Complement System Flashcards

(47 cards)

1
Q

Complement system is defense against

A

mainly bacteria

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2
Q

proteins for CS are synthesized in

A

the liver

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3
Q

many CS proteins are present as

A

inactive form in blood and other fluids and require activation for effect

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4
Q

activation pathways

A

classical(CP), Alternative(AP) and Terminal(TP)

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5
Q

a deficiency in the terminal pathway components leads to

A

susceptibility to Neisseria Sp infections

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6
Q

Membrane attack complex (MAC)=

A

in terminal/common C5b, C6, C7, C8, C9

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7
Q

activation of classical pathway leads to

A

convergence with terminal pathway

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8
Q

Activation of classical pathway starts with

A

IgG(2 Fc’s needed) or IgM(only 1 needed) complex binds to C1

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9
Q

Pentameric IgM=

A

5Fc-mu’s available to bind

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10
Q

C1 cleaves

A

C4 to C4a and C4b and C2 to C2a and C2b

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11
Q

C1 Cleavage forms

A

C4b2a= C3 convertase(CP)

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12
Q

C3 convertase cleaves

A

C3 to C3a and C3b and forms C4b2a3b (C5 convertase)

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13
Q

C5 convertase cleaves

A

C5a and C5b

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14
Q

C5b binding to

A

the microbe surface initiations formation of MAC of the Terminal pathway

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15
Q

Alternative pathway is activated by

A

spontaneously generated C3b deposits on activating surface

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16
Q

Factor B binds to

A

C3b

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17
Q

Factor B is cleaved by

A

Factor D and forms teh C3bBb

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18
Q

C3bBbis also called

A

C3 convertase

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19
Q

Poperdin extends

A

the half life of C3bBb by 6-10 fold

20
Q

C3bBb cleaves

A

C3 to C3a and C3b and forms C3bBb3b (C5 convertase)

21
Q

C3bBb3b cleaves

A

C5 to C5a and C5b

22
Q

classical proteins

23
Q

Terminal proteins

24
Q

Alternative proteins

A

C3b,3,5 Factor B, D Properdin

25
role of C3b
opsonin mediated phagocytosis and elimination of immune complexes
26
role of C3a, 4a, 5a
degranulation of mast cells and basophils
27
Role of C5a
chemotaxis of neutrophils
28
role of MAC
Osmotic lysis of bacteria
29
role of regulatory complement proteins
protect autologous cells from complement mediated damage
30
C1 INH, C1 esterase inhibitor binds
C1 to prevent spontaneous activation
31
C4bp(binding protein binds
the fluid phase of C4b preventing attachment to cells and formation of C3 convertase
32
Factor H binds
to C3b in fluid phase preventing the binding to the microbe
33
Factor H competitively binds
C3b which leads to dissociation of C3bBb if it has formed.
34
Decay accelerating Factor (DAF)
binds to membrane bound C3b or C4b blocking formation of C3 convertase or dissociating C3 convertases that formed.
35
Anaphylatoxin inhibitor binds
C3a, C4a and C5a and inhibits binding to Cr3a/4a. C45a
36
Factor I cleaves
C4b and C3b to inactive forms in presence of cofactors
37
S- protein, CD59, and Homolgous restriction factor (HRF
inihibit formation of MAC on autologous cells.
38
CR1
receptor on phagocytes and RBC that binds to C3b or C4b and is part of the opsonin/immune complex elimination
39
CR2
receptor on B cells that binds C3bi- is a mode of epstein barr virus infection
40
C3a/4a binds
C3a and C4a and is found on mast cells and basophils, it leads to degranulation and histamine release (CR5a binds C5a on mast cells and basophils for the same effect
41
CR5a on neutrophils binds
C5a which is used as a chemotaxis for neutrophils
42
Ch50 complement test
measures overall complement activity and whether or not it is low for c3 and c4
43
Tissue damage activates
the intrinsic coagulation system and activates factor XII
44
factor XII(a) activates
zymogen prekallikrein to kallikrein
45
role of kallikrein
- -cleave kininogen to kininogena and brady kinin | - -cleaves C5 to C5a and C5b because C5a is chemotactic for neutrophils
46
bradykinin increases
vascular permeability which is critical in inflammation
47
Killikrein is inactivated by
C1INH