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Pedi Rheum Boards > Sherry > Flashcards

Sherry Flashcards

1
Q

4-8 yrs, sclerotic margins

A

Fibrous Cortical Defect (Nonossifying Fibroma)

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2
Q

low T1 & T2 evidence of hemosiderin

A

Pigmented villonodular synovitis
overexpressin of CSF1

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3
Q

most common soft tissue sarcoma
5% of pediatric cancer
age 5, painless

A

Rhabdomyosarcoma

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4
Q

Expansile +/- pain
Metaphysis of proximal humerus or femur

A

Unicameral bone cyst

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5
Q

Adolescent girls, expansile, pain
Lack distinct margins, fluid levels
Recur 60%

A

Aneurysmal bone cyst

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6
Q

Bone mineral

A

70% hydroxyapatite

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7
Q

Bone organic component

A

98% matrix, mostly type 1 collagen

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8
Q

Distal 1/3 of radius %

A

95% cortex, 5% trabecular

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9
Q

Vertebral bodies %

A

5% cortex, 95% trabecular

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10
Q

Bone formation markers

A

Alk phos, osteocalcin

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11
Q

Bone resorption markers

A

TRAP, hydroxyproline

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12
Q

RANKL

A

made by osteoBlasts
When bind to RANK on osteoClasts – chew up bone
Blocked by Osteoprotegerin
Induced by T cell activation

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13
Q

blocks RANK-RANKL which causes osteoporosis, DECREASED in menopause

A

Osteoprotegerin

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14
Q

Q angle 15-17⁰

A

Patella-femoral syndrome

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15
Q

Activity related MEDIAL knee pain, snapping, catching

A

plica (ultrasound)

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16
Q

Activity related LATERAL
Knee pain

A

Iliotibial band syndrome

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17
Q

Osteochondritis desiccans

A

MEDIAL femoral condyle

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18
Q

Tennis elbow

A

LATERAL epicondylitis

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19
Q

Golfer elbow

A

MEDIAL epicondylitis

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20
Q

de Quervain tenosynovitis

A

abductor pollicis longus & extensor pollicis brevis

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21
Q

diskitis

A

toddlers, L4-5, MRI

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22
Q

Schurmann

A

juvenile kyphosis, adolescent boys, T7-9, Schmorl nodes, pain with activity

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23
Q

Kienböck

A

Lunate [?post trauma –Karate] avascular necrosis

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24
Q

Kohler

A

Tarsal navicular avascular necrosis

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25
Q

Frieberg

A

Metatarsal head (2nd, 3rd) avascular necrosis

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26
Q

Legg-Calvé-Perthes

A

proximal femur avascular necrosis, 4-10, no prolonged bracing

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27
Q

Slipped capital femoral epiphysis

A

puberty, obese, bilateral 30%, thyroid, growth hormone, AVN

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28
Q

Carpal Tunnel Syndrome

A

Mucopolysaccharidoses
Mucolipidosis

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29
Q

90% bone matrix collagen

A

Type I collagen

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30
Q

articular cartilage, vitreous, discs collagen

A

type 2 collagen

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31
Q

Intramembranous ossification

A

clavicle, skull, face

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32
Q

Th17 effects

A

bone resorption
↑ IL-1, IL-6, IL-17, RANKL

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33
Q

Tregs

A

bone formation
↓ inflammation IL-4, IL-10, TGF-β

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34
Q

Tidemark

A

in cartilage between deep zone and calcified zone

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35
Q

Fibrocartilage

A

triangular fibrocartilage wrist, TMJ, iliac side SI joint, labrum, menisci

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36
Q

chondroitin sulfate, keratan sulfate, heparan sulfate

A

Proteoglycans

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37
Q

Metalloproteinases stabilized by _ , activated by _

A

stabilized by zinc, activated by calcium

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38
Q

Most abundant proteoglycan

A

Decorin – cross-linking between collagen fibers in tendon

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39
Q

insert into bone (entheses, ligaments, capsule, tendons, periosteum)

A

Sharpey fibers

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40
Q

functional unit of muscle

A

Sarcomere

41
Q

slow, red, thick z bands, lots of mitochondria, oxidative enzymes

A

Muscle type I fibers

42
Q

fast, white, rich in glycogen, phosphorylases, Atrophic with steroid myopathy (normal CK)

A

Muscle type II fibers

43
Q

poly & oligo JIA, encodes lymphoid protein tyrosine kinase, that negatively regulates T cells. Mutation associated with T-cell activation & promotion of autoimmune disease.

A

PTPN22

44
Q

differentially influence susceptibility to SLE & SLE nephritis

A

Fc-γIII receptor polymorphisms

45
Q

IgG4 and Complement activation

A

IgG1,2,3 but not IgG4 activate
Classic pathway (as does IgM, CRP & serum amyloid protein

46
Q

present endogenous antigen via MHCI to CD8+ T Cells
Present phagocytized endogenous antigen via MHCII to CD4+ T Cells
Cross presentation presents EXOGENOUS peptides via MHCI to CD8+ T cells

A

Dendritic cells

47
Q

subtype of DC that produces large amount of type I interferon (IFN-α & IFN-β)

A

Plasmacytoid dendritic cells

48
Q

if bind to MHCI – stand down – does not kill. If cell has no MHCI (if infected) will kill

A

natural killer cells

49
Q

produce type II interferon (IFN-γ)

A

natural killer cells

50
Q

_ recognize antibody coated cells, make IFN-γ, this stimulates macrophage to make IL-12, which induces _ cells

A

natural killer cells

51
Q

Lectin C’ activation

A

mannose binding lectin, pathogen associated molecular patterns, ficolins

52
Q

C3a, C5a actions

A

chemotaxis, anaphylatoxins C5a critical to anti-phospholipid antibody syndrome

53
Q

C3b, iC3b actions

A

opsonization, phagocytosis

54
Q

Adhesion sequence

A

injury, macrophages make TNF, IL-1, chemokines, then selectins slow down leukocytes, integrins more adhesive, then transmigration into tissue

55
Q

bacterial infections, no pus, delay in umbilical cord sloughing

A

Leukocyte adhesion Deficiency

56
Q

IL-5 action

A

eosinophils

57
Q

IL-2 action

A

proliferation and activation of T cells
Increases transcription and expression of Fas Ligand

58
Q

IL-4 action

A

Th2 differentiation
Isotype switching to IgE in B cells

59
Q

IL-12 action

A

Th1 differentiation
Synthesis of IFN-γ by T & NK cells

60
Q

IL-18 action

A

Synthesis of IFN-γ by T & NK cells

61
Q

IL-23 action

A

Th17 differentiation

62
Q

Pro-inflammatory cytokines

A

IL-1, IL-1β, TNF-α, IL-6, IL-17,
IL-22

63
Q

Anti-inflammatory cytokines

A

IL-10, TGF-β

64
Q

IFN-γ action

A

Th1 differentiation,
Induces MHCI on somatic cells, MHCII on antigen presenting cells [in SLE & JDMS – so more MHCI on muscle cells in JDMS]

65
Q

CD4+ - Th1 differentiation

A

IL-12, INF-γ

66
Q

CD4+ - Th2 differentiation

A

IL-4

67
Q

Plasmacytoid dendritic cell action

A

makes up to 1000 times more type I INF (IFN-α & IFN-β) than any other cell

68
Q

Type I INF (IFN-α & IFN-β) action

A

activate NK cells, antiviral

69
Q

Positive selection (1st)

A

thymic medulla, double positive T cells (CD4+CD8+) are positively selected if they recognize MCH I or MHCII (turn into CD4+ OR CD8+) [most die here]

70
Q

Negative selection (2nd)

A

thymic cortex, the CD4+ or CD8+ cells meet thymic epithelioid cells who present self peptides – if bind to these self peptides, they die – too autoreactive.

71
Q

Memory T cells

A

cells that, after presented with an antigen, rather than differentiate into effector (active) helper or cytotoxic cells, form memory T cells (either CD4+ or CD8+) that survive in an inactive stage until re-encounter same antigen

72
Q

Regulatory T cells

A

mediate tolerance, restrict the adaptive immune responses, make IL-10, express FOXP3

73
Q

Th1

A

CD4+ (helper) makes IFN-γ (differentiation driven by IL-12 & IFN-γ)

74
Q

Th2

A

CD4+ (helper) makes IL-4, IL-5, IL-13 (differentiation driven by IL-4)

75
Q

Th17

A

CD4+ (helper) makes IL-17, IL-22, TNF, GM-CSF, (differentiation driven by IL-23, IL-1, IL-6)

76
Q

T independent antigens

A

elicit plasma cell differentiation and antibody production without T-cell help – make low affinity IgM
[lipopolysaccharide, poly-immune complexes, polysaccharides]

77
Q

B effector type 1

A

primed by Th1 – make IFN-γ, IL-12, TNF-α, IL-6

78
Q

B effector type 2

A

primed by Th2, make IL-2, IL-4, IL-13, lymphotoxin

79
Q

B regs

A

make antiinflammatory cytokines, IL-10, TGF-β, IL-35

80
Q

Hypogammaglobulinemia

A

bacterial infections
X-linked – at birth
CVID – gradually lose IgG

81
Q

OmEnn syndrome

A

Erythroderma (like GVHD)
IgE high
Eosinophilia
Low T cells, No B cells,
Mutant RAG genes
[smells bad – wrapped in RAGs]

82
Q

X-linked SCID

A

most common form
IL-2r gene
Low T cells, no NK cells, non-functioning B cells

83
Q

Bare lymphocyte syndrome

A

Type 1 – MHCI not expressed
Type 2 – MHCII not expressed

84
Q

Mutation in JAK3

A

leads to SCID

85
Q

family history discoid lupus
measure superoxide anion generation (respiratory burst) in neutrophils
Staph, Serratia, Nocardia

A

CGD

86
Q

Herpes, HLH, SCID

A

NK cell deficiency

87
Q

XIAP X-linked inhibitor
Of apoptosis protein

A

HLH with EBV

88
Q

Wiskott-Aldrich syndrome

A

thrombocytopenia, eczema, ENT infections
Low CD8+, high IgA, low IgM
x-linked WASP [Wiskott-Aldrich syndrome protein]

89
Q

low IgG, mutations in NFκB pathway, ITP 15%, lung disease if haplosufficiency of CTLA4

A

CVID

90
Q

mutation in Fas mediated apoptotic pathway
Double negative T cells (no CD4+, CD8+). Hypergammaglobulinemia, high B12, sFASL,
Use MMF or mTOR inhibitor sirolimus (rapamycin) or rituximab

A

ALPS

91
Q

Autoimmune Polyendocrinopathy Candidiasis Ectodermal Dysplasia (APECED)
half Sjögren syndrome
HSCT not indicated

A

AIRE mutation

92
Q

FOXP3 mutation

A

Immunodysregulation Polyendocrinopathy Enteropathy X-linked Syndrome (IPEX), Day 1 of life enteropathy – diabetes, rash, cytopenia

93
Q

HLH

A

inefficient CD8 and NK cells
High IFN-γ, IL-18, IL-1, IL-6, IL-33, TNF (cytokine storm)

94
Q

IL-10 deficiency

A

very early IBD, arthritis, lymphoma

95
Q

CTLA4 deficiency

A

enteropathy, adenopathy, hepatosplenomegaly, diabetes, arthritis, lung disease. Treat with abatacept

96
Q

Positive Schirmer

A

≤ 5 mm in 5 minutes, without anesthesia

97
Q

in localized scleroderma but not systemic scleroderma

A

Papillary dermis sclerosis

98
Q

Diseases associated with microchimerism

A

limited scleroderma, neonatal lupus, JDMS

99
Q

Generalized morphea

A

≥ 4 individual lesions

Pedi Rheum Boards (4 decks)

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