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Mercy CLS 1: Immunology > 12) Complement > Flashcards

12) Complement Flashcards

1
Q

3 C’ pathways

A
  • classical
  • alternative
  • common
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2
Q

current definition of complement

A

a system of plasma proteins which mediate a variety of inflammatory effects in addition to bacteriolysis

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3
Q

discovered classical pathway

A

1894
Pfeiffer

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4
Q

discovered alternative pathway

A

1954
Pillemer

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5
Q

Ab dependent and independent C’ pathways

A

classical: dependent
alternative: independent

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6
Q

pathway that evolved earlier
more primitive

A

alternative

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7
Q

why does complement become functional in a cascade?

A

too destructive to exist in plasma in activated form

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8
Q

3 general functions of C’ system

A
  • lysis of bacteria/enveloped viruses
  • opsonization (phagocytes have receptors for C3)
  • anaphylatoxins cause inflammation (vasodilation, permeability, chemotaxis)
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9
Q

requirements for classical pathway

A
  • antigenic surface
  • Ab bound to antigenic surface (1 IgM, or 2 IgGs closeby)
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10
Q

IgG subclasses best at fixing C’

A
  1. IgG3
  2. IgG1
  3. IgG2
  4. IgG4 (not at all)
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11
Q

3 units/phases of classical pathway

A
  1. recognition unit (C1 binding, activation)
  2. activation unit
  3. MAC
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12
Q

trimolecular complex that initiates classical pathway

components?

A

C1

C1q
C1r
C1s

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13
Q

Classical Pathway Steps
(Not including common pathway)

A
  1. C1q binds Fc of Ab bound to antigenic surface
  2. C1 is activated, and molecule twists
  3. Activated C1r then activates C1s
  4. C1s activates C4, and then (with C4) C2
  5. Complex C42 forms and attaches to the surface —the C3 convertase
  6. C3 convertase cleaves C3
  7. C3a is released; C3b binds to membrane surface (C5 convertase proximal, opsonin distal)

Common pathway begins

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14
Q

Common Pathway Steps

A
  1. C5 convertase cleaves C5
  2. C5a is released; C5b forms focal point for MAC
  3. C5b fuses with C6 and C7
  4. Complex attaches to target cell membrane
  5. C8 and C9 bind, forming transmembrane channel
  6. Cell lyses
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15
Q

Alternative Pathway Steps
(Not including common pathway)

A
  1. Spontaneous cleavage of C3; C3b binds surface
  2. C3b binds factor B and factor D
  3. New C3b binds membrane surface proximally; binds properdin to stabilize C5 convertase (distal binding is opsonin)
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16
Q

best C1q binding configuration

A

IgM + IgG3

17
Q

C1s activates —–, which is required to then activate —–

A

C4
C2

18
Q

determines whether C3b is an opsonin or part of C5 convertase

A

whether it attaches to membrane proximal or distal to C42/C3bBD

19
Q

how does MAC cause lysis?

A
  • water flows in
  • K+ flows out
  • Na+ flows in
  • gross swelling of cell
  • contents leak out

empty cell sack is phagocytized

20
Q

requirements for the alternative pathway

A
  • surface with repeating polysaccharide units (bacteria, fungi, viruses)
  • spontaneous cleavage of C3 (0.2-0.4% total C3/hour)
21
Q

functions of anaphylatoxins C3a and C5a

A
  • degranulation of masts (histamine) - smooth muscle contraction, permeability
  • induce local edema - fluid contains more Ab and C’
  • chemotaxis
22
Q

examples of C’ system regulators

A
  • C1 esterase inhibitor
  • Beta 1 H
  • DAF
  • cAb inhibitor
  • anaphylatoxin inhibitor
  • S protein
  • C8 binding protein
  • C3b inhibitor
23
Q

indications for C’ lab tests

A
  • suspected hyper-utilization due to complement-activating disease
  • suspected hyposynthesis due to genetic deficiency
24
Q

3 parts of C’ panel

A
  • total hemolytic complement (CH50 assay)
  • C3 quantitative
  • C4 quantitative
25
Q

only pathway measured by total hemolytic complement

A

classical + common

26
Q

method used for C3 and C4 quantitation

A

nephelometry

measures presence only, not function

27
Q

measures rate of Ag-Ab complex formation by measuring amt of light scattered as they are formed

A

C3/C4 nephelometry

28
Q

special C’ assays done in reference labs

A
  • all complement components, immunochemical or functional
  • C1 esterase inhibitor, immunochemical or functional
29
Q

measures ability of test sample to lyse 50% of sheep rbcs coated with rabbit anti-srbc

A

CH50 total hemolytic complement

30
Q

CH50 steps

A
  • mix srbc-Ab with standard, control or pt serum
  • incubate
  • centrifuge
  • read hemolysis at 415 nm
  • calculate CH50 value
31
Q

CH50 precautions

A
  • collect on ice; C1q and C5 are heat-labile
  • reconstitute reagents with cold water
  • follow procedure exactly
  • pipette carefully
32
Q

causes of elevated complement levels

A
  • acute inflammatory conditions (acute phase proteins)
  • rheumatic diseases
  • viral hepatitis
  • MI
  • cancer
  • DM
  • pregnancy
  • sarcoidosis
  • amyloidosis
  • thyroiditis
  • IBD
  • typhoid
  • pneumococcal pneumonia
33
Q

causes of decreased complement levels

A
  • hypercatabolism (severe rheumatic disease, subacute bacterial endocarditis, HBV, GN sepsis, malaria, cryoglobulinemia)
  • liver disease (decreased synth)
  • protein malnutrition
  • genetic deficiency
34
Q

seriousness of genetic C’ defiency depends on…

A

whether component is involved in 1 pathway or the common pathway

35
Q

sx of genetic C’ deficiency

A

recurrent infections

36
Q

deficiency of C1 esterase inhibitor

A

hereditary angioedema (HANE)

37
Q

uncontrolled activation of C4 and C2, resulting in local edema

life threatening if in larynx

A

hereditary angioedema (HANE)

38
Q

HANE tx

A
  • synthetic C1 esterase inhibitor
  • non-masculinizing androgenic steroids

Mercy CLS 1: Immunology (19 decks)

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