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Can you name the MDTI - ALL OF RHEUMATOLOGY?

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

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