Hematology Q
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| 1. What is Hematopoiesis? | The process of the formed elements that are produced of blood.
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| 2. How does the process of Hematopoiesis occur? | The process occurs through a series of intricate steps that initiate with stem cell.
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| 3. What does the stem cell produce? | The stem may produced red cells, all classes of granulocytes, monocytes, platelets and cells of the immune system
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| 4. Where does hematopoiesis occur? | In the yolk sack, then liver, and eventually the bone marrow. In normal adults it occurs in marrow and lymphatic tissues.
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| 5. What are the characteristics of RBC? | In humans, RBC takes the form of flexible biconcave disks, lack a cell nucleus, subcellular organelles and the ability to synthesize protein.
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| 6. Where is RBC developed? | Bone Marrow
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| 7. How does a RBC live? | About 120 days
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| 8. Does RBC have a red cell precursor? | Yes
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| 9. What is the initial recognizable red cell precursor for RBC? | pronormoblast
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| 10. What will the pronormoblast cell undergo? | This cell will undergo 4/5 division before, in result of production of 16-32 RBC
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| 11. Along with the division, what else occurs with the pronormoblast? | Concomitant with the stimulation of erythropoietin the early progenitor cell production can be amplified.
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| 12. What is Erythropoietin? | A dalton glycoprotein hormone that is produced and released by the peritubular capillary linining of the kidney
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| 13. Where is EPO produced? | liver and kidney
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| 14. What does EPO regulate? | It governs the day to day production of RBC
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| 15. What does EPO measure? | The ambient level of the hormone
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| 16. How is EPO measured? | By very sensitive immunoassays
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| 17. How is EPO production controlled? | By the tissue availability of oxygen
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| 18. What is the function of EPO? | To bind to receptors on the marrow erythroid precursors
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| 19. What can occur under the stimulus of EOP? | Red cell production can increase 4-5 fold in one week time
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| 20. What happens when hemoglobin falls below 10g per dl? | a stimulus to enhance EPO production is initiated
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| 21. What is a erythron? | A dynamic organ made of a pool of marrow erythroid precursor cells and a large mass of mature circulating red blood cells
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| 22. What is the function of erythron? | It depends on EPO and functional erythroid marrow, and adequate supply of nutrients for red cell production
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| 23. What are the disorders of hematological system? | Nutrient Disorders, Hemoglobinopathies, Metabolic Defects, Autoimmune Related Disorders, Disorders of Cell Production, Mylelothistic Disorder ( Malignancies), Hemolytic Anemias
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| 24. What are the 3 major nutrients of RBC production? | Iron, B12 and folate
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| 25. What does Iron binds to? | Iron binds to hemoglobin and facilitates the biological activity of EPO
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| 26. What does Iron Deficiency cause? | hypo-proliferative anemia
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| 27. What causes megaloblastic anemias? | Both folic and coblamin B12
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| 28. What is the major role of Iron? | To carry oxygen as part of the heme protein that turns into hemoglobin
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| 29. What is Iron a critical element of? | Iron is a critical element in the cytochrome system in mitochrondria
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| 30. What happens to sans iron cells in Iron Deficiency Anemia? | Sans iron cells lose their capacity for electron transport and hemoglobin synthesis is impaired
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| 31. Where does the Iron absorbed from the diet circulate? | In the plasma bound to transferin
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| 32. What is a transferrin? | It is a bi-lobed glycoprotein with two binding sites
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| 33. Where is majority of the iron transported by transferring delivered? | To the erythroid marrow
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| 34. What is the clearance of tranferrin directly related to? | marrow activity and plasma Fe
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| 35. Where does the Iron transferrin complex circulate? | In the plasma until they interact with transferrin receptors on the surface of the erythroid marrow cells
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| 36. What has the greatest number of receptors? | The developing erythroblast
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| 37. Why is Iron made available upon interacting with the receptor? | For heme synthesis
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| 38. Where does excess of amounts of hemoglobin synthesis of Iron bind to? | storage protein
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| 39. How is ferritin formed? | By a storage protein apoferritin
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| 40. What occurs when apoferritin forms ferritin? | It is binds with the excess Fe
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| 41. Where else does Iron storage occur? | In the liver
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| 42. How does Iron incorporated into hemoglobin enter the circulation? | As a new red blood cell that are released in the circulation
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| 43. What does the iron incorporated into hemoglobin become a part of? | Becomes a part of red cell mass and cannot be re-utilized until red cell dies
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| 44. What is the life span of RBC? | 120 days
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| 45. What causes megaloblastic anemias? | Impaired DNA synthesis
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| 46. What kinds of cells are affected in megaloblastic anemia? | Cells with rapid turnover – hemopoietic precusors and gastrointestinal epithelial cells
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| 47. How are cells affected in megaloblastic anemia? | Cells are larger with greater RNA to DNA ratio
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| 48. What is the end result of megaloblastic anemias? | The end result is ineffective erythropoesis
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| 49. What does Hemoglobin Oxygen Dissociation Curve do? | It plots the proportion of hemoglobin in saturated form on its vertical axis against the prevailing oxygen tension on the horizontal axis
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| 50. What will changes in physiological condition do to the curve? | It will shift the curve to the left or right indication decreased or increase oxygen affinity
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| 51. What will happen to the curve is there is an increase temperature, 2,3-BPG, or pC02, or a decrease in pH? | It will shift the curve to the right, which demonstrated decrease oxygen affinity
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| 52. What does the right shift do? | It decreases the oxygen affinity of hemoglobin thus increasing the requirement oxygen to obtain the same saturation.
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| 53. What does the right shift enhance? | The ability of hemoglobin to release oxygen into the tissues
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| 54. Who has a higher oxygen affinity, adult hemoglobin or fetal hemoglobin? | Fetal hemoglobin, which shifts the curve to the left
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| 55. What does the fetal hemaglobin physiological ability to shift the curve to the left mean? | It compensates for the lower oxygen tension that are in the human placenta
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| 56. What is apparent at 6 weeks of fetal life? | 3 hemoglobin variants appear that are subsequently transformed into fetal hemoglobin
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| 57. When does fetal hemoglobin appear? | At 10 weeks and persistent until 38 weeks after which adult hemoglobin is predominately synthesized
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| 58. What causes Spleenic Sequestration Syndrome? | Caused by engorgement of RBCs in un-infarcted spleen.
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| 59. In who does SSS present in? | children under 5 years of age.
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| 60. If a child has a grossly enlarged spleen and profound anemia, what is possible? | shock is possible
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| 61. What is the first line of therapy? | Immediate transfusion with packed RBC
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| 62. What are the Classification of Hemoglobinopathies? | 1-Structural hemaglobinopathies, 2-Thalassemias, 3-Combination Thalassemia variants, 4-Hereditary Persistent of HgbF, and 5-Aquired Hemaglobinopathies
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| 63. What is structural hemoglobinopathies? | A specific single amino acid defects in the Beta chain
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| 64. What is Thalassemias? | A defective biosynthesis of the globin chains
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| 65. What hemaglobinopathies does no clinically present before six months of age? | B chain hemaglobinopathies
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| 66. What has a much higher oxygen affinity, Fetal Hemoglobin (gamma chain) or hemoglobin A? | Fetal hemoglobin (gamma chain)
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| 67. When does the gamma chain switch to B chain? | 6 months of age
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| 68. What can happen after 6 months of age? | A child can begin to express one of the B chain hemoglobinopathies
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| 69. What is B chain Hemoglobinopathies? | The B chain hemaglobinopathies are inherited as autosomal recessive due to a single amino acid substitution.
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| 70. What is the basic mechanism for sickle cell anemia? | The B chain changes from hemaglobin A to hemaglobin S from single amino acid substitution of valine for glutamic acid at position 6 of B chain.
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| 71. Does Sickle cell hemoglobin have a significantly decrease oxygen carrying capacity? | Yes
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| 72. In what conditions does sickle sell hemoglobin tend to lose their capability of deformability that predisposes them to a sickle? | Under adverse physiological conditions such as infection, surgery and stress.
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| 73. What occurs in the first 5 years of life to a sickle cell anemia patient? | Infarction of the spleen, which results in auto spleenectomy and is associated with immunodeficiency
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| 74. What does chronic hemolytic anemia result in a sickle cell anemia patient? | excessive number of RBC that must be catabolized which subsequently overloads the RE system and potentiates the spleenic dysfunction
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| 75. What are sickle RBC capable of? | Obstructing capillaries resulting in a pathology of increased adhesion and local microinfarction
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| 76. What does the process of microinfarction in sickle cell anemia patients involve? | Progressive and preferentially involves the spleen, the long bones, CNS and chest
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| 77. Is the process of microinfarction in sickle cell anemia patients progressive? | Yes
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| 78. What are the clinical syndromes of sickle cell anemia? | Hand Foot Syndrome, Spleenic Sequestration Syndrome, Pain Crises( tubular bones), Hypoplastic Crises, Chest Syndrome, CNS infarctions, Osteomyelitis, Sepsis
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| 79. When does the Hand Foot Syndrome occur? | It occurs in the 1st two years of life
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| 80. What does the Hand Foot Syndrome initiate? | It initiates pain and swelling of the small tubular bones of the hand and feet.
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| 81. What does a child with Hand Foot Syndrome present with? | Child presents with swollen hands or the inability to walk
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| 82. What is the treatment for Hand Foot Syndrome? | Treatment with analagesics and fluid therapy is usually effective
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| 83. What does pain crisis principally involve? | Pain crises principally involve the long bones
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| 84. Why does pain crisis occur? | These crises are result of capillary obstruction by increased number sickled red blood cells
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| 85. How are the pain crisis initiated? | These crises are initiated by infection, dehydration and stress.
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| 86. How are Pain Crisis treated? | Pain crises are treated with hydration and pain management.
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| 87. What causes Hypoplastic Crisis? | These crises are caused by intercurrent viral infection in particular Parvo B19.
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| 88. What does Parvo B19 initiate? | red cell production at the level of the bone marrow
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| 89. What does a patient with Hypoplastic Crisis present with? | Patient present with fever, lethargy, occasionally gastroenteritis and pallor
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| 90. What will a patient with Hypoplastic Crisis’ laboratory evaluation demonstrate? | A fall in Hgb, Hct and reticulocyte count.
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| 91. What is the cause of Chest Syndrome? | Chest syndrome is caused by multiple micro-infarctions in the lung resulting in perfusions defects that may result in respiratory failure
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| 92. What does a child with Chest Syndrome present with? | Children with chest syndrome present with acute chest pain, dyspnea, tachypnea, pallor and occasionally cyanosis
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| 93. How is Chest Syndrome best diagnosed? | Chest syndrome is best diagnosed by chest Xray( infiltrates) or more specifically with MRI
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| 94. Are children with sickle cell disease more susceptible to strokes? | Yes
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| 95. Are patients with more malignant genotypes( Central African) more prone to the devastating complication of stroke and major infections? | Yes
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| 96. Are all children with sickle cell disease have an increase prevalence to micro brain infarcts that may lead to both brain functional impairments or physiologic impairment? | Yes
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| 97. Should every child with sickle cell disease be monitored with transdermal Doppler yearly? | Yes
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| 98. Why are sickle cell patients susceptible to infection? | because of splenetic dysfunction, impairment of the RE system secondary to failure of clearing immune complexes from the RE system and possible Factor B deficiency
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| 99. What do children with sickle cell disease present with? | pneumococcal sepsis, H. influenza disease and osteomyelitis due to salmonella
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| 100. In hemoglobinopathies, what is critical for oxygen delivery? | Hemoglobin
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| 101. In hemoglobinopathies, what can happen to hemoglobin? | Hemoglobin can alter the shape, deformability and viscosity of RBC
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| 102. What are hemoglobinopathies? | Disorders that affect the structure, function or production of hemoglobin
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| 103. Where does neutrophils evolve from? | Neutrophils evolve in the marrow from the myeloblast into a mature neutrophil
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| 104. What does promyelocyte have? | The promyelocyte has a large nucleus with the development of primary granules
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| 105. What does a band form consist of? | The Band form has condensed band shaped nucleus and is the analog to the reticulocyte
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| 106. Is mature neutrophil is segmented? | Yes
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| 107. Where and how is neutrophils released? | The neutrophil is released from the bone marrow by G-CSF, steroid, infection( endotoxin)
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| 108. In what sort of pool does neutrophil circulate? | Circulating pool
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| 109. How are neutrophils induced to leave the circulating pool? | By inflammatory mediators
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| 110. How are neutrophils egressed from the circulation to the tissue? | Adhesion molecules
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| 111. The bone marrow represents how many pools? | 3 dynamic pools
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| 112. What are the three dynamic Marrow pools? | Circulating Pool, Tissue Pool, and Marginal Pool
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| 113. What is the marrow pool? | The Marrow pool is the development and storage facility for neutrophil and its’ precursors
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| 114. Where are the marrow pools? | Normally 90% of the marrow pool is in the bone marrow
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| 115. The circulating pool consists of two dynamic pools? | Yes
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| 116. What percent is the free flowing pool? | Approximately 50%
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| 117. What is marginal pool? | The marginal pool are neutropils that are in close contact with the endothelium
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| 118. How does Infection affect the marrow pools? | Infection expands the circulating and marginal pools as well as tissue pool.
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| 119. Does Infection expands the tissue pool? | Yes
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| 120. How does Epinephrine affect the marrow pools? | It expands the circulating pool and Contracts the marginal pool
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| 121. How does Steroid affect the marrow pools? | Expands the marginated pool and the circulating pool
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| 122. How does Leucocyte Adhesion Deficiency affect the marrow pools? | It expands the Circulating Pool and contracts the Tissue Pool and Marginated Pool
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| 123. What are the Plasma Cell disorders? | Basic Mechanism of Plasma Cell Dycrasias, Immunological Mechanisms Involved, Monoclonal gammapathies of Undetermined Significance(MGSU), Multiple Myeloma, Waldenstrom’s Macrogloblinemia, Heavy Chain Disease, Cryoglobulinemia
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| 124. How are each M protein characterized? | Each M protein is characterized by two Heavy Chains and two Light Chains of the identical class.
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| 125. How are the heavy chains designated? | use Greek letter
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| 126. How are the Light Chains designated? | Either Kappa or Lambda.
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| 127. Are Plasma Cell Disorder neoplastic? | Plasma Cell Disorders are either neoplastic or potentially neoplastic
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| 128. What are plasma cell disorders associated with? | These disorders are associated with the proliferation of a single clone of immunoglobulin secreting plasma cells derived from B cell immunocytes.
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| 129. How are plasma cell disorders characterized? | These disorder are characterized by immunologically homogenous proteins(M).
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| 130. What is the previous terminology for MGUS? | Benign Monoclonal Gammapathy
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| 131. How is MGUS defined? | A disease process that produces less than 3 g/dl of M protein and fewer than 10% plasma cells in the BM.
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| 132. What is there a absence of in MGUS? | lytic lesions, hypercalcemia, renal insufficiency and stablization of the M protein concentration.
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| 133. How is Multiple Myeloma characterized? | By the neoplastic proliferation of single clone of plasma cell engaged in the production a monoclonal immunoglobulin
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| 134. In Multiple Myeloma, what is involved in the process? | Involves bone marrow proliferation, with invasion of the adjacent bone.
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| 135. What are the features of Multiple Myeloma? | Anemia, hypercalcemia and renal insufficiency
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| 136. What does the Multiple Myeloma represent? 1 | % of all cancers and 10% of all hematologic cancers.
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| 137. What is the incidence of Multiple Myeloma? | The incidence is 4 per 100,000.
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| 138. What is the average age of onset of Multiple Myeloma? | 65 years.
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| 139. Is Multiple Myeloma more common in men or female? | It is more common( slightly in men)
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| 140. In Multiple Myeloma, is the incidence 2X greater in African Americans? | Yes
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| 141. What is the clinical manifestation of Multiple Myeloma? | bone pain that spares the patient during sleep, anemia, weakness and fatigue.
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| 142. What is the most common physical finding? | most common is pallor.
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| 143. In Multiple Myeloma, what is present from an allergic stand point? | generalized pruritis.
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| 144. How is Multiple Myeloma caused? | environmentally and hereditary
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| 145. What is Multiple Myeloma linked to? | To hydrocarbons and aliphatic chemical. Ex: Herbicides.
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| 146. How is Multiple Myeloma linked to family clusters? | Reported in first degree relative and in identical twins
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| 147. What are the basic Immunology plasma cells? | The plasma cell are cytoplasmic Ig+, CD38+, CD 138+, and PCA 1+
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| 148. What does the smaller % of cells express? | CD 10, HLADR
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| 149. What does the 20% of cells express? | CD 20.
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| 150. Where does the premyeloma cell circulate? | In the microenvironment of the marrow
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| 151. What cells are reduced? | CD4 + Tcell
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| 152. What are the over produced myeloma? | Il6, TNFa, Il-1B
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| 153. What are the results of increased osteoclast activity? | Lytic lesions, osteopenia, and hypercalcemia and fractures
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| 154. How are the Osteoclast activated? | By the transmembrane receptor RANK( receptor activator of nfkb)
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| 155. What controls the osteoclast production? | Receptor RANK
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| 156. What is the newly discovered member of the TNf-R family? | Oteoprotegerin OPG or receptor of activator of RANK.
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| 157. How is Oteoprotegerin expressed? | osteoclasts, macrophages and dendritic cell
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| 158. What increases the receptor activator? | Cytokines Il-6, TNfa and Il-1b
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| 159. What increases osteoclast proliferation? | Cytokines Il-6, TNfa and Il-1b
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| 160. How is Oseosclerotic Myeloma (POEMS) characterized? | by polyneuropathy, organomegaly, endocrinopathy, M protein and skin changes.
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| 161. What is the clinical features of Oseosclerotic Myeloma (POEMS)? | Chronic inflammatory demyelinating polyneuropathy, hepatomegaly, optic neuritis, gyneocomastia, testicular atrophy, and hyperpigmentation and hypertrichosis.
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| 162. In Oseosclerotic Myeloma (POEMS), do the patients have elevated mu protein? | Yes
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| 163. In Oseosclerotic Myeloma (POEMS), the patient does not have bone marrow involvement, anemia, hypecalcemia? | True
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| 164. What is Waldenstrom’s Macroglobulinemia the result of? | from an uncontrolled proliferation of lymphocytes and plasma cells resulting in a large lgM M protein.
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| 165. What are the clinical manifestations of Waldenstrom’s Macroglobulinemia? | weakness, fatigue, bleeding( oronasal), blurred vision , heart failure and recurrent infections.
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| 166. In Waldenstrom’s Macroglobulinemia, there is no lytic lesions and renal involvement. | True
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| 167. What are the physical examination of Waldenstrom’s Macroglobulinemia? | pallor, hepatospleenomegaly, retinal hemorrhages, exudates and vascular segementation.Sensimotor periheral neuropathy and extensive pulmonary involvment
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| 168. What is the most common physical examination? | Extensive pulmonary involvement
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| 169. What is evident in the laboratory for Waldenstrom’s Macroglobulinemia? | severe normocytic normochromic anemia.
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| 170. What is evident in electrophoresis for Waldenstrom’s Macroglobulinemia? | It reveals a tall narrow peak(g)mobility.
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| 171. T/F. In Waldenstrom’s Macroglobulinemia 75% of Ig M has k light chains? | True
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| 172. In Waldenstrom’s Macroglobulinemia, Is the bone marrow is hypocellular(apirate)? | Yes
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| 173. In Waldenstrom’s Macroglobulinemia , the biopsy is hypercellular with lymphoid, plasma cells and mast cells? | Yes
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| 174. Is the formation of Rouleaux present on Waldenstrom’s Macroglobulinemia? | Yes
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| 175. In Waldenstrom’s Macroglobulinemia patients, how many % produce cryoglobulins? | 10%
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| 176. In Waldenstrom’s Macroglobulinemia, what does the lymphoplasmacytic cells express? | CD 19, CD 20, and CD 22
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| 177. How does Myeloma and Heavy Chain Disease differ? | These disease differ from myeloma due the production of M protein characterized only by portions of the heavy chain in the serum and urine.
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| 178. In Heavy Chain Disease, how are the Gamma HCD characterized? | By an M protein that contains on amino acid deletions and the CH1 domain
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| 179. What are the clinical manifestation of Heavy Chain Disease? | Severe anemia, coombs + anemia, hepatospleenomegaly and bone marrow(hypercellular)
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| 180. T/F. Alpha Heavy Chain Disease is the most common and occurs in Mediterranean region? | True
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| 181. What is Alpha Heavy Chain Disease most commonly present with? | GI disease mal-absorption, diarrhea, steatorrehea and weight loss.
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| 182. Is there a Pathology infiltration of the jejunum with plasma cells in Alpha Heavy Chain Disease? | True
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| 183. What is the diagnosis depend on in a patient of Alpha Heavy Chain Disease? | The identification alpha heavy chain
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| 184. Is Alpha Heavy Chain Disease a frequent, progressive and fatal disorder that responds to treatment with early diagnosis? | True
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| 185. What does the diagnosis of Mu Heavy Chain Disease depend on? | The detection of a mu heavy chain in the serum.
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| 186. What do the patients of Mu Heavy Chain Disease present with? | Chronic lymphocytic leukemia or lymphoma.
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| 187. Does a patients with Mu Heavy Chain Disease frequently present with? | Significant hypogammaglobulinemia
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| 188. In Cryglobinemia, what proteins are present? | Cryglobulins
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| 189. What are Cryglobulins? | Proteins that precipitate when cooled and dissolve with heat.
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| 190. How many types of patients are there? | Type 1 and Type 2
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| 191. How is Type 1 disease characterized? | By IgM and Ig G.
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| 192. Are 80% of the patients with Type 1 Cryoglobulin asymptomatic? | Yes
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| 193. What is the range in Type 1 patients with monoclonal cryoglobulins? | 1-2 dL
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| 194. What does a Type 1 patient Cryoglobulins present with? | pain, purpura, and ulceration of skin on exposure to cold
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| 195. What is a Type 1 patient Cryoglobulin associated with? | WMG,MM, and MGUS
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| 196. How are the characteristized of a Type 2 Cryoglobulin? | IgM and polyclonal IgG/A.
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| 197. What is Type 2 Cryoglobulins associated with? | Severe renal disease glomerular damage, vasculitis, and lymphoproliferative disease
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| 198. What are the Causes of Neutropenia? | Decreased production, peripheral destruction, peripheral pooling and hereditary
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| 199. How is the production decreased? | drug induced Hematologic disorders( aplastic anemia)
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| 200. What is peripheral destruction? | Autoimmune disorders
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| 201. What are the Hereditary disorders? | Kostmann’s Syndrome, Shachman’s Syndrome, cyclic neutropenia
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To hide a column, click on the column name.
To hide the entire table, click on the "Hide All" button.
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
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