patho exam 3 - hematology

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patho exam 3 - hematology
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2014-11-11 22:10:24
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  1. what is the normal range for hemaglobin (Hgb)?
    12-18 g/dl
  2. what is the normal range for hematocrit (Hct)?
    37-52%
  3. what is a reduction in number or circulating RBC's or a decrease in quality/quantity of Hgb?
    anemia
  4. why do women have lower RBC's and hematocrit?
    periods
  5. what are some causes of anemia from chronic diseases?
    AIDS, neoplasms (cancer), and chronic hepatitis
  6. what are some symptoms of hemolytic anemia?
    jaundice, splenomegaly
  7. what is microcytic-hypochromic and what are 2 anemias classified under it?
    small cell-low hemaglobin. iron-deficiency and siberoblastic
  8. what causes folate (folic acid) anemia?
    dietary deficiency of folic acid
  9. how do you treat pernicious anemia?
    give vitamin B12 shots
  10. what are the symptoms for pernicious anemia?
    typical symptoms (fatigue, weakness, dyspnea, and pallor), peripheral neuropathy, tingling, numbness, and loss of vibratory senses, glossitis
  11. what are two causes of pernicious anemia?
    chronic gastritis and they lack intrinsic factor in the stomach
  12. what type of anemia is insufficient influence of vitamin B12 on developing cells?
    pernicious anemia
  13. what does macrolytic-normochromic mean and name 2 anemias that are classifed under this type:
    large RBC's-normal hemaglobin. pernicious anemia and folate deficiency (folic acid)
  14. what does normochromic mean?
    normal amounts of hemaglobin
  15. what does hypochromic mean?
    contains abnormally low concentration of Hgb because not enough iron and B12
  16. what does hyperchromic mean?
    contains unusally high concentration of Hgb in cytoplasm because there's not enough RBC's
  17. what does normolytic mean when referring to anemia?
    cells of normal
  18. what does microlytic mean when referring to anemia?
    abnormally small
  19. what does macrolytic mean when referring to anemia?
    abnormally large
  20. what dies "chromic" mean when referring to anemia?
    describes hemaglobin
  21. what does "cytic" mean when referring to anemia?
    cellular size
  22. what are the typical symptoms of anemia?
    fatigue and weakness - Ois not getting to the brain and muscles, dyspnea - body is starving for Oand pallor - decreased RBC and Hct
  23. what are the symptoms of aplastic anemia?
    typical symptoms (fatigue, weakness, dyspnea, and pallor), petechiae, purpura, ecchymosis, bleeding, and infection
  24. what causes aplastic anemia?
    radiation, viruses, lesions in red bone marrow that depress its action - quit producing
  25. what is aplastic anemia associated with?
    pancytopenia
  26. what is normocytic-normochromic and what 4 anemias are are classified under it?
    normal size-normal hemaglobin. aplastic anemia, posthemorrhagic anemia, hemolytic anemia, and anemia of chronic disease (ACD)
  27. what are the symptoms of sideroblastic anemia?
    typical symptoms (fatigue, weakness, dyspnea, and pallor), mild hepatomegaly, and splenomegaly
  28. what type of anemia is characterized by decreased heme synthesis (genetic), acquired from lead, chloramphenicol (Chloromycetin), antitubercular drugs?
    sideroblastic
  29. what are some social/physical risk factors for iron-deficiency anemia?
    poverty, alcohol abuse, poor dentition, candle burning, GIT disease, and depression
  30. what are some dietary risk factors for iron-deficiency anemia?
    low-iron, low vitamin C, excess phytate, excess tea/coffee, fad diets
  31. what are some demographic risk factors for iron-deficiency anemia?
    elderly, teenager, female, immigrant, aborigine, and widower
  32. what are the symptoms of iron-deficiency anemia?
    the typical symptoms (fatigue, weakness, dyspnea, and pallor)
  33. who are the most at risk for iron-deficiency anemia?
    individuals of all ages with minor chronic blood loss
  34. what is another name for absolute polycythemia and what can it cause?
    polycythemia vera, causes leukemia
  35. what causes primary absolute polycythemia?
    results from abnormality of bone marrow stem cells (stem cells all want to be a RBC)
  36. what causes relative polycythemia?
    dehydration for any reason
  37. what are the two forms of polycythemia?
    relative and absolute
  38. what is the blood like in someone with polycythemia?
    thicker, increased BP and increased risk for clots
  39. what is polycythemia?
    increased RBC's
  40. what symptoms would someone have if they had decreased O2 supple to the GI tract (hypoxia in the GI tract)?
    abdominal pain, n/v, and anorexia
  41. is the neurologic system affected in someone with a B12 deficiency?
    yes
  42. when you have tissue hypoxia and decreased blood flow, what happens in the kidneys?
    the kidneys sense the decreased blood flow and activate the renin-angiotensin response
  43. what happens to the character of someone's breathing when someone has tissue hypoxia?
    rate and depth of breathing increases in attempt to make more O2 available to remaining RBC's
  44. what does tissue hypoxia cause?
    inadequate cellular O2
  45. what is the end result of anemia?
    tissue hypoxia
  46. reduced O2 in blood causes arterial dilation which results from what?
    hypoxemia
  47. what is a diagnosis for infectious mononucleosis based on?
    atypical lymphocytes and classic symptoms
  48. what is an absolute rise in lymphocyte count and presence of atypical lymphocytes a result of?
    proliferation of B and T cells
  49. how does infectious mononucleosis begin?
    begins with invasion of B lymphocytes that possess an EBV receptor site
  50. with symptomatic infectious mononucleosis, what age group does it normally affect?
    young adults between 15-35
  51. what is infectious mononucleosis?
    acute infection of B lymphocytes
  52. what disease is lymphocytopenia a major problem in?
    AIDS
  53. what does lymphocytosis occur most often with?
    viral infections such as Esptein-Barr virus (infectious mononucleosis)
  54. what is monocytopenia?
    hairy cell leukemia/prednisone therapy
  55. what is monocytosis?
    increase in monocytes and is most common in late stages of bacterial infections
  56. what is eosinopenia?
    decreased eosinophil count (1-5%) due to migration into inflammatory sites
  57. what is eosinophilia associated with?
    allergic disorders associated with asthma, hay fever, and parasitic invasions
  58. what is eosinophilia?
    absolute increase in total numbers of eosinophils in blood
  59. what does a shift to the left mean?
    when demand for neutrophils > circulatory supply. marrow releases immature WBC's into blood and blood smears look similar to leukemia
  60. what is agranulocytosis?
    neutrophils < 500... very serious
  61. what is neutropenia?
    low neutrophil count <2000 r/t decreased marrow production
  62. what is granulocytosis or neutraphilia?
    prevalent in early stages of infection  or inflammation when stored neutrophils from venous sinuses released into circulating blood
  63. what does increased WBC's 24 hours after surgery indicate versus 3 days after surgery?
    • 24 hours - inflammation
    • 3 days - infection
  64. is leukopenia ever good?
    no, put them on neutrapenic precautions
  65. what is leukopenia?
    lower than normal <5,000
  66. what can cause leukocytosis?
    invading microorganisms, allergic responses, inflammatory response after surgery, and anesthesia
  67. what is leukocytosis?
    higher than normal > 10,000
  68. what may leukocytosis indicate?
    malignancy/hematologic disorders
  69. what are some treatment options for absolute polycythemia?
    minimize risk of thrombosis and prevent progression to acute leukemia
  70. what causes secondary absolute polycythemia?
    increase in erythropoietin in response to chronic hypoxia (high altitude, smokers, COPD) or erythropoietin tumors
  71. is primary or secondary absolute polycythemia more common?
    secondary
  72. people affected with primary absolute polycythemia have a mutation in what gene? what does that gene do?
    Janus kinase 2 (JAK2), it increases erythropoietin receptors in bone marrow regardless of the level of erythropoietin
  73. what is thrombocythemia?
    platelet count > 600,000
  74. how do you treat immune thrombocytopenic purpura?
    replace platelets
  75. when is chronic immune thrombocytopenic purpura more common?
    in females ages 20-40
  76. what is immune thrombocytopenic purpura preceded by?
    viral infection
  77. what age group is acute immune thrombocytopenic purpura common in?
    children and young adults
  78. can Immune thrombocytopenic purpura (IPT) be acute, chronic, or both?
    both
  79. what are some secondary causes to thrombocytopenia?
    viral infections that destroy platelets, bacterial infections that consume platelets, IgG autoantibodies, or drug hypersensitivities (ex. heparin)
  80. when can hemorrhage occur in thrombocytopenia?
    from minor trauma and when platelet count is < 50,000
  81. what is thrombocytopenia?
    platelet count <100,000
  82. what does Waldenstrom macroglobulinemia do?
    produces IgM that leads to high blood viscosity that interferes with circulation to eyes, brain and kidneys
  83. what type of bone tumor is Waldenstrom macroglobulinemia?
    malignant myeloma
  84. what are the most common initial symptoms for malignant myelomas?
    bone pain in single or entire skeletal system, pathologic fractures (bones can break by just turning them in bed), renal failure, recurrent bacterial infections (most common cause of death)
  85. in malignant myelomas, what abnormal antibody becomes protein and is at its highest level in the blood?
    M-protein
  86. what causes malignant myelomas?
    bone lesions and hypercalcemia
  87. is lymphoblastic lymphoma common in males or females?
    males
  88. the majority of lymphoblastic lymphoma originates from what cell?
    T-cell
  89. what age group and region is Non-Hodgkin Lymphoma most prevalent in?
    children, East Africa and New Guinea
  90. what is Burkitt Lymphoma?
    B cell tumor involving jaw and facial bones
  91. what symptoms are specific to Non-Hodgkin Lymphoma?
    pleural effusion, abdominal pain, and splenomegaly
  92. which cells are deviated in Non-Hodgkin Lymphoma?
    B cells, T cells, and NK cells
  93. what are some causes of Non-Hodgkin Lymphoma?
    cancer causing viruses, immunodeficiency, H. pylori infection
  94. are there Reed-Sternburg cells in non-Hodgkin lymphoma?
    no
  95. how do you confirm if someone has Hodgkins Lymphoma and why?
    get a sample of lymph to verify because that's where Reed-Sternburg cells are
  96. what are some symptoms for Hodgkins lymphoma?
    night sweats, fever, weight loss, and weakness
  97. in Hodgkins lymphoma, are lymph nodes painful or painless?
    painless
  98. which lymph nodes are involved in Hodgkins lymphoma?
    neck nodes; single or chain, cervical, inguinal, axillary, and retroperitoneal - abdominal pain
  99. what happens to B cells in Hodgkins lymphoma?
    B cells are deviated
  100. what causes Hodgkins Lymphoma?
    caused by Reed-Sternburg cells that are malignant tissue macrophages that are scattered among normal cells
  101. how does malignant lymphomas develop?
    proliferation of malignant lymphocytes in lymphoid system, classified by cell type
  102. is chronic myelogenous leukemia generic?
    yes
  103. what is a common complication in chronic myelogenous leukemia?
    hyperuricemia which produces gouty arthritis
  104. what chromosomes are affected in chronic myelogenous leukemia and in how many cases?
    9 and 22 (Philadelphia chromosome) in >95% of cases
  105. how does someone get chronic myelogenous leukemia?
    clonal and believed to arise from hematopoietic stem cell
  106. in chronic lymphocytic leukemia, what does hypogammaglobulinemia affect the body? what is someone more at risk for?
    is affects humoral immunity, and someone is at higher risk for infection with encapsulated bacteria
  107. why does someone get chronic lymphocytic leukemia?
    B cells fail to mature into plasma cells that synthesize immunoglobulin
  108. what are the symptoms for acute myelogenous leukemia?
    fatigue, fever, night sweats, petechial hemorrhages, weight loss, uricemia, pallor r/t bone marrow depression
  109. why does someone get pancytopenia with acute myelogenous leukemia?
    bone marrow involvement, bleeding, anemia, and infection
  110. is acute myelogenous leukemia more common in adults or children?
    adults
  111. what happens to the liver, spleen and lymph nodes in acute lymphocytic leukemia?
    enlarge
  112. is it harder to get adults or children into remission in acute lymphocytic leukemia and why?
    adults, dealing with B AND T cells
  113. where does acute lymphocytic leukemia originate from?
    transformed precursor B cells in children and from precursor B and T cells in adults
  114. how do you define acute lymphocytic leukemia as far as lymphoblast count?
    > 30% lymphoblasts in marrow or blood
  115. is acute lymphocytic leukemia more common in adults or children?
    children
  116. what is acute lymphocytic leukemia?
    progressive neoplasm
  117. which drug can predispose someone to getting leukemia and why?
    the antibiotic chloramphenicol, causes bone marrow depression
  118. the most common genetic abnormality is on which chromosomes?
    9 and 22 (the Philadelphia chromosomes)
  119. is leukemia usually familial?
    yes
  120. what are the 4 types of leukemia?
    • AML - acute myeloid leukemia
    • ALL - acute lymphoid leukemia
    • CML - chronic myeloid leukemia
    • CLL - chronic lymphoid leukemia
  121. how is leukemia classified?
    • 1) predominant cell of origin: myeloid (from bone marrow) and lymphoid (from lymph)
    • 2) rate of progression (acute or chronic)
  122. what does uncontrolled proliferation of dysfunctional WBC's in leukemia result in?
    pancytopenia or reduction in all blood cells
  123. what is leukemia?
    malignant disorder of the blood and blood forming organs
  124. why does someone have coagulation disorders?
    usually caused by defects/deficiencies of one or more of clotting factors (genetic)
  125. where does DIC happen, in the intrinsic or extrinsic pathway?
    extrinsic pathway
  126. when is the only time a clot should form?
    when something is wrong, not for no reason
  127. when does thrombocythemia clot?
    when nothing is wrong
  128. what does it mean if a PT test is decreased?
    doesn't take as long to clot
  129. in someone with thrombocytopenia, is a PT increased or decreased and what does that indicate?
    increased, takes longer to clot
  130. in a simplified version, what is going in with someone who has DIC?
    they bleed then clot, bleed then clot. clotting and hemorrhaging are simultaneously occuring
  131. in DIC, what does plasmin do?
    it degrades fibrin before stable clot can develop and pieces of it are released
  132. what can cause DIC?
    gram-negative sepsis, septic chock, hypoxia can damage endothelium and precipitate DIC by activating clotting pathway
  133. what are the 3 pathologic processes in DIC?
    • -endothelial damage
    • -exposure to tissue factor (TF) which complexes with Factor VII. Excess TF activates clotting pathway
    • -direct activation of factor x
  134. how does someone get disseminated intravascular coagulation (DIC)?
    acquired with variety of predisposing conditions
  135. what happened to the clotting cascade in liver disease?
    clotting cascade takes longer or has no cascade at all which impacts platelet function, and fibrinolytic systems
  136. Why are the containers that TPN come in a risk factor for vitamin K deficiency?
    the containers are sterile which inhibit E. coli in the GI tract which is needed to produce vitamin K
  137. what is the most common cause of a deficiency in vitamin K?
    parenteral nutrition combined with broad-spectrum antibiotic that destroy normal gut flora
  138. what is the Triad of Virchow?
    • -loss of vessel wall integrity from injury (tissue factor released)
    • -blood flow abnormalities such as obstruction
    • -blood constituent alterations such as polycythemia
  139. what is secondary hypercoagulability?
    conditions that promote venous stasis (immobility, DVT)
  140. what does hypercoagulability result from?
    deficiency of anticoagulation proteins (too much ability to clot)
  141. what is thromboembolic disease?
    occur from a fixed clot (thrombus) or moving clot (embolus) that obstructs blood flow
  142. is a d-dimer test increased or decreased in someone with DIC?
    increased
  143. what is the max range for d-dimer test in adults?
    0.5 is max
  144. what is a D-dimer?
    neoantigen produced by plasmin lysis of fibrin clots
  145. what is the most reliable and specific test for diagnosing DIC?
    D-dimer test

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