Just For Fun / MDTI - ALL OF RHEUMATOLOGY

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Can you name the MDTI - ALL OF RHEUMATOLOGY?

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PromptsDiseases
environmental influence of vinyl plastics, hair dyes
30% associated with HepB infection
Bouchard's Node
slow progression over time
Cytokines Involved: IL-1, IL-6, IL-17, TNFalpha
Can be caused by increase in enzyme PRPP
Vascular injury may be initiating factor
6% concordance among MZ twins
20-200 white cells in joint fluid
Type I/III collagen production
HLADRB1 association
Anti-SCl-70 (Topoisomerase 1)
Raynaud's Phenomenon precedes it
interferon signature connects viral infection to lymphocyte invasion
Interferon Signature (1)
increase vascularization of cartilage which allows cytokine spread
Allopurinol
2000-100,000 white cells in joint fluid
treat with physical therapy, braces, NSAIDs
msu crystals
HLA DQ7/DR5 associated
crescentic glomerulonephritis
estrogen and prolactin cause activation/proliferation of lymphocytes
Defect in clearance of apoptosis
CXCL 12 - T-cells
ANA test involves permeabilizing cells
90% male, correlated with obesity and alcohol use
NALP3
fibroblasts turn to myofibroblasts
Pyrazinamide, Nicotinate, Lactate all stimulate URAT1
Comes in both diffuse/limited versions
lack of DHEA
antibiotic resistant arthritis possibly due to mimcry between OspA and LFA
discoid rash
IFNalpha upregulates TLR7/IRF7 to help uptake of DNA/RNA containing complexes
Heberden's Node
lymphepithelial lesion
Possible mimicry between retroviruses and anti-SCL70
malar rash
200-2000 white cells in joint fluid
PromptsDiseases
Can be caused by increase in enzyme XO
cast nephritis
monoarthritic arthritis, usually 1st MTP/Knee/Ankle
transmural inflammation
Genetic defect in COL1A2, TGFb, Fibrillin 1
focus
cartilage fragments mediate inflammation
sicca
Mainly affects DIP, Knee, and 1st MCP joints
BAFF
cells inappropriately express both MHC1 and 2
fibroblasts upregulate PDGFr in response to TGFb
TGFb/CTGF sensitize fibroblasts and increases collagen production
cppd
40% twin concordance
Anti-Smith, Anti-dsDNA, Anti-SSB
anti-M3
TGFb/SMAD signaling
IFN signal induced by DNA/RNA containing complexes
associated with previous damage (RA, OA), diabetes mellitus, immunosuppression
Oxypurinol
cytoplasmic and perinuclear antibodies
A20 mutation leads to too much NfKb
CXCL 13 - B-cells
sialadenitis
osteophytes
Belimumab (2)
Alcohol increases conversion of ATP to AMP; produces lactate that acts on URAT1
Acute Uric Acid nephropathy (especially in cancer patients with chemo drugs)
Inflammasomes
fibrinoid kidney necrosis causes hypertension
Characterized by immune dysregulation/vascular dysfunction/fibrosis
karryohexis
URAT1
Fibrosis leading to ischemia and organ damage
cholinesterase
Probenecid
renal hypertension due to medium vessel closure
>50,000 cells, >95% PMN's
problems in the WNT pathway
PromptsDiseases
two causal reasons: highly vascularized synovium, no basement membrane
hypertrophy of chondrocytes, but decrease in collagen production
Anti-centromere antibodies seen in limited version
treat acute flair up with NSAIDs, colchicine, corticosteroids
Sex hormones/chromosomes are important
Febuxostat
TGFb downregulated metalloproteinase release
4:1 female to male ratio
spares lung/kidneys
anti-ANA are first important sign
Occurrence linked to ingestion of purine/pyrimidines, endogenous production of urate, and breakdown of tissues
Cytokines: IL-6, IL-17, IFN-alpha
African Americans have particularly high anti-SCL70, bad prognosis
75% of people get this
Tophi in olecranon bursa
Blys
Uric Acid Kidney Stones
Vital Dye test
cytokines: TGFb, CTGF, PDGF(r)
Defect in Complement Receptor 1, FCyR
fibrillations
environmental triggers are UV exposure/DNA or RNA viruses/Medication
Interferon Signature (2)
Can be caused by increase in enzyme APRT
ectopic lymphoid follicles in salivary glands
subchondral sclerosis
3 stages, last one develops B cell Lymphoma
anti-ssa/ssb (not lupus)
Pathway: Nalp3 -> IL-1b -> NfkB -> attracting of neutrophils
Schirmer's test
cells express Bax, lymphocytes express BCLxl
Can be caused by deficiency of HGPRT
polymorphisms in HLA DR2/DR3
CREST
polymorphisms in C2/C4 genes
Cytokines Involved: IL-1, IL-6, IL-17, TNFalpha, with TNF-alpha being the boss
Belimumab (1)
early, early disseminated, late disseminated spread
IFN-g/TNFa both inhibit SMAD activity

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