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Immunology > Quiz 1 > Flashcards

Quiz 1 Flashcards

1
Q

Isolated congenital asplenia

A
  • due to ribosomal protein SA and laminin mutations
  • increased susceptibility to encapsulated bacteria
  • immunizations are important
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2
Q

Properdin deficiency

A

recurrent infections

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3
Q

Factor H or I deficiency

A
  • unchecked complement activation

- renal disease and recurrent infections

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4
Q

C5-9 deficiency

A

Neisseria infections susceptibility

-meningitis and gonorrhea

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5
Q

Paroxysmal Nocturnal Hemoglobinuria

A
  • PIGA gene mutation impairs HRF, protectin, and DAF function
  • complement mediated RBC lysis, hemoglobinuria, symptomatic anemia, thrombosis
  • Tx: eculizumab (anti-C5)
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6
Q

C3 deficiency

A

recurrent bad infections, Ag-Ab complex (lupus like) disease

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7
Q

Inappropriate complement activation

A

C5a, C3a, C4a mediated anaphylaxis

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8
Q

MBL deficiency

A

recurrent infections

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9
Q

C4A or C4B gene deficiency

A

propensity to develop SLE

genes located in MHC Class III area

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10
Q

C1INH deficiency

A
  • Hereditary angioedema
  • increases C2 kinin and bradykinin levles
  • painless swelling that does not respond to antihistamines
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11
Q

C1INH treatment

A
  • C1INH: Berinert, Cinryse, Ruconest
  • bradykinin B2 receptor antagonist: icatibant
  • Kallikrein inhibitor: Ecallantide
  • 2nd line is fresh frozen plasma
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12
Q

C1INH Types

A

1: less C1INH
2: less functional C1INH
3: level and function are normal, females Facton XII gain of function triggers kallikrein-kinin system
acquired: anti-C1INH Ab, excessive C1 activation

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13
Q

IRAK4 or MyD88 deficiency

A

strep, staph, gram negative susceptibility in children

typically by age 14 adaptive immune system takes over

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14
Q

NEMO deficiency

A

aka IKK-gamma subunit deficiency
incontinentia pigmenti (worsening skin condition)
anhidrotic ectodermal dysplasia (conical teeth, skin, hair)
impaired Ab class switching
recurrent infections

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15
Q

Septic shock

A

due to systemic bacterial infection and TNF-alpha release

increased susceptibility with TLR4 mutation

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16
Q

UNC-93B deficiency

A

needed for TLR3, TLR7-9

increased susceptibility to HSV

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17
Q

Familial cold autoinflammatory syndrome 1

A

gain of function NLRP3 mutation (cryopyrin)
rash, fever, arthralgias following cold exposure
Tx: canakinumab (antiIL-1beta), rilanocept (IL1 inhibitor)

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18
Q

Chediak-Higashi syndrome

A

large cytoplasmic granules in neutrophils impede diapedisis

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19
Q

Chronic Granulomatous Disease (CGD)

A

deficiency in NADPH oxidase subunit impairs H2O2 production in neutrophils, prevents respiratory burst

  • Sx: boils, abscesses, pneumonia, osteomyelitis
  • typically X-linked recessive
  • Susceptibility to: Staphyloccocus aureus, Aspergillus fumigatus, Serratia marcescens, Nocardia asteroides, Burkholderia cepacia
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20
Q

CH50

A

screens classical pathway defect
near 0 in C1-C8 deficiency
half normal in C9 deficiency
low in factor I or H deficiency

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21
Q

AH50

A

screen for alternative pathway defect

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22
Q

C3d

A

marker for classical pathway activation

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23
Q

Ba

A

marker for alternative pathway activation

24
Q

C1q

A

detects immune complexes

25
Q

IRAK4

A

test for TLR deficiency

26
Q

DHR (dihyrorhodamine)

A

tests for respiratory burst

27
Q

Properdin

A

stabilizes C3bBb

28
Q

DAF and MCP

A

kicks C3b off of C3b2Bb

-MCP also recruits factors I

29
Q

Factors H and I

A

inactivate C3b to iC3b

30
Q

C3b2Bb

A

alternative C5 convertase

31
Q

S protein, clusterin, factor J

A

prevent C5b67 from inserting into membrane

32
Q

HRF and protectin

A

prevent C9 polymerization

33
Q

anaphylatoxins

A

C5a>C3a>C4a

inflammatory response

34
Q

alpha2-macroglobulin

A

inactivates bacterial proteases

35
Q

defensins

A

family of antimicrobial peptides

36
Q

pentraxis

A

circulating proteins bind pathogen and immune cell

37
Q

C4b2b3b

A

classical C5 convertase

38
Q

C1INH

A

binds to C1r and C1s and dissociate from C1q, also inhibits clotting and kinin systems

39
Q

lectins

A

recognize carbohydrates

40
Q

scavenger receptors

A

SR-A, SR-B, MARCO

recognize negatively charged microbial ligands

41
Q

CR1

A

recognizes C3b

42
Q

CR3 and CR4

A

recognize iC3b and LPS

43
Q

TLR4

A

recognizes LPS

44
Q

TLR3

A

recognizes dsRNA including HSV

45
Q

TLR9

A

recognizes unmethylated CpG

46
Q

TLR pathway

A

TLR activation - intracellular TIR domain - MyD88 - IRAK4 - TRAF6 - phosphorylation of IKK - degradation of IkB from NFkB - NFkB increases transcription of cytokines and adhesion proteins

47
Q

Pyrogens

A

IL1beta, IL-6, TNF-alpha

48
Q

IL-12

A

activates NK cells and IFN-gamma production

49
Q

CXCL8

A

chemokine recruits basophils and neutrophils

50
Q

NLRs (NOD-like receptors)

A

recognize intracellular PAMPs

51
Q

NLRP3

A

recognizes intracellular PAMP and forms inflammasome to activate pro-IL-1beta –> inflammation

52
Q

Sialyl-Lewis-x

A

on neutrophils, interaction with endothelial selectin to slow

53
Q

LFA-1

A

on neutrophil, binds ICAM-1 on endothelium for extravasation

54
Q

lipofuscin

A

age-related pigment associated with atrophy

55
Q

nuclear changes with cell death

A
  1. pyknosis: chromatin condensation
  2. karyorrhexis: nuclear fragmentation
  3. karyolysis: fading of nucleus
56
Q

Coagulative necrosis

A

architecture remains, greater protein denaturation than enzymatic digestion

57
Q

Liquefactive necrosis

A

architecture is lost early, greater enzymatic digestion than protein denaturation

Immunology (10 decks)

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