella osteomyelitis
    21. 21. THALASSEMIAS • A WIDE VARIETY of diseases involving GLOBIN synthesis, COMPLEX genetics • Alpha or beta chains deficient synthesis involved • Often termed MAJOR or MINOR, depending on severity, silent carriers and “traits” are seen • HEMOLYSIS is uniformly a feature, and microcytic anemia, i.e, LOW MCV (just like iron deficiency anemia has a low MCV) • A “crew cut” skull x-ray appearance may be seen in severe erythroid hyperplasia.
    22. 22. Hemoglobin H Disease • Deletion of THREE alpha chain genes • HGB-H is primarilly Asian H HIGH • HGB- has a affinity for oxygen • HGB-H is unstable and therefore has classical hemolytic behavior
    23. 23. HYDROPS FETALIS • FOUR alpha chain genes are deleted, so this is the MOST SEVERE form of thalassemia • Many/most never make it to term • Children born will have a SEVERE hemolytic anemia as in the erythroblastosis fetalis of Rh disease: – Pallor (as in all anemias), jaundice, kernicterus – Edema (hence the name “hydrops”) – Massive hepatosplenomegaly (hemolysis)
    24. 24. Paroxysmal Nocturnal Hemoglobinuria (PNH) GlycosylphosPhatidylInositol (lipid rafts) • ACQUIRED, NOT INHERITED like all the previous hemolytic anemias were • ACQUIRED mutations in phosphatidylinositol glycan A (PIGA) • Note: It is “P” and “N” only 25% of the time!
    25. 25. Immunohemolytic Anemia • All of these have the presence of antibodies and/or compliment present on RBC surfaces • NOT all are AUTOimmune, some are caused by drugs • Antibodies can be – WARM AGGLUTININ (IgG) – COLD AGGLUTININ (IgM) – COLD HEMOLYSIN (paroxysmal) (IgG)
    26. 26. IMMUNOHEMOLYTIC ANEMIAS • WARM AGGLUTININS (IgG), will NOT hemolyze at room temp – Primary Idiopathic (most common) – Secondary (Tumors, especially leuk/lymph, drugs) • COLD AGGLUTININS: (IgM), WILL hemolyze at room temp – Mycoplasma pneumoniae, HIV, mononucleosis • COLD HEMOLYSINS: (IgG) Cold Paroxysmal Hemoglobinuria, hemo-LYSIS in body, ALSO often follows mycoplasma pneumoniae
    27. 27. COOMBS TEST • DIRECT: Patient’s CELLS are tested for surface Ab’s • INDIRECT: Patient’s SERUM is tested for Ab’s.
    28. 28. HEMOLYSIS/HEMOLYTIC ANEMIAS DUE TO RBC TRAUMA • Mechanical heart valves breaking RBC’s • MICROANGIOPATHIES: – TTP – Hemolytic Uremic Syndrome
    29. 29. • • • • • • • • NON-Hemolytic Anemias: i.e., DE-creased Production “Megaloblastic” Anemias B12 Deficiency (Pernicious Anemia) Folate Deficiency Iron Deficiency Anemia of Chronic Disease Aplastic Anemia “Pure” Red Cell Aplasia OTHER forms of Marrow Failure
    30. 30. MEGALOBLASTIC ANEMIAS • Differentiating megaloblasts (marrow) from macrocytes (peripheral smear, MCV>94) • Impaired DNA synthesis • For all practical purposes, also called the anemias of B12 and FOLATE deficiency • Often VERY hyperplastic/hypercellular marrow* (* exception to the rule)
    31. 31. Decreased intake Inadequate diet, vegetarianism Impaired absorption Intrinsic factor deficiency   Pernicious anemia     Gastrectomy     Malabsorption states   Diffuse intestinal disease, e.g., lymphoma, systemic sclerosis Ileal resection, ileitis   Competitive parasitic uptake   Fish tapeworm infestation     Bacterial overgrowth in blind loops and diverticula of bowel Increased requirement Pregnancy, hyperthyroidism, disseminated cancer
    32. 32. Vit-B12 Physiology • Oral ingestion • Combines with INTRINSIC FACTOR in the gastric mucosa • Absorbed in the terminal ileum • DEFECTS at ANY of these sites can produce a MEGALOBLASTIC anemia
    33. 33. Please remember that ALL megaloblastic anemias are also MACROCYTIC (MCV>94 or MCV~100), and that not only are the RBC’s BIG and hyperplastic/hypercellular, but so are the neutrophils, and neutrophilic precursors in the bone marrow too, and even more so, HYPERSEGMENTED!!!
    34. 34. PERNICIOUS ANEMIA • • • • • • • • MEGALOBLASTIC anemia LEUKOPENIA and HYPERSEGS JAUNDICE…??? NEUROLOGIC posterolateral spinal tracts ACHLORHYDRIA Can’t absorb B12 LOW serum B12 Flunk Schilling test, i.e., can’t absorb B12, using a radioactive tracer
    35. 35. FOLATE DEFICIENCY MEGALOBLASTIC AMEMIAS • • • • • • Decreased Intake: diet, etoh-ism, infancy Impaired Absorption: intestinal disease DRUGS: anticonvulsants, BCPs, CHEMO Increased Loss: hemodialysis Increased Requirement: pregnancy, infancy Impaired Usage 
    36. 36. Fe Deficiency Anemia • Due to increased loss or decreased ingestion, almost always, in USA, nowadays, increased loss is the reason • Microcytic (low MCV), Hypochromic (low MCHC) • THE ONLY WAY WE CAN LOSE IRON IS BY LOSING BLOOD, because FE is recycled!
    37. 37. Fe Transferrin Ferritin/apo- (GREAT test) Hemosiderin
    38. 38. Clinical Fe-Defic-Anemia • Adult men: GI Blood Loss • PRE menopausal women: menorrhagia • POST menopausal women: GI Blood Loss
    39. 39. 2 BEST lab tests: • Serum Ferritin • Prussian blue hemosiderin stain of marrow (also called an “iron” stain)
    40. 40. ?
    41. 41. Anemia of Chronic Disease* • CHRONIC INFECTIONS • CHRONIC IMMUNE DISORDERS • NEOPLASMS • LIVER, KIDNEY failure * Please remember these patients may very very much look like iron deficiency anemia, BUT, they have ABUNDANT STAINABLE HEMOSIDERIN in the marrow!
    42. 42. APLASTIC ANEMIAS • ALMOST ALWAYS involve platelet and WBC suppression as well • Some are idiopathic, but MOST are related to drugs, radiation • FANCONI’s ANEMIA is the only one that is inherited, and NOT acquired • Act at STEM CELL level, except for “pure” red cell aplasia
    45. 45. MYELOPHTHISIC ANEMIAS • Are anemias caused by metastatic tumor cells replacing the bone marrow extensively
    46. 46. POLYCYTHEMIA • Relative (e.g., hemoconcentration) • Absolute – POLYCYTHEMIA VERA (Primary) (LOW EPO), mutation in tyrosine kinase, making RBCs hyper responsive to EPO – POLYCYTHEMIA (Secondary) (HIGH EPO) • HIGH ALTITUDE • EPO TUMORS • EPO “Doping” • CVAC, the trendy California bubble pods
    47. 47. P. VERA • A “myeloproliferative” disease • ALL cell lines are increased, not just RBCs
    48. 48. BLEEDING DISORDERS (aka, Hemorrhagic “DIATHESES”) • Blood vessel wall abnormalities √ • Reduced platelets √ • Decreased platelet function √ • Abnormal clotting factors √ • DIC (Disseminated INTRA-vascular Coagulation), also has ↓ plats.
    49. 49. VESSEL WALL ABNORMALITIES (angiopathic thrombocytopenias) (NON-thrombotic purpuras) • • • • • • Infections, especially, meningococcemia, and rickettsia Drug reactions causing a leukocytoclastic vasculitis Scurvy, Ehlers-Danlos, Cushing syndrome Henoch-Schönlein purpura (mesangial deposits too) Hereditary hemorrhagic telangiectasia Amyloid
    50. 50. THROMBOCYTOPENIAS • Like RBCs: – DE-creased production – IN-creased destruction – Sequestration (Hypersplenism) – Dilutional • Normal value 150K-300K
    53. 53. THROMBOCYTOPENIAS • ITP (Idiopathic Thrombocytopenic Purpura) • Acute Immune • DRUG-induced • HIV associated • TTP, Hemolytic Uremic Syndrome
    55. 55. ACUTE ITP • • • • CHILDREN Follows a VIRAL illness (~ 2 weeks) ALSO have anti-platelet antibodies Platelets usually return to normal in a few months
    56. 56. DRUGS • Quinine • Quinidine • Sulfonamide antibiotics •HEPARIN
    57. 57. HIV • BOTH DE-creased production AND IN-creased destruction factors are present
    58. 58. Thrombotic Microangiopathies • BOTH are very SERIOUS CONDITIONS with a HIGH mortality: – TTP (THROMBOTIC THROMBOCYTOPENIC PURPURA) – H.U.S. (HEMOLYTIC UREMIC SYNDROME) • These can also be called “consumptive” coagulopathies, just like a DIC
    59. 59. “QUALITATIVE” platelet disorders • Mostly congenital (genetic): – Bernard-Soulier syndrome (Glycoprotein1-b deficiency) – Glanzmann’s thrombasthenia (Glyc.IIB/IIIA deficiency) – Storage pool disorders, i.e., platelets misfunction because of defective granulation • ACQUIRED: ASPIRIN, ASPIRIN, ASPIRIN
    60. 60. PTT PT/INR
    61. 61. BLEEDING DISORDERS due to CLOTTING FACTOR DEFICIENCIES • NOT spontaneous, but following surgery or trauma • ALL factor deficiencies are possible • Factor VIII and IX both are the classic X-linked recessive hemophilias, A and B, respectively • ACQUIRED disorders often due to Vitamin-K deficiencies (II, VII, IX, X) • von Willebrand disease the most common, 1%
    62. 62. • • • • • • von Willebrand Disease 1% prevalence, most common bleeding disorder Spontaneous and wound bleeding Usually autosomal dominant Gazillions of variants, genetics even more complex Prolonged BLEEDING TIME, NL platelet count vWF is von Willebrand Factor, which complexes with Factor VIII, to join platelets with the exposed ECM in endothelial disruption. it is the von Willebrand Factor which is defective in von Willebrand disease • Usually BOTH platelet and FactorVIII-vWF disorders are present
    63. 63. PTT PT/INR
    64. 64. • • • • • • HEMOPHILIA A The “classic” HEMOPHILIA Factor VIII decreased Co-factor of Factor IX to activate Factor X Sex-linked recessive Hemorrhage usually NOT spontaneous Wide variety of severities • Prolonged PTT (intrinsic) only • Rx: Recombinant Factor VIII
    65. 65. • • • • • HEMOPHILIA B The “Christmas” HEMOPHILIA Factor IX decreased Sex-linked recessive Hemorrhage usually NOT spontaneous Wide variety of severities • Prolonged PTT (intrinsic) only • Rx: Recombinant Factor IX
    67. 67. DIC, Disseminated INTRA-vascular, Coagulation • Extremely SERIOUS condition • NOT a disease in itself but secondary to many conditions – Obstetric: MAJOR OB complications, toxemia, sepsis, abruption – Infections: Gm-, meningococcemia, RMSF, fungi, Malaria – Many neoplasms, acute promyelocytic leukemia – Massive tissue injury: trauma, burns, surgery • “Consumptive” coagulopathy
    68. 68. Common Coagulation TESTS • PTT (intrinsic) • PT INR (extrinsic) • Platelet count, aggregation • Bleeding Time, so EASY to do • Fibrinogen • Factor Assays
    69. 69. RBC LAB http://www.chronolab.com/hematology/2_1.htm