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Can you name the MDTI - ALL OF RHEUMATOLOGY?

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

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