Hematology Q
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| show | The process of the formed elements that are produced of blood.
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| 2. How does the process of Hematopoiesis occur? | show 🗑
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| 3. What does the stem cell produce? | show 🗑
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| 4. Where does hematopoiesis occur? | show 🗑
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| show | 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? | show 🗑
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| show | About 120 days
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| show | Yes
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| show | pronormoblast
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| 10. What will the pronormoblast cell undergo? | show 🗑
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| 11. Along with the division, what else occurs with the pronormoblast? | show 🗑
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| 12. What is Erythropoietin? | show 🗑
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| show | liver and kidney
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| 14. What does EPO regulate? | show 🗑
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| show | The ambient level of the hormone
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| 16. How is EPO measured? | show 🗑
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| show | By the tissue availability of oxygen
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| show | To bind to receptors on the marrow erythroid precursors
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| 19. What can occur under the stimulus of EOP? | show 🗑
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| show | a stimulus to enhance EPO production is initiated
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| 21. What is a erythron? | show 🗑
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| 22. What is the function of erythron? | show 🗑
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| show | 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? | show 🗑
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| show | Iron binds to hemoglobin and facilitates the biological activity of EPO
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| show | hypo-proliferative anemia
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| 27. What causes megaloblastic anemias? | show 🗑
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| 28. What is the major role of Iron? | show 🗑
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| show | Iron is a critical element in the cytochrome system in mitochrondria
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| show | Sans iron cells lose their capacity for electron transport and hemoglobin synthesis is impaired
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| show | In the plasma bound to transferin
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| 32. What is a transferrin? | show 🗑
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| show | To the erythroid marrow
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| show | marrow activity and plasma Fe
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| show | 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? | show 🗑
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| show | For heme synthesis
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| 38. Where does excess of amounts of hemoglobin synthesis of Iron bind to? | show 🗑
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| show | By a storage protein apoferritin
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| 40. What occurs when apoferritin forms ferritin? | show 🗑
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| 41. Where else does Iron storage occur? | show 🗑
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| 42. How does Iron incorporated into hemoglobin enter the circulation? | show 🗑
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| show | Becomes a part of red cell mass and cannot be re-utilized until red cell dies
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| show | 120 days
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| show | Impaired DNA synthesis
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| show | Cells with rapid turnover – hemopoietic precusors and gastrointestinal epithelial cells
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| show | Cells are larger with greater RNA to DNA ratio
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| show | The end result is ineffective erythropoesis
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| 49. What does Hemoglobin Oxygen Dissociation Curve do? | show 🗑
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| show | 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? | show 🗑
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| 52. What does the right shift do? | show 🗑
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| 53. What does the right shift enhance? | show 🗑
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| 54. Who has a higher oxygen affinity, adult hemoglobin or fetal hemoglobin? | show 🗑
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| 55. What does the fetal hemaglobin physiological ability to shift the curve to the left mean? | show 🗑
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| 56. What is apparent at 6 weeks of fetal life? | show 🗑
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| show | At 10 weeks and persistent until 38 weeks after which adult hemoglobin is predominately synthesized
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| show | Caused by engorgement of RBCs in un-infarcted spleen.
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| show | children under 5 years of age.
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| show | shock is possible
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| 61. What is the first line of therapy? | show 🗑
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| 62. What are the Classification of Hemoglobinopathies? | show 🗑
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| show | A specific single amino acid defects in the Beta chain
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| show | A defective biosynthesis of the globin chains
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| show | B chain hemaglobinopathies
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| 66. What has a much higher oxygen affinity, Fetal Hemoglobin (gamma chain) or hemoglobin A? | show 🗑
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| 67. When does the gamma chain switch to B chain? | show 🗑
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| show | A child can begin to express one of the B chain hemoglobinopathies
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| 69. What is B chain Hemoglobinopathies? | show 🗑
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| show | 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? | show 🗑
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| show | 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? | show 🗑
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| 74. What does chronic hemolytic anemia result in a sickle cell anemia patient? | show 🗑
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| 75. What are sickle RBC capable of? | show 🗑
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| 76. What does the process of microinfarction in sickle cell anemia patients involve? | show 🗑
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| show | Yes
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| show | 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? | show 🗑
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| 80. What does the Hand Foot Syndrome initiate? | show 🗑
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| 81. What does a child with Hand Foot Syndrome present with? | show 🗑
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| show | Treatment with analagesics and fluid therapy is usually effective
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| show | Pain crises principally involve the long bones
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| 84. Why does pain crisis occur? | show 🗑
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| 85. How are the pain crisis initiated? | show 🗑
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| show | Pain crises are treated with hydration and pain management.
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| show | These crises are caused by intercurrent viral infection in particular Parvo B19.
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| 88. What does Parvo B19 initiate? | show 🗑
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| 89. What does a patient with Hypoplastic Crisis present with? | show 🗑
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| show | A fall in Hgb, Hct and reticulocyte count.
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| 91. What is the cause of Chest Syndrome? | show 🗑
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| show | Children with chest syndrome present with acute chest pain, dyspnea, tachypnea, pallor and occasionally cyanosis
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| show | Chest syndrome is best diagnosed by chest Xray( infiltrates) or more specifically with MRI
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| show | 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? | show 🗑
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| show | Yes
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| 97. Should every child with sickle cell disease be monitored with transdermal Doppler yearly? | show 🗑
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| show | 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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| show | pneumococcal sepsis, H. influenza disease and osteomyelitis due to salmonella
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| show | Hemoglobin
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| 101. In hemoglobinopathies, what can happen to hemoglobin? | show 🗑
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| 102. What are hemoglobinopathies? | show 🗑
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| show | Neutrophils evolve in the marrow from the myeloblast into a mature neutrophil
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| 104. What does promyelocyte have? | show 🗑
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| 105. What does a band form consist of? | show 🗑
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| show | Yes
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| show | The neutrophil is released from the bone marrow by G-CSF, steroid, infection( endotoxin)
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| show | Circulating pool
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| show | By inflammatory mediators
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| 110. How are neutrophils egressed from the circulation to the tissue? | show 🗑
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| 111. The bone marrow represents how many pools? | show 🗑
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| 112. What are the three dynamic Marrow pools? | show 🗑
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| 113. What is the marrow pool? | show 🗑
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| 114. Where are the marrow pools? | show 🗑
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| show | Yes
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| 116. What percent is the free flowing pool? | show 🗑
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| 117. What is marginal pool? | show 🗑
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| show | Infection expands the circulating and marginal pools as well as tissue pool.
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| 119. Does Infection expands the tissue pool? | show 🗑
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| 120. How does Epinephrine affect the marrow pools? | show 🗑
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| 121. How does Steroid affect the marrow pools? | show 🗑
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| 122. How does Leucocyte Adhesion Deficiency affect the marrow pools? | show 🗑
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| 123. What are the Plasma Cell disorders? | show 🗑
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| show | 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? | show 🗑
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| show | Either Kappa or Lambda.
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| 127. Are Plasma Cell Disorder neoplastic? | show 🗑
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| 128. What are plasma cell disorders associated with? | show 🗑
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| show | These disorder are characterized by immunologically homogenous proteins(M).
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| 130. What is the previous terminology for MGUS? | show 🗑
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| 131. How is MGUS defined? | show 🗑
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| 132. What is there a absence of in MGUS? | show 🗑
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| show | 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? | show 🗑
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| 135. What are the features of Multiple Myeloma? | show 🗑
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| show | % of all cancers and 10% of all hematologic cancers.
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| 137. What is the incidence of Multiple Myeloma? | show 🗑
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| 138. What is the average age of onset of Multiple Myeloma? | show 🗑
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| show | It is more common( slightly in men)
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| 140. In Multiple Myeloma, is the incidence 2X greater in African Americans? | show 🗑
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| 141. What is the clinical manifestation of Multiple Myeloma? | show 🗑
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| show | most common is pallor.
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| show | generalized pruritis.
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| show | environmentally and hereditary
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| 145. What is Multiple Myeloma linked to? | show 🗑
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| show | Reported in first degree relative and in identical twins
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| 147. What are the basic Immunology plasma cells? | show 🗑
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| show | CD 10, HLADR
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| show | CD 20.
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| show | In the microenvironment of the marrow
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| 151. What cells are reduced? | show 🗑
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| 152. What are the over produced myeloma? | show 🗑
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| 153. What are the results of increased osteoclast activity? | show 🗑
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| show | By the transmembrane receptor RANK( receptor activator of nfkb)
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| show | Receptor RANK
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| show | Oteoprotegerin OPG or receptor of activator of RANK.
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| show | osteoclasts, macrophages and dendritic cell
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| show | Cytokines Il-6, TNfa and Il-1b
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| 159. What increases osteoclast proliferation? | show 🗑
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| 160. How is Oseosclerotic Myeloma (POEMS) characterized? | show 🗑
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| show | 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? | show 🗑
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| show | True
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| show | 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? | show 🗑
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| 166. In Waldenstrom’s Macroglobulinemia, there is no lytic lesions and renal involvement. | show 🗑
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| 167. What are the physical examination of Waldenstrom’s Macroglobulinemia? | show 🗑
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| show | Extensive pulmonary involvement
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| show | severe normocytic normochromic anemia.
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| 170. What is evident in electrophoresis for Waldenstrom’s Macroglobulinemia? | show 🗑
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| show | True
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| 172. In Waldenstrom’s Macroglobulinemia, Is the bone marrow is hypocellular(apirate)? | show 🗑
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| show | Yes
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| show | Yes
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| 175. In Waldenstrom’s Macroglobulinemia patients, how many % produce cryoglobulins? | show 🗑
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| 176. In Waldenstrom’s Macroglobulinemia, what does the lymphoplasmacytic cells express? | show 🗑
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| show | 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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| show | By an M protein that contains on amino acid deletions and the CH1 domain
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| show | Severe anemia, coombs + anemia, hepatospleenomegaly and bone marrow(hypercellular)
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| show | True
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| show | GI disease mal-absorption, diarrhea, steatorrehea and weight loss.
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| show | True
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| show | The identification alpha heavy chain
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| show | True
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| show | The detection of a mu heavy chain in the serum.
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| show | Chronic lymphocytic leukemia or lymphoma.
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| 187. Does a patients with Mu Heavy Chain Disease frequently present with? | show 🗑
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| show | Cryglobulins
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| show | Proteins that precipitate when cooled and dissolve with heat.
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| 190. How many types of patients are there? | show 🗑
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| show | By IgM and Ig G.
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| show | Yes
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| show | 1-2 dL
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| 194. What does a Type 1 patient Cryoglobulins present with? | show 🗑
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| 195. What is a Type 1 patient Cryoglobulin associated with? | show 🗑
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| 196. How are the characteristized of a Type 2 Cryoglobulin? | show 🗑
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| show | Severe renal disease glomerular damage, vasculitis, and lymphoproliferative disease
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| show | Decreased production, peripheral destruction, peripheral pooling and hereditary
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| 199. How is the production decreased? | show 🗑
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| show | Autoimmune disorders
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| show | Kostmann’s Syndrome, Shachman’s Syndrome, cyclic neutropenia
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