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Can you name the MDTI - ALL OF RHEUMATOLOGY?

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

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