1. What are the 4 main classes of microorganisms?
    Bacteria, Fungi, Viruses, Parasites(worms)
  2. Name the DNA and RNA viruses.
    DNA: parvo, papova, pox, herpes, hepadn, and adenoviruses

    RNA: picorna, calici, astro, toga, flavi, corona, paramyxo, retroviruses
  3. What is the difference between gram-positive and gram negative bacteria?
    The cell wall, gram + have a thick peptidoglycan cell wall, the gram - have a thin cell wall.
  4. What is a spore? (endospore = spore)
    A dormant bacterium cell that is resistant to adverse conditions.
  5. What cells are initially present in acute inflammation?
    Mast cells, sparse macrophages and lymphocytes.

    Neutrophils, monocytes/macrophages and lymphocytes are then recruited.
  6. Which cells dominate a chronic inflammation?
    Lymphocytes and macrophages
  7. What are the main recruiters and activators in an acute inflammation?
    Cytokines, chemokines and complement
  8. What mediators lead to vascular changes?
    Eicosanoids and Histamine
  9. Why is vasodilation important for mitigating inflammation?
    Causes enhanced adhesion and transmigration of leukocytes
  10. What things limit the spread of infection?
    Cortisol, Soluble TNF receptor, Lipoxins
  11. What are the systemic effects of an immune response?
    • Fever
    • acute phase reactants made by liver(IL-6)
    • increase metabolism
    • leukocytosis
    • thrombocytosis
  12. What is the purpose of a fever?
    • Increased infection resistance
    • enhanced coaguability and other various immune responses
    • Increased intracellular expression of chaperones that enhance antigen presentation, prevent protein denaturation and protects cells from stress
    • Also many pathogens grow better at lower temps.
  13. What is the mechanism of a fever?
    Cytokines and infectious agents lead to activation of endothelium in hypothalamus, which makes PgE2, which signals hypothalamus to release cyclic AMP which alters hypothalamic thermal set point.
  14. At what temperature can a fever cause CNS damage?
    At about 41.5, or 107
  15. Along with the liver secreting response cytokines (TNF, IL-1, and IL-6), it decreases the synthesis of what?
  16. What is the result of the cytokines released by the liver in an acute phase?
    Increased synthesis of: Fibrinogen, clotting factors, complement factors, C-reactive protein, MBL, and other opsonins.
  17. What does a sedimentation rate tell us, and how does it work?
    It is a nonspecific indicator of dz.

    The sedimentation rate changes because of the increase in Fibrinogen, which reduces the charge on RBCs, which makes them stick together and so the sink faster than they normally would.
  18. What does a mild increase in C-reactive protein indicate in a healthy subject?
    Increased risk of atherolsclerotic changes (high sensitivity to CRP, different units and normal range)
  19. What are the harmful effects of a systemic immune response?
    • Circulatory problems (shock) caused by generalized vasodilation and a negative inotropic effect
    • Increased atherosclerosis and cancer risk
    • Vascular activation and leakage induced tissue damage (ARDS)
    • DIC (Disseminated intravascular coagulopathy)
  20. What should be established with a Pt before prescribing them an antimicrobial drug?
    • The disorder is caused by an infection
    • the infection represents a threat
    • there is a drug that works for that type of infection
    • there is a way to get the req. [ ] to the site of infection
  21. What req. does a microbial drug need to meet to be an appropriate Rx choice?
    • least toxic
    • narrowest spectrum of action
    • least $$
    • won't make Pt's other pathologies worse
    • that the choice between bactericidal or bacteriostatic is appropriate for the state of the Pt's immune system
  22. When would it be appropriate to choose a bactericidal agent?
    When the hosts immune system is impaired
  23. Is a negative rapid strep test convincing evidence that the Pt doesn't have strep?
    No, specificity is only 70%
  24. Ideally you will be able to identify the specific organism causing an infection before prescribing antimicrobials, but in the case of a severe infection, how should you proceed?
    First initiate cultures, then make the best educated guess using the Medical Letter's Antimicrobial Handbook. Often a broad spectrum or combination of drugs is used, but once the pathogen has been identified it is imperative that the single most effective drug be given and any that are not necessary are stopped.
  25. What is the Minimum Inhibitory Concentration (MIC)?
    the smallest amount that needs to be used to prevent bacterial growth in vivo, it is estimated from a disc diffusion test and the size of the bacteria-free zone.
  26. What is the MBC (minimal bactericidal concentration)?
    The [ ] that kills 99.5% of the microbes, determined from a bactericidal dilution test, where the bacteria grows in the presence of different [ ] of the drug.
  27. Why might the MIC not give you the correct dose?
    Acidic/basic conditions, poor absorption, pus, binding of penicillins and tetracyclines to Hb all might alter the efficacy of the drug.
  28. In general, should you use more or less drug than the MIC suggests?
    More if possible, but be sure its less than the toxic level!
  29. Why is the earliest possible tx beneficial?
    Cells growing in the log phase (as opposed to the plateau phase) are more sensitive.
  30. What is the shortest amount of time after cure that a drug regimen can be stopped?
    2 days, but it is often longer
  31. What circumstances would make monitoring the dose necessary?
    Using a drug with a narrow therapeutic index, or an infection in the CNS. Knowing the plasma [ ] of the drug makes it easier to choose the smallest possible dose that will have the desired effect.
  32. What are the important things to remember when considering a drugs ability to be distributed across the BBB?
    • Lipid solubility, [ ] in CNS is almost = to [ ] in plasma.
    • the rate the drug will be actively transported out of the CNS by the choroid plexus, drugs such as penicillin cannot reach an adequate [ ] in the CNS.
  33. What factors affect distribution of drugs into urine?
    • Resorption, lipid soluble drugs are more readily resorbed so urine [ ] = plasma [ ].
    • Water soluble drugs are not readily resorbed so urine [ ] can be 10-60x greater than plasma [ ].
    • Active transport of drugs into the urine can lead to toxic [ ].
  34. What impacts the drugs ability to get to it's target for both gram + and gram - bacteria?
    • Gram +: drug must permeate porous peptidoglycan envelope; size, polarity, active transport must be considered.
    • Gram -: Beta-lactams (penicillin) need only cross 1 of the 2 plasma membranes (usually by diffusion). Gentamicin on the other hand must cross both membranes.
    • Once the agent has reached its target it is important that it stays there, increased drug efflux is a common mechanism of resistance.
  35. Is the efficacy of a drug lost if the [ ] of the drug at the site of infection falls below the MIC?
    Not always, aminoglycosides can be given once a day in a large dose w/out compromising efficacy.
  36. Augmentin, Sulbactam and Primaxin have what common unique property?
    • Augmentin (ampicillin + clavulanate) and Sulbactam (ampicillin + sulbactam) are antimicrobials + inhibitors of bacterial enzymes that inactive antimicrobials.
    • Primaxin (imipenem + cilastatin) is similar but it also inhibits an enzyme that produces an agent that is nephrotoxic, so it kills 2 birds w/ one stone.
  37. Why would a drug be classified as "broad spectrum"?
    it acts on several pathogens on both sides of the gram fence. (tetracycline)
  38. Tetracycline is effective against many gram + and gram - organisms, but it is rarely used to treat infection, why?
    • Spectrum of action refers to # of pathogens are drug can target, therapeutic range is how a effective a drug is against a specific action.
    • While tetracycline has a large spectrum of action, it does not have a great therapeutic range, so there are generally better antimicrobials to use.
  39. Penicillins, cephalosporins, monobactams, carbapenems, cycloserine, vancomycin, ristocetin, and fosfomycin all work by a similar mechanism, what is it?
    They all interfere with bacterial cell wall synthesis (some trigger a suicide pathway via autolysins), they are known as bactericidal.
  40. What are the mechanisms of action of antimicrobial agents?
    • Interfere w/ synthesis of bacterial wall
    • increase plasma membrane permeability
    • interfere w/ protein synthesis
    • interfere w/ nucleic acid syn
    • block metabolic steps by serving as antimetabolites.
  41. Why would you consider using a combination of drugs to treat an infection?
    • target many pathogens while culture is perfromed
    • It increase efficacy
    • to treat mixed infections
    • enable use of lower, less toxic doses(however drugs can interact synergistically, so be careful)
    • delay emergence of resistance
  42. What are the disadvantages to using drug combinations?
    • Increased risk of toxicity due to adverse effects or drug interactions
    • may cause supra-infection
    • antagonistic interactions between bactericidal and bacteriostatic drugs
    • $$$
  43. What is chemoprophylaxis, and when is it appropriate?
    • use of antimicrobials to prevent infection.
    • >5% chance of infection
    • drugs have high therapeutic index
    • situation where prophylaxis has previously had success
    • surgery
  44. What is the significance of AMDR? (acquired microbial drug resistance)
    Bacteria can become resistant to antimicrobials, the more drugs used the more resistant the pathogens become.
  45. Why does AMDR occur more often in populations that use more antimicrobial agents?
    • Because in the presence of a drug, growth of the parent cell is suppressed while that of the drug-resistant progeny is unaffected. An example of evolution.
    • Resistance is NOT induced by the drug, but resistant strains are selected for by the drug.
  46. What are the mechanisms by which AMDR is acquired?
    • Mutation
    • Transformation (incorporation of DNA from environment into genome)
    • Transduction (viral transfer of a gene into a microbe, ie E coli O157:H7)
    • Plasmid transfer during conjugation
  47. Why is plasmid transfer during conjugation considered the most important?
    • They lead to MDR, as plasmids have been found to contain many combinations of drug resistant mechanisms. Resistance of up to 9 different drugs has been found in a single plasmid.
    • Plasmid transfer is common and can occur between different species.
  48. What are the 4 main mechanism of AMDR?
    • Drug-inactivating enzymes (phosphorylation, acetylation, etc.)
    • Reduction of cytoplasmic drug concentration by: Decreasing cell permeability, Pumping the drug out
    • Alteration of the protein-binding site for the drug
    • Antibiotic-specific mechanisms
  49. What could cause a superinfection?
    • Broad-spectrum antibiotics (cause wide-spread alterations in a microbial system)
    • High [ ] of norrower spectrum antibiotics can also cause SI.
  50. How do you determine the likelihood of overcoming 2 antibiotics at one time?
    P1+2 = P1 x P2
  51. Is Cox-1 or Cox-2 associated with inflammation and cytokines?
    Cox-2, Cox-1 inhibition leads to GI problems.
  52. What are analgesics good for?
    Pain from injury or inflammation (reduce inflammatory mediators and have vasodilatory effects)
  53. If a patient has a low platelet count, is more likely to have taken tylenol, ibuprofin or aspirin?
    Aspirin (NSAIDs also have some anti-coagulative effect, but not as strong as aspirin)
  54. A Pt presents with impaired peripheral edema, acute renal failure, interstitial nephritis and analgesic nephropathy; you suspect he has been taking too many OTC pain pills. What drugs should you ask the Pt about?
    Acetaminophen and NSAIDs (not aspirin)
  55. What is sometimes used to prevent or treat GI injury caused by NSAIDs?
    Misoprostol and proton pump inhibitors like prilosec.
  56. Aspirin has been shown to have beneficial cardiovascular and myocardial effects, but it also can lead some negative side effects, what are these? and what dose leads to the negative side effects?
    • Increased risk of hemorrhagic stroke, bleeding, GI toxicities, renal, hepatic, hypersensitivity (rarely CNS effects like Tinnitus or hyperventilation and Reye's syndrome)
    • 325 mgs leads to GI toxicities (81 good for beneficial CV effects)
  57. Which drug are pediatricians likely to avoid giving to Pts?
    Aspirin (also not good for pregnant women)
  58. What is the toxic dose of Aspirin and how do you treat it?
    • 20-30g for adults, 250 mg/kg for kids
    • Emesis, activated charcoal
    • Aspirin also has many drug interactions
  59. Aspirin is effective for what common ailments?
    fever, pain, inflammation
  60. How much tylenol leads to hepatotoxicity?
    • 10-15g (150-250 mg/kg),
    • 20-25g can be fatal
  61. What factors can contribute to hepatotoxicity due to tylenol and how is it treated?
    • 1/2 life of drug increases w/ liver damage,
    • Acetaminophen is in many OTC drugs,
    • Hepatic necrosis occurs if 1/2 life >4 hrs. (normal = 2-3 hrs)
    • Tx = activated charcoal (<4 hrs after overdose), N-acetylcysteine
  62. Bioactivation of acetaminophen through which pathway leads to a hepatotoxic agent?
    metabolism via cytochrome p450 => NAPQI
  63. What are the maximum dosages of acetaminophen?
    • Adults/Adolescents: 1000 mgs/dose (4x/day)
    • Children(6-12): 75 mg/kg/day or 4 g/day, whichever is less
    • Children(<6): same as older children, but don't use extended-release tab
    • Infants: 75 mg/kg/day
  64. Naproxen, sulindac, diflunisal, oxaprozin, nabumetone, and ketorolac are NSAIDs that have what in common?
    Long half-life (>5 hrs)
  65. Which NSAID has low toxicity, but can inhibit CYP2C9?
  66. Which NSAID is used for gout, but otherwise avoided due to frequent adverse effects?
  67. Which NSAID might be used on a post-opp Pt who does not respond to opiates?
  68. Which NSAIDs appear to be effective for the regression of colorectal polyps?
    Sulindac and celecoxib (celecoxib is the the only COX-2 selective NSAID on the market)
  69. Match the inhibitor to the toxicity:
    COX-1 & COX-2

    GI/kidney/Renal & Myocardial
    COX-1 => GI/Kidney/Renal toxicities

    COX-2 => Myocardial toxicities
  70. What is the general mechanism of action of penicillins?
    cause a bactericidal inhibition of cell wall synthesis (attach to PBP)
  71. How does the access to PBP differ between gram + and gram - bacteria?
    • Gram + have no outer membrane => easier access
    • Gram - have an outer lipid membrane => more limited access
  72. Penicillin G and V are said to be natural penicillins. What are they most effective at targeting?
    Sterptococci (however some streptococci pneumoniae are developing resistance)
  73. Nafcillin and Oxacillin are Penicillinase-resistant penicillins, for what type infection would you prescribe them?
    Staphylocoous aureus and staphlococcus epidermidis producing penicillinase.
  74. What are the broad spectrum penicillins? When would you use them?
    • Aminopenicillins (Ampicillin, Amoxicillin)
    • Most common Streptoccoci, as well as
    • H influenza,
    • proteus,
    • E coli,
    • Proteus Mirabilis,
    • Salmonella, and
    • Shigella
  75. Expanded spectrum or antipsuedomonal penicillins (piperacillin, ticarcillin) are good for what?
    targeting gram - bacteria (pseudomonas and klebsiella)

    Combinations of these drugs w/ B-lactamase inhibitors expands their activity to cover pencillinase-producing staphylococci and other B-lactamase producing pathogens.
  76. A Pt comes in w/ prophylaxis of rheumatic fever and a history of cardio valve damage. What should you prescribe?
    Natural penicillin (G or V)

    Also effective against upper respiratory infections due to staphylococci
  77. A Pt presents with a systemic infection due to staphylococci, what penicillin should you choose?
    Penicillinase-resistant penicillin (Nafcillin, Oxacillin)
  78. Pts w/ UTIs Salmonella, Shagella, or kids w/ pharyngitis or otitis media (due to streptococci or H influenza) should be prescribed what type of penicillin?
    Aminopenicillins (Ampicillin or Amoxicillin)
  79. Which type of penicillins should you avoid using except in the case of a gram - bacillary infection?
    Expanded-spectrum penicillins
  80. Name some of the ways pathogens become resistant to penicillins.
    • Altered PBPs (penicillin binding proteins),
    • Mutated porins (porins produce holes in the outer membrane of gram - bacteria),
    • Presence of penicillinase or specific B-lactamases,
    • Antibiotic efflux pumps (Gram - bacteria only),
    • Lack of apoptosis mechanism in bacteria,
    • Bacteria that have exited the log growth phase.
  81. A bacterium that causes a common dz in a pop. that has previously been exposed to it is called:

    E. endemic
  82. Name 3 epithelia in the human body that act as barriers to infection.
    Skin, mucosal epithelium (of GI, respiratory tract and urogenital tract)
  83. Name the 3 main ways in which the epithelia carry out the barrier function.
    • 1) Physical barrier - tight junctions, cilia-mucosal.
    • 2) Chemical barrier - lysozyme, pH, defensins.
    • 3) Microbiological barrier - normal flora
  84. An antimicrobial peptide that protects epithelial surfaces from pathogens is called a _____.

    E. defensin
  85. Describe the characteristics commonly associated w/ inflammation and what causes them.
    • Head, redness, pain and swelling.
    • These are caused by a combination of vasodilation and increased vascular permeability which leads to infiltration of fluid and leukocytes from the blood into the infected site (which leads to swelling and pain).
  86. Which of the following are characteristics of innate immunity? (select all that apply)

    a. inflammation
    b. recognition of the pathogen improves during response
    c. fast response
    d. highly specific for a particular pathogen
    e. cytokine production
    a, c, e
  87. Which of the following statements about neutrophils is false?

    A. (Neutrophils are active in aerobic AND anaerobic conditions)
  88. What are the main differences between innate and adaptive immunity?
    Innate: fast response, less specific, unable to eradicate infection completely(usually), no memory.

    Adaptive: slower response, high specificity, often completely eradicates infection, has memory.
  89. A. What are the 2 major progenitor subsets of leukocytes?

    B. Where do they originate in adults?

    C. Name the white blood cells that differentiate from these 2 progenitor lineages.
    a. Lymphoid and myeloid

    b. bone marrow (from pluripotent hematopoietic stem cells)

    c. Lymphoid => B/T cells and NK cells. Myeloid => basophils, eosinophils, neutrophils, mast cells, dendritic cells, and monocytes (monocytes => macrophages)
  90. Primary lymphoid tissues are the sites where lymphocytes ______, whereas secondary lymphoid tissues are the sites where lymphocytes _______.

    B. primary => develop and mature, secondary => become stimulated
  91. The spleen differs from other secondary lymphoid organs in which of the following ways?

  92. How do clonal selection and clonal expansion shape the adaptive immune response?
    Clonal selection describes the fact that only the lymphocytes that can recognize the particular pathogen respond as part of the immune response. Clonal expansion describes proliferation and differentiation of the original lymphocytes into a large # of effector lymphocytes.
  93. What type of bacterial infection is most dangerous for a Pt w/ a ruptured spleen?

    what type of antimicrobials should be administered?
    Encapsulated bacteria (the spleen is very important for protection against this type of bacteria)

    booster immunization w/ DPT (dyphtheria toxoid)
  94. An older Pt has been taking broad-spectrum antibiotics for the last 4 months. This morning she presents w/ severe abdominal cramping, vomiting, offensive smelling non-bloody diarrhea and a fever. Which of the following is NOT likely associated w/ her condition?

    E. E coli causes bloody diarrhea.
  95. Which of these pairs are mismatched?

  96. The 3 complement pathways converge on a common enzymatic reaction known as complement fixation.
    A. Describe this reaction
    B. Describe the enzyme responsible for this rxn in the alternate pathway.
    C. Identify the 3 effector mechanisms of complement that are enabled by this common pathway.
    A. All 3 pathways result in the cleavage of C3 into C3a and C3b, this and the covalent bonding of C3b to the pathogen surface = complement fixation.

    B. Alternative convertase = C3bBb (the classical and lectin pathways use the classical C3 convertase C4b2a)

    • C.(1) C3b binds and tags pathogens for destruction by phagocytes through binding to a C3b receptor, (2) C3b contributes to a multi-component enzyme, C5 convertase, which catalyzes the assembly of the terminal complement componenets and leads to the formation of the MAC (membrane attack complex).
    • (3) C3a is an inflammatory mediator that serves as a chemoattractant and recruits inflammatory cells to the infection site.
  97. Which of the following is the soluble form of C3 convertase of the alternative pathway?

    A. iC3Bb
  98. Explain the steps that take place when a bacterium is opsonized via C3b:CR1 interaction between the bacterium and a resident macrophage in tissues.
    The C3b, which is coating the bacterial surface after complement activation, is bound by the CR1 on the macrophage. The bacteria is engulfed by the macrophage in an intracellular vesicle known as a phagosome. The phagosome fuses w/ lysosome form phagosysosome, which dumps toxic mediators and degradative enzymes into the phagosome, killing the bacterium.
  99. Which soluble factors of the alternative pathway inhibit C5b, C6 and C7 from binding to cell membranes?
    S protein, clusterin, and factor J.
  100. Human cell membranes contain CD59. This is important so that membranes are not perforated by the complement system. How does CD59 inhibit perforation?
    It inhibits C9, which catalyzes the final step in the formation of the MAC (membrane attack complex).
  101. Briefly explain how the 3 complement pathways are activated.
    • 1. Alternative - requires an activating surface of a pathogen, which stabilizes complement components (B&D).
    • 2. Classical - activated by the presence of Crp, or the presence of antibody bound to a microorganism.
    • 3. Lectin - activated by MBL, which is made by the liver (in response to IL-6) during an acute-phase immune response.
  102. Why is the classical pathway considered part of the adaptive immune response as well as the innate immune response?
    because it can be activated by the presence of antibody. (neither the lectin or alternative pathways respond to antibodies)
  103. Lectin receptor binds to what?
    mannose and glucan (carbohydrates)
  104. CR3 binds to what ligand?
    iC3b, lipophosphoglycan, hemagglutinin, LPS
  105. CR4 binds to what ligands?
    iC3b, lipophosphoglycan, hemagglutinin, LPS
  106. CR1 binds to what?
  107. TLR4:TLR4 binds to what?
    LPS (lipopolysaccharide)
  108. TLR5 binds to what?
  109. TLR3 binds to what?
  110. Other than ligand specificity, what is the key difference between TLR5, TLR4, TLR1:TLR2, and TLR2:TLR6, when compared to TLR3, TLR7, TLR8, and TLR9?
    TLR5, TLR4, TLR1:TLR2, and TLR2:TLR6 are transmembrane receptors anchored on the plasma surface of human cells that interact w/ pathogens in extracellular locations.

    TLR3, TLR7, TLR8, and TLR9 are anchored in endosomal membranes located in the cytosol (where intracellular degradation of pathogens occurs).
  111. Explain the relationship between NFkB and TLRs.
    NFkB is a transcription factor found in the cytoplasm of macrophages. Signaling through TLRs => phosphorylation cascade => NFkB activation. Once active NFkB turns on genes that enable the effector capacity of the macrophage.
  112. How are TLRs able to recognize so many different species w/ such a limited number of receptor proteins?
    Because groups of pathogens tend to have similar characteristics. (i.e. LPS in gram - bacteria, 1 TLR can recognize a whole class of bacteria)
  113. What is the difference between macrophages and neutrophils?
    Macrophages reside in tissues, are long live, have many important functions other than killing pathogens (cytokine production, attract neutrophils, help initiate adaptive response, act as antigen presenting cells) and macrophages have TLRs.

    Neutrophils circulate in the blood (entering tissues after infection), are short-lived, and have no TLRs.
  114. In response to TNF-alpha, vascular endothelium produces ______, which induces localized blood clotting?

    A. platelet-activating factor is produced by vascular endothelium in response to TNF-alpha.
  115. A. What induces the production of type-1 interferon by virus-infected cells?

    B. Do normal cells produce this inducer?

    C. What are the antiviral effects of type-1 interferon?
    A. Type 1 interferon genes are transcribed as a result of the presence of double-stranded RNA.

    B. No, since normal cells never have double stranded RNA, viral cells either contain dsRNA or use it as an intermediate in replication.

    C. Type 1 interferons block virus replication in affected cells and prevent adjacent cells from being infected. IFN also activates NK cells by releasing cytotoxic granules and cytokines.
  116. Which of the following are closely associated w/ NK cells? (select all that apply)

    C. NK cells are responsible for lysis of virus-infected cells
  117. Eradicating encapsulated bacteria is dependent on what?
    Opsonization (complement, C3b, etc)
  118. Image Upload 1
    • a. lymphatics
    • b. capsule
    • c. subcapsular sinus
    • d. cortex
    • e. medulla
  119. What are the characteristics of an infected lymph node?
    >2 cm, tender, rubbery, mobile

    (tumor infected nodes are >3-4 cm, non-tender, hard and fixed)
  120. A. Where are B cells in lymph nodes?

    B. T cells?
    A. Germinal centers

    B. Periphery (macrophages seem to be in these areas as well?)
  121. What are the functions of the spleen?
    Synthesize IgG, remove bacteria, particles, old/abnormal RBCs from blood,

    (in kids they are involved in hepatopoiesis)
  122. What are the differences between Splenomegaly & Asplenia?
    Splenomegaly: usually result of immune response (mono, endocarditis), incresed RBC destruction, congestion, can rupture and bleed massively.

    Asplenia (small or absent spleen): result of splenectomy (sickle cell/Betal thal) or congenital. Increased risk of sepsis w/ bacterial infection (especially from pneumococcus, meningococcus, H influenza)
  123. Image Upload 2
    Thymus: atrophies in early teens, major function is T cell maturation
  124. Image Upload 3
  125. What are immature neutrophils called?

    and what is their significance?

    can be only hint of infection in elderly people
  126. Monocytes are a precursor for this lymphoctye?
    Image Upload 4
  127. Eosinophils respond primarily to what type of infection?
    parasitic (also present in allergic reactions)
  128. (clayton)
    B cells make ____, and become _____.
    immunoglobin and plasma cells
  129. (clayton)
    T cells receive antigen, leading to 3 types of activation. What are these 3 types?
    • 1) Helper T (CD4) - make cytokines (TH2:parasite/allergies, TH1:cell mediated)
    • 2) Cytotoxic T cells (CD8) - important for viral immunity, kill cells expressing certain antigens.
    • 3) Regulatory T cells (CD4) suppress immune response.
  130. What is the role of dendritic cells in the immune response?
    Phagocytose antigen, then migrate to lymph node to present antigen to T cells (initiating the adaptive immune response)

    They are found in epithelial tissues.
  131. Mast cells are rare blood leukocytes. How do they initiate an antiparasitic infection?

    What are their other functions?
    They become coated w/ IgE.

    • They are also activated by direct tissue injury => histamine release (edema & vasidilation), release of serotonin, proteases, prostoglandin and cytokines
    • They are also involved in allergic reactions.
  132. (clayton)
    Acute inflammation:

    what are the subsequent effects?

    effects: swelling, redness, warm to touch, pain, loss of function (tumor, rubor, calor, dolor)
  133. (clayton)
    Chronic inflammation:

    what cells are present?

    cells: lymphocytes, macrophages, often plasma cells.
  134. (clayton)
    A. What are 3 common causes of Gramulomatous inflammation?

    B. and what is a common charactistic?
    A. Tuberculosis, myobacteria, and most fungi.

    B. they are often caseating.
  135. Which cells are most prone to injury?
    • Highly metabolic cells (cardiac myocytes, renal tubular cells & hepatocytes) and
    • Rapidly proliferating cells (testicular germ cells, intestinal epithelium, hepatopoietic cells)
  136. What types of cell injury are irreversible and generally cause cell death?
    • Holes in cell membrane
    • long Ca++ efflux
    • mitochondrial loss
  137. Why do injured cells swell up?
    Lack of ATP leads to loss of function of Na pumps.
  138. Image Upload 5
    Apoptosis vs Necrosis
  139. What temp = fever?

    At what temp would a physician worry?
    • >37.2 or 98.9(AM)
    • >37.7 or 99.9 (PM)

  140. What is the best time to get a culture sample?
    Ideally right before the fever spikes, but shortly after is okay as well.
  141. Adult Respiratory Distress Syndrome (ARDS) is when the lung capillaries become very leaky(30-40% mortality rate). When is this seen?
    Commonly seen w/ sever infection as well as other disorders w/ cytokine release.
  142. What causes DIC? (disseminated intravascular coagulopathy)
    increased clotting factors (endothelium releases them in response to TNF, IL-1, LPS) during a severe systemic inflammatory response.
  143. A. Leukocytopenias:

    B. Bacteremia:

    C. Septicemia:
    A. Low white cell counts (can be real or an actifact from clumping of intravascular leukocytes)

    B. bacteria cultured from blood

    C. bacteria cultured from blood or toxin detected in blood
  144. A. SIRS (systemic inflammatory response syndrome) is 2 or more of what 4 symptoms?

    B. Is it always caused from an infection?
    • A. Fever (oral temp >38) or Hypothermia (<36)
    • Tachypnea (>24 breaths/min)
    • Tachycardia (>90 beats/min)
    • Leukocytosis (>12,000/nL) or Leukopenia (<4,000/nL) or bands (>10%)

    B. No (pancreatitis, trauma, amniotic fluid embolism)
  145. A.Sepsis is SIRS + what?

    B. What is the difference between Sepsis, Severe Sepsis and Septic shock?
    A. an infection

    • B. Severe sepsis is associatae w/ one or more of a list of systemic responses to an infection,
    • Septic shock is Sepsis + hypotension.
  146. The process by which a pathogen stimulates only those lymphocytes with receptors specific for that pathogen is called

    B. clonal selection
  147. When is the host most vulnerable to infection from an unrecognized pathogen?
    The first several days, after clonal selection, clonal expansion takes a while.
  148. The process of _____ results in the recombination of gene segments of the T cell receptor and immunoglobulin genes giving rise to lymphocytes with unique specificities for antigens:

    D. somatic recombination
  149. Which of the following statements about B and T cell receptors is incorrect?

    A. easy, constant region is conserved, variable region differs. The rest are true.
  150. During a typical infection, dendritic cells first encounter a pathogen in __________and then transport the pathogen to _________ where the pathogen-derived peptide fragments are presented to ________.

    C. T cells
  151. Explain the differences between CD4 and CD8 T cells in terms of (a) their effector function and (b) their interaction w/ MHC molecules.
    • (a) CD4 (helper T cells) secrete cytokines that instruct other cells to acquire effector function, CD8 (cytotoxic T cells) cells kill the target cells they recognize.
    • (b) CD4 T cells resognize only antigens presented by MHC class II molecules. CD8 T cells recognize only antigens presented by MHC class I molecules.
  152. What are the 2 major sources of the pathogen-derived antigens recognized by T cells?
    • Intracellular (recognized by CD8 T cells)
    • Extracellular/interstitial (CD4 recognized)
  153. True or False, CD4 T cells are activated only when pathogen peptides are presented on the surface of antigen-presenting cells together w/ MHC class II molecules.
    True, CD4 : MHC II
  154. How does neutralization differ from opsonization?
    In neutralization the antibody binds an antigen that blocks it from binding a native antigen, so uptake is blocked.
  155. If there are no receptors on macrophages for the constant region of IgM, then how does the IgM coating a pathogen promote phagocytosis?
    IgM induces the classical pathway of complement activation. (so C3b binds to pathogen surface, which is recognized by the CR1 receptor on phagocytes)
  156. Briefly describe wich antibodies are made against an infecting pathogen, and how that leads to phagocytosis.
    • IgM is the first antibody made agaisnst an infecting pathogen,
    • Somatic hypermutation selects for antibodies that bind more tightly to the pathogen,
    • Switching antibody isotype to IgG, IgA or IgE allows for delivery of the pathogen to phagocytes.
  157. What is the diffence between antibodies and immunoglobulins?
    • Immunoglobulins: membrane bound form of the antigen receptors of B cells.
    • Antibodies: plasma cell produced secreted form of the same immunoglobulins.
  158. Briefly describe the series of events that leads to antibody secretion.
    Resting B cell (with Ig); encounter w/ antigen => stimulated B cell => antibody secreting plasma cells
  159. The molecules to which antibodies bind are called:

    A. antibodies bind to antigens
  160. A. What is an epitope?

    B. Define the term multivalent antigen.

    C. How does a linear epitope differ from a conformational epitope?

    D. Do antibodies bind their antigens via noncovalent bonding or via covalent bonding?
    A. The epitope is the specific part of the antigen that is recognized by an antibody and binds to the complementarity-determining regions in the antibody variable domains.

    B. Multivalent antigens are complex macromolecules that contain more than one epitope.

    C. Linear or continuous epitopes comprise a contiguous amino acid sequence. (in contrast to conformational epitopes, which result from protein folding)

    D. Non-covalent bonds (H-bonding, etc)
  161. The process of gene rearrangement in immunoglobulin and T cell receptor genes is called

    A. somatic recombination
  162. Somatic recombination allows for an almost unlimited variety of different variable regions, which is key for producing antibodies that can recognize a huge repertoire of antigens. Briefly explain the roles of V, D, and J gene segments and how this is accomplished.
    • Heavy-chain loci contain gene segments called V (variable), D (diversity), and J (joining), while light chain loci contain only V and J segments.
    • In somatic recombination in developing B cells one of each family of gene segments is randomly selected and joined together to give complete variable-region sequence (expressed as an Ig heavy or light chain).
    • Ig gene rearrangement is irreversible, leading to permanent alteration of the chromosome.
  163. What is the final arrangement of gene segments in the rearranged Ig heavy-chain gene V region, and in what order do these gene segment rearrangments occur?
    a D gene segment first joins to a J (forming a DJ), this is followed by a V joining to the DJ =>VDJ (which encodes a complete variable region).
  164. In what order to various Ig loci rearrange?
    Heavy-chain before Light-chain.
  165. What problem in somatic recombination leads to severe combined immuno deficiency?
    Lack of RAG genes. (RAG is a telomerase-like enzyme)

    The end result is no mature B and T cells.
  166. Junctional diversity during gene rearrangement results from addition of

    D. P and N nucleotides
  167. Which of the following statements is incorrect?

    E. Effector function depends on isotype.
  168. Indicate which of the following statements are T and which are F with reference to immunoglobulin structure.
    A. the antibody secreted by a plasma cell has a different specificity for antigen than the immunoglobulin expressed by its B cell precursor.
    B. the amino-terminal regions of heavy and light chains of different immunoglobulins all differ in amino acid sequence.
    C. a flexible hinge region holds the heavy chain and light chain together.
    D. the heavy-chain constant region is responsible for the effector function of immunoglobulins.
    E. gamma and kapa light chains have different function.
    • A = F
    • B = T
    • C = F
    • D = T
    • E = F
  169. Which of the following is mismatched

  170. Which of the following statements about the production and use of monoclonal antibodies is incorrect?

    A. it does not require a purified form of an antigen
  171. What is the process used to produce either surface or secreted forms of the Ig heavy-chain called?
    alternative RNA processing.
  172. AID (activation-induced cytidine deaminase) is required for what to vital steps in immunoglobulin maturation?
    Isotype switching and somatic hypermutation
  173. Why is isotype switching important?
    it is the way a B cell changes the immunoglobulin class while preserving the antigenic specificity of the Ig.
Card Set
Week 1, Phase 2.2 (Immunology)