RBC abnormalities

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corbin19
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13736
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RBC abnormalities
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2010-04-12 01:37:18
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MLT 10005
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Medical conditions associated with red blood cell abnormalities
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  1. a general increase in RBC's
    pancytosis
  2. a general decrease in RBC's
    pancytopenia
  3. storage form of iron in tissue
    Ferritin
  4. Disorders in production of myelod stem cells
    myelodysplastic syndromes
  5. what are the four aspects of RBC evaluation
    • Size
    • Color
    • Shape
    • Inclusion bodies
  6. The color of an RBC depends on what?
    the amount of Hgb
  7. any variation in size due to deficiency in the raw material; associated with increased RDW.
    anisocytosis
  8. Normal RDW range.
    11.5-14.5%
  9. an RBC that is, <6 microns, MCV is <80fL, and seen in Iron deficiency, Thalassemia, Lead Poisoning, and sideroblastic anemia.
    Microcyte
  10. An RBC that is >8 microns, MCV is 99fL, and seen in liver disease, megaloblastic process, hypothyroidism, Chemotherapy and newborns.
    macrocytes
  11. RBC's have decreased Hgb, increased central pallor, and MCHC is <32%.
    hypochromasia
  12. RBC's decreased surface-to-volume ration, decreased to absent central pallor, increaed Hgb, MCHC is >36%, usually spherical, not biconcave.
    hyperchromasia
  13. This refers to the entire red cell morphology in the scanned area of a peripheral smeal.
    poikilocytosis
  14. Grading scale for RBC morphology
    Normal:
    Slight:
    1+:
    2+:
    3+:
    4+:
    • Normal: 5%
    • Slight: 5-10%
    • 1+: 10-25%
    • 2+: 25-50%
    • 3+: 50-75%
    • 4+: >75%
  15. An RBC that has an irreversible defect or loss of the cell membrane resulting in no central pallor.
    Spherocytes
  16. This abnormality is seen in hereditary spherocytosis, immune hemolytic anemia, and post transfusion.
    Spherocytes
  17. These are also called crenated, or burr cells and may be artifact in origin.
    echinocytes.
  18. True forms of this abnormality occur in small numbers and have unevenly spaced spicules.
    echinocytes
  19. These abnormalities are associated with uremia, heart disease, dehydration, and untreated hypothyroidism.
    echinocytes
  20. These are RBC's with 3-12 blunt, irregularly spaced spicules that result from LCAT enzyme deficiency.
    acanthocytes
  21. These cells have contain excess cholesterol and are associated with abetalipoproteinemia, pyruvate kinase deficiency, zieve's syndrome, and vitamin E deficiency.
    acanthocytes.
  22. These abnormalities also called dacrocytes are pair shaped and associated with thalassemia and iron deficiency.
    Tear Drop
  23. These are RBC's that have been caught in fibrin strands in circulation and fuses together to create a vacuole that resembles a blister.
    keratocyte
  24. These cells are formed when the spleen bites off large RBC inclusion like Heinz bodies. They are associated with G6PD and pulmonary emboli. also called bite cells.
    helmet cells
  25. these cells, also called codocytes, may be artificially induced on a slide or caused by excess membrane cholesterol.
    Target cells
  26. This abnormality is associated with liver disease, thalassemia, Hgb C, and iron deficiency anemia.
    Target cells
  27. These cells have been transformed by hemoglobin polymerization into a ridged and inflexible crescent shape. also called a drepanocyte.
    sickle cell
  28. These are extreme fragmentations of RBC's that have been split, cut or cloven due to trauma to the cell membrane.
    Schistocytes
  29. This abnormality is associated with DIC, hemolytic anemia, heart valve surgery, and severe burns.
    schistocytes
  30. The name for these abnormalities is used interchangeably but one is more egg shaped while the other is more pencil shaped.
    • ovalocyte
    • elliptocyte
  31. These abnormalities are belived to be a result of mechanical weakness or fragility of the membrane skeleton.
    ovalocyte/elliptocyte
  32. This abnormality is associated with thalassemia and the megaloblastic process
    ovalocyte
  33. This abnormality is associated with hereditary elliptocytosis and iron deficiency anemia
    elliptocyte
  34. These cells have an oval or rectangular central pallor as the result of membrane defect or artifactual origin; they are associated with acute alcoholism and hereditary stomatocytosis.
    stomatocyte
  35. in a stomatocyte cause by membrane defect how will the central pallor appear?
    slit like area of pallor appear shaded.
  36. if artifactual in origin how will the central pallor appear in a stomatocyte?
    slit like area of pallor
  37. RBC's arranged in stacks like coins due to abnormal protein coating on the cell's surface.
    rouleaux formation
  38. This is associated with multiple myeloma, waldentrom's macroglobulinemia, and chronic inflammatory disorders.
    rouleaux formation
  39. This is when RBC's are clumped and results from Ab-Ag interaction associated with cold agglutinins and paroxysmal cold hemoglobinuria.
    RBC agglutination
  40. This is a round purple staining body seen single or doubly in peripherary of cell membrane that is normally pitted by the spleen.
    howell-jolly bodies
  41. This inclusion is associated with splenectomy, megaloblastic anemia, thalassemia, hemolytic anemia, and sickle cell anemia
    howell jolly bodies
  42. These are small irregular, magenta colored inclusions seen in periphery of cell usually in clusters.
    pappenheimer bodies.
  43. these inclusions are referred to as siderotic granules if stained with prussian blue which is the confrimation test.
    pappenheimer bodies
  44. These inclusions consist of nonheme iron, resulting from excess of available iron throught the body.
    pappenheimer bodies
  45. These inclusions are associated with sideroblastic anemia, sickle cell anemia, thalassemia and splenectomy.
    pappenheimer bodies
  46. This is a coarse or diffuse blue staining body that consists of percipitated ribosomes that occurs when smear is drying.
    basophilic stippling
  47. this inclusion is associated with thalassemia, lead poisoning, alcoholism, and megaloblastic anemia.
    basophilic stippling
  48. This is a purple thread-like loop that is remnants of microtubules found in stippled cells.
    cabots ring
  49. This inclusion is associated with megaloblastic anemia, post splenectomy,and homozygous thalassemia.
    Cabot's ring
  50. This inclusion is aggregates of precipitated hemoglobin only seen in crystal violet stain or cresyl blue.
    heinz bodies
  51. This inclusion is associated with G6PD deficiency under oxidative stress and alpha thalassemia.
    heinz bodies
  52. this is the most common protozoal infection, contracted thru mosquito bites.
    malaria
  53. This is caused by four species fo plasmodium that invade RBC's.
    malaria
  54. This parasite may be mistaken for platelets.
    malaria
  55. This parasite is caused by infection thru tick bites, organism is called babesia microti.
    babesiosis
  56. Condition in which there is reduced oxygen delivery to the tissues
    anemia
  57. what are three things anemia may result from?
    • destruction of RBC's
    • Excessive blodd loss
    • decreased production of red cells
  58. what is classification of anemias based on?
    RBC morphology
  59. what are the three types microcytic hypochromic anemias?
    • Iron deficiency anemia
    • anemia of chronic diseases
      sideroblastic anemia
  60. This is a microcytic hypochromic anemia that develops in 3 stages, it is acquired and prgessive.
    iron deficiency anemia
  61. what are the three stages that lead to iron deficiency anemia?
    • iron depletion (w/o anemia)
    • iron deficient erythropoiesis (w/ mild anemia)
    • Iron deficiency anemia develops (w/severe anemia)
  62. this anemia occurs in:
    decreased iron intake
    inadequate absorption
    increased iron utilization
    loss of iron
    iron deficiency anemia
  63. Which type of anemia will result in weakness and dyspnea, increased TIBC, and decreased Hgb and retics.
    iron deficiency anemia
  64. This is a microcytic, hypochromic anemia that in sex linked and congenital.
    sideroblastic anemia
  65. what is the cause of primary sideroblastic anemia?
    idiopathic
  66. what is the cause of secondary sideroblastic anemia?
    toxins or drugs
  67. This microcytic hypochromic anemia will cause dismorphic RBC's, decreased TIBC, and increased serum iron and ferritin.
    hereditary sideroblastic anemia
  68. This microcytic hypochromic anemia will cause dismorphic RBC's basophilic stippling and ringed sideroblasts.
    acquired sideroblastic anemia
  69. This anemia is associated with infections, and autoimmune disorders.
    anemia of chronic disorders.
  70. This anemia is caused by a failure of kidneys to produce erythropoetin, or a renal disease that leads to chemical imbalance or uremia
    anemia of chronic renal problems.
  71. This anemia may cause burr cells due to uremia and hemolysis due to mechanical trauma or adverse metabolic environment.
    anemia of chronic renal problems
  72. This anemia is associated with diseases of the thyroid, pituitary, adrenals, and gonads which produce hormones for erythropoiesis.
    anemia of endocrine diseases.
  73. Macrocytic normochromic anemia is also know as what?
    megaloblastic anemia
  74. This anemia has defective nuclear maturation caused by impared DNA synthesis due to Vit B12 and folic acid deficency
    • macrocytic normochromic anemia
    • (megaloblastic)
  75. This Anemia is seen in strict vegetarians, fish tapeworm, and pernicious anemia patients.
    • macrocytic normochromic anemia
    • (megaloblastic)
  76. The lab findings in this anemia are slight ovalocytosis and tear drops, abnormal schilling test, increased MCV, and hypersegmented neutrophils in more than 98% of cases.
    • macrocytic normochromic anemia
    • (megaloblastic)
  77. This anemia is a failure of bone marrow to produce blood cells.
    aplastic anemia
  78. the congenital form of aplastic anemia is known as what?
    fanconi's anemia
  79. The Lab findings of this anemia include pancytopenia, normocytic normochromic RBC's, polychromasia, and decreased retic count, Hgb, and Hct.
    Aplastic anemia
  80. This is a group of anemia characterized by increased destruction of RBC's.
    hemolytic anemias
  81. This is the most common hereditary hemolytic anemia in northern europe.
    spherocytosis
  82. This hemolytic anemia is due to defective spectrin, it causes jaundic durring hemolytic episodes and is diagnosed in early childhood.
    spherocytosis
  83. In this hemolytic anemi RBC's are spherical instead of biconcave which makes them hyperpermeable to sodium.
    spherocytosis
  84. Lab finding of this hemolytic anemia include spherocytes, an MCHC >36% in 50% of cases, and osmotic fragility is increased.
    spherocytosis
  85. This anemia is caused by a defective cytoskeleton, 90% have no clinical, 10% have symptoms similar to spherocytosis.
    elliptocytosis
  86. The Lab findings of this anemia are elliptocytes and increased reticulocytes.
    elliptocytosis
  87. This hemolytic anemia is characterized by a sodium potassium imbalance that causes RBC's to swell.
    Stomatocytosis
  88. The lab finding of this hemolytic anemia are stomatocytes, MCV increased, and MCHC decreased.
    stomatocytosis
  89. This is the most common RBC enzyme disorder that is generally seen in black populations.
    G6PD deficiency
  90. This hemolytic anemia is harmless unless exposed to oxidative stress such as antimalarial drugs and fava beans.
    G6PD
  91. The lab finding of this Hemolytic anemia include heinz bodies, basophilic stippling, and hemoglobinuria.
    G6PD
  92. In this hemolytic anemia deficiency in PK causes reduced ATP and RBC's become fragile.
    pyruvate kinase (PK) deficiency
  93. This anemia results from infection and causes a loss of self recognition of individual's own RBC's, auto-antibody's are produced against own RBC's,
    autoimmune hemolytic anemia
  94. What are the three types of auto immune hemolytic anemia?
    • Warm agglutinin auto-immune hemolytic anemia (WAIHA)
    • Cold Agglutinin auto-immune hemolytic anemia (CAIHA)
    • Paroxysmal cold hemoglobinuria (PCH)
  95. This very rare hemolytic anemia involves antibodies with optimal serological activity at 37oC has Lab findings of schistocytes and Retculocytes.
    WAIHA
  96. This Hemolytic anemia involves antibodies with optimal serological activity at 4oC, (also seen at 25-31oC, and has lab findings of rouleaux formation and RBC agglutination.
    CAIHA
  97. This is the least common of the AIHA and is seen almost exclusively in children.
    PCH
  98. This animia involves anti-P which attaches to RBC's at low temperatures and as body temp increases it causes RBC hemolysis that results in severe and rapid anemia
    PCH
  99. what is the test for PCH?
    donath-landstier test
  100. This Hemolytic anemia is caused a blood type incompatiblity betwen the mother and fetus.
    Hemolytic Disease of Newborns (HDN)
  101. In HDN administration of this drug prior to a fetal-maternal hemorrhage can prevent the other from producing anti-D.
    rhogam
  102. What is it called when rhogam is administered prior to a fetal-maternal hemmorhage?
    maternal sensitization
  103. Rhogam is usually given when durring pregnancy to D-negative mother
    • at 28 weeks
    • again within 72hrs of birth.
  104. This fairly rare hemolytic anemia has an insidious onset, the RBC membrane is abnormal, and is confired by the HAM's test.
    Proximal Nocturnal Hemolysis (PNH)
  105. This Hemolytic anemia's Lab findings are hematuria (worst in the morning), leukopenia, thrombocytopenia, and slight macrocytosis.
    Proximal Nocturnal Hemolysis (PNH)
  106. This anemia is caused by drugs that lead to immune complex formation, autoimmunity, or membrane modification.
    drug induced IHA
  107. This anemia has lab findings of extravascular hemolysis, spherocytosis and a positive DAT test.
    Drug induced IHA
  108. This is a diverse group of conditions that shorten RBC survial such as infections, mechanical damage or chemical and physical agents. Lab findings are dependent on causative factor.
    Acquired Non-IHA
  109. This anemia is caused by a sudden loss of blood in a short period of time.
    acute blood loss anemia
  110. In acute blood loss anemia reticulocytes will increase ____ days after blood loss and peak at ______ days.
    • 2-3 days
    • 6-10 days
  111. this anemia is caused by a loss of small quantities of blood over a long period of time.
    chronic blood loss anemia
  112. This is synthesized in mitochondria and contains iron.
    hemoglobin
  113. This is synthesized in ribosomes and is twisted along the heme group, each has an exact number and sequence of amino acid.
    globin
  114. what are the four types of globin?
    • alpha
    • beta
    • delta
    • gamma
  115. This hemoglobin consists of two alpha chains, and two beta chains and is 95-97% of all hemoglobin.
    Hgb A
  116. This hemoglobin consists of two alpha chains and two delta chains and is 2-3% of all Hgb.
    Hgb A2
  117. This Hemoglobin consists of 2 alpha chains and two gamma chains and is 1-2% of all hemoglobin.
    Hgb F
  118. Anemias characterized by a structural defect in the hemoglobin.
    hemoglobinopathies
  119. what type of Hgb chain defects are usually clinically significant?
    alpha or beta
  120. what type of Hgb chain defects are usually not clinically significant?
    gamma and delta
  121. these are hgb structural defects due to amino acid substitutions.
    qualitative structural defects
  122. These are hgb structural defects due to impared production of the globin chain.
    quantitative structural defects
  123. what are the types of qualitative structural defects.
    • Hgb S
    • Hgb C
    • Hgb SC
    • Hgb E
  124. What are the types of quantitative structural defects?
    • Beta Thalassemia (major and minor)
    • Alpha Thalassemia
  125. This is due to substitution of amino acid valine for glutamic acid on the 6th position of beta chain, also known as sickle cell.
    Hgb S
  126. This condtion leads to chronic hemolytic anemia, decreased O2 causes RBC's to sickle and become rigid, sickle cells plug small vessels in joints and abdomen.
    Sickle Cell Anemia
  127. in this conditon sickle cells, target cells, howell-jolly bodies, and NRBC's are seen along with a positive sickle cell. electrophoresis shows no Hgb A, 80% or more Hgb S, and 1-20% Hgb F.
    Sickle Cell anemia
  128. In this condition no sickle cells will be in the smear unless in crisis, sickle cell test is positive and electrophoresis shows 60% Hgb A and 40% Hgb S.
    Sickle cell Trait
  129. This is the substitution of lysine for glutamic acid on the 6th position of beta chain mostly in black populations.
    Hgb C
  130. in this conditon 50-90% target cells are seen, increased retics are noted as well as Hgb C crystals, electrophoresis shows no Hgb A, 95% Hgb C plus A2, and <7% Hgb F.
    Hgb C disease
  131. In this condtion there are no clinical symptoms and electrophoresis shows 60% Hgb A and 40% Hgb C plus A2.
    Hgb C trait
  132. This condition mostly seen in blacks has symptoms like sickle cell and is caused by two abnormal beta chains, Hgb S and Hgb C.
    Hgb SC
  133. This condition will have Target cells, Hgb C crystals, Folded RBC's, and sickle cells. electrophoresis will show 50% Hgb S and 50% Hgb C.
    Hgb SC
  134. This is the substitution of lysine for glutamic acid at the 26th position of beta chain, mostly seen in south east asia.
    Hgb E
  135. This condition has mild anemia and moderate target cells, electrophoresis shows 95-97% Hgb E plus A2 and 3-5% Hgb F.
    Hgb E
  136. Electrophoresis of this condition will show 70% Hgb A and 30% Hgb E plus A2
    Hgb E trait
  137. This is the decreased production of one globin chain that causes decreased production of normal hemoglobin.
    Thalassemia
  138. In this condition the beta chain is decreased or absent, and excess A2 causes apoptosis of red cell precursors which leads to ineffective erythropoiesis.
    Beta Thalassemia
  139. This is a homozygous state that occurs in people of Mediterranean decent and causes severe anemia.
    Thalassemia major
  140. Symptoms of this conditon are splenomegaly, retarded growth and mongoloid facial features.
    Thalassemia major
  141. Lab findings of this condition include basophillic stippling, many target cells, howell jolly bodies, pappenheimer bodies, NRBC's and increased Retic count.
    Thalassemia Major
  142. In this condition Alpha chains are reduced or absent and there is an excess of Fetal and beta chains.
    Alpha thalassemia
  143. In this condition Beta chains form stable nonfunctional tetramers.
    Alpha Thalassemia
  144. what are some stable nonfunctional tetramers seen in alpha thalassemia?
    • Hgb H: 4 beta chains
    • Hgb Bart's: 4 Gamma Chains
  145. Absence of all alpha chains is ___________.
    incompatible with life
  146. which type of thalassemia occurs in the uterus
    Alpha
  147. Who is ID of alpha thalassemia minor important to? why?
    • Women of childbearing years or pregnant of mediterranean decent.
    • at risk for hydrop fetalis
    • prevent unnecessary treatment of Iron deficency anemia
  148. This is a chronic life shortening myeloproliferative disorder involving all bone marrow elements, characterized by an increase in RBC mass and Hgb concentration.
    polycythemia vera
  149. what are the types of polycythemia?
    • polycythemia vera
    • secondary polycythemia
  150. this is a chronic disease with insidious onset, symptoms are headaches, epistaxis, myocardial infarction, thrombosis, splenomegaly, hepatomegaly, and erythromelalgia.
    polycythemia vera
  151. Lab findings of this condition are an elevated RBC count, Hgb, and Hct. thrombocytosis, leukocytosis, decreased erythopoesis, and increased red cell mass.
    polycythemia vera
  152. in polycythemia vera this must be seperated from a true increase in red cell mass.
    hemoconcentration
  153. This condition is caused by hypoxic situations such as COPD, cyanosis and CHF, and an excess production of erythropoietin causes an increase in RBC's.
    Secondary polycythemia
  154. This condition is also known as hypoxic erythrocytosis.
    secondary polycythemia
  155. this condition has an increased red cell mass, increased erythropoietin, and a normal plt/WBC count.
    secondary polycythemia
  156. In this condtion an increased Hct is secondary to a decrease in plasma volume.
    relative polycythemia
  157. This condition is seen in acute and subacute dehydration and also middle aged men with a history of smoking, hypertension, and obesity.
    relative polycythemia
  158. This test measures the ability of the RBC's to take up fluid without lysing, it is used to diagnose hemolytic anemias specifically spherocytosis.
    osmotic fragility test
  159. in this test whole blood is added to saline dilutions which lyses RBC's Hgb is measured.
    osmotic fragility test
  160. what is an effective measure of erythrocyte susceptibility to hypotonic damage?
    the presence or absence of hemolysis
  161. In normal RBC's
    inital hemolysis occurs at:
    complete hemolysis occurs at:
    • inital hemolysis: 0.45% NaCl
    • Complete hemolysis: 0.30% NaCl
  162. In spherocytes
    initial hemolysis occurs at:
    Complete heolysis occurs at:
    • initial hemolysis: 0.65% NaCl
    • Complete hemolysis: 0.45% NaCl
  163. In this test lysing agent and sodium dithionate is added to RBC to release Hgb and reduce Hgb S which forms turbid crystals.
    Sickle cell test
  164. This test is used to determine the different types of Hgb present in blood.
    Hgb Electrophoresis
  165. What is the specimen of choice for Hgb electrophoresis?
    EDTA whole blood
  166. using cellulose acetate at pH 8.4 Hgb migration pattern is:
    • A2=C=E
    • S
    • E
    • A
  167. Using citrate agar pH 6.0-6.2 migration pattern is:
    • C
    • S
    • A=E=A2
    • F

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