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Pathoma > Pathoma 2 > Flashcards

Pathoma 2 Flashcards

1
Q

acute vs chronic inflamm: edema and neutrophils in tissue

A

acute

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2
Q

acute vs chronic inflamm: innate immunity w/limited specificity

A

acute

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3
Q

TLR’s activated by:

A

PAMPs = pathogen associated molecular patterns

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4
Q

TLR on macrophages that recognizes LPS

A

CD14

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5
Q

TLR’s are present on cells of innate/adaptive/both?

A

both

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6
Q

TLR activation upregulates:

A

NF-kB

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7
Q

arachidonic acid is released via what enzymes?

A

phospholipase A2 and C

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8
Q

COX produces _______, which mediate:

A

PGI2, D2, E2 (also pain & fever): vasodilation, inc. vasc. permeability

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9
Q

5-lipoxygenase produces ________, which mediate:

A

LTB4: attracts/activates neutrophils; LTC4, D4, E4: vasoconstriction, bronchospasm, inc. vasc. permeability (anaphylaxis)

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10
Q

mast cells activated by what 3 things:

A

tissue trauma, C3a/C5a, cross-linking of IgE by antigen

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11
Q

immediate mast cell response:

A

preformed histamine granules

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12
Q

delayed mast cell response:

A

arachidonic acid metabolites, esp. LT’s

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13
Q

mannose-binding lectin complement pathway

A

MBL binds mannose on microorganisms

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14
Q

alternative complement pathway

A

microbial products directly activate complement

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15
Q

classical complement pathway

A

C1 binds IgG or IgM bound to antigen

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16
Q

all complement pathways result in production of:

A

C3 convertase (C3–> C3a + C3b)–> C5 convertase (C5–> C5a + C5b)

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17
Q

MAC made up of:

A

C5b-C9

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18
Q

neutrophil chemotaxis

A

C5a, LTB4, IL-8, 5-HETE, bacterial products

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19
Q

opsonins for phagocytosis

A

IgG, C3b

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20
Q

hageman factor

A

factor XII, role in DIC w/acute gram neg sepsis, complement and kinin systems

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21
Q

kinin system

A

kinin cleaves HMWK–> bradykinin (vasodilation, inc. vasc. permeability, pain)

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22
Q

mediators of pain:

A

PGE2, bradykinin

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23
Q

rubor

A

redness

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24
Q

calor

A

warmth

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25
Q

mediators of rubor and calor:

A

histamine, PGI/E/D, bradykinin

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26
Q

mediators of tumor (swelling):

A

histamine, tissue damage

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27
Q

dolor

A

pain

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28
Q

mediators of fever:

A

pyrogens (LPS)–> IL-1, TNF–> inc. COX–> inc. PGE2

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29
Q

phases of acute inflammation: 12 hrs, 24 hrs, 48 hrs

A

edema, neutrophils, macrophages

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30
Q

speed bumps in neutrophil rolling

A

P-selectin from Weibel-Palade bodies (histamine); E-selectin (TNF, IL-1)

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31
Q

selectins bind ______ on WBC’s

A

sialyl lewis X

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32
Q

ICAM and VCAM upregulated by

A

TNF, IL-1

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33
Q

firm adhesion via:

A

CAMS, integrins

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34
Q

integrins upregulated by:

A

C5a, LTB4, IL-8, 5-HETE, bacterial products

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35
Q

leukocyte adhesion def. (LAD)

A

AR defect of integrins (CD18); delayed separation of umbilical cord, inc. neutrophils, recurrent bacterial infections lacking pus

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36
Q

protein trafficking defect w/impaired phagolysosome formation

A

chediak higashi syndrome, AR

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37
Q

chediak higashi sx:

A

neutropenia, defective primary hemostasis, albinism, peripheral neuropathy

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38
Q

oxidative burst

A

O2–> O2 radical by NADPH oxidase–> H2O2 by SOD–> HOCl radical by MPO

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39
Q

CGD

A

NADPH oxidase defect, X linked or AR

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40
Q

catalase positive organisms:

A

s. aureus, pseudomonas cepacia, serratia marcescens, nocardia, aspergillus

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41
Q

screening for CGD:

A

nitroblue tetrazolium test (colorless is there’s a defect)

42
Q

MPO def. increases risk for:

A

Candida infections

43
Q

anti-inflammatory cytokines:

A

IL-10, TGF-beta from macrophages

44
Q

cytokine released from macrophages for continued acute inflamm:

A

IL-8

45
Q

acute vs chronic inflamm: lymphocytes and plasma cells in tissue

A

chronic

46
Q

acute vs chronic inflamm: delayed adaptive immunity w/specificity

A

chronic

47
Q

where does TCR undergo rearrangement–> CD4 vs CD8?

A

thymus

48
Q

TCR and CD3 is used for:

A

antigen surveillance

49
Q

2nd activation signal for CD4 T cells:

A

B7 on APC binds CD28 on CD4 T cell

50
Q

TH1 secretes:

A

IL-2 (T cell growth factor and CD8 activator), IFN-gamma (macrophage activator)

51
Q

TH2 secretes:

A

IL-4 (B cell class switching–> IgG, IgE), IL-5 (eosinophil chemotaxis/activation, B cell–> plasma cell w/class switching to IgA), IL-10 (inh. TH1)

52
Q

expressed by all nucleated cells and PLT’s

A

MHC I

53
Q

2nd activation signal for CD8 T cells:

A

IL-2 from CD4 TH1

54
Q

how do CD8 T cells kill?

A

perforin, granzyme, FasL

55
Q

where do B cells undergo Ig rearrangements?

A

bone marrow

56
Q

naïve B cells express:

A

IgM, IgD

57
Q

2nd activation signal for B cells:

A

CD40 rec. on B cell binds CD40L on TH cell

58
Q

epithelioid histiocytes

A

macrophages w/abundant pink cytoplasm–> granuloma

59
Q

noncaseating granulomas:

A

rxn to FB, sarcoidosis, beryllium exposure, crohn’s disease, cat scratch disease

60
Q

caseating granulomas:

A

TB and fungal infections

61
Q

granuloma formation

A

IL-12 from macrophages–> TH1 cells–> IFN-gamma–> epithelioid histiocytes and giant cells

62
Q

digeorge syndrome

A

3rd/4th pharyngeal pouches, 22q11 microdeletion, T cell def. and hypocalcemia

63
Q

SCID etiologies:

A

cytokine rec. defects, ADA def., MHC class II def.

64
Q

SCID tx:

A

sterile isolation and stem cell transplantation

65
Q

X-linked agammaglobulinemia

A

disordered B cell maturation, mutated bruton tyrosine kinase (Btk), X-linked

66
Q

CVID

A

low Ig’s due to B cell or TH cell defects; inc. risk for autoimmune dz and lymphoma

67
Q

most common Ig def.

A

IgA

68
Q

hyper-IgM syndrome

A

mutated CD40L or CD40 rec. = no cytokines for class switching

69
Q

WAS

A

thrombocytopenia, eczema, recurrent infections, WASR gene, X-linked

70
Q

C5-C9 def.

A

neisseria infections

71
Q

C1 inh. def.

A

hereditary angioedema of skin and mucosal surfaces

72
Q

anergy of lymphocytes is due to:

A

recognition of antigen in peripheral lymphoid tissue w/no 2nd signal

73
Q

SLE hypersensitivity

A

type II and III

74
Q

SLE most common cause of death

A

diffuse proliferative GN and infection

75
Q

small sterile deposits on both sides of mitral valve

A

libman-sacks endocarditis w/SLE

76
Q

specific antibody for SLE

A

anti-dsDNA

77
Q

ANA

A

sensitive for SLE but not specific

78
Q

antihistone Ab

A

drug-induced SLE due to: hydralazine, procainamide, INH

79
Q

anticardiolipin and lupus anticoagulant

A

antiphospholipid antibody syndrome: false pos. syphilis, falsely inc. PTT

80
Q

sjogren’s hypersensitivity

A

type IV

81
Q

SSA (Ro)/SSB (La)

A

anti-ribonucleoprotein antibodies

82
Q

sjogren’s w/inc. risk for _____ w/unilat. enlargement of parotid

A

B cell (marginal zone) lymphoma

83
Q

most commonly involved organ w/diffuse scleroderma:

A

esophagus

84
Q

anti-centromere Ab’s

A

CREST syndrome

85
Q

anti-topo I (Scl-70) Ab’s

A

diffuse scleroderma

86
Q

Ab’s against U1-ribonucleoprotein

A

mixed CT disease (SLE, systemic scleroderma, polymyositis)

87
Q

labile tissues

A

continuously regenerate: bowels, skin, bone marrow

88
Q

stable tissues

A

regenerate when necessary: liver by compensatory hyperplasia after resection

89
Q

permanent tissues

A

myocardium, skeletal m., neurons

90
Q

scar formation

A

type III collagen (granulation, embryonic, uterus, keloids) replaced w/type I collagen (skin, bone, tendons, organs)

91
Q

what removes type III collagen, using _____ as a cofactor?

A

collagenase, zinc

92
Q

TGF-alpha

A

EGF and FGF

93
Q

TGF-beta

A

FGF, inh. Inflamm.

94
Q

PDGF

A

endothelium, smooth m., fibroblasts

95
Q

FGF

A

angiogenesis, skeletal dev.

96
Q

VEGF

A

angiogenesis

97
Q

healing via secondary intention

A

edges not approximated, granulation tissue, myofibroblast contraction w/scar

98
Q

what vitamin/mineral def. result in delayed wound healing?

A

vit. C (hydroxylation), copper (lysyl oxidase), zinc (collagenase)

99
Q

dehiscence

A

rupture of a wound

100
Q

hypertrophic scar

A

excess scar tissue localized to wound

101
Q

keloid

A

excess type III collagen, african americans, earlobes/face/UE’s

Pathoma (3 decks)

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