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Hematology Q

1. What is Hematopoiesis? The process of the formed elements that are produced of blood.
2. How does the process of Hematopoiesis occur? The process occurs through a series of intricate steps that initiate with stem cell.
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
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.
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.
6. Where is RBC developed? Bone Marrow
7. How does a RBC live? About 120 days
8. Does RBC have a red cell precursor? Yes
9. What is the initial recognizable red cell precursor for RBC? pronormoblast
10. What will the pronormoblast cell undergo? This cell will undergo 4/5 division before, in result of production of 16-32 RBC
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.
12. What is Erythropoietin? A dalton glycoprotein hormone that is produced and released by the peritubular capillary linining of the kidney
13. Where is EPO produced? liver and kidney
14. What does EPO regulate? It governs the day to day production of RBC
15. What does EPO measure? The ambient level of the hormone
16. How is EPO measured? By very sensitive immunoassays
17. How is EPO production controlled? By the tissue availability of oxygen
18. What is the function of EPO? To bind to receptors on the marrow erythroid precursors
19. What can occur under the stimulus of EOP? Red cell production can increase 4-5 fold in one week time
20. What happens when hemoglobin falls below 10g per dl? a stimulus to enhance EPO production is initiated
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
22. What is the function of erythron? It depends on EPO and functional erythroid marrow, and adequate supply of nutrients for red cell production
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
24. What are the 3 major nutrients of RBC production? Iron, B12 and folate
25. What does Iron binds to? Iron binds to hemoglobin and facilitates the biological activity of EPO
26. What does Iron Deficiency cause? hypo-proliferative anemia
27. What causes megaloblastic anemias? Both folic and coblamin B12
28. What is the major role of Iron? To carry oxygen as part of the heme protein that turns into hemoglobin
29. What is Iron a critical element of? Iron is a critical element in the cytochrome system in mitochrondria
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
31. Where does the Iron absorbed from the diet circulate? In the plasma bound to transferin
32. What is a transferrin? It is a bi-lobed glycoprotein with two binding sites
33. Where is majority of the iron transported by transferring delivered? To the erythroid marrow
34. What is the clearance of tranferrin directly related to? marrow activity and plasma Fe
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
36. What has the greatest number of receptors? The developing erythroblast
37. Why is Iron made available upon interacting with the receptor? For heme synthesis
38. Where does excess of amounts of hemoglobin synthesis of Iron bind to? storage protein
39. How is ferritin formed? By a storage protein apoferritin
40. What occurs when apoferritin forms ferritin? It is binds with the excess Fe
41. Where else does Iron storage occur? In the liver
42. How does Iron incorporated into hemoglobin enter the circulation? As a new red blood cell that are released in the circulation
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
44. What is the life span of RBC? 120 days
45. What causes megaloblastic anemias? Impaired DNA synthesis
46. What kinds of cells are affected in megaloblastic anemia? Cells with rapid turnover – hemopoietic precusors and gastrointestinal epithelial cells
47. How are cells affected in megaloblastic anemia? Cells are larger with greater RNA to DNA ratio
48. What is the end result of megaloblastic anemias? The end result is ineffective erythropoesis
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
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
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
52. What does the right shift do? It decreases the oxygen affinity of hemoglobin thus increasing the requirement oxygen to obtain the same saturation.
53. What does the right shift enhance? The ability of hemoglobin to release oxygen into the tissues
54. Who has a higher oxygen affinity, adult hemoglobin or fetal hemoglobin? Fetal hemoglobin, which shifts the curve to the left
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
56. What is apparent at 6 weeks of fetal life? 3 hemoglobin variants appear that are subsequently transformed into fetal hemoglobin
57. When does fetal hemoglobin appear? At 10 weeks and persistent until 38 weeks after which adult hemoglobin is predominately synthesized
58. What causes Spleenic Sequestration Syndrome? Caused by engorgement of RBCs in un-infarcted spleen.
59. In who does SSS present in? children under 5 years of age.
60. If a child has a grossly enlarged spleen and profound anemia, what is possible? shock is possible
61. What is the first line of therapy? Immediate transfusion with packed RBC
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
63. What is structural hemoglobinopathies? A specific single amino acid defects in the Beta chain
64. What is Thalassemias? A defective biosynthesis of the globin chains
65. What hemaglobinopathies does no clinically present before six months of age? B chain hemaglobinopathies
66. What has a much higher oxygen affinity, Fetal Hemoglobin (gamma chain) or hemoglobin A? Fetal hemoglobin (gamma chain)
67. When does the gamma chain switch to B chain? 6 months of age
68. What can happen after 6 months of age? A child can begin to express one of the B chain hemoglobinopathies
69. What is B chain Hemoglobinopathies? The B chain hemaglobinopathies are inherited as autosomal recessive due to a single amino acid substitution.
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.
71. Does Sickle cell hemoglobin have a significantly decrease oxygen carrying capacity? Yes
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.
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
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
75. What are sickle RBC capable of? Obstructing capillaries resulting in a pathology of increased adhesion and local microinfarction
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
77. Is the process of microinfarction in sickle cell anemia patients progressive? Yes
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
79. When does the Hand Foot Syndrome occur? It occurs in the 1st two years of life
80. What does the Hand Foot Syndrome initiate? It initiates pain and swelling of the small tubular bones of the hand and feet.
81. What does a child with Hand Foot Syndrome present with? Child presents with swollen hands or the inability to walk
82. What is the treatment for Hand Foot Syndrome? Treatment with analagesics and fluid therapy is usually effective
83. What does pain crisis principally involve? Pain crises principally involve the long bones
84. Why does pain crisis occur? These crises are result of capillary obstruction by increased number sickled red blood cells
85. How are the pain crisis initiated? These crises are initiated by infection, dehydration and stress.
86. How are Pain Crisis treated? Pain crises are treated with hydration and pain management.
87. What causes Hypoplastic Crisis? These crises are caused by intercurrent viral infection in particular Parvo B19.
88. What does Parvo B19 initiate? red cell production at the level of the bone marrow
89. What does a patient with Hypoplastic Crisis present with? Patient present with fever, lethargy, occasionally gastroenteritis and pallor
90. What will a patient with Hypoplastic Crisis’ laboratory evaluation demonstrate? A fall in Hgb, Hct and reticulocyte count.
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
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
93. How is Chest Syndrome best diagnosed? Chest syndrome is best diagnosed by chest Xray( infiltrates) or more specifically with MRI
94. Are children with sickle cell disease more susceptible to strokes? Yes
95. Are patients with more malignant genotypes( Central African) more prone to the devastating complication of stroke and major infections? Yes
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
97. Should every child with sickle cell disease be monitored with transdermal Doppler yearly? Yes
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
99. What do children with sickle cell disease present with? pneumococcal sepsis, H. influenza disease and osteomyelitis due to salmonella
100. In hemoglobinopathies, what is critical for oxygen delivery? Hemoglobin
101. In hemoglobinopathies, what can happen to hemoglobin? Hemoglobin can alter the shape, deformability and viscosity of RBC
102. What are hemoglobinopathies? Disorders that affect the structure, function or production of hemoglobin
103. Where does neutrophils evolve from? Neutrophils evolve in the marrow from the myeloblast into a mature neutrophil
104. What does promyelocyte have? The promyelocyte has a large nucleus with the development of primary granules
105. What does a band form consist of? The Band form has condensed band shaped nucleus and is the analog to the reticulocyte
106. Is mature neutrophil is segmented? Yes
107. Where and how is neutrophils released? The neutrophil is released from the bone marrow by G-CSF, steroid, infection( endotoxin)
108. In what sort of pool does neutrophil circulate? Circulating pool
109. How are neutrophils induced to leave the circulating pool? By inflammatory mediators
110. How are neutrophils egressed from the circulation to the tissue? Adhesion molecules
111. The bone marrow represents how many pools? 3 dynamic pools
112. What are the three dynamic Marrow pools? Circulating Pool, Tissue Pool, and Marginal Pool
113. What is the marrow pool? The Marrow pool is the development and storage facility for neutrophil and its’ precursors
114. Where are the marrow pools? Normally 90% of the marrow pool is in the bone marrow
115. The circulating pool consists of two dynamic pools? Yes
116. What percent is the free flowing pool? Approximately 50%
117. What is marginal pool? The marginal pool are neutropils that are in close contact with the endothelium
118. How does Infection affect the marrow pools? Infection expands the circulating and marginal pools as well as tissue pool.
119. Does Infection expands the tissue pool? Yes
120. How does Epinephrine affect the marrow pools? It expands the circulating pool and Contracts the marginal pool
121. How does Steroid affect the marrow pools? Expands the marginated pool and the circulating pool
122. How does Leucocyte Adhesion Deficiency affect the marrow pools? It expands the Circulating Pool and contracts the Tissue Pool and Marginated Pool
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
124. How are each M protein characterized? Each M protein is characterized by two Heavy Chains and two Light Chains of the identical class.
125. How are the heavy chains designated? use Greek letter
126. How are the Light Chains designated? Either Kappa or Lambda.
127. Are Plasma Cell Disorder neoplastic? Plasma Cell Disorders are either neoplastic or potentially neoplastic
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.
129. How are plasma cell disorders characterized? These disorder are characterized by immunologically homogenous proteins(M).
130. What is the previous terminology for MGUS? Benign Monoclonal Gammapathy
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.
132. What is there a absence of in MGUS? lytic lesions, hypercalcemia, renal insufficiency and stablization of the M protein concentration.
133. How is Multiple Myeloma characterized? By the neoplastic proliferation of single clone of plasma cell engaged in the production a monoclonal immunoglobulin
134. In Multiple Myeloma, what is involved in the process? Involves bone marrow proliferation, with invasion of the adjacent bone.
135. What are the features of Multiple Myeloma? Anemia, hypercalcemia and renal insufficiency
136. What does the Multiple Myeloma represent? 1 % of all cancers and 10% of all hematologic cancers.
137. What is the incidence of Multiple Myeloma? The incidence is 4 per 100,000.
138. What is the average age of onset of Multiple Myeloma? 65 years.
139. Is Multiple Myeloma more common in men or female? It is more common( slightly in men)
140. In Multiple Myeloma, is the incidence 2X greater in African Americans? Yes
141. What is the clinical manifestation of Multiple Myeloma? bone pain that spares the patient during sleep, anemia, weakness and fatigue.
142. What is the most common physical finding? most common is pallor.
143. In Multiple Myeloma, what is present from an allergic stand point? generalized pruritis.
144. How is Multiple Myeloma caused? environmentally and hereditary
145. What is Multiple Myeloma linked to? To hydrocarbons and aliphatic chemical. Ex: Herbicides.
146. How is Multiple Myeloma linked to family clusters? Reported in first degree relative and in identical twins
147. What are the basic Immunology plasma cells? The plasma cell are cytoplasmic Ig+, CD38+, CD 138+, and PCA 1+
148. What does the smaller % of cells express? CD 10, HLADR
149. What does the 20% of cells express? CD 20.
150. Where does the premyeloma cell circulate? In the microenvironment of the marrow
151. What cells are reduced? CD4 + Tcell
152. What are the over produced myeloma? Il6, TNFa, Il-1B
153. What are the results of increased osteoclast activity? Lytic lesions, osteopenia, and hypercalcemia and fractures
154. How are the Osteoclast activated? By the transmembrane receptor RANK( receptor activator of nfkb)
155. What controls the osteoclast production? Receptor RANK
156. What is the newly discovered member of the TNf-R family? Oteoprotegerin OPG or receptor of activator of RANK.
157. How is Oteoprotegerin expressed? osteoclasts, macrophages and dendritic cell
158. What increases the receptor activator? Cytokines Il-6, TNfa and Il-1b
159. What increases osteoclast proliferation? Cytokines Il-6, TNfa and Il-1b
160. How is Oseosclerotic Myeloma (POEMS) characterized? by polyneuropathy, organomegaly, endocrinopathy, M protein and skin changes.
161. What is the clinical features of Oseosclerotic Myeloma (POEMS)? Chronic inflammatory demyelinating polyneuropathy, hepatomegaly, optic neuritis, gyneocomastia, testicular atrophy, and hyperpigmentation and hypertrichosis.
162. In Oseosclerotic Myeloma (POEMS), do the patients have elevated mu protein? Yes
163. In Oseosclerotic Myeloma (POEMS), the patient does not have bone marrow involvement, anemia, hypecalcemia? True
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.
165. What are the clinical manifestations of Waldenstrom’s Macroglobulinemia? weakness, fatigue, bleeding( oronasal), blurred vision , heart failure and recurrent infections.
166. In Waldenstrom’s Macroglobulinemia, there is no lytic lesions and renal involvement. True
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
168. What is the most common physical examination? Extensive pulmonary involvement
169. What is evident in the laboratory for Waldenstrom’s Macroglobulinemia? severe normocytic normochromic anemia.
170. What is evident in electrophoresis for Waldenstrom’s Macroglobulinemia? It reveals a tall narrow peak(g)mobility.
171. T/F. In Waldenstrom’s Macroglobulinemia 75% of Ig M has k light chains? True
172. In Waldenstrom’s Macroglobulinemia, Is the bone marrow is hypocellular(apirate)? Yes
173. In Waldenstrom’s Macroglobulinemia , the biopsy is hypercellular with lymphoid, plasma cells and mast cells? Yes
174. Is the formation of Rouleaux present on Waldenstrom’s Macroglobulinemia? Yes
175. In Waldenstrom’s Macroglobulinemia patients, how many % produce cryoglobulins? 10%
176. In Waldenstrom’s Macroglobulinemia, what does the lymphoplasmacytic cells express? CD 19, CD 20, and CD 22
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.
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
179. What are the clinical manifestation of Heavy Chain Disease? Severe anemia, coombs + anemia, hepatospleenomegaly and bone marrow(hypercellular)
180. T/F. Alpha Heavy Chain Disease is the most common and occurs in Mediterranean region? True
181. What is Alpha Heavy Chain Disease most commonly present with? GI disease mal-absorption, diarrhea, steatorrehea and weight loss.
182. Is there a Pathology infiltration of the jejunum with plasma cells in Alpha Heavy Chain Disease? True
183. What is the diagnosis depend on in a patient of Alpha Heavy Chain Disease? The identification alpha heavy chain
184. Is Alpha Heavy Chain Disease a frequent, progressive and fatal disorder that responds to treatment with early diagnosis? True
185. What does the diagnosis of Mu Heavy Chain Disease depend on? The detection of a mu heavy chain in the serum.
186. What do the patients of Mu Heavy Chain Disease present with? Chronic lymphocytic leukemia or lymphoma.
187. Does a patients with Mu Heavy Chain Disease frequently present with? Significant hypogammaglobulinemia
188. In Cryglobinemia, what proteins are present? Cryglobulins
189. What are Cryglobulins? Proteins that precipitate when cooled and dissolve with heat.
190. How many types of patients are there? Type 1 and Type 2
191. How is Type 1 disease characterized? By IgM and Ig G.
192. Are 80% of the patients with Type 1 Cryoglobulin asymptomatic? Yes
193. What is the range in Type 1 patients with monoclonal cryoglobulins? 1-2 dL
194. What does a Type 1 patient Cryoglobulins present with? pain, purpura, and ulceration of skin on exposure to cold
195. What is a Type 1 patient Cryoglobulin associated with? WMG,MM, and MGUS
196. How are the characteristized of a Type 2 Cryoglobulin? IgM and polyclonal IgG/A.
197. What is Type 2 Cryoglobulins associated with? Severe renal disease glomerular damage, vasculitis, and lymphoproliferative disease
198. What are the Causes of Neutropenia? Decreased production, peripheral destruction, peripheral pooling and hereditary
199. How is the production decreased? drug induced Hematologic disorders( aplastic anemia)
200. What is peripheral destruction? Autoimmune disorders
201. What are the Hereditary disorders? Kostmann’s Syndrome, Shachman’s Syndrome, cyclic neutropenia
Created by: sap_213