Rheumatology Flashcards
Osteoarthritis joints
DIP (Herberden's) PIP (Bouchard's) 1st CMC Hips and knees Spine First MTP
OA mechanism
No systemic features MMP breakdown of type II collagen in cartiladge: increased chondrocytes increased MMP increased water content decreased proteoglycan decreased TIMP
OA synovial fluid
noninflammatory
type I fluid (200-2,000 WBCs)
OA cytokine factors and MMP effects
IL-1: stimulates MMPs and NO, PG, IL-6 production
NO: increases MMPs and inhibits proteoglycan/chondro
Prostaglandins: produce and activate MMPs
OA radiographs
joint space loss
sclerosis
osteophytes
RA joints
Non-symmetric, inflammatory joints
Spare DIP
Medium/large joints can be involved
RA genetics
shared epitope QKRAA with HLA-DR4/HLA-DR1
damage mediated by RF-IgG immune complexes (rheumatoid nodules)
RA markers
RF (IgM) not specific
Anti-CCP more specific
Both = very specific
Anti-CCP corresponds well with shared epitope
RA mechanism (intra and extra articular)
Inflammed synovium
Pannus invasion and damage
Cytokine release -> B cell -> RF, Anti-CCP release
Immune complexes, complement activation
MMP stimulation and damage
Extra-articular: RF-IgG complex=vasculitis, rheum nodules
RA cell types
CD4 - modulate/amplify local response via antigen recognition
Th17
B cells and plasma cells (RF, anti-CCP)
Gout joints
1st MTP (podagra) Cool, peripheral joints
Gout hyperuricemia causes
Over-production (Xlinked): PRPP synthease overactivity, HGPRT deficiency
Under-excretor: 90%
Gout mechanism
Purine metabolism byproduct, humans lack uricase
MSU recognized by TLR2/TLR4
NLRP3 Inflammasome activation resulting in caspase-1 pathway and IL-1ß production
Gout synovial fluid
Dx by arthrocentesis
MSU crystals - needle shaped, negatively birefrigent
Gout self limiting treatment
Protein coat: IgG or Apolipoprotein B
More phagocytosis = less concentration
Inflammatory heat
ACTH secretion suppresses inflammation
Calcium Pyrophosphate Dihydrate Deposition Disease mechanism and crystal formation
Abnormal PPi metabolism
ANK gene mutation resulting in excess PPi leaking from chondrocytes
PPi precipitate with Ca2+ = CPPD crystals
Shedding, enzymatic strip mining
CPPD crystals: rhomboid, positively birefrigent
Spondyloarthropathies joints and signs/symptoms
Spine and SI joints Small and large peripheral joints Enthesitis Mucocutaneous lesion, rash, conjuctivitis Anterior uveitis
SAP genetics
HLA-B27
Negative RF and ANA
Ankylosing Spondylitis chance of development
2% if HLA-B27 positive
20% if HLA-B27 and first degree relative affected
Other HLA-B27 risks
Skin, nail, genital tract involvement
IBD
Heart involvement
Reactive Arthritis joints and signs/symptoms
Asymmetric, oligo, lower extremity arthritis
Dactylitis - sausage digits
Can’t pee, can’t see, can’t climb tree
ReactA mechanisms
molecular mimicry Arthrogentic peptide: processed HLA-B27 HLA-B27 heavy chain, NK activation ***Unfolded protein - ER stress, Th17 activation*** Th2 response
Systemic Lupus Erythematous defect
autoimmune (foreign as self) T and B cell process antigen driven (CD4+ T cells) Loss of T cell tolerance allowing autoreactive B cell
SLE pathogenesis
dsDNA as foreign
Ex. PMN death, DNA release to kill bacteria
