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Quick Notes for Step 1 > Immunology > Flashcards

Immunology Flashcards

1
Q

Mutations in Fas

A

Decrease extrinsic apoptosis pathway → decreased apoptosis of autoreactive lymphocytes → autoimmune processes

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2
Q

BRCA

A
  • Tumor suppressor (2 hit) DNA repair gene
  • Repairs double stranded DNA breaks
  • AD inheritance
  • Risk of breast and ovarian cancer
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3
Q

ERBB/HER2

A
  • Protooncogene (1 hit) Tyrosine kinase receptor

- Acquired (not inherited)

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4
Q

MPO (myeloperoxidase)

A
  • In neutrophil granules catalyzes intracellular killing by producing bleach (HOCl) from H2O2 and chlorine
  • Gives sputum greenish color
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5
Q

Acute Graft Rejection

A

Dense interstitial lymphocytic infiltrate

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6
Q

Chronic Graft Rejection

A

Scant inflammatory cells + interstitial fibrosis

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7
Q

IL-2 exclusively produced by:

A

Antigen-stimulated lymphocytes

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8
Q

Tumor Suppressors: 2 Hit Hypothesis

A

If inherited syndrome, one hit is genetic, 2nd hit is sporadic

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9
Q

Invariant Chain

A

During antigen processing in macrophages, invariant chain of the MHC II is removed and replaced by an external proteins in acidified endosomes

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10
Q

Ataxia Telengectasia

A

DNA more susceptible to breaks from ionizing radiation

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11
Q

Thymus derived from

A

3rd Pharyngeal Pouch

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12
Q

PSGN: Hypersensitivity Type ___

A

Type 3 Hypersensitivity: immuno complexes deposit as humps on EM

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13
Q

Serum Sickness: Hypersensitivity Type ____

A

Type 3 hypersensitivity

- characterized by vasculitis, from a reaction to nonhuman proteins (eg. Infliximab)

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14
Q

IgG4

A
  • membranous nephropathy
  • Reidel thyroiditis
  • autoimmune pancreatitis
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15
Q

X-linker Agammaglobulinemia

A

(Bruton): mutation in tyrosine kinase that blocks B-cell maturation → immunodeficiency

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16
Q

IFN- a and IFN-b

A
  • stimulates neighboring cells to synthesize antiviral proteins that degrade intracellular mRNA (host and viral) and impair protein synthesis
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17
Q

Chediak Higashi

A

failure of phagosome-lysosome fusion → recurrent infection

- Albinism, neurological defects, and infections

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18
Q

Neutrophilia may occur w/:

A

Glucocorticoid use

- due to “demargination” of leukocytes previously attached to wall

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19
Q

IL-2 Transcription inhibitor/Inhibit calcineurin

A

Cyclosporine and Tacrolimus

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20
Q

Inhibits signaling/Inhibits MTOR

A

Sirolimus

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21
Q

Binds FKBP

A

Sirolimus and Tacrolimus

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22
Q

CGD

A

Dx: DHR (preferred) or NBT

  • Recurrent infections of catalase + enzymes (because defect in NADPH oxidase)
  • Candida, Staph, Klebsiella, Burkholderia
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23
Q

p-ANCA/MPO

A

Churg Strauss and Microscopic polyangiitis

  • Churg: allergy, and granulomatous, adult onset asthma, eosinophilia, and neuropathy
  • Polyangitis: use cyclophosphamide (also for polyarteritis)
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24
Q

c-ANCA/PR3

A

Wegeners: upper respiratory and granulomatous, use cyclophosphamide

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25
Q

Tight binding of neutrophils and crawling via:

A

ICAM (to LFA, MAC1) or VCAM (to VLA)

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26
Q

Transmigration via:

A

PECAM (aka CD31)

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27
Q

Margination and Rolling via:

A

E and P selectins (on endothelium) to sialyly lewis on leukocytes

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28
Q

DiGeorge: Abnormal Development of _______

A

3rd and 4th Pharyngeal Pouches

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29
Q

HyperIgM

A

defective CD40L on Th cell → no isotype switching so low IgG, IgE, and IgA (high IgM)

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30
Q

Hypersensitivity: Immediate, IgE, eosinophilia

A

Type I

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31
Q

Hypersensitivity: Autoantibodies

A

Type II

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32
Q

Hypersensitivity: Immune complex deposites

A

Type III

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33
Q

Hypersensitivity: T-cell or delayed (TH1 or CD8/CTL)

A

Type IV

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34
Q

Leukotriene B4

A

attracts neutrophils

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35
Q

Leukotriene C4, D4, E4

A

Bronchoconstriction

36
Q

C5a, IL8, and Kallikrein

A

released in response to bacteria

37
Q

IL-6

A

mediates inflammatory response (acute phase protein)

38
Q

IL-10

A

anti-inflammatory

39
Q

TGF-B

A

anti-inflammatory

40
Q

IL-2

A

stimulates growth/proliferation of helper T cells and B cells (which activate macrophages and NK cells)

41
Q

IFN-gamma

A

activates macrophages

42
Q

TH2 Cytokines: B cell class switching

A
  • IL-4 → IgE and IgG

- IL-5 → IgA and eosinophils

43
Q

Selective IgA Deficiency

A
  • MC deficiency

- anaphylaxis to IgA containing products (should get blood products from another IgA deficient person)

44
Q

Phenotypic Mixing

A

2 viruses that infect the same cell can make resulting progeny that can have nucleocapsid proteins from one strain and the genome form another (but there is not change in viral genome so the next generation will go back to the unmixed phenotype)

45
Q

T Cells in Lymph Node

A

Paracortex

46
Q

Hypercalcemia in Granulomatous Diseases

A

In granulomatous diseases (eg. Sarcoidosis), macrophages are activated and they have increased activity of 1-alpha hydroxylase → hypercalcemia

47
Q

During anaphylaxis, Mast Cells Release:

A

histamine, heparin, and tryptase (specific)

48
Q

HLA A3

A

Hemochromatosis

49
Q

HLA B27

A

psoriatric arthritis, ankylosing spondylitis, IBD, reactive (reiter) arthritis (PAIR)

50
Q

HLA DQ2/8

A

Celiac

51
Q

HLA DR4

A

Rheumatoid Arthritis

52
Q

HLA DR2

A

Autoimmune type diseases: Goodpasture, SLE, MS, hay fever

53
Q

HLA DR3

A

Graves and SLE

54
Q

HLA DR3/4

A

Type I Diabetes

55
Q

HLA DR 5

A

Pernicious anemia, Hashimoto

56
Q

3 Actions of Antibodies

A

opsonize for phagocytosis, neutralize to prevent attachment, or activate complement to kill

57
Q

Antibody: Idiotype

A

the specific antigen it binds

58
Q

Antibody: Allotype

A

Minor changes in constant regions of Ab that are different in each person

  • IgG in one person will be different from another
  • Used in paternity testing
59
Q

Antibody: Isotype

A

Class of antibody (E, M, D, G, A)

60
Q

Antibody: Complement

A

Complement binds to Fc region of heavy chain

61
Q

Antibody: Heavy chain

A

VDJ-C; Light chain: VJ

62
Q

IgA

A

Prevents attachment to mucosa (does not fix complement)

63
Q

IgE: Hypersensitivity vs Helminth

A
  • If hypersensitivity reaction: then does not activate complement, only crosslinks and causes degranulation of Mast cells and basophils
  • If activated by TH2, then does complement to kill helminth
64
Q

C3b

A

Opsonization (also done by IgG)

65
Q

C5a

A

Neutrophil chemotaxis (also anaphylaxis)

66
Q

DAF (CD55) and C1 esterase inhibitor

A

Prevent complement

67
Q

Macrophages release:

A

IL-1, 6, 8, 12, TNFa

68
Q

TH1 activates:

A

NK cells, Macrophages, and CTLs

69
Q

TH2 effects:

A

B cell class switching and eosinophil recruitment

  • IgE/IgG (from IL 4)
  • IgA/eosinophils (from IL5)
70
Q

CD40L on ______

A

Helper T cells

71
Q

CD40 on ______

A

APCs (B cells)

72
Q

Type III Hypersensitivity

A

antigen + soluble IgG + complement → complex → damage to tissue

73
Q

MHC II

A
  • extracellular antigen presentation

- loaded with antigen within an acidified endosome

74
Q

ANCA

A

Anti- Neutrophil Cytoplasmic Antibody

75
Q

Immediate Hypersensitivity w/ Blood Transfusion

A

Seen w/ Selective IgA deficiency

patients often have IgG antibodies against IgA

76
Q

Individuals with HLA haplotypes that cannot bind certain polypeptide fragments:

A

will be unable to mount a T-cell dependent (IgG, IgA) immune response against these antigens
- unable to present an antigen if it cannot recognize it

77
Q

Posterior calf and dorsolateral foot Drains to: _________ lymph nodes

A

Popliteal

78
Q

Below pectinate line, and skin below umbilicus (except popliteal area) Drain to: _______ lymph nodes

A

Superficial Inguinal

79
Q

Testes, Ovaries, Kidneys, and Uterus Drain to: ________ lymph nodes

A

Para-aortic

80
Q

Edema at a site of injury or inflammation

A

Endothelial tight junctions permeability is increased in response to injury and inflammation, allowing migration of white blood cells to site

81
Q

C3 Deficiency

A

SLE

82
Q

IL8

A

Chemotactic factor for neutrophils

83
Q

Type III Hypersensitivity (5)

A 
SLE
Polyarteritis nodosa
PSGN
Arthus Reaction
Serum Sickness
84
Q

Type IV Hypersensitivity (5)

A 
MS
Guillain Barre
PPD
Graft vs Host
Contact Dermatitis
85
Q

Hyper IgE

A

AD
Deficiency of TH17 due to STAT3 mutation –> impair neutrophil recruitment
coarse facies, noninflamed staph abcesses, primary teeth rentention, eczema

86
Q

SCID: X linked Mutation vs Auto Recessive Mutation

A

X linked: IL2R gamma chain problem (MC)

Auto recessive: Adenosine deaminase

Quick Notes for Step 1 (18 decks)

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