MDTI - ALL OF RHEUMATOLOGY

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Can you name the MDTI - ALL OF RHEUMATOLOGY?

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

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