Assesment 5 Rheumatology Module Professor Hints
Metabolic Bone disease
Know biochem markers of bone turnover
Formation: BSALP, Osteocalcin, carboxyterminal propeptide of type 1 collagen
(P1NP)
Resorption: Pyridinium crosslinks, n-telopeptide, carboxyterminal of type 1
collagen (CTX-1)
Recognize key clinic features of the metabolic bone disorders
Know about OI, Paget’s etc.
Know the pathophys basis of each
Know about OI, Paget’s etc.
Regional Rheumatic Pain Syndromes
know the anatomy and name of common regional non-articular pain syndromes
Rotator cuff tendinitis (recall Neer’s sign), Bicipital tendonitis (Yergason’s sign,
Speeds test, Popeye’s sign), Adhesive capsulitis (frozen shoulder, associated with
diabetes), Olecranon bursitis (golf ball elbow), Lateral (tennis elbow) epicondylitis,
medial epicondylitis, Ulnar nerve entrapment, Flexor tenosynovitis, de Quervain’s
tenosynovitis (abductor pollicis longus, extensor pollicis brevis, recall finklestein’s
test), Ganglion, Carpal Tunnel syndrome (Tinel’s sign and Phalen test), Dupuytren
contracture, Trochanteric bursitis (point tenderness over greater trochanter), Meralgia
parasthetica, Baker’s cyst, prepatellar bursitis (can be septic), Achilles Tendinitis
(Thompson sign), Plantar fasciitis (pain in plantar area of heel), Pes planus (flat foot),
mortons neuroma, Hammertoe (flexion of PIP and tip of toe points down), Bunionette
(prominence of metatarsal head)
know the clinical features of fibromyalgia
Widespread pain>3mo., 11/18 tender points, could be involved with cortical centers
involved in pain stimulation, tx. educate patients,exercise, improve sleep,
Normal Joint Structure and Lab Testing
understand the structure of the normal diarthrodial joint
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Have a synovial lining, freely movable, includes all peripheral joints
Synarthrosis has no synovial lining, fixed joints (skull,tooth socket, tibiofibula
jxn., manubriosternal joint, symphysis pubis)
Assesment 5 Rheumatology Module Professor Hints
understand the components and properties of cartilage
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Avascular, no nerve supply, low cell content (chondrocytes only), rich in
matrix
Matrix composed of 60-85% water, collagen, proteoglycans (hyaluronic acid,
link proteins), other glyoproteins, lipids
know which autoantibodies are present in which rheumatic diseases
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RF present in RA (80%), SLE (40%), Sjogren’s (90%), Cryoglubinemia
(>90%)
o RF should only be used to confirm, not diagnose
ANA sensitive for SLE (95%)
o Can be drug induced or caused by MCTD, Sjogrens, scleroderma,
myositis, vasculitis
SSA-A/Ro
o Sjogrens (75%), SLE (25%), Congenital heartblock (remember this)
Sm
o Lupus in African Americans (more specific)
U1RNP
o MCTD, SLE
Anti-dsDNA
o More specific, less sensitive for SLE
o Correlates with renal disease
o Usually negative in drug induced lupus
Jo1
o Inflammatory myositis
o Directed against tRNA histidyl synthetase
Anti-Centromere
o Scleroderma
Antiphospholipid antibody
o Lupus
o Actually a pro-coagulant
C-ANCA
o Proteinase 3
o Wegener’s
P-ANCA
o Myeloperoxidase
o Microscopic polyangiitis (glomerulonephritis happens)
o Churg-Strauss (remember eosinophilia and asthmatics)
Cryoglobulin
o Ig precipitate when serum is cooled to 4 degrees or lower
o Associated with malignancy and Hep C
understand the limitations of laboratory tests in rheumatology
Assesment 5 Rheumatology Module Professor Hints
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CRP more sensitive than ESR
Laboratory tests can’t always diagnose, many test are used to confirm (e.g.,
RF and FANA) if they are used as screening procedures we will get many
false positives
Rheumatoid Arthritis (RA)
recognize articular and extra articular features of RA
Inflammatory condition affecting synovium, symptoms >6 wks, symmetrical
presentation, MCP, PIP, wrists affected most. Swelling usually confined to joint
cavity. Ulnar deviation, swan neck, boutonnière deformity, flexion contractures etc. ,
cervical spine subluxation, Felty’s (neutropenia, leucopenia), Keratoconjunctivitis
sica, xerostomia, episcleritis, scleritis,
understand the pathogenesis of RA, including the role of cytokines, T cells
HLA-DR4 (0401,0404,0408) bind and present antigens to T cells leading to
activation, second signal (CD86/28) leads to T cell activation and cytokine release.
Recall CTLA4 inhibits this second signal. RA is involved with Th17 and Th1
pathways. Cytokines destroy synovium and cause pannus formation. B cells also
involved in RA, Th1 pathway (TNF-alpha, IFN-gamma). Drugs exist to inhibit TNFalpha (infliximab) and CD20 on B cells.
understand the inflammatory nature of RA
See above.
Spondyloarthropathy
recognize the key clinical features of each of the spondyloarthropathies
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Common features
o RF negative
o HLA-B27 association
o Axial involvement with sacroiliac joint
o Enthesitis
o Dactylitis
o TNF alpha
Ankylosing Spondylitis
o Inflammation of spinal joints, fusion of bony spine
o More common in first degree relatives of HLA-B27
o Back pain, stiffness, worse in morning and improves with exercise
o Anterior uveitis
o Aortic regurg, apical lung fibrosis secondary amyloidosis,
o Sacroiliac tenderness, limited spine motion, loss of lumbar lordosis
Assesment 5 Rheumatology Module Professor Hints
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o Abnormal schober’s tes
o Reduced chest expansion
Enteropathic arthritis
o Crohn’s, IBS, etc.
o Peripheral arthritis
o Asymmetric
o Pyoderma gangrenosum
o E. nodosum
Reactive arthritis
o Arthritis, Urethritis, conjunctivitis
o Shigella, salmonella, campylobacter,
o Asymmetric
o Enthesitis, Oral ulcerations, Keratoderma blennorrhagica
o Oncholysis
Psoriatic arthritis
o Synovial inflammation
o DIP involvement
o Arthritis mutilans
o Axial involvement
o Nail pitting!
o Pencil in a cup
o Enthesitis, Dactylytis
understand the role HLA-B27 plays in spondyloarthropathies
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Class I MHC that binds peptides and presets to CD8+ T cells
Scleroderma
understand the role of fibrosis in scleroderma
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Thickening and fibrosis is main defect in scleroderma.
Sclerodactyly
Raynauds (fibrosis of vessels)
Telangectasias
Nailfolds
Calcinosis
Watermelon stomach
Pulmonary fibrosis * cause of death
PDGF, Collagenase 1, important in pathogenesis, Th2 and CD4 mediated
recognize scleroderma renal crisis
o IF blood pressure rises slightly, put on ACE-I
Assesment 5 Rheumatology Module Professor Hints
distinguish between limited and diffuse forms of scleroderma
o Limited
o Not with systemic disease
o Scl-70 negative
o Generalized
o Scl-70 positive
Infectious Arthritis
distinguish between gonococcal and non gonococcal septic arthritis
Gonococcal typically seen in pt. who are sexual active (younger). Non-gonococcal is
primarily S. auerus (except for prosthetic joints which is coag. Neg. staph, and
i.V.DA which is candida and pseudomonas). Non-gonococcal is typically isolated in
aspiration, gonococcal is not (have to look to sites of primary infection).
understand the role of synovial fluid analysis in the diagnosis of septic arthritis –
interpret results
Typically purulent in bacterial arthritis. >80k WBC’s, >75% PMN’s, Gram stain + in
60-80%, crystals may co-exist.
Note: Parvovirus can mimic RA, Rubella is involved with squatting pose, and Hep B
/C can mimic OA distribution (knees). Hep C is in hands, wrists, knee’s also
associated with cryoglobunemia (I and II). Lyme disease is monoarticular or
pauciarticulr (usually involves Knee and TMJ), TB commonly infects spine/knee.
Gout
distinguish between under excretors and over producers of uric acid, recognize
urate crystals under polarizing microscopy, know pathophys basis of the disease
Urate crystals under polarizing microscopy when parallel to polarizer are negatively
birefringement (yellow). Under excretors are those who can’t get rid of uric acid (e.g,
URAT1 mut., low dose ASA, Hctz, over producers make too much (HGPRT def.,
PRPP synthetase over active).
Uric acid accumulates in joints and crystallizes at the appropriate Ksp producing
monosodium urate crystals. PMN’s engulf these crystals and release cytokines and
enzymes which cause inflammation, pain, and damage to surrounding tissues.
sUA can be normal in acute gout attacks. Never start chronic treatment in acute
attacks.
Assesment 5 Rheumatology Module Professor Hints
distinguish between gout and other crystalline arthropathies
Gout and pseudogout more present in men. Family history is often present in
gout but not pseudogout. Primary site of pseudogout is knee, primary of gout is
MTP. Both present with fever, tophi are not common in pseudogout. Bursa
affected in gout, tendons in pseudogout.
know the effects of diet on urate production, other non-pharm treatments
At best diet decrease sUA 1-2mg/dl. Allopurinol, Febuxostate both decrease uric
acid production (inhibit XO)
Other Crystalline Arthropathies
recognize calcium pyrophosphate crystals under polarizing microscopy
Positively birefringement (blue when parallel, yellow when perpendicularbirefringment means has two different colors).
know clinical features of the various non-urate crystal diseases
See above for pseudogout. Most attacks of pseudogout are spontaneous.
Synovial fluid has poor viscosity, and is moderatey cloudy. WBC>20k. Rhomboid shaped
crystals (CPPD) in pseudogout. No erosions in pseudogout, but yes in gout. BCP
accumulates sometimes in OA. BCP stain with azilarin red stain. They also accumulate in
Milwaukee shoulder syndrome which can mimic rotator cuff tendinitis. It is not known
whether the tear’s in Milwaukee shoulder syndrome correlate with crystals, or if the crystals
actually cause the tears. MSS is a disease of older white women*. CPPD comes from
transglutaminase-2 enzyme. Primary oxalis is a rare calcification of articular joints (typically
hand) and renal calcifications, can also be acquired due to secondary conditions.
Systemic Lupus Erythematosus (SLE) and Sjogren’s Syndrome
understand the role of immune complexes in the pathogenesis of SLE
o Complement is deposited, ADCC causes inflammatory cascade.
recognize clinical features of SLE and Sjogren’s syndrome
o SLE: Malar rash, oral ulcers, alopecia, dermatitis, arthralgias, arthritis, muscle pain,
serositis, renal disease (correlates to dsDNA Ab), Neuropsychiatric, Hematologic
(anemia), GI, pulmonary effusions, Neonatal lupus associated with SSA/Ro and
congenital heart block. FANA is helpful for screening, use Anti-Sm to rule in (better
in African Americans). All SLE has + FANA.
o Sjoergen’s: Keratoconjunctivitis sicca (schirmer test), xerostomia, parotid
enlargement, +FANA,+RF, +SSA/Ro, SSB/La
Assesment 5 Rheumatology Module Professor Hints
o Recall: DILS in HIV has dry eyes also (CD8 mediated)
understand the role of autoantibodies in Sjogren’s syndrome
o AutoAb destroy exocrine glands (salivary/lacrimal)
o Mainly CD4+
Osteoarthritis (OA)
understand the pathogenesis of OA, and the contributors to secondary causes
o Hemochromatosis, Wilson’s disease (OA in wrist), Ochronosis (Alkaptonuria),
acromegaly
o Cystic changes in bone, osteophyte formation, increased water in collagen early on,
join space narrowing, bony sclerosis, misalignment
o DISH
o Excessive tendon calcification
Vasculitis
recognize the key clinical features of Wegeners, HSP, PAN, PMR, temporal arteritis,
Kawasaki’s, Takayasu’s
This objective basically says recap the entire vasculitis lecture, which we have in our
handout.
Note to self:
Remember polymyalgia rheumatic can lead to temporal arteritis.
Takayasu’s not associated with GMN. Multiple aneurysm’s seen on arteriogram.
Kawasaki: Strawberry tongue, desquamation, ertythema, coronary disease.