Complement Flashcards

1
Q

What is complement?

A

A system of interacting proteins that play a role in innate immunity and inflammation (p.199)

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2
Q

What types of bacteria does the Membrane attack complex (MAC) of complement specifically protect against?

A

Gram negative bacteria (p.199)

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3
Q

What immunoglobulins mediate activation of the classic pathway of complement?

A

IgG or IgM (pneumonic: GM makes classic cars) (p.199)

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4
Q

What activates the alternative pathway of complement?

A

Microbe surface molecules (p.199)

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5
Q

What activates the lectin pathway of complement activation?

A

Mannose or other sugars on the microbe surface (p.199)

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6
Q

What are the three pathways of complement activation?

A

Classic, Alternative, Lectin pathways (p.199)

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7
Q

What is the function of C3b?

A

Opsonization (p.199)

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8
Q

What is the function of C3a and C5a together?

A

Anaphylaxis (p.199)

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9
Q

What is the function of C5a individually?

A

Neutrophil chemotaxis (p.199)

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10
Q

What complement factors are involved in cytolysis by MAC?

A

C5b- C9 (p.199)

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11
Q

Name the two primary opsonins in bacterial defense.

A

C3b and IgG (p.199)

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12
Q

Name another important function of C3b.

A

C3b helps clear immune complexes (p.199)

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13
Q

What two factors inhibit complement activation on self cells (e.x. RBCs)?

A

Decay accelerating factor (DAF) and C1 esterase inhibitor (p.199)

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14
Q

Describe the steps of the alternative pathway of complement activation.

A

Spontaneous and microbial surfaces act on C3. C3 –> C3b –> C3 Convertase –> C3a + C3b. C3b –> C5 convertase –> C5b –> MAC –> lysis, cytotoxicity (p.199)

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15
Q

Describe the steps of the classic pathway of complement activation.

A

Antigen antibody complexes cause C1 to convert C2 –> C2a which when added to C4b becomes C3 convertase –> C3b + C3a. C3b –> C5 convertase –> C5b –> MAC –> lysis, cytotoxicity (p.199)

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16
Q

Describe the steps of the alternative pathway of complement activation.

A

Microbial surfaces (ex. Mannose) turns a C1 like complex into C1. C1 converts C2 –> C2a which when added to C4b becomes C3 convertase –> C3b + C3a. C3b –> C5 convertase –> C5b –> MAC –> lysis, cytotoxicity (p.199)

17
Q

What are the clinical manifestations of a C1 esterase inhibitor deficiency?

A

Hereditary angioedema (p.200)

18
Q

What types of medications are contraindicated in a patient with a C1 esterase inhibitor deficiency?

A

ACE inhibitors (p.200)

19
Q

What are the clinical manifestations of a C3 deficiency?

A

Severe, recurrent pyogenic sinus and respiratory tract infections; increased susceptability to type III hypersensitivity reactions (p.200)

20
Q

What are the clinical manifestations of a C5-C9 deficiency?

A

Recurrent Neisseria bacteremia (p.200)

21
Q

What type of bacterial infection is most common in patients with a C5-C9 deficiency?

A

Neisseria bacteremia (p.200)

22
Q

What are the clinical manifestations of a DAF (GPI anchored enzyme) deficiency?

A

Complement mediated lysis of RBCs and paroxysmal nocturnal hemoglobinuria (PNH) (p.200)