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Unit 2 Exam Review

Josefina Gonzalez Immunology Freshmen Englisch 199 Karten

Karten in diesem Stapel (199)

  1. 1THE SITE OF HEMATOPOIESIS IN THE FIRST MONTH OF GESTATION IS THE?YOLK SAC
  2. 2THE PRINCIPAL TYPE OF LYMPHOCYTE IN THE PROCESS OF PHAGOCYTOSIS IS THE?NEUTROPHIL
  3. 3CHRONIC GRANULOMATOUS DISEASE REPRESENTS A DEFECT OF?OXIDATIVE METABOLISM
  4. 4A PRIMARY FUNCTION OF THE EOSINOPHIL IS?SUPPRESSION OF THE INFLAMMATORY RESPONSE
  5. 5THE CELLS OF THE MONONUCLEAR PHAGOCYTE SYSTEM INCLUDE?BOTH A AND B: MONOCYTES, PROMONOCYTES, AND MACROPHAGES
  6. 6THE HOST DEFENSE FUNCTION OF MONOCYTES-MACROPHAGES INCLUDE?ALL OF THE ABOVE: ANTIGEN PRESENTATION , PHAGOCYTOSIS, AND SECRETION OF BIOLOGICALLY ACTIVE MOLECULES
  7. 7THE SURFACE MHC CLASS 2 GENE PRODUCT IS IMPORTANT IN?ANTIGEN RECOGNITION BY T LYMPHOCYTES
  8. 8WHAT IS THE APPROPRIATE MONOCYTE-MACROPHAGE ABNORMALITY ASSOCIATED WITH WISKOTT-ALDRICH SYNDROME?DEFECTIVE MONOCYTE CYTOTOXICITY
  9. 9WHAT IS THE APPROPRIATE MONOCYTE-MACROPHAGE ABNORMALITY ASSOCIATED WITH BURNS OR DIABETES?DEPRESSED MIGRATION
  10. 10WHAT IS THE APPROPRIATE MONOCYTE-MACROPHAGE ABNORMALITY ASSOCIATED WITH SYSTEMIC LUPUS ERYTHEMATOSUS?IMPAIRED PHAGOCYTOSIS
  11. 11WHAT IS THE APPROPRIATE MONOCYTE-MACROPHAGE ABNORMALITY ASSOCIATED WITH CORTICOSTEROID THERAPY?DEFECT IN PHAGOCYTIC KILLING
  12. 12WHAT IS THE APPROPRIATE MONOCYTE-MACROPHAGE ABNORMALITY ASSOCIATED WITH INTRACELLULAR INFECTIONS?DEFECTIVE RELEASE OF MACROPHAGE-ACTIVATING FACTORS
  13. 13ARRANGE THE STEPS OF PHAGOCYTOSIS IN ORDER?INCREASE IN CHEMOATTRACTANTS AT SITE OF TISSUE DAMAGE - MOVEMENT OF PHAGOCYTIC CELLS - INGESTION OF BACTERIA - DIGESTION OF BACTERIA
  14. 14WHAT IS THE FUNCTION OF POLYMORPHONUCLEAR NEUTROPHIL LEUKOCYTES (PMN)?PRIMARY PHAGOCYTIC CELLS
  15. 15WHAT IS THE FUNCTION OF LYMPHOCYTES?RECOGNITION OF FOREIGN ANTIGEN AND PRODUCTION OF ANTIBODY
  16. 16WHAT IS THE FUNCTION OF MONONUCLEAR MONOCYTES-MACROPHAGES?PRIMARY PHAGOCYTIC CELLS
  17. 17WHAT IS THE FUNCTION OF PLASMA CELLS?ANTIBODY-SYNTHESIZING CELLS
  18. 18WHAT IS THE SITE OF INITIAL RBC PRODUCTION IN A FETUS/EMBRYO?YOLK SAC
  19. 19WHAT IS THE PREDOMINANT SITE FOR HEMATOPOIESIS FROM 2-5 MONTHS OF FETAL LIFE?LIVER AND SPLEEN
  20. 20WHAT IS THE ULTIMATE SITE OF PRIMARY HEMATOPOIESIS?BONE MARROW
  21. 21PATIENTS WITH A MARKED DECREASE IN NEUTROPHILS OR SEVERE DEFECTS IN NEUTROPHIL FUNCTION HAVE?ALL OF THE ABOVE: A HIGH RATE OF INFECTION, RECURRENT SYSTEMIC BACTERIAL INFECTIONS, RECURRENT LIFE-THREATENING FUNGAL INFECTIONS
  22. 22WHAT ARE THE CHARACTERISTICS OF CHRONIC GRANULOMATOSUS DISEASE?FAILURE TO EXHIBIT INCREASED ANAEROBIC METABOLISM DURING PHAGOCYTOSIS
  23. 23WHAT ARE THE CHARACTERISTICS OF LAZY LEUKOCYTE SYNDROME?DEFECTIVE LEUKOCYTE LOCOMOTION
  24. 24WHAT ARE THE CHARACTERISTICS OF CHEDIAK-HIGASHI ANOMALY (SYNDROME)?MARKED DEFECT IN CELLULAR RESPONSE TO CHEMOTAXIS
  25. 25WHAT ARE THE CHARACTERISTICS OF MYELOPEROXIDASE DEFICIENCY?MILD OR MARKED DEFECT IN BACTERICIDAL ABILITY OF NEUTROPHILS
  26. 26T/F: EOSINOPHILS PARTICIPATE IN HYPERSENSITIVITY REACTIONS?FALSE
  27. 27T/F: BASOPHILS REACT WITH TWO ADJACENT IgA MOLECULES ON MAST CELLSFALSE
  28. 28THE CELLS THAT CONSTITUTE THE PHYSIOLOGIC, MONONUCLEAR PHAGOCYTE SYSTEM DO NOT INCLUDE?POLYMORPHONUCLEAR NEUTROPHILS
  29. 29WHAT MONONUCLEAR PHAGOCYTIC CELL IS FOUND IN THE BRAIN REGION?MICROGLIAL CELLS
  30. 30WHAT MONONUCLEAR PHAGOCYTIC CELL IS FOUND IN THE NECK REGION?MACROPHAGES
  31. 31WHAT MONONUCLEAR PHAGOCYTIC CELL IS FOUND IN THE LIVER REGION?MACROPHAGES AND KUPFFER CELLS
  32. 32WHAT MONONUCLEAR PHAGOCYTIC CELL IS FOUND IN THE INTESTINAL REGION?HISTIOCYTES (TISSUE MACROPHAGES)
  33. 33WHAT IS THE PROCESS OF PHAGOCYTOSIS?CHEMOTAXIS - ADHERENCE - ENGULFMENT - PHAGOSOME FORMATION - FUSION - DIGESTION AND DESTRUCTION
  34. 34A FUNCTION OF THE CELL-MEDIATED IMMUNE RESPONSE NOT ASSOCIATED WITH HUMORAL IMMUNITY IS?INITIATION OF REJECTION OF FOREIGN TISSUES AND TUMORS
  35. 35THE PRIMARY OR CENTRAL LYMPHOID ORGANS IN HUMANS ARE THE?BONE MARROW AND/OR FETAL LIVER AND THYMUS
  36. 36T/F: SYNTHESIS OF ANTIBODY IS A FUNCTION OF T CELLS?FALSE
  37. 37WHAT IS THE FUNCTION OF T CELLS?CELLULAR IMMUNE RESPONSE
  38. 38WHAT IS THE FUNCTION OF B CELLS?HUMORAL RESPONSE
  39. 39WHAT IS THE FUNCTION OF K-TYPE LYMPHOCYTES?ANTIBODY-DEPENDENT, CELL-MEDIATED CYTOTOXICITY (ADCC) REACTION
  40. 40WHAT IS THE FUNCTION OF NATURAL KILLER (NK) CELLS?CYTOTOXIC REACTION
  41. 41WHAT SURFACE MEMBRANE MARKER IS ASSOCIATED WITH ALL OR MOST T LYMPHOCYTES?CD3
  42. 42WHAT SURFACE MEMBRANE MARKER IS ASSOCIATED WITH HELPER-INDUCER T CELLS?CD4
  43. 43WHAT SURFACE MEMBRANE MARKER IS ASSOCIATED WITH SUPPRESSOR-CYTOTOXIC T CELLS?CD8
  44. 44T/F: CD4 IS A B CELL SURFACE MEMBRANE MARKER?FALSE
  45. 45WHICH MAJOR TYPE OF LYMPHOCYTE IS AFFECTED BY THYMIC HYPOPLASIA? CONGENITAL OR ACQUIRED?CONGENITAL T CELL DISORDER
  46. 46WHICH MAJOR TYPE OF LYMPHOCYTE IS AFFECTED BY AIDS? CONGENITAL OR ACQUIRED?ACQUIRED T CELL DISORDER
  47. 47WHICH MAJOR TYPE OF LYMPHOCYTE IS AFFECTED BY CHRONIC LYMPHOCYTIC LEUKEMIA? CONGENITAL OR ACQUIRED?ACQUIRED T CELL DISORDER
  48. 48WHICH MAJOR TYPE OF LYMPHOCYTE IS AFFECTED BY SYSTEMIC LUPUS ERYTHEMATOSUS? CONGENITAL OR ACQUIRED?ACQUIRED T CELL DISORDER
  49. 49WHICH MAJOR TYPE OF LYMPHOCYTE IS AFFECTED BY MULTIPLE MYELOMA? CONGENITAL OR ACQUIRED?AQUIRED B CELL DISORDER
  50. 50WHICH MAJOR TYPE OF LYMPHOCYTE IS AFFECTED BY BRUTONS AGAMMAGLOBULINEMIA? CONGENITAL OR ACQUIRED?CONGENITAL B CELL DISORDER
  51. 51MOST DISEASES ASSOCIATED WITH A PRIMARY DEFECT ARE ___ DISORDERS?B CELL
  52. 52SEVERE COMBINED IMMUNODEFICIENCY IS CAUSED BY?INAPPROPRIATE DEVELOPMENT OF STEM CELLS
  53. 53DIGEORGES SYNDROME IS CAUSED BY?FAULTY EMBRYOGENESIS
  54. 54THE MAJOR CLINICAL MANIFESTATION OF A B CELL DEFICIENCY IS?INCREASED SUSCEPTIBILITY TO BACTERIAL INFECTIONS
  55. 55BRUTONS AGAMMAGLOBULINEMIA IS A?SEX-LINKED GENETIC DISORDER
  56. 56DOES POISON IVY HYPERSENSITIVITY RESULT IN A SECONDARY IMMUNODEFICIENCY?NO
  57. 57THE SECONDARY LYMPHOID TISSUES IN MAMMALS ARE?BOTH B AND C: LYMPH NODES AND SPLEEN
  58. 58IN MAMMALIAN IMMUNOLOGIC DEVELOPMENT, THE PRECURSORS OF LYMPHOCYTES ARISE FROM PROGENITOR CELLS OF THE?BOTH B AND C: LYMPH NODES AND SPLEEN
  59. 59THE THYMUS IS EMBRYOLOGICALLY DERIVED FROM THE?PHARYNGEAL POUCHES
  60. 60WHAT ARE THE SITES OF SECONDARY TISSUE ON THE BODY?SPLEEN, LYMPH NODES, AND PEYERS PATCHES (INTESTINES)
  61. 61THE PROCESS OF AGING CAUSES THE THYMUS TO?BOTH A AND C: DECREASE IN SIZE AND LOSE CELLULARITY
  62. 62T LYMPHOCYTES CAN ALSO BE REFERRED TO AS?MEMORY CELLS
  63. 63T/F: T LYMPHOCYTES CAN SYNTHESIZE AND SECRETE IMMUNOGLOBULIN?FALSE
  64. 64WHICH CELLS FUNCTION TO SECRETE A VARIETY OF CYTOKINES?HELPER OR REGULATOR T CELLS
  65. 65WHICH CELLS FUNCITON TO RECOGNIZE ANTIGENS ASSOCIATED WITH MHC CLASS 1?CYTOTOXIC OR EFFECTOR T CELLS
  66. 66WHICH CELLS FUNCTION TO INHIBIT RESPONSE OF HELPER T CELLS?SUPPRESSOR T CELLS
  67. 67NATURAL KILLER CELLS DO WHAT?ALL OF THE ABOVE: PRODUCE INTERFERON, PRODUCE IL-2, AND WERE PREVIOUSLY CALLED NULL CELLS
  68. 68K-TYPE CELLS DO WHAT?DESTROY BY CYTOTOXIC REACTION
  69. 69WHICH TESTS ARE USED TO EVALUATE ALL SUSPECTED IMMUNODEFICIENCIES?ESR, CBC WITH PLATELET EVALUATION
  70. 70WHICH TESTS ARE USED TO EVALUATE ANTIBODY DEFICIENCY?SCREENING FOR ANTI-A AND ANTI-B ISOAGGLUTININS, SCREENING FOR ANTIBODIES TO DIPHTHERIA OR TETANUS TOXOIDS
  71. 71WHICH TESTS ARE USED TO EVALUATE T CELL DEFICIENCY?ABSOLUTE LYMPHOCYTE COUNT, INTRADERMAL SKIN TEST
  72. 72WHICH TESTS ARE USED TO EVALUATE PHAGOCYTIC CELL DEFICIENCY?ABSOLUTE NEUTROPHIL COUNT
  73. 73WHAT % OF IMMUNODEFICIENCIES DO T CELL DISORDERS ACCOUNT FOR?7%
  74. 74WHAT % OF IMMUNODEFICIENCIES DO B CELL DISORDERS ACCOUNT FOR?53%
  75. 75WHAT % OF IMMUNODEFICIENCIES DO SEVERE COMBINED IMMUNODEFICIENCIES (SCIDS) ACCOUNT FOR?23%
  76. 76WHAT % OF IMMUNODEFICIENCIES DO DISORDERS OF PHAGOCYTOSIS ACCOUNT FOR?14%
  77. 77THE COMPLEMENT SYSTEM IS?ALL OF THE ABOVE: A HEAT-LIABLE SERIES OF PLASMA PROTEINS, COMPOSED OF MANY PROTEINASES, AND COMPOSED OF THREE INTERRELATED PATHWAYS
  78. 78T/F: CD3 IS A COMPLEMENT CONTROLLING PROTEIN?FALSE
  79. 79THE THREE COMPLEMENT ACTIVATION PATHWAYS CONVERGE AT THE POINT OF CLEAVAGE OF COMPLEMENT COMPONENT ___?CD3
  80. 80T/F: DECREASED CELL SUSCEPTIBILITY TO PHAGOCYTOSIS RESULTS FROM COMPLEMENT ACTIVATION?FALSE
  81. 81WHAT IS THE ACTIVATION SEQUENCE OF THE CLASSIC COMPLEMENT PATHWAY?C1 - C4 - C2 - C3 - C5 - C6 - C7 - C8 - C9
  82. 82WHAT COMPLEMENT COMPONENT IS PRESENT IN THE GREATEST QUANTITY IN PLASMA?C3
  83. 83WHAT IS THE CORRECT ORDER OF SEQUENCE OF THE CLASSIC COMPLEMENT PATHWAY?RECOGNITION - ENZYMATIC ACTIVATION - MEMBRANE ATTACK
  84. 84T/F: FIXATION OF THE C1 COMPLEMENT COMPONENT IS RELATED TO THE MOLECULAR WEIGHT OF THE ANTIBODY?FALSE
  85. 85AT WHICH STAGE DOES THE COMPLEMENT SYSTEM REACH ITS FULL AMPLITUDE?C3
  86. 86THE FINAL STAGES (C8 AND C9) IN COMPLEMENT ACTIVATION LEAD TO?CELL LYSIS
  87. 87WHICH PATHWAY IS ACTIVATED BY ANTIGEN-ANTIBODY COMPLEXES?CLASSIC PATHWAY
  88. 88WHICH PATHWAY GENERATES AN ACTIVE (C3b, Bb) C3 CONVERTASE AND IS ACTIVATED BY MICROBIAL AND MAMMALIAN CELL SURFACES?ALTERNATIVE PATHWAY
  89. 89WHICH PATHWAY TERMINATES IN A MEMBRANE ATTACK COMPLEX?CLASSIC AND ALTERNATIVE PATHWAYS
  90. 90THE ALTERNATIVE COMPLEMENT PATHWAY IS?BOTH B AND C: PREDOMINANTLY A NON-ANTIBODY-INITIATED PATHWAY AND IS ACTIVATED BY FACTORS SUCH AS ENDOTOXINS
  91. 91WHICH CONDITION CAN BE ASSOCIATED WITH HYPERCOMPLEMENTEMIA?MYOCARDIAL INFARCTION
  92. 92WHICH DEFICIENT COMPONENT IS ASSOCIATED WITH XERODERMA PIGMENTOSA?C8
  93. 93WHICH DEFICIENT COMPONENT IS ASSOCIATED WITH LEINERS DISEASE?C5 DYSFUNCTION
  94. 94WHICH DEFICIENT COMPONENT IS ASSOCIATED WITH RAYNAUDS PHENOMENON?C6 AND C7
  95. 95WHICH DEFICIENT COMPONENT IS ASSOCIATED WITH RECURRENT PYROGENIC INFECTIONS?C2
  96. 96A NONSPECIFIC COMPONENT OF THE IMMUNE SYSTEM IS?BOTH A AND B: COMPLEMENT AND T CELLS
  97. 97T CELL GROWTH FACTOR IS THIS IL AND IT ENHANCES CYTOLYTIC ACTIVITY OF LYMPHOKINE-ACTIVATED KILLER CELLS (LAK)?IL-2
  98. 98LYMPHOCYTE-ACTIVATING FACTOR IS THIS IL AND IT IS A POTENT MEDIATOR IN ACUTE-PHASE RESPONSE?IL-1
  99. 99B CELL GROWTH FACTOR 2 IS AND ACTIVATES EOSINOPHILS??IL-5
  100. 100MULTICOLONY COLONY-STIMULATING FACTOR IS WHICH IL AND IT STIMULATES HEMATOPOIETIC CELLS?IL-3
  101. 101NK CELL STIMULATORY FACTOR IS AND IT ENHANCES THE ACTIVITY OF CYTOTOXIC EFFECTOR T CELLS?IL-12
  102. 102WHICH IL STIMULATES NEUTROPHILS IN CHEMOTAXIS AND STIMULATES EARLY B CELL PROGENITOR CELLS?IL-8
  103. 103WHICH IL INDUCES ACUTE PHASE RESPONSE AND INDUCES THE SECRETION OF Ig?IL-6
  104. 104WHICH IL STIMULATES EXPANSION OF IMMATURE T AND B CELLS AND ACTIVATES THE RESPIRATORY BURST?IL-7
  105. 105WHICH IL ENHANCES PRODUCTION OF IgG ND INHIBITS PRODUCTION OF IgE BY ACTIVATED B CELLS?IL-4
  106. 106WHICH IL INHIBITS CYTOKINE SYNTHESIS?IL-10
  107. 107WHICH IL INCREASES THE NUMBER OF IgG-SECRETING B LYMPHOCYTES?IL-11
  108. 108WHICH IL STIMULATES PROLIFERATION OF T CELLS AND MAST CELLS?IL-9
  109. 109WHICH IL INHIBITS ACTIVATION OF MACROPHAGES?IL-13
  110. 110WHICH IL IS PRODUCED IN RESPONSE TO VIRAL INFECTION?IL-15
  111. 111WHICH IL ACTS AS A T CELL CHEMOATTRACTANT?IL-16
  112. 112WHICH IL ACTS AS A B CELL GROWTH FACTOR?IL-14
  113. 113WHICH IL ACTS AS A SYNERGIST WITH IL-12?IL-18
  114. 114WHICH IL SUPPRESSES ACTIVITIES OF Th1 AND Th2?IL-19
  115. 115WHICH IL IS ASSOCIATED WITH SKIN INFLAMMATION?IL-20
  116. 116WHICH IL INDUCES GRANULOPOIESIS?IL-17
  117. 117WHICH IL PROMOTES INCREASED PRODUCTION OF T CELLS?IL-21
  118. 118WHICH IL IS SOMEWHAT SIMILAR TO IFN-a, IFN-b, AND IFN-y?IL-22
  119. 119WHICH IL IS A MEMBER OF THE IL-17 CYTOKINE FAMILY?IL-25
  120. 120WHICH IL SHARES SOME IN VIVO FUNCTIONS WITH IL-12?IL-23
  121. 121T/F: CYTOKINES SECRETED BY LYMPHOCYTES ARE ALSO CALLED LYMPHOKINES?TRUE
  122. 122T/F: CYTOKINES ARE POLYPEPTIDE PRODUCTS OF ACTIVATED CELLS.TRUE
  123. 123T/F: CYTOKINES ARE RELEASED ONLY IN RESPONSE TO SPECIFIC ANTIGENS.FALSE
  124. 124T/F: MOST CYTOKINES HAVE MULTIPLE ACTIVITIES AND ACT ON NUMEROUS CELL TYPES.TRUE
  125. 125WHAT IS UNABLE TO STIMULATE T CELL PROLIFERATION?TUMOR NECROSIS FACTOR
  126. 126WHAT ACTS BETWEEN LEUKOCYTES?INTERLEUKINS
  127. 127WHAT WAS DISCOVERED IN VIRALLY INFECTED CELLS?INTERFERONS
  128. 128WHAT PROVIDES A LINK BETWEEN THE LYMPHOID HEMATOPOIETIC SYSTEM?COLONY-STIMULATING FACTORS
  129. 129TRANSFORMING GROWTH FACTORS?ALL OF THE ABOVE: ARE PRODUCTS OF VIRALLY TRANSFORMED CELLS, CAN BE A POTENT INHIBITOR OF IL-1-INDUCED T CELL PROLIFERATION IN THEIR BETA FORM, AND ARE IMPORTANT IN INFLAMMATION, TUMOR DEFENSE, AND CELL GROWTH
  130. 130WHICH ACTIVITY IS ASSOCIATED WITH INTERFERON?INTERFERES WITH VIRAL REPLICATION
  131. 131TUMOR NECROSIS FACTOR (TNF) DIFFERS FROM IL-1 IN THAT TNF IS NOT ABLE TO?STIMULATE T CELL PROLIFERATION
  132. 132WHAT STIMULATES HEMATOPOIETIC GROWTH FACTOR?COLONY-STIMULATING FACTORS
  133. 133WHAT IS THE ENCODING GENE LOCATED IN THE HLA REGION BETWEEN THE HLA-DR AND HLA-B LOCITUMOR NECROSIS FACTOR
  134. 134WHAT INDUCES PHENOTYPIC TRANSFORMATION IN NON-NEOPLASTIC CELLSTRANSFORMING GROWTH FACTORS
  135. 135T/F: THE QUALITY OF TEST RESULTS IN AN AGGLUTINATION REACTION DEPENDS ON WHETHER THE CARRIER IS ARTIFICIAL OR BIOLOGICAL.FALSE
  136. 136FLOCCULATION PROCEDURES DIFFER FROM LATEX AGGLUTINATION PROCEDURES BECAUSE?SOLUBLE ANTIGEN REACTS WITH ANTIBODY
  137. 137IN A HEMAGGLUTINATION TECHNIQUE, ANTIHUMAN GLOBULIN IS USED AS AN ENHANCEMENT MEDIUM TO DETECT ___?IgM
  138. 138THE PROZONE PHENOMENON CAN RESULT IN A?FALSE-NEGATIVE REACTION
  139. 139THE EFFECT OF COMPETING ANTIBODIES SEEKING TO ATTACH TO ANTIGEN SITES IS CALLED?STERIC HINDRANCE
  140. 140THIS METHOD CAN NOT BE USED TO ENHANCE THE AGGLUTINATION OF IgG ANTIBODIES?ACIDIFYING THE MIXTURE
  141. 141ALL THE ERYTHROCYTES ARE COMBINED INTO ONE SOLID AGGREGATE; CLEAR SUPERNATENT IS WHAT GRADE?4+
  142. 142FEW ISOLATED AGGREGATES; SUPERNATENT APPEARS RED IS WHAT GRADE?MIXED FIELD
  143. 143MEDIUM-SIZED AGGREGATES; CLEAR SUPERNATENT IS WHAT GRADE?2+
  144. 144A FEW SMALL AGGREGATES; TURBID AND REDDISH SUPERNATENT IS WHAT GRADE?1+
  145. 145A CLASSIC TECHNIQUE FOR THE DETECTION OF VIRAL ANTIBODIES IS?INDIRECT HEMAGGLUTINATION
  146. 146PRECIPITATION IS?AGGREGATION OF SOLUBLE TEST ANTIGENS
  147. 147AGGLUTINATION IS?AGGREGATION OF PARTICULATE TEST ANTIGENS
  148. 148COAGGLUTINATION IS?USES ANTIBODIES BOUND TO A PARTICLE TO ENHANCE VISIBILITY OF AGGLUTINATION
  149. 149FLOCCULATION IS?BASED ON THE INTERACTION OF SOLUBLE ANTIGEN WITH ANTIBODY, RESULTING IN FORMATION OF A PRECIPITATE OF FINE PARTICLES
  150. 150HEMAGGLUTINATION IS?AGGLUTINATION OF ERYTHROCYTES IN TESTS FOR ANTIBODY DETECTION
  151. 151ARTIFICIAL OR BIOLOGICAL CARRIERS THAT CAN BE USED IN AN AGGLUTINATION REACTION INCLUDE?ALL OF THE ABOVE: LATEX PARTICLES, COLLOIDAL CHARCOAL, AND ERYTHROCYTES COATED WITH ANTIGEN IN A CONSTANT AMOUNT
  152. 152SENSITIZATION IS?BOTH A AND B: IS THE FIRST PHASE OF AGGLUTINATION AND REPRESENTS THE PHYSICAL ATTACHMENT OF ANTIBODY MOLECULES TO ANTIGENS ON THE RBC MEMBRANE
  153. 153T/F: AGGLUTINATION CAN BE USED TO ENHANCE REACTIONS BY INCREASING PH OF THE REACTIONFALSE
  154. 154TINY AGGREGATES THAT ARE BARELY VISIBLE MICROSCOPICALLY IS WHAT GRADE?WEAK (1+ OR 2+)
  155. 155SEVERAL LARGE AGGREGATES IS WHAT GRADE?3+
  156. 156NO AGGREGATES IS WHAT GRADE?NEGATIVE
  157. 157T/F: THE PRESENCE OF HCG IN MATERNAL URINE OR SERUM PERSISTS THROUGHOUT PREGNANCYFALSE
  158. 158T/F: HCG IS DETECTABLE WITHIN 102 HOURS AFTER THE LAST EXPECTED MENSTRUAL PERIODFALSE
  159. 159THE MOST COMMON LABORATORY METHOD FOR DETECTING HCG IS?LATEX AGGLUTINATION
  160. 160IN THE LATEX AGGLUTINATION METHOD FOR THE DETECTION OF HCG, NO AGGLUTINATION INDICATES THE?PRESENCE OF HCG
  161. 161CAN A URINE SPECIMEN FOR PREGNANCY TESTING BE FROZEN?YES
  162. 162T/F: A FALSE-POSITIVE REACTION IN A LATEX AGGLUTINATION TEST FOR HCG CAN BE CAUSED BY TAKING ORAL CONTRACEPTIVEFALSE
  163. 163If the first line of nonspecific body defense, intact skin, is cut with a piece of glass contaminated with Staphylococcus aureus, which cellular component of the immune system quickly responds?NEUTROPHILS
  164. 164Place the stages of phagocytosis in the correct sequence of occurrencechemotaxis, adherence, engulfment, phagosome formation, fusion, and digestion and destruction
  165. 165Primary phagocytic cellsPMN leukocytes AND Mononuclear monocytes-macrophages
  166. 166Recognition of foreign antigenLYMPHOCYTES
  167. 167Antibody-synthesizing cellsPLASMA CELLS
  168. 168Homeostatic regulator of inflammationEOSINOPHIL
  169. 169High concentrations of heparin and histamineBASOPHIL
  170. 170Principal leukocyte associated with phagocytosisNEUTROPHIL
  171. 171What is the source of undifferentiated T lymphocytes?BONE MARROW
  172. 172Surface markers on lymphocytes can be used to:a. identify and count CD4+ and CD8+ cells.
    b. classify leukemic cells.
    c. monitor patients on immunotherapy.
  173. 173Cluster designation (CD) antigens are involved in various lymphocyte functions, which can include:a. promotion of cell to cell interactions and adhesion.
    b. transduction of signals that lead to lymphocyte activation.
  174. 174When mature T lymphocytes leave the thymus, their T cell receptors are either CD4+ or _______.CD8+
  175. 175Play a greater role in the regulation of antibody production and the release of cytokines required for B cell differentiationHelper T type 2 (Th2)
  176. 176Responsible for cell-mediated effector mechanismsHelper T type 1 (Th1)
  177. 177Regulatory T (Treg)Are an immunoregulatory type of helper T cells (Th cells)
  178. 17880% OF T LYMPHOCYTESBLOOD
  179. 17960% OF T LYMPHOCYTESLYMPH NODES
  180. 18010% OF T LYMPHOCYTESBONE MARROW
  181. 181Complement is characterized by all except:normally present in the circulation as an active enzyme
  182. 182Functions of the complement system include:a. host defense against infection, such as chemotaxis.
    b. clearance of apoptotic cells.
    c. clearance of immune complexes from the tissues.
  183. 183The classic complement pathway is activated by:factor B
  184. 184The alternate complement pathway is activated by:bacterial exotoxins
  185. 185The physiologic or cellular consequences of complement activation can include:a. production of inflammatory mediators.
    b. cytolysis or hemolysis.
    c. opsonization.
  186. 186The membrane attack complex (MAC) is characterized by all except:the complement cascade reaches full amplitude at this stage
  187. 187Increased susceptibility to pyogenic infections can be caused by:a. deficiency of the opsonic activities of complement.
    b. any deficiency that compromises the lytic activity of complement.
    c. deficient function of the mannose-binding lectin pathway.
  188. 188Interferons:mediate the early immune response to viral infections.
  189. 189Which of the following characteristics is representative of C-reactive protein (CRP)?a. The first acute-phase reactant to become elevated
    b. Nonspecific indicator of inflammation
    c. Acute-phase reactant
  190. 190The measurement of C-reactive protein (CRP) can be used for all except:diagnosis of viral septicemia.
  191. 191The definition of the term agglutination is?ALL OF THE ABOVE: a. visible expression of the aggregation of antigens and antibodies.
    b. formation of a framework in which antigen particles or molecules alternate with antibody molecules.
    c. term used to describe the aggregation of particulate test antigens.
  192. 192Precipitation is the term applied to?aggregation of soluble test antigens
  193. 193An artificial carrier could be:BOTH A AND B: a. latex particles.
    b. colloidal charcoal.
  194. 194With agglutination inhibition in pregnancy testing, a negative result is evidenced by _____________________.agglutination
  195. 195The first phase of agglutination represents:BOTH A AND C:
    a. physical attachment of antibody molecules to antigens on the erythrocytic membrane.
    c. a reversible chemical reaction.
  196. 196The most efficient type of antibodies in agglutination reactions are _________.IgM
  197. 197Anti–human globulin (AHG) is used to:form cross-links between antibodies bound to the surface of erythrocytes.
  198. 198Prozone phenomenon?An excessive antibody concentration produces a false-negative reaction
  199. 199Postzone phenomenon?An excessive antigen concentration results in no lattice formation

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Immunology
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Josefina Gonzalez
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