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Immunology > L4 Complement > Flashcards

L4 Complement Flashcards

1
Q

Complement is a biochemical pathway that is a key part of the innate/adaptive immune system and assists with the innate/adaptive immune system

A

innate; adaptive

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2
Q

complement enhances/eliminates the inflammatory response, enhances/eliminates pathogens and enhances/eliminates the immune response

A

enhances, eliminates, enhances

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3
Q

three steps of complement

A
  1. opsonization
  2. inflammation
  3. lysis
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4
Q

opsonization

A

acts like a glue to attach substances or antibodies to pathogens to phagocytosis by macrophages (poly-mononuclear neutrophils)

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5
Q

inflammation

A

induces acute inflammation to dilate blood vessels by activating mast cells/basophils and to recruit inflammatory phagocytic cells to eat the invading organism

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6
Q

lysis

A

generates a group of proteins able to penetrate the invading organisms cell wall and induce lysis

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7
Q

the order of activation for complement pathways

A
  1. alternating
  2. lectin
  3. classical
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8
Q

alternating pathway

A

uses C3, activated spontaneously or via microbial surfaces
c3 –> c3a + c3b (c3b binds to pathogen and can help in opsonization or be converted to C3 convertase), or form C5 convertase whiich can help form membrane attack complex

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9
Q

C3 is present in the circulation system and is produced by the

A

liver

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10
Q

lectin pathway

A

activated via microbial surfaces
ex. mannose
mannose binding protein binds to mannose present on bacteria surface, C2 –> C2a + C2B and C4 –> C4a + C4b, C4b and C2b combine to form C3 convertase whcih helps convert C3 to C3b and C3a, C3b will eventually help form C5 convertase which can lead to MAC

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11
Q

classical pathway

A

activated via antibody attachment and Fc portion, C1
C2 –> C2a + C2B and C4 –> C4a + C4b, C4b and C2b combine to form C3 convertase which helps convert C3 to C3b and C3a, C3b will eventually help form C5 convertase which can lead to MAC

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12
Q

lectins activate the _____ pathway

A

lectin

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13
Q

the common goal of the three pathways is to deposit clusters of _________ on a target

A

C3b

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14
Q

anaphylatoxins

A

increase vascular permeability

C3a, C4a, and C5a

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15
Q

chemoattractants

A

attract neutrophils and monocytes

C3a C5a

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16
Q

membrane attack complex (MAC)

A

final phase of complement- C5b-9
lysis
creates perforations in cellular membranes

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17
Q

C3b functions as an

A

opsonin

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18
Q

microbes coated in C3b are ________ by virtue of C3b being recognized by complement receptor type I (CR1)

A

phagocytosed

19
Q

____________ helps to down-regulate the C3 convertase

A

decay accelerating factor (DAF)

20
Q

people with lack of DAF

A
  • uncontrolled complement

- leads to RBC lysis

21
Q

RBC lysis

A

paroxysmal nocturnal hemoglobinuria (PNH)

22
Q

C1 inhibitor

A

protease inhibitor that down regulated C1 activation in the classical pathway of complement

23
Q

people who lack C1 inhibitor

A

uncontrolled C1 activation
excessive vasoactive peptides
can lead to angiodema

24
Q

how does C1 inhibitors regulate angiodema?

A

C1 inhibits bradykinin pathway

25
Q

assay for alternative pathway

A

AH50

26
Q

assay for lectin pathway

A

MBL

27
Q

assay for classical pathway

A

CH50

28
Q

C3 deficiency

A

profound risk of encapsulated bacteria infection

29
Q

C1, C2, C4 DEFICIENCY

A

associated with increased risk of immune complex disease example would be systemic lupus erythematosus (SLE)

30
Q

C1 inhibitor deficiency

A

excess of vasoactive peptides (bradykinin)

31
Q

C5b, C6, C7. C8, C9 deficiency

A

increased susceptibility to Neisseria and meningitidis infections due to not being able to form MAC

32
Q

MAC can induce lysis only on cells that have thin cell walls such as

A

neisseria species

33
Q 
The Classical pathway of Complement is activated following antibody:antigen interaction with what component?
C1q (and C1r-C1s)
C3 convertase
C5a
C5b, C6, C7, C8, C9
A

C1q (and C1r-C1s)

34
Q

T/F Complement activation typically occurs in the order of Alternative, Lectin, and Classical pathways, respectively.

A

T

35
Q

t/f Complement components C6, C7, C8, and C9 comprise the anaphylatoxins.

A

false

36
Q

T/F Complement component C5a is an opsonin because it coats/labels bacteria.

A

false

37
Q 
Invasive meningococcal (Neisseria meningitidis) disease and disseminated gonococcal (Neisseria gonorrheae) infections are the only conditions (i.e. no autoimmune diseases) known to be associated with complement deficiencies in:
C3
C1q
C8
C4
C1 inhibitor
A

C8

38
Q

The highest rates of meningococcal disease are seen in infants, who have little natural antibody against Neisseria. Older teens and young adults have much higher rates of colonization (on mucous membranes), higher levels of antibody, but lower levels of disease. Which pathway of complement activation could involve this specific antibody?

A

classical

39
Q

You are called to see a patient with severe disease due to meningococcemia in the ICU. He has purpura fulminans and sequelae of sepsis including multisystem organ disease including liver and kidney failure. The resident ordered a CH50 and the result is low. You are trying to decide if this is more likely an acquired or inherited terminal complement deficiency. Which of the following is FALSE:

  1. Testing for decreased levels of multiple complement components may help distinguish acquired from the inherited defect
  2. Testing total complement after recovery of this illness may help distinguish acquired from inherited defect
  3. Liver failure is a cause of low CH50
  4. Vasculitis is a cause of low CH50
  5. Obtaining an AH50 to test function of the alternate pathway may help to distinguish acquired from the inherited defect
A
  1. Obtaining an AH50 to test function of the alternate pathway may help to distinguish acquired from the inherited defect
40
Q

The three main anatomic locations involved in attacks of hereditary angioedema are:
Lower extremities, genitalia, abdomen
Eyelids, upper extremity, upper airway
Upper extremity, neck, gastrointestinal tract
Lower extremities, gastrointestinal tract, skin
Skin, upper airway, gastrointestinal tract

A

Skin, upper airway, gastrointestinal tract

41
Q 
Pathogenesis of angioedema in hereditary angioedema is predominantly mediated by excess:
Histamine
C1 Inhibitor
C3
Bradykinin
Membrane Attack Complex
A

Bradykinin

42
Q 
In Hereditary C1 Inhibitor Deficiency, on would expect the following complement levels:
Low C4, Low C1 Inh
Low C4, High C1 Inh
Normal C4, Low C1 Inh
Normal C4, High C1 Inh
High C4, High C1 Inh
A

Low C4, Low C1 Inh

43
Q

hereditary angioedema

A

disease due to defect in C1 inhibitor
decreadsed levels of C4 and C2
autosomal dominant
plasma derived C1 inhibitor

44
Q

neisseria meningitidis

A

gram negative cocci
produces polysaccharide capsule - major virulence factor
complement deficiencies in C8

Immunology (14 decks)

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