Heme - May.txt

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Heme - May.txt
2011-06-14 15:21:59
May Microbiology

Hematology/Immunology Dr. May's Review
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  1. TCRs only recognize and bind peptide antigens complexed with what?
    Special cell-surface proteins called major histocompatibility complex (MHC) molecules (unlike B cells)
  2. MHC class I molecules on APCs present what type of pathogen to which type of cell?
    Presents intracellular pathogens to CD8+ cells (cytotoxic T cells)
  3. MHC class II molecules on APCs present what type of pathogen to which type of cell?
    Presents extracellular pathogens to CD4+ cells (helper T cells)
  4. What is the function of CD8+ cytotoxic T cells?
    They kill intracellular pathogens (viral & bacterial), tumor cells, & foreign tissue grafts (from MHC I)
  5. What transports peptides across the ER membrane to associate with newly formed MHC I molecules?
    A specialized protein called the transporter associated with antigen processing (TAP)
  6. What is bare lymphocyte syndrome?
    A rare genetic disease in which the TAP protein is nonfunctional. Patients have less than 1% of normal MHC class I molecules on cell surfaces, so develop weak CD8+ T cell responses to intracellular pathogens.
  7. What interacts with MHC class II molecules on the surface of APCs, and what type of antigen is affected?
    The T-cell co-receptor CD4; antigens of extracellular origin
  8. Which antigen presenting cells (APCs) are associated with MHC class II?
    Dendritic cells, macrophages, and B cells (presented to CD4+ T cells)
  9. What is another term for the human leukocyte antigen complex (HLA) class I and class II molecules?
    Human major histocompatibility complex (MHC) molecules, class I and class II, respectively
  10. What are the isotypes of the MHC class I molecule?
    There are 6: HLA-A, -B, & -C, and HLA-E, -F, & -G
  11. What are the isotypes of the MHC class II molecule?
    There are 5: HLA-DM, -DO, -DP, -DQ, & -DR
  12. What is a haplotype?
    The particular combination of HLA alleles that an individual inherits
  13. In a cross-match test, what is assessed?
    Blood serum from the prospective donor
  14. In a cross-match test, what is a positive result?
    Occurrence of complement-mediated lysis, indicating reactive antibodies present against donor T or B cells
  15. In a mixed lymphocyte reaction, what is assessed?
    A tissue sample of recipient lymphocytes is mixed in vitro with irradiated (dead) cells from the potential donor
  16. In a mixed lymphocyte reaction, what is a positive result?
    Measurement of high levels of recipient T cell proliferation (MHC II) and recipient cytotoxicity (MHC I)
  17. What is the mechanism of action of a superantigen?
    Bacteria bind simultaneously to MHC class II molecules and T cell receptors, causing a massive, ineffective polyclonal (T cell) response.
  18. What are two examples of superantigens?
    Staphylococcal enterotoxins and toxic shock syndrome toxin
  19. What changes occur in the T cell receptor after it has been stimulated by an antigen?
    None. (Different from immunoglobulins which can undergo somatic hypermutation = class switching)
  20. What signals are required for T lymphocyte activation?
    1) peptide binds to MHC and 2) co-stimulation of the T cell's CD28 molecules by the APC's B7 cell-surface molecule
  21. What is anergy?
    A nonresponsive state that a T cell can enter
  22. Under what conditions does anergy occur?
    When an APC has the required peptide:MHC complex but does not have B7 on its surface for co-stimulation
  23. What is positive selection?
    Marking a T cell with a TCR that binds self-MHC class I for survival; occurs in cortex of thymus
  24. What is the purpose of positive selection?
    It's necessary so that an individual has T cells that can interact with self-MHC molecules.
  25. What is negative selection?
    Deletion of strongly self-reactive T cells; occurs in the thymus
  26. What is the purpose of negative selection?
    It's necessary so that an individual's T cells do not bind self-MHC molecules too strongly.
  27. What is CTLA-4 and what is its role?
    Cytotoxic T lymphocyte-associated antigen-4 protein; it can bind to B7, shutting off T cell responses
  28. What do most regulatory T cells have in common?
    They are CD4+ and express high levels of CD25.
  29. What is the development and function of regulatory cells dependent on?
    A transcription factor called Foxp3 and the cytokine IL-2
  30. With respect to transplantation, what is a donor?
    The individual who provides the graft
  31. With respect to transplantation, what is a recipient or host?
    The individual in whom the graft is placed
  32. With respect to transplantation, what does syngeneic mean?
    Animals (or grafts) that are genetically identical to one another
  33. With respect to transplantation, what does allogeneic mean?
    Animals (or grafts) of one species that differ genetically from other animals of the same species
  34. With respect to transplantation, what does xenogeneic mean?
    Animals (or grafts) of different species
  35. With respect to transplantation, what are allografts?
    Grafts between members of the same species
  36. With respect to transplantation, what are xenografts?
    Grafts between members of two different species
  37. What is the most likely cause of acute rejection of transplanted tissues or organs?
    The direct pathways of allorecognition; involves activation of recipient T cells by donor dendritic cells
  38. What is the most likely cause of hyperacute rejection of transplanted tissues or organs?
    It's mediated by circulating antibodies; it occurs within minutes.
  39. What is yellow fever and how is it transmitted to humans?
    It is a viral hemorrhagic fever; it's transmitted via the bite of an infected mosquito.
  40. What ensures the transmission of yellow fever from one year to the next?
    An infected mosquito can pass the virus in its eggs, which lie dormant when dry and hatch in the rainy season.
  41. How many people enter the toxic phase of yellow fever and under what time frame? How many die?
    15% enter the toxic phase within 24 hours; half of these patients die within 10-14 days
  42. What is affected in the toxic phase of yellow fever?
    Several body systems: jaundice & abdominal pain ? bleeding from mouth, nose, eyes, stomach ? blood in vomit & feces ? kidney function deteriorates (albuminuria or anuria)
  43. What are some key facts about the vaccine for yellow fever?
    It's safe & highly effective; it's a live attenuated virus (17D); one dose gives 10+ years protection (probably life); not given to infants < 6mo, pregnant women, immunocompromised patients, and patients allergic to eggs
  44. What does recovery from dengue imply?
    Lifelong immunity against that serotype; partial & transient protection against the other three serotypes
  45. What are the risks of sequential infection of dengue?
    Increased risk of more serious disease resulting in dengue hemorrhagic fever (DHF)
  46. What is the predominant vector for dengue?
    The urban mosquito Aedes aegypti.
  47. How can an Aedes aegypti mosquito transmit dengue to her offspring?
    Via transovarial transmission (through the eggs)
  48. What are the Arenaviruses and how are they transmitted to humans?
    Lassa virus & others (Junin, Machupo, Guanarito, Sabia); shed into environment in the urine or droppings of infected Old World rats & mice (the rodents don�t show signs of illness)
  49. What is the animal host for Lassa Virus?
    The "multimammate rat" of the genus Mastomys
  50. How is Crimean-Congo Hemorrhagic Fever (CCHF) transmitted to humans?
    The reservoir & vector are Ixodid (hard-bodied) ticks, eps. genus Hyalomma; amplifying hosts include many animals (cattle, goats, sheep, hares); transmission occurs through contact with animal or human blood or ticks
  51. How is Hemorrhagic Fever with Renal Syndrome (HFRS) transmitted to humans?
    Carried & transmitted by rodents; infection occurs after exposure to aerosolized urine, droppings, or saliva
  52. What are the most common epidemologic associations with Rift Valley Fever (RVF)?
    Mosquito-borne epidemics during years of unusually heavy rainfall
  53. How is Rift Valley Fever (RVF) transmitted to humans?
    Usually through bites from infected mosquitoes (& possibly other biting insects)
  54. Which drug used to treat HIV is a fusion inhibitor and what is its mechanism of action?
    Enfuvirtide; binds to gp41, blocking fusion of virus envelope with host cell membrane
  55. Which drugs used to treat HIV are nucleoside(/-tide) reverse transcriptase inhibitors?
    Didanoside (ddI), Abacavir, Zidovudine (AZT, ZDV), Lamivudine (3TC), Emtricitabine, Stavudine (d4T), Tenofovir
  56. Which drugs used to treat HIV target integrase (catalyzes integration of virus ds cDNA into host genome)?
    Raltegravir & Elvitegravir
  57. Which drugs used to treat HIV inhibit the viral protease?
    Indinavir, Saquinavir, Lopinavir, Atazanavir, Nelfinavir, Darunavir; Ritonavir, Amprenavir, Fosamprenavir, Tipranavir
  58. What may cause resistance to HIV infection?
    A 32-bp deletion variant of the CCR5 co-receptor (about 1% of Caucasians are homozygous, 10% heterozygous)
  59. During the primary infection of HIV, what cells are affected?
    Langerhans cells (dendritic) in the mucosa; they spread to establish infection in lymphatic tissues (GALT)
  60. What constitutes a definitive diagnosis of HIV?
    "Western blot" analysis of serum for antibodies against specific viral proteins (gp120, gp41, p24)
  61. How is a diagnosis made for a Streptococcus pneumoniae infection?
    Gram stain of sputum reveals gram-positive diplococci surrounded by an unstained capsule.
  62. What is a quelling reaction and what is it used for?
    A reaction performed by mixing bacteria with anticapsular antibody & observing for an increase in refractiveness; it can be used to confirm the gram stain of a Strep. pneumoniae infection.
  63. How is a definitive diagnosis made for tuberculosis?
    Positive cultures for Mycobacterium tuberculosis on Lowenstein-Jensen medium
  64. What is the gold standard for diagnosis of Pneumocystis jiroveci (= P. carinii; PCP)?
    Bronchoalveolar lavage (BAL) performed with a fiberoptic bronchoscope
  65. Excluding the gold standard, what can be used to diagnose Pneumocystis jiroveci (= P. carinii; PCP)?
    Various stains (Gomori methenamine-silver, Toluidine blue O, modified Wright-Giemsa, monoclonal fluorescent antibody) revealing presence of cysts and/or trophozoites
  66. What is sufficient to confirm a diagnosis of Candida albicans?
    Appearance of "the lesion" and presence of yeast forms on microscopic examination of the oropharynx
  67. What structure is seen upon microscopic examination of Cryptococcus neoformans?
    India ink stain outlines the polysaccharide capsule.
  68. What is used to dianose invasive Cryptococcus neoformans infection with >95% sensitivity and specificity?
    Detection of cryptococal antigen (in serum or CSF)
  69. How is a diagnosis made for a Histoplasma capsulatum infection?
    Direct microscopic identification of budding yeast cells in sputum, BAL fluid, blood smears, bone marrow, or tissue, usually intracellular and clustered together
  70. How is a diagnosis made for a Cryptosporidium parvum infection?
    A modified acid-fast stain of freshly excreted feces
  71. How is a diagnosis made for a Toxoplasma gondii infection?
    Serologic tests for anti-T. gondii IgG (gold standard) & IgM; IgG peaks in 1-2 months, but is elevated for life
  72. How is a diagnosis made for a Cytomegalovirus infection?
    Histology reveals a cytomegalic cell (enlarged cell with dense, central "owl's eye" = basophilic inclusion body); found in any tissue and in urine (thought to be epithelial in origin)
  73. How is a diagnosis made for a Polyomavirus JC (JC virus) infection?
    It's based on clinical and radiographic features; routine CSF evaluation is nondiagnostic, but CSF PCR detection of JC virus DNA is very useful