Patho Exam 2 - anemia

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Patho Exam 2 - anemia
2013-03-26 15:06:46
boston college CRNA program

for the first part of the hematologic system...
Show Answers:

  1. What is the process of making RBCs called?
  2. Where does erythropoiesis occur?
    in the bone marrow
  3. How long does it take for the stem cell to become a reticulocyte?
    1 week
  4. How long does it take for a reticulocyte to become a mature ERYTHROCYTE?
    1-2 days
  5. What percentage of circulating RBCs are reticulocytes?
  6. What hormone does the kidney release that is critical in RBC formation?
  7. How long does an RBC live?
    120 days
  8. What is the daily percentage of RBC destruction?
  9. What is the daily percentage rate of RBC production?
  10. What is one disease that causes the life span of an RBC to be shorter?
    hemolytic anemia
  11. Where does RBC destruction occur?
    in the spleen
  12. When RBCs are destroyed, is the iron destroyed?
    It can be recycled by the bone marrow or stored in the spleen and liver.
  13. Are the amino acids from hemoglobin destruction destroyed?
    No, they are recycled too
  14. What happens to the heme when hemoglobin is destroyed?
    It is converted to FREE BILIRUBIN
  15. Why is free bilirubin called UNCONJUGATED?
    because it is insoluble in the plasma
  16. If there is too much free/unconjugated bilirubin, what can occur?
  17. Where does bilirubin get conjugated?
  18. If you secrete too much bilirubin what can happen?
    gall stones
  19. What percentage of blood is plasma?
  20. What percentage of blood is erythrocytes?
    45% (aka rbc, aka hematocrit)
  21. What percentage of blood is leukocytes & platelets?
  22. Is anemia a disease?
    No, it is a symptom
  23. What stimulates erythropoietin secretion?
  24. What size and color RBCs will an acute hemorrhage have?
    normocytic, normochromic (it takes 48-72 hours for the reticulocyte count to start to increase)
  25. How long for RBC to return to normal after an acute hemorrhage if iron stores are available?
    3-4 weeks
  26. What size and color are RBCs in a chronic hemorrhage?
    microcytic, hypochromic (iron isn't absorbed as fast as it is lost; less iron means hgb has less carrying capacity (low color) and smaller size (less ability for gas exchange)).
  27. Is the blood volume affected in chronic hemorrhage?
    No. The volume is the same, though there is iron deficiency.
  28. What is the main cause of iron deficiency anemia?
    chronic blood loss
  29. What size/color does hemolytic anemia present?
    normocytic and normochromic (the RBC itself is not altered, there is just an increased destruction or a shorter lifespan)
  30. What is hemoglobinemia?
    Excess hemoglobin in the plasma (it's supposed to be in the RBC, but it has separated from the RBC and is now in the plasma)
  31. What is hemoglobinuria? What causes it?
    Hemoglobin in the urine. Caused by hemoglobinemia; hgb from plasma goes through the kidneys to be excreted in the urine.
  32. If jaundiced too long what can happen?
    gall stones, pulmonary HTN
  33. Is jaundice a S&S of hemolytic anemia?
    It can be, if the heme destruction exceed's the liver's capacity to conjugate the bilirubin.
  34. Why do skeletal abnormalities occur in chronic hemolytic anemia?
    Increased destruction of RBCs leads to increased production (which happens in the bone marrow). The expansion of bone marrow leads to the skeletal abnormalities.
  35. What kind of genetic transmission is hereditary spherocytosis?
    autosomal dominant
  36. What vitamin deficiencies can lead to decreased reticulocytes?
    b12, folic acid
  37. A patient with a hgb level of 9 will be symptomatic.
    Usually, asymptomatic until hgb <8.
  38. What does it mean to have an intrinsic cause of hemolytic anemia? Name 2 examples.
    the cause is hereditary; hereditary spherocytosis, hemoglobinopathies (thalassemia, sickle cell anemia, 6-GPD deficiency)
  39. What is an extrinsic cause of hemolytic anemia? Name 2 examples.
    One that is immune-mediated, or caused by certain meds

    • Examples of anemias with extrinsic causes:
    • hemolytic blood transfusion reaction, immunohemolytic anemia (autoimmune)
  40. What is another name for Vit B12?
  41. What size and color are RBCs from if Vit B12 deficiency?
    Macrocytic, normochromic

    B12 is essential for DNA synthesis and nuclear maturation or normal RBC. Without it, you get large ineffective cells.
  42. Where is Vit B12 found?
    all foods of animal origin
  43. Is Vit B12 deficiency always a result of a dietary deficiency?
    No, it can be caused by lack of intrinsic factor from parietal cells of stomach, which is called pernicious anemia). Intrinsic factor is a protein.
  44. What size/color are the RBCs in iron deficiency?
    microcytic, hypochromic
  45. What size/color RBCs for folic acid deficiency?
    macrocytic, normochromic
  46. What is another name for VitB12/folic acid anemia?
    megaloblastic anemia
  47. What can perpetuate iron deficiency anemia in infants?
    maternal deficiency, diet of only cow's milk
  48. How does renal failure lead to anemia?
    deficient erythropoietin (hormone from kidneys that stimulates RBC production)
  49. Does decreased hct always indicate an anemia?
    No, it can indicate hemodilution
  50. True or false: Anemia leads to decreased plasma volume
    False. The fluid shifts to the intravascular space to compensate, plasma volume expands.
  51. What type of genetic transmission is responsible for sickle cell anemia (SCA)?
    autosomal recessive (has to be received from father and mother to clinically manifest)
  52. In sickle cell disease there is a point mutation of A for T which results in the abnormal substitution of amino acid _________ for _________
    glutamic acid (normal) is replaced by valine (sickle)
  53. how long does a sickle cell live?
    10-20 days (normal RBCs live 90-120 days)
  54. The most two important interventions for sickle cell disease:
    hydration, oxygenation
  55. True or false: Sickle cell carries are usually symptomatic.
    False, they are usually asymptomatic. Hypoxic or hypovolemic conditions can cause sickling. Hydration and oxygenation are important!!
  56. In sickle-cell trait, what % of hgb is hgbS?
  57. In sickle cell disease, what % of hgb is HgbS?
  58. Can sickled cells return to normal shape?
    Yes, with re-oxygenation, they can return to normal. However, after repeated episodes, they can permanently sickle.
  59. What is the leading cause of death in sickle cell anemia?
    Acute Chest Syndrome (atypical pneumonia)
  60. What type of genetic transmission is thalassemia, and what is thalassemia?
    autosomal recessive, condition where too few hgb are synthesized
  61. Can you be heterozygous for both sickle cell and thalessemia?
    Yes, and it can produce an atypical presentation
  62. Which genetic transmission of sickle cell disease is protective against malaria?
    heterozygous (homozygotes are uniquely vulnerable and should get prophylactic anti-malarial treatment)
  63. What is one of the first symptoms of SCA?
    Dactylitis (edema of hands and feet)
  64. What does hydroxyurea do?
    increases HgbF (instead of HgbS) for sickle cell disease
  65. What medication is prophylactic treatment for SCD?
    pcn daily from birth until 5 years old to prevent infection, 1mg folic acid daily for life
  66. Hemochromocytosis leads to iron ________.
  67. The most common mutation for hemochromatosis is:
    autosomal recessive (HFE gene on chromosome 6)
  68. This is what iron forms in the plasma.
  69. This is what iron is stored as in the liver

    Serum ferritin levels provide an index of body iron and storage.
  70. Important lab tests to get if HH is suspected...
    transferrin saturation, total iron binding capacity, serum ferritin
  71. If a person with hemochromatosis has severe anemia (hgb <10, hct <30), how do you remove the iron?
    Desferal (iron chelator)