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Can you name the MDTI - ALL OF RHEUMATOLOGY?

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A20 mutation leads to too much NfKb
cells express Bax, lymphocytes express BCLxl
90% male, correlated with obesity and alcohol use
6% concordance among MZ twins
Defect in clearance of apoptosis
Comes in both diffuse/limited versions
polymorphisms in C2/C4 genes
treat acute flair up with NSAIDs, colchicine, corticosteroids
Fibrosis leading to ischemia and organ damage
2000-100,000 white cells in joint fluid
Type I/III collagen production
problems in the WNT pathway
Tophi in olecranon bursa
Interferon Signature (2)
subchondral sclerosis
environmental influence of vinyl plastics, hair dyes
transmural inflammation
IFNalpha upregulates TLR7/IRF7 to help uptake of DNA/RNA containing complexes
TGFb/CTGF sensitize fibroblasts and increases collagen production
fibrinoid kidney necrosis causes hypertension
Characterized by immune dysregulation/vascular dysfunction/fibrosis
Can be caused by deficiency of HGPRT
20-200 white cells in joint fluid
two causal reasons: highly vascularized synovium, no basement membrane
Anti-Smith, Anti-dsDNA, Anti-SSB
Possible mimicry between retroviruses and anti-SCL70
African Americans have particularly high anti-SCL70, bad prognosis
early, early disseminated, late disseminated spread
Can be caused by increase in enzyme PRPP
3 stages, last one develops B cell Lymphoma
Interferon Signature (1)
30% associated with HepB infection
Cytokines: IL-6, IL-17, IFN-alpha
Defect in Complement Receptor 1, FCyR
associated with previous damage (RA, OA), diabetes mellitus, immunosuppression
>50,000 cells, >95% PMN's
hypertrophy of chondrocytes, but decrease in collagen production
Sex hormones/chromosomes are important
Occurrence linked to ingestion of purine/pyrimidines, endogenous production of urate, and breakdown of tissues
increase vascularization of cartilage which allows cytokine spread
Heberden's Node
Cytokines Involved: IL-1, IL-6, IL-17, TNFalpha, with TNF-alpha being the boss
cast nephritis
HLA DQ7/DR5 associated
anti-ssa/ssb (not lupus)
fibroblasts turn to myofibroblasts
Pathway: Nalp3 -> IL-1b -> NfkB -> attracting of neutrophils
Cytokines Involved: IL-1, IL-6, IL-17, TNFalpha
40% twin concordance
IFN-g/TNFa both inhibit SMAD activity
cells inappropriately express both MHC1 and 2
Uric Acid Kidney Stones
anti-ANA are first important sign
Vascular injury may be initiating factor
TGFb/SMAD signaling
msu crystals
ANA test involves permeabilizing cells
Genetic defect in COL1A2, TGFb, Fibrillin 1
Can be caused by increase in enzyme XO
slow progression over time
environmental triggers are UV exposure/DNA or RNA viruses/Medication
lymphepithelial lesion
200-2000 white cells in joint fluid
Acute Uric Acid nephropathy (especially in cancer patients with chemo drugs)
ectopic lymphoid follicles in salivary glands
Can be caused by increase in enzyme APRT
polymorphisms in HLA DR2/DR3
TGFb downregulated metalloproteinase release
HLADRB1 association
Raynaud's Phenomenon precedes it
malar rash
Belimumab (2)
spares lung/kidneys
fibroblasts upregulate PDGFr in response to TGFb
estrogen and prolactin cause activation/proliferation of lymphocytes
4:1 female to male ratio
Alcohol increases conversion of ATP to AMP; produces lactate that acts on URAT1
Vital Dye test
treat with physical therapy, braces, NSAIDs
Belimumab (1)
renal hypertension due to medium vessel closure
cytoplasmic and perinuclear antibodies
CXCL 13 - B-cells
Schirmer's test
antibiotic resistant arthritis possibly due to mimcry between OspA and LFA
monoarthritic arthritis, usually 1st MTP/Knee/Ankle
cytokines: TGFb, CTGF, PDGF(r)
75% of people get this
IFN signal induced by DNA/RNA containing complexes
Mainly affects DIP, Knee, and 1st MCP joints
Anti-centromere antibodies seen in limited version
interferon signature connects viral infection to lymphocyte invasion
crescentic glomerulonephritis
CXCL 12 - T-cells
Anti-SCl-70 (Topoisomerase 1)
Bouchard's Node
discoid rash
lack of DHEA
Pyrazinamide, Nicotinate, Lactate all stimulate URAT1
cartilage fragments mediate inflammation

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Created Feb 5, 2012ReportNominate
Tags:disease, prompt