Bio 251 - EXAM 2
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1. Which of the following statements about b) the skin is the most com-
how the skin prevents disease is false? mon route for organisms to
a) salt in sweat retards microbial growth penetrate the body
b) the skin is the most common route for
organisms to penetrate the body
c) oil glands on the skin make it waterproof
d) native microbes that live on your skin
help protect you from infection
2. This antimicrobial protein is found at high a) lysozyme
levels in lacrimal secretions (tears)
a) lysozyme
b) defensins
c) sebum
d) C3b
3. Which component of the compliment sys- d) C3b
tem would stimulate neutrophils to phago-
cytize an attached cell?
a) C5a
b) C5b
c) C3a
d) C3b
4. Which of the following would prevent a mi- c) a bacteria that can prevent
crobe from activating the Alternative path- C3b from binding to it
way of the compliment system?
a) a bacteria that has an enzyme that de-
grades antibodies
b) a bacteria that has a thick cell wall
c) a bacteria that can prevent C3b from bind-
ing to it
d) a bacteria that contain no mannose
5. Which of the following is NOT a feature of a) melanin in the skin is toxic
the skin that allows it to serve as a barrier to a bacteria
to infection?
a) melanin in the skin is toxic to a bacteria
b) sweat creates a sling environment that
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prevents non-halotolerant bacteria from
growing
c) tight junctions in keratinocytes make the
skin waterproof
d) resident flora produce bacteriocins
6. The immune system cell most commonly c) basophil
associated with allergies is:
a) neutrophil
b) eosinophil
c) basophil
d) macrophage
7. Which of the following would be an example c) peptidoglycan
of a PAMP?
a) GaGs on the surface of eukaryotic of a
PAMP
b) C3b bound to bacteria
c) peptidoglycan
d) tissue factor
8. This cytokine is released by virally infected interferon
cells, anti-viral
9. Suppose that someone's blood stem cells c) colony stimulating factor
in their marrow ware dividing and devel-
oping into B cells. What cytokine might be
responsible for this?
a) chemokines
b) tumor necrosis factor
c) colony stimulating factor
d) interferon
10. Which of the following cells would likely mast cells, dendritic cells
have Toll-like receptors (TLRs)?
a) mast cells
b) dendritic cells
c) neutrophils
d) T-lymphocytes
e) hepatocytes
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11. Which of the following would be most likely c) double stranded RNA
to be detected by a Rig-like receptor (RLR)
a) bacterial DNA
b) helminth proteins
c) double stranded RNA
d) LPS
12. What event during inflammation is respon- b) increasing vascular perme-
sible for swelling? ability
a) diapedesis
b) increasing vascular permeability
c) vasodilation
d) increased sensitivity of nociceptors
13. Put the steps of Phagocytosis in order. Chemotaxis
Chemotaxis Recognition and Attachment
Exocytosis Engulfment (endocytosis)
Recognition and Attachment Phagosome maturation and
Engulfment (endocytosis) phagolysosome formation
Destruction and Digestion Destruction and Digestion
Phagosome maturation and phagolyso- Exocytosis
some formation
14. What are examples of Antigen Presenting Mast cells, Dendritic cells,
Cells? Macrophages, B-cells
15. Which of the following is NOT a way that b) poking holes in the cell
antibodies assist the immune system in get- membrane and lysing bacte-
ting rid of pathogens? ria directly
a) labelling pathogens for phagocytosis
(opsonization)
b) poking holes in the cell membrane and
lysing bacteria directly
c) binding to viral coat proteins and pre-
venting them from being able to enter cells
d) binding to flagella and fimbrae and pre-
venting movement and adherence
16. b) Gram- organisms
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Which of the following pathogens could ini-
tiate an antibody response without Helper
T-cells?
a) HIV
b) Gram- organisms
c) Gram+ organisms
d) Helper T-cells are not normally for an an-
tibody response
17. Which of the following statements about b) B-cell receptors are all
B-cells is false? identical
a) B-cells mature in the bone marrow
b) B-cell receptors are all identical
c) When activated, B-cells differentiate into
plasma cells
d) B-cells present foreign antigens on an
MHCII
18. Suppose you are observing a patient who The patient's immune reac-
has a bacterial infection that begins to sub- tion happened through the
side fairly quickly after becoming sympto- T-independent pathway
matic. An analysis of their blood shows
high levels of IgM specific to the bacteria,
but undetectable levels of IgG and IgD. Two
months after being discharged, the patient
returns with another infection by the same
bacteria. What would be reasonable to con-
clude?
19. Know the following: IgM- first antibody produced
IgM, IgG, IgA, IgE, IgD in response to an infection
IgG- antibody that penetrates
the placenta; abundant in
blood and fluids; antibody of
memory
IgA- found in body secretions:
mucus, tears, saliva, breast-
milk for infants
IgE- involved in allergic reac-
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tions
IgD- poorly understood func-
tion
20. Suppose that an antibody binds to a toxin d) neutralization
molecule and prevents the toxin from bind-
ing to a receptor where it would have a neg-
ative effect. This is an example of:
a) cross-linking
b) opsonization
c) immobilization
d) neutralization
21. In the thymus, T-cells that bind self antigens c) eliminated through nega-
are: tive selection
a) stimulated to proliferate (divide)
b) sent to the spleen
c) eliminated through negative selection
d) shunted back into the thymus for a sec-
ond round of selection
22. An HIV positive individual with low CD4 c) they were unable to gen-
T-cell count is infected with a normally erate antibodies through the
non-fatal virus and later dies. What likely T-dependent pathway due to
occurred? lack of helper T-cells
a) they were unable to release histamine
and could don't mount an inflammatory re-
sponse
b) their immune system became hyper-ac-
tive through the T-independent pathway and
they died due to a cytokine storm
c) they were unable to generate antibod-
ies through the T-dependent pathway due to
lack of helper T-cells
d) their macrophages were unable to stimu-
late Helper T-cells due to insufficient MHC II
23. Once you have recovered from influenza, a) natural active immunity
you have acquired immunity to that strain.
This is an example of
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a) natural active immunity
b) artificial active immunity
c) natural passive immunity
d) artificial passive immunity
24. When would an inactivated vaccine be d) in a disaster situation
preferable to an attenuated vaccine? where electricity is unavail-
a) when cost is a factor able
b) when the patient has a well developed
immune response
c) when rapid immunization must be ob-
tained
d) in a disaster situation where electricity is
unavailable
25. Which of the following cells would posses a) red blood cell
NEITHER an MHCII NOR an MHCI
a) red blood cell
b) hepatocyte
c) dendritic cell
d) neutrophil
26. Which of the following would be a common c) steroids
treatment for an autoimmune disorder?
a) epinephrin
b) antihistamines
c) steroids
d) theyroidectomy
27. Suppose that someone has a contact der- d) No, because latex allergies
matitis latex allergy. Would you expect this work through cytotoxic T cells
condition to be diagnosable via a basophil
degranulation assay?
a) Yes, because latex allergies are localized
type 1 hypersensitivities
b) Yes, because although latex allergies are
not IgE dependent they still operate through
a basophil induced inflammation
c) No, because as a localized reaction latex
allergies only work through mast cells
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d) No, because latex allergies work through
cytotoxic T cells
28. Mother/fetus Rh factor incompatibility is an b) Type 2
example of what hypersensitivity:
a) Type 1
b) Type 2
c) Type 3
d) Type 4
29. What would likely be an appropriate treat- a) Epi-pen
ment for a systemic type 1 hypersensitivity
a) Epi-pen
b) RhoGAM
c) Anti-histamine cream
d) there is no effective treatment for type 1
hypersensitivities
30. Which of the following would be an example c) someone with a mutation
of a primary immunodeficiency? in the gene that codes for the
a) someone in the advanced stages of AIDS C3 protein of the compliment
b) someone on immunosuppressive thera- system
py for an organ transplant
c) someone with a mutation in the gene that
codes for the C3 protein of the compliment
system
d) all of these primary immunodeficiencies
31. Which of the follow statements is false? c) children do not need vac-
a) herd immunity only protects a population cines if they breastfeed from
if most of the members have been vaccinat- a vaccinated mother
ed
b) inactivated vaccines primarily work
through humoral immunity
c) children do not need vaccines if they
breastfeed from a vaccinated mother
d) vaccines are often ineffective in immuno-
compromised patients
32.
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What are the three pathways of the compli- Classical, Lectin, and Alterna-
ment system? tive pathway
33. Which of the following is NOT a way that the b) preventing viral replication
compliment system acts to protect you?
a) stimulating inflammatory response
b) preventing viral replication
c) opsonization
d) direct lysis of cells
34. (T/F) The compliment system can be activat- False
ed by antigen presenting cells
35. What is a chemokine? chemotaxis of immune cells
36. What are colony-stimulating factors multiplication and differentia-
(CSFs)? tion of leukocytes
37. What is an interferon? cytokine with anti-viral func-
tion
38. What is an interleukin? involved in regulation and co-
ordination of the immune sys-
tem
39. What is tumor necrosis factor (TNF)? stimulates inflammation and
apoptosis
40. Suppose someone has a very high fever b) prostaglandin
that threatens to kill them. Which chemical
would it be most useful to suppress?
a) bradykinin
b) prostaglandin
c) histamine
d) CRP
41. What serves as chemical signals between cytokines
cells and stimulate a wide range of nonspe-
cific defenses?
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42. Bacteriocins and defensins are types of d) antimicrobial peptides
which of the following?
a) leukotrienes
b) cytokines
c) inflammation-eliciting mediators
d) antimicrobial peptides
43. What is a chemical mediator that is secreted sebum
onto the surface of the skin?
44. Identify the complement activation path- c) lectin
way that is triggered by the binding of an
acute-phase protein to a pathogen.
a) classical
b) alternative
c) lectin
45. Histamine, leukotrienes, prostaglandins, chemical mediators that pro-
and bradykinin are examples of what? mote inflammation
46. What are bacteriocins? antimicrobial peptides pro-
duced by normal microbiota
47. TLRs (toll-like receptors) found on surface of sentinel
cells, used to find infectious
molecules/cell, OUTSIDE the
cell
48. NLRs (NOD-like receptors) found in cytoplasm of most
cells, detects INSIDE the cell
(flagella, peptidoglycan)
49. RLRs (RIG-like receptors) found in cytoplasm to detect
VIRAL components (ds RNA)
50. Neutrophils most abundant circulating
WBC
NK cells- kills cells that fail to
display self antigens on their
surface
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Macrophages- phagocytic
sentinel cell
51. Basophils releases histamine in re-
sponse to infection, involved
in allergic reactions
52. Macrophages sentinel cells that phagocy-
tize foreign substances, dead
cells, debris
53. Eosinophils has an anti parasitic function
54. B cells a lymphocyte processed in
bone marrow and responsible
for producing antibodies.
55. Cytotoxic T-cells destroy cells infected with in-
tracellular pathogens, made
in thymus
56. NK cells (natural killer cells) a lymphocyte that kills cells
that do not present anti-
gens/proteins (virally infect-
ed/cancerous)
57. Type 1 hypersensitivity IgE mediated, triggering
mast cell degranulation ex)
food/drug allergies
58. Type 2 hypersensitivity IgG and IgM antibodies di-
rected against cellular anti-
gens, leads to cell dam-
age ex) red blood cell dam-
age after transfusion w/ mis-
matched blood
59. Type 3 hypersensitivity immune complexes of IgG
and IgM antibodies and anti-
gens are deposited in tissues,
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cascades into tissue damage
ex) rheumatoid arthritis
60. Type 4 hypersensitivity T cell mediated , TH1 cells
secrete cytokines, which ac-
tivate macrophages and cy-
totoxic T cells
61. Which of the following is the type of cell b) mast cell
largely responsible for type I hypersensitiv-
ity responses?
a) erythrocyte
b) mast cell
c) T cell
d) antibody
62. Type I hypersensitivities require which of a) sensitization
the following initial priming events to oc-
cur?
a) sensitization
b) secondary immune response
c) cellular trauma
d) degranulation
63. Which of the following are the main me- a) antibodies
diators/initiators of type II hypersensitivity
reactions?
a) antibodies
b) mast cells
c) erythrocytes
d) histamines
64. Which of the following is a common treat- a) anti-inflammatory steroid
ment for type III hypersensitivity reactions? treatments
a) anti-inflammatory steroid treatments
b) antihistamine treatments
c) hyposensitization injections of allergens
d) RhoGAM injections
65.
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Which of the following is NOT an example of d) hemolytic disease of the
a type 4 hypersensitivity? newborn
a) latex allergy
b) contact dermatitis (contact w/ poison ivy
c) a positive tuberculin skin test
d) hemolytic disease of the newborn
66. Allergy shots work by shifting antibody re- IgG
sponses to produce ________ antibodies.
67. Primary immunodeficiency congenital; usually genetic er-
rors that impair development
(antibody deficiencies)
68. secondary immunodeficiency acquired later in life; result of
infection (sometimes viral) or
other stress on system (AIDs,
malnutrition)
69. natural active immunity immunity gained through ill-
ness and recovery
70. natural passive immunity immunity gained from anti-
bodies through placenta or
breastmilk
71. artificial active immunity immunity gained through a
vaccine
72. artificial passive immunity immunity gained from an ani-
mal or another person
73. Bacteriostatic a substance that inhibits bac-
teria from spreading
74. Bacteriocidal a substance that kills bacteria
75. Sterilization removal of ALL microbial life,
including virus but not prions
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76. disinfection getting rid of MOST
pathogens from a non-living
object (kitchen)
77. antisepsis getting rid of pathogens from
skin or another living entity
78. Sanitization removal of pathogens from
objects to meet public health
standards
79. degerming removing, NOT killing, organ-
isms through mechanical ac-
tion (hwndwwashing)
80. Pasteurization use of heat to destroy
pathogens and reduce the
number of spoilage microor-
ganisms in foods and bever-
ages
81. preservation action that inhibits microbial
growth in the future
82. T-independent activation -the activation of B cells with-
out helper T cells, only pro-
duces IgM, but DANGEROUS
-no class switching and no
memory TH cells
83. T-dependent activation high affinity B cells with
class-switched antibodies
84. Which of the following would have an MHC macrophages, dendritic cells,
II? monocytes
a) neutrophils
b) macrophages
c) dendritic cells
d) basophils
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e) mast cells
f) monocytes
85. Which of the following chemical control d) heavy metals
agents is no longer in common use?
a) peroxides
b) halogens
c) aldehydes
d) heavy metals
86. ALCOHOLS intermediate-level disinfec-
tant that denatures proteins
and disrupts cell membranes,
not a sterilant
87. PHENOLICS low- to intermediate-level dis-
infectants, used in household
applications
88. HALOGENS intermediate level disinfec-
tant, damages enzymes by
oxidation and denaturation,
bleach, chlorine
89. SURFACTANTS soaps, detergents, quads:
degerming agents
90. selective toxicity antibiotics that target compo-
nents of bacteria and not the
host, interferes with biological
structures & processes
91. Penicillin inhibits cell wall synthesis
92. Tetracycline inhibit protein synthesis,
cause discolored teeth
93. Chloramphenicol inhibit protein synthesis, drug
of last resort: aplastic anemia
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94. Ciporfloxacin inhibit nucleic acid synthesis,
last resort
95. Rifampin Antituberculosis, blocks RNA
polymerase
96. Sulfa drugs Inhibits the synthesis of folic
acids
97. Isoniazid inhibits mycolic acid synthe-
sis
98. Explain, in physiological detail, how the On first exposure to the aller-
body reacts to PB gen, APCs process and pre-
sent the allergens on MHC
II to helper T cells. B cells
are also able to process and
present these on an MHC
II to helper T2 cells that
releases cytokines. The cy-
tokines then stimulate dif-
ferentiation and proliferation
in the IgE-secreting plasma
cells. The IgE antibodies then
bind to mast cells, sensitizing
them for subsequent expo-
sure to the allergen. On sec-
ond exposure, the allergens
cross-links IgE antibodies on
the mast cells causing activa-
tion. This then releases gran-
ules and inflammatory mole-
cules that causes signs and
symptoms type 1 hypersensi-
tivity reactions.
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