WorksheetsISD2-P1
Total questions: 79
Worksheet time: 40mins
Name
Class
Date
1.
no antibody is detectable
a)
Lag phase
b)
Log phase
c)
Plateau phase
d)
Decline phase
2.
– the antibody titer increases logarithmically
a)
Lag phase
b)
Log phase
c)
Plateau phase
d)
Decline phase
3.
– the antibody titer stabilizes
a)
Lag phase
b)
Log phase
c)
Plateau phase
d)
Decline phase
4.
the antibody is catabolized
a)
Lag phase
b)
Log phase
c)
Plateau phase
d)
Decline phase
5.
First encounter and immune response to a specific immunogen
a)
primary antibody response
b)
secondary antibody response
6.
It refers to the initial challenge of the immune system
a)
primary antibody response
b)
secondary antibody response
7.
Shorter lag phase
a)
primary antibody response
b)
secondary antibody response
8.
Increased antibody titer
a)
primary antibody response
b)
secondary antibody response
9.
Predominant antibody: IgG
a)
primary antibody response
b)
secondary antibody response
10.
Slow decrease
a)
primary antibody response
b)
secondary antibody response
11.
The immune response to subsequent exposure to the same antigenic stimulus
a)
primary antibody response
b)
secondary antibody response
12.
▪ Purified antibodies cloned from a single cell
a)
Hybridoma technology
b)
Monocloonal Antibodies
c)
Polymerase Chain Reaction
d)
Toni fowler
13.
Formation of a hybridoma in monoclonal antibody production
a)
Hybridoma technology
b)
Monocloonal Antibodies
c)
Polymerase Chain Reaction
d)
Toni fowler
14.
A mouse is immunized, and spleen cells are removed. These cells are fused with non-secreting myeloma cells and then plated in a restricted medium. Only the hybridoma cells will grow in this medium, where they synthesize and secrete a monoclonal immunoglobulin specific for a single determinant on an antigen
a)
Hybridoma technology
b)
Monocloonal Antibodies
c)
Polymerase Chain Reaction
d)
Toni fowler
15.
These antibodies exhibit exceptional purity and specificity and are able to recognize and bind to a specific antigen
a)
Hybridoma technology
b)
Monocloonal Antibodies
c)
Polymerase Chain Reaction
d)
Toni fowler
16.
Abrupt decrease
a)
primary antibody response
b)
secondary antibody response
17.
Predominant antibody: IgM
a)
primary antibody response
b)
secondary antibody response
18.
Decreased or low antibody titer
a)
primary antibody response
b)
secondary antibody response
19.
Longer lag phase
a)
primary antibody response
b)
secondary antibody response
20.
Order of discovery
a)
C 1 2 3 4 5 6 7 8 9
b)
C 1 4 2 3 5 6 7 8 9
c)
C 1 3 2 4 5 6 7 8 9
d)
C 1 4 2 5 3 6 7 8 9
21.
Order of activation
a)
C 1 2 3 4 5 6 7 8 9
b)
C 1 4 2 3 5 6 7 8 9
c)
C 1 3 2 4 5 6 7 8 9
d)
C 1 4 2 5 3 6 7 8 9
22.
▪ It was the first complement pathway to be described
a)
Classical pathway
b)
Alternative pathway
c)
Lectin pathway
23.
Originally thought to be initiated by Properdin
a)
Classical pathway
b)
Alternative pathway
c)
Lectin pathway
24.
Triggers include bacterial cell walls, fungal cell walls, yeast, viruses, virally infected cells, tumor cell lines, some parasites (esp. Trypanasomes), and aggregation of IgA
a)
Classical pathway
b)
Alternative pathway
c)
Lectin pathway
25.
Initiated by IgG and IgM, CRP
a)
Classical pathway
b)
Alternative pathway
c)
Lectin pathway
26.
Binds to Fc of IgM and IgG
a)
C1q
b)
C1r
c)
C1s
d)
C4
e)
C2
27.
Activates C1s
a)
C1q
b)
C1r
c)
C1s
d)
C4
e)
C2
28.
Cleaves C4 and C2
a)
C1q
b)
C1r
c)
C1s
d)
C4
e)
C2
29.
Part of C3 convertase
a)
C1q
b)
C1r
c)
C1s
d)
C4
e)
C2
30.
Binds to C4b – form C3 convertase
a)
C1q
b)
C1r
c)
C1s
d)
C4
e)
C2
31.
Key intermediate in all pathways
a)
C3
b)
C5
c)
C6
d)
C7
e)
C8
32.
Initiates membrane attack complex
a)
C3
b)
C5
c)
C6
d)
C7
e)
C8
33.
Binds to C5b in MAC
a)
C3
b)
C5
c)
C6
d)
C7
e)
C8
34.
Binds to C5bC6 in MAC
a)
C3
b)
C5
c)
C6
d)
C7
e)
C8
35.
Polymerizes to cause cell lysis
a)
C3
b)
C5
c)
C6
d)
C7
e)
C9
36.
Starts pore formation on membrane
a)
C3
b)
C5
c)
C6
d)
C7
e)
C8
37.
Binds C3b to form C3 convertase
a)
Factor B
b)
Factor D
c)
Properdin
38.
Cleaves factor B
a)
Factor B
b)
Factor D
c)
Properdin
39.
Stabilizes C3 convertase
a)
Factor B
b)
Factor D
c)
Properdin
40.
Cleaves C4 and C2
a)
MBL
b)
MASP-1
c)
MASP-2
41.
Unknown
a)
MBL
b)
MASP-1
c)
MASP-2
42.
Binds to mannose
a)
MBL
b)
MASP-1
c)
MASP-2
43.
C3a, C4a, C5a
a)
Anaphylatoxin
b)
Chemotaxin
c)
Opsonins
d)
Immune adherence
e)
Kinin activator
44.
C5a, C5b, C6, C7
a)
Anaphylatoxin
b)
Chemotaxin
c)
Opsonins
d)
Immune adherence
e)
Kinin activator
45.
C3b, C4b, C5b
a)
Anaphylatoxin
b)
Chemotaxin
c)
Opsonins
d)
Immune adherence
e)
Kinin activator
46.
C3b
a)
Anaphylatoxin
b)
Chemotaxin
c)
Opsonins
d)
Immune adherence
e)
Kinin activator
47.
C2b
a)
Anaphylatoxin
b)
Chemotaxin
c)
Opsonins
d)
Immune adherence
e)
Kinin activator
48.
Kinin activator
a)
C3a, C4a, C5a
b)
C5a, C5b, C6, C7
c)
C3b, C4b, C5b
d)
C3b
e)
C2b
49.
Opsonins
a)
C3a, C4a, C5a
b)
C5a, C5b, C6, C7
c)
C3b, C4b, C5b
d)
C3b
e)
C2b
50.
Chemotaxin
a)
C3a, C4a, C5a
b)
C5a, C5b, C6, C7
c)
C3b, C4b, C5b
d)
C3b
e)
C2b
51.
Anaphylatoxin
a)
C3a, C4a, C5a
b)
C5a, C5b, C6, C7
c)
C3b, C4b, C5b
d)
C3b
e)
C1, C4b
52.
Virus neutralization
a)
C3a, C4a, C5a
b)
C5a, C5b, C6, C7
c)
C3b, C4b, C5b
d)
C3b
e)
C1, C4b
53.
Immune adherence
a)
C3a, C4a, C5a
b)
C5a, C5b, C6, C7
c)
C3b, C4b, C5b
d)
C3b
e)
C2b
54.
Ions involved in complement activation
a)
Calcium
b)
Potassium
c)
Magnesium
d)
Sodium
55.
Dissociates C1r and C1s from C1q
a)
C1 inhibitor
b)
Factor I
c)
Factor H
d)
C4-binding protein
e)
S protein
56.
Cleaves C3b and C4b
a)
C1 inhibitor
b)
Factor I
c)
Factor H
d)
C4-binding protein
e)
S protein
57.
Cofactor with I to inactivate C3b; prevents binding of B to C3b
a)
C1 inhibitor
b)
Factor I
c)
Factor H
d)
C4-binding protein
e)
S protein
58.
principal soluble regulator of alternative pathway
a)
C1 inhibitor
b)
Factor I
c)
Factor H
d)
C4-binding protein
e)
S protein
59.
Acts as a cofactor with I to inactivate C4b
a)
C1 inhibitor
b)
Factor I
c)
Factor H
d)
C4-binding protein
e)
S protein
60.
Prevents attachment of the C5b67 complex to cell membrane
a)
C1 inhibitor
b)
Factor I
c)
Factor H
d)
C4-binding protein
e)
S protein
61.
Vitronectin
a)
C1 inhibitor
b)
Factor I
c)
Factor H
d)
C4-binding protein
e)
S protein
62.
Protects the cells from bystander lysis
a)
DAF
b)
MIRL
c)
HRF
d)
CR1
e)
MCP
63.
Prevents insertion of C9 into cell membrane
a)
DAF
b)
MIRL
c)
HRF
d)
CR1
e)
MCP
64.
Cofactor with I, mediates transport of immune complexes It binds C3b and C4b but has greatest affinity for C3b. Once bound to CR1, both C3B and C4b can be degraded by factor I
a)
DAF
b)
MIRL
c)
HRF
d)
CR1
e)
MCP
65.
Most efficient cofactor for Factor I-mediated cleavage of C3b It also helps to control the alternative pathway because binding of factor B to C3b is inhibited
a)
DAF
b)
MIRL
c)
HRF
d)
CR1
e)
MCP
66.
prevents formation of C3 convertase
a)
DAF
b)
MIRL
c)
HRF
d)
CR1
e)
MCP
67.
Inhibitor of MAC
a)
DAF
b)
MIRL
c)
HRF
d)
CR1
e)
MCP
68.
Lupuslike syndrome; recurrent infections
a)
C1 (q, r, or s)
b)
C2
c)
C3
d)
C4
e)
C5-C8
69.
Lupuslike syndrome; recurrent infections, atherosclerosis
a)
C1 (q, r, or s)
b)
C2
c)
C3
d)
C4
e)
C5-C8
70.
Severe recurrent infections; glomerulonephritis
a)
C1 (q, r, or s)
b)
C2
c)
C3
d)
C4
e)
C5-C8
71.
Lupuslike syndrome
a)
C1 (q, r, or s)
b)
C2
c)
C3
d)
C4
e)
C5-C8
72.
Neisseria infections
a)
C1 (q, r, or s)
b)
C2
c)
C3
d)
C4
e)
C5-C8
73.
No known disease association
a)
C9
b)
C1NH
c)
DAF
d)
MIRL
74.
Hereditary angioedema
a)
C9
b)
C1NH
c)
DAF
d)
MIRL
75.
Paroxysmal nocturnal hemoglobinuria
a)
C9
b)
C1NH
c)
DAF
d)
MIRL
76.
Recurrent pyogenic infections
a)
Factor H or Factor I
b)
MBL
c)
Properdin
d)
MASP-2
77.
Pneumococcal diseases, sepsis, Neisseria infections
a)
Factor H or Factor I
b)
MBL
c)
Properdin
d)
MASP-2
78.
Neisseria infections
a)
Factor H or Factor I
b)
MBL
c)
Properdin
d)
MASP-2
79.
Pneumococcal diseases
a)
Factor H or Factor I
b)
MBL
c)
Properdin
d)
MASP-2
100 %
