RA Flashcards
RA Etiology:
- Genetic
- Enviro
- Antibodies
Genetic: MHC region for HLA-DR genes, SNPs of STAT4, PTPN22, TRAF1
Enviro: smoking, silica, pollution, viruses, bacteria
Antibodies to citrullinated/ carbamylated proteins –> immune complex, complement activation, inflammation, NETosis, osteoclast-genesis/activation, adaptive immune system
RA Classification Criteria
2010: ACR/EULAR: 6 or more
- Swollen/tender joint
* One medium to large joint (shoulders, elbows, hips, knees, ankles) = 0
* 2–10 medium to large joints = 1
* 1–3 small joints (MCP, PIP, 2–5 MTP, or wrist with or without large joint involvement) = 2
* 4–10 small joints (with or without large joint involvement) = 4
* >10 joints (at least one small joint involved) = 5 - Serology
* -RF and -ACPA = 0
* Low +RF or low +ACPA (<=3 x ULN) = 2
* High +RF or high +ACPA (>3 x ULN) = 3 - Acute-phase reactants
* Normal CRP and normal ESR = 0
* Abnormal CRP or abnormal ESR = 1 - Duration of self-reported symptoms
* <6 weeks = 0
* ≥6 weeks = 1
DDx RA
- Seroneg (PEAR)
- Crystal (CPPD, polyarticular gout)
- CTD (SLE, SSc, PM, Vasc, MCTD, PMR)
- Infectious (EBV, HIV, Parvo, rubella, Hep C)
- FM, OA
Uncommon:
- Infectious: endocarditis, rheumatic fever, Lyme
- Metabolic: hypothyroid, hemochromatosis, hyperlipoproteinemias (types II, IV), amyloid arthropathy
- Infiltrative: sarcoidosis,
- Vascular: hemoglobinopathies (sickle cell disease)
- Malignant: malignancy, paraneoplastic syndrome, hypertrophic osteoarthropathy,
- Inflamm: Behçet’s disease, Relapsing polychondritis, R3SPE, FMF, SAPHO
RA Epidemiology (race, age, prevalence)
All races (higher in Native Americans)
Age: 40-60 in F, older in M
1% of US
RA Patterns
- Insidious (55%–65%): Arthritis over weeks to months.
- Subacute (15%–20%): Similar to insidious onset but more systemic symptoms.
- Acute (10%): Severe onset, some have fever.
b) Variant patterns of onset (10% of patients)
* Palindromic (episodic) pattern: Usually <5 joints and resolves within several days.- Tx: HCQ may decrease frequency of attacks and progression to RA.
* Insidious onset of elderly (>65 years): Pain/stiffness of limb girdle joints often with swelling of UE (difficult to differentiate from PMR & RS3PE)
* Arthritis robustus: Typically seen in men: bulky, proliferative synovitis –> erosions/ deformities with little pain or disability.
* Rheumatoid nodulosis: recurrent joint pain/swelling in, subcutaneous nodules, and subchondral bone cysts on XR.
RA Hand/Wrist deformities
Wrist:
- Volar subluxation (due to articular cartilage degradation and ligamentous laxity)
- Radial deviation (extensor carpi ulnaris tendon weakness = unopposed radial)
- Piano key ulnar head (radioulnar ligament damage –> floating ulnar styloid)
-Vaughan-Jackson deformity
MCPs:
- Subluxation (metacarpal head dorsally, prox phalanx head volar)
- Ulnar deviation
Fingers
- Ulnar drift (with wrist radial deviation, finger tendons pull fingers ulnarly)
- Fusiform swelling—PIP synovitis (spindle-shaped)
- Boutonnière
- Swan-neck
- Hitchhiker thumb (Z thumb)
Opera glass hands - bone resorption/shortening
RA XR findings
A—Alignment, abnormal; no ankylosis
B—Bones—periarticular (juxtaarticular) osteopenia; no periostitis or osteophytes
C—Cartilage—uniform (symmetric) joint space loss in weight-bearing joints; no cartilage or soft tissue
calcification
D—Deformities (swan neck, ulnar deviation, boutonnière) with symmetrical distribution
E—Erosions, marginal
S—Soft-tissue swelling; nodules without calcification.
RA C spine involvement
- subluxation
- impaction
- which joints
- neurologic manifestations
- C1–C2 atlantoaxial subluxation (60%–65%) –> anterior: C1 arch and C2 odontoid gap >3mm 2/2 synovial proliferation around odontoid –> stretch/rupture of transverse/alar ligaments; >9mm anterior atlantodontoid interval or <14mm posterior atlantodontoid interval risks spinal cord compression
- C1–C2 impaction: superior migration of odontoid from destroyed occipitoatlantal and atlantoaxial joint articulations between C1 and C2 –> impinge brainstem if moves into foramen magnum (worst neuro prognosis = odontoid ≥5 mm above Ranawat’s line)
- Subaxial involvement: involves C2–C3 and C3–C4 facets and intervertebral disks –> “stair-stepping” vertebrae (important if >3.5mm)
Manifestations:
-neck pain to occiput
-painless sensory loss (hands/feet)
- syncope/death
- cerebral ischemia w vertebral insufficiency
Rheumatoid Nodules
- Histology / Layers
- Inner: Central area of fibrinoid necrosis
- Middle: Palisading macrophages and histiocytes
- Outer: Monocytes and cellular connective tissue
RA Ocular Manifestations
- MOST COMMON: Sicca
- Episcleritis (painless)
- Scleritis –> scleromalacia perforans
- Choroid and retinal nodules,
- Ulcerative keratitis (corneal melt)
RA Pulmonary Manifestations
- Pleura: thickening, pleuritis, exudative effusion
- Interstitium: IPF/UIP >NSIP, COP, nodules, pneumoconiosis (Caplan’s syndrome), apical fibrobullous dz, lymphocytic interstitial PNA (LIP)
- Airway: criocoarytenoid arthritis, dysphagia, hoarseness, stridor, bronchiolitis (proliferative and obstructive), bronchiectasis
- Vascular: PH, vasculitis
- Other: infection, drug related, amyloid
RA Cardiac Manifestations
- Pericarditis: constriction, effusion, tamponade
- Myocarditis: CHF, afib
- Coronary: CAD, arteritis, vasculitis
- Nodules on valves: valvulopathy, conduction, endocarditis
RA Neuro Manifestations
- Entrapment neuropathy: median nerve (carpal tunnel), posterior tibial nerve (tarsal tunnel), ulnar nerve (cubital tunnel), and posterior interosseous branch of the radial nerve
- Peripheral neuropathy
- Mononeuritis multiplex
- CNS vasculitis
- C1/C2 subluxation or impaction
- Subaxial subluxation (C2/C3 and C3/C4)
RA Heme Manifestations
- Felty’s syndrome (leukopenia, splenomegaly, RA)
- Lymphomas
- Large granular lymphocyte syndrome: neutropenia, splenomegaly, susceptibility to infections
RA Other manifestations
- Sjögren’s syndrome
- Amyloidosis
- Osteoporosis
- Ossicles of ear: tinnitus and decreased hearing.
RA Derm Manifestations
- Palmar erythema,
- Subcutaneous nodules,
- Vasculitis
Tx of Felty
- If RA and infxn: MTX –> +Ritux –> +Steroids as needed (unless infxn). TNF not effective.
- G-CSF if severe infxn (risk of arthritis/vasculitis)
- Splenectomy (for severe infxns and nonhealing ulcers)
- Others: LEF, CNI, CYC, Abatacept > TNF
DC SSZ (neutropenia)
RA Disease activity measures
DAS28
SDAI
CDAI
RAPID3
RA Markers of poor prognosis
- Poor functional status (HAQ >1) at presentation
- Long dz duration prior to tx
- Low education level (<gr 11)
- Male
- Smokers
- Polyarthritis (small and large) >13
- Erosions within 2 years of onset
- Extraarticular dz: nodules, vasculitis
- HLA-DR4 genetic marker
- RF & CCP +
- ANA + (if also RF+)
- Persistently elevated ESR or CRP
RA Treatment targets
-how soon treatment
-activity level
Therapy within 3-6 mo of synovitis
Aim for LDAS or remission
SDAI calculation
Simplified disease activity index: TJC (0–28) + SJC (0–28) + PtGA (0–10) + PhGA (0–10) + CRP (mg/dL)
i.e. CDAI + CRP
CDAI calculation
Clinical disease activity index: TJC (0–28) + SJC (0–28) + PtGA (0–10) + PhGA (0–10)
RAPID calculation and cutoffs
Routine assessment of patient index data: MDHAQ (0–10) + patient pain (0–10) + PtGA (0–10)
Cutoff: <1, 1.3-2, 2.3-4, 4.3-10
RA Mortality causes
CV
Infection: PNA
Cancer: lymphoma, leukemia, lung, melanoma
Renal: amyloid
GI bleed: NSAID
RA synovium histology
Hyperplasia (1-2 –> 6-10 cells thick
Hypercellularity (T-lymph and macrophages mainly, but also plasma cells, activated fibroblasts, dendritic cells)
Neovascularization/angiogenesis
RA synovium cytokines elevated
Which responsible for systemic fx
TNF, IFNg
IL-1, 2, 6
IL6 - fatigue, cognitive dysfunction, and altered HPAA function
** RA: adhesion molecules in synovium**
M6- leukocyte activation antigen, is a potent inducer of enzymes for degrading cartilage and bone in RA
RANKL (Receptor Activator of Nuclear Factor-kappaB ligand) expressed on activated T cells and synovial fibroblasts and on bone lining cells for osteoclast activation
VCAM, ICAM
MTX lung:
-Manifestations
- Imaging findings
- BAL
- Biopsy
- Tx
- SOB, fever, cough over weeks after starting drug
- CXR - bilateral interstitial opacities or mixed interstitial/alveolar pattern; NSIP
- CT - GGO
- BAL: lymphocytosis w low CD4/8, +/-eos
- Biopsy - Interstitial pneumonitis w granuloma, occasional eos and bronchiolitis
- Tx: stop MTX, give steroids
RA effusion features
- Subclinical: small-mod size, unilateral, asymptomatic
- Exudative (high prot and LDH, low gluc and pH <7.2)
- RF positive
- Cell count <5000, mostly lymh but PMN and eos initially
- Cholesterol > 5.2 (chol crystals)
4-5 clinical manifestations that help to differentiate amyloidosis from RA on physical exam
and biopsy results
- Macroglossia
- Shoulder pad sign
- Enlarged liver
- CHF, periph edema (also from nephrotic syndrome and prot losing enteropathy)
- Arthropathy similar to RA: symmetric, shoulders, knees, wrists, MTP and PIP’s, lesser degree elbows and hips, tender w AM stiffness
- Amyloid nodules ( biopsy positive for Congo red birefringemnt
- Periorbital purpura
RA Pregnancy
- When remit vs flare
2/3 remit from T1-T3 –> 2/3 flare in 1st 6mo
1/3 flare during pregnancy (mostly T1)
RA Ulnar deviation pathogenesis
3 reasons
- Extensor carpi ulnaris weakness from laxity and erosion –> radial deviation of the wrist and compensatory ulnar pull of finger tendons
- Failure of radial collateral ligament from MCP synovitis causing stretching/thinning –> imbalance favouring ulnar collateral ligaments
- Weakened radial collateral ligament –> unopposed abductor digiti minimi muscle –> drift of little finger
- MCP synovitis and subluxation
Boutonnière
Pathogenesis and DDx
PIP synovitis –> extensor tendon elongation and rupture dorsally –> lateral and volar displacement of lateral bands ie shortens –> flexes PIP and hyperextends DIP
DDx: RA, trauma (blunt/laceration), burns.
Pathogenesis: Swan-neck
Lateral and DORSAL displacement of lateral bands –> shortening –> flexes DIP and hyperextends PIP
Felty Triad and other features
- RA, leukopenia, splenomegaly,
- RA assoc’d: erosions, wt loss, sicca, episcleritis, eye lid necrosis, pleuritis, vasculitis, neuropathy, nonhealing ulcers, hyperpigmentation
- Leukopenia assoc’d: Infection, NHL risk
- Splenomegaly assoc’d: LN, hepatomegaly/cirrhosis, portal HTN, varices
LGL (pseudo Felty) vs Felty
- LGL: lymphocytosis in periph blood and BM.
- FS: hypocellular BM
- LGL leukemia - Monoclonal T-cell
- FS: Polyclonal T cell
- LGL CD2, 3, 8, 16, and 57 surface phenotypes in the peripheral blood smear (BM bx required to confirm)
Vaughan-Jackson deformity
- Features
- Mx
Extensor tendon rupture (D3-D5) from chronic wrist tenosynovitis + damaged ulnar styloid –> rupture (surgical emergency)
- Scallop sign
- Prevention via screening for extensor tendon weakness or restriction
- Tenosynovectomy +/- ulnar head surgery if high risk.
- After rupture: surgical repair
RA Vasculitis Types and manifestations
- Leukocytoclastic - papable purpura. Vasculitis of post capillary venules
- Small arteriolar - infarcts of digital pulp and nailfolds (rarely gangrene), distal sensory neuropathy (due to vasculitis of vasa nervorum)
- Medium vessel - resembles PAN (visceral arteritis), mononeuritis multiplex, livedo reticularis
- Pyoderma gangrenosum
Pathogenesis: Z thumb
1st MCP synovitis weakens capsule/ ligament → stretching EPB allowing EPL to sublux volarly → flexing MCP and hyperextending IP
Rheumatoid Nodules DDx
Nodule + arthritis:
- MTX-induced accelerated rheumatoid nodulosis (–> multinucleated giant cell formation via a1 adenosine R)
- RA,
- Xanthoma,
- Gout (tophi),
- SLE (rare), IIm, SSc (calcinosis)
-Amyloidosis, Sarcoid
- Rheumatic fever (rare), Leprosy
- Multicentric reticulohistiocytosis,
No arthritis: Granuloma annulare
**IL6 role RA **
- Autoimunity: Induce B cell maturation and TH17 differentiation
- Systemic fx: acute phase rxn and anemia via hepcidin, fatigue via HPAA
- Bones: Recruits osteoclasts and induces MMPs for erosions
- Blood vessels: Induce vascular permeability via VEGF production; Activate neutrophil migration to tissue
MTX-induced accelerated rheumatoid nodulosis Tx
- DC MTX and switch DMARD/biologic
- Continue MTX if cosmetic only
- If pain, mass effect: steroid injxn
- Case series: IL6, JAKi, RTX
** How to calculate HAQ**
41 total items:
-20 four‐point Likert‐scale Qs for specific ADL in 8 functional categories (each category scored based on highest sub-question)
-13 Qs for use of assistive devices
- 8 Qs assessing help received
Responses options/scale.
0 = without difficulty,
1 = some difficulty,
2 = much difficulty
3 = unable to do.
Scoring.
1) Use highest subcategory score for category. If used aids/help, increase score from 0/1 to 2 (no change if alrdy 2 or 3)
2) sum category scores;
3) divide final sum by the number of categories for final HAQ score rounded to the nearest value evenly divisible by 0.125.
**Requires a minimum of 6 categories answered; if less, do not score.
Score interpretation.
Total score is between 0–3.0, in 0.125 increments. Increasing scores indicate worse functioning with 0 indicating no functional impairment and 3 indicating complete impairment.
Claw toe deformity
- Pathogenesis
- DDx
Chronic MTP hyperextension leads to unopposed flexion of the DIP and PIP.
Atrophy/weakness of intrinsic muscles overpowered by extrinsinc (EDL, EDB, FDL)
DDx:
Synovitis,
-Trauma
- Delayed/missed compartment syndrome of deep posterior compartment of leg/foot
- Cavus deformity
- Neuromuscular disease
Foot pain DDx
Synovitis,
MTP subluxation,
Bunion (Hallux valgus),
Stress fracture of MTP,
Toe deformities,
Enthesitis/plantar fasciitis,
Tendonitis,
Bursitis,
Rheumatoid nodules,
Neuropathy (eg Tarsal tunnel, vasculitic, drug-related)
Preop Screening
- C-spine XR (flex/extend) if pain
- Screen cardiac disease
- Cricoartyenoid joint disease
Claw vs Mallet vs Hammer
Claw: MTP extended, PIP flexed, DIP flexed
Mallet: DIP flexed, others neutral
Hammer: PIP flexed, others extended or neutral
Pregnancy + Breastfeeding (BF) Meds
- NSAIDs
- ACE/ARB
- Pred
- TNFi
- Continue
- Discontinue
- Not compatible
NSAIDs - DC in 3rd to prevent premature fetal ductus arteriosus closure (ok 1-2), ibuprofen for BF
ACE6ARB - DC in T2/3 - fetal renal fx
Pred <20mg (if >20mg, hold BFfor 4h)
TNFi: DC in 3rd (ok 1-2), ok for BF
Continue: HCQ, SSZ, colch, AZA, CNI (preterm, low birth weight, NOT for BF)
Discontinue at conception and in preg: anakinra, belimumab, abatacept, anti IL6, anti IL17, JAKi
NOT COMPATIBLE preg and breastfeeding: MTX, MMF, LFN, CYC, Thalidomide, Tofa, apremilast, baricitinib
RA ILD:
-Risk factors to DEVELOP
-Poor prognosis
Smoking
Age
High anti CCP-RF
Fam Hx RA
Male
MUC5B promoter variant
-Male, older
-Hx of exacerbation
-Low DLCO
-UIP (honeycombing)
- Extent of fibrosis
Drugs to avoid in ILD
MTX, LFN
Gold
TNFi
Felty DDx
LGL-L
EBV/HIV
Meds: TNFi, MTX
SLE
Pathogenesis:
-Hallux valgus
-Splay foot
- Hindfoot valgus
-Pes planus
-Hallux valgus: sznovitis 1st MTP, lax ligament, lateral deviation prox phalanx
-Splay foot: MTP laxity + intrinsic muscle weakness
- Hindfoot valgus: synovitis midtarsal, subtalar, ankle; tibialis posterior rupture, lax ligament
-Pes planus: synovitis peritalar joints and tib post –> midtarsal, subtalar instability –> navicular pushed anterior/down depressing medial longitudinal arch
Tx for
LGL-L
Rheumatoid robustus with amyloid
RA w/ vasculitis
RA w/ nodules on MTX
RA with cricoarytenoid disease
LGL-L: MTX, CNi, CYC, +/- pred
Amyloid: MTX, CYC, TNFi, Toci,
Vasculitis: pulse steroids +/- ritux/cyc
Nodules on MTX: DC MTX, can inject nodules w steroids or surgically remove, maybe colchicine, SSZ, HCQ can shrink nodules
Cricoarytenoid: treat RA, inject vocal cords, ENT
Indications for C spine fusion in RA
-Atlantoaxial subluxation w/ posterior antlantodens interval of <14mm
OR 5mm of basilar invagination
-Subaxial subluxation and sagittal diameter of spinal canal of <14mm
RA mech of wrist radial deviation
Extensor carpi ulnaris tendon weakness = unopposed radial
RA mech of Piano key ulnar head
Radioulnar ligament damage –> floating ulnar styloid
RA mech of ulnar drift of fingers
With wrist radial deviation changes line of pull –> finger tendons pull fingers ulnarly
Cutoffs for DAS28, SDAI, CDAI, RAPID 3
DAS28: ≤2.6, ≤3.2, >3.2 to ≤5.1, >5.1
-*change must >0.6 to be meaningful
SDAI: ≤3.3, ≤11, >11 to ≤26, >26
CDAI: ≤2.8, ≤10, >10 to ≤22, >22
RAPID3: ≤1, <6, ≥6 to ≤12, >12
List 3 proteases produced by synovial fibroblasts
- MMP (matrix metalloproteinases)
- Serine proteinases (Granzymes A/B, trypsin, tryptase)
- Cysteine proteinases (Cathepsins B, D, K, L)
- Aggrecanases (fibronectin)
Define pannus
- Proliferative synovium: mononuclear cells (CD4+ T lymphocytes, activated macrophages, B cells, plasma cells, and dendritic cells)
- Can invade bone/cartilage to cause destruction via fibroblast like synoviocyte and proteinases
5 cells found in pannus/synovium
Mononuclear cells:
- CD4+ T lymphocytes
- Activated macrophages,
- B cells,
- Plasma cells
- Dendritic cells
- Osteoclasts
- Mast cells
- Fibroblast like synoviocyte
Rheumatoid nodule
- Where (and manifestations)
- Forearm extensor surface, olecranon bursa, over joints, and over pressure points (e.g. sacrum, occiput, and heel)
- Lung (effusion, PTX, fistula, hemoptysis)
- Cardiac (valvulopathy, stroke, syncope,
- CNS (SC compression, stenosis)
Cytokine with antiinflamm fx
Major anti-inflammatory cytokines include IL-4, IL-10, IL-11, and IL-13
TNFa roles in RA
- Blood vessel related
- Angiogenesis
- Activate endothelial cell adhesion molecules (VCAM, ICAM)
- Inflammation related
- Proinflammatory cytokine release (1,6,23)
- Hepcidin induction (acute phase response)
- PGE2 production
- Erosion related
- Osteoclast activation
- Chondrocyte activation —> MMP production and cartilage destruction
Draw and describe a rheumatoid factor
RF = autoantibody (IgM, G, A, E) against antigenic determinants on Fc fragment of immunoglobulin G forming immune complex
Nonrheum causes of positive RF
CHRONIC
CH: chronic dz: hepatic (PBC), pulmonary (IPF, silicosis, asbestosis)
R: RA
O: Other CTD: SLE, SSc, MCTD< SS, PM, Sarcoid N: neoplastm
I: infxn - TB, IE, Hep B/C, HIV, Mono, Parasitic (toxo, malaria), syphilis, Leprosy, Parvo, Rubella
C: cryo
Chronic liver and renal disease
Elderly
What are anti-citrullinated antibodies (ACPA)
Proteins directed against citrullinated peptides (eg fibrinogen, T2collagen, vimentin) –> immune complex to start innate/adaptive response, cytokine production, and activation of fibroblast like synoviocytes
(Citrulline formed by deimination of arginine by peptidylarginine deiminase in mucosal surfaces)
**DDX of positive Anti-CCP **
CTD: RA, SLE, SS, PsA,
Infection: TB
Lung disease: IPAF, RA-ILD
**Anti-CCP significance in RA (new and old)
New RA:
- Specific for RA
- More severe disease course
- Erosive disease
Old RA:
- Less likely to achieve drug free remission
- Assoc’d w/ ILD and CVD
Why cyclic configuration of Ag in assays that test for antiCCP
Peptides in peptide-AB complexes adopt beta-turn conformation
This increases ACPA binding affinity (ie increase sensitivity without sacrificing specificity)
1 genetic and 1 environmental factor associated with CCP
Genetic:
- HLA-DR4,
- PADI4,
- PTPN22
Environmental:
- Smoking (increases PADI), pollution, silica
- Microbiome,
- Infections
- Perionditis - porphyromonas gingivalis can form citrullinated neo antigen –> ACPA
Role of smoking in RA
Increases risk of ACPA+ RA
Activates innate immune pathway
Induces PADI expression in airway –> more protein citrullination and stimulation for generating ACPAs
2 advantages of antiCCP over RF
More specific but equally sensitive
Predicts severity and erosive disease
Difference between synovial path in PsA vs RA
PsA
- LESS cellular infiltrate (T/B cells) with MORE TH17 cells
- MORE vascular tissue in PsA (increased expression of VEGF, ANG2, BFGF)
- LESS hyperplasia of synovium in PsA
- Proliferation of existing vessels by EXTENSION vs/ in RA vessels show BRANCHING = NEOVASCULARIZATION
- NO antibodies to citrinullated peptides
Drug induced pneumonitis vs RA-ILD
- MTX pneumonitis happens in 1st year vs more chronic in RA-ILD
- NSIP (vs UIP in RA-ILD)
- BAL: lymphocytic (vs neutrophilic or lymphocytic in RA ILD)
Drugs safe to use in RA ILD
CYC
Steroids
MMF
AZA
Ritux
How to diagnose cricoarytenoid arthritis
HRCT
PFT
Laryngoscopy
**MC tendon rupture in RA **
Ulnar extensor tendons (extensor digiti minimi is first)
Then radial extensor tendons
Flexor policis longis = MC flexor to be ruptured (Mannerfelt lesion)
Mechanism of stenosing flexor tenosynovitis
Thickening/hypertrophy of A1 pulley
Presence of nodules
Windswept deformity of the knee
Rare complication of untreated RA
Abnormal valgus deformity in one knee with varus in the other
PsA vs RA - clinical/lab manifestations
DIP involvement
Asymmetric oligoarticular
No RF or CCP
HLAB27, IL23
Nail pitting/dystrophy
Dactylitis and Enthesitis
Axial involvement
Psoriasis
PsA vs RA - XR manifestations
RA
- Periarticular osteopenia
- Marginal erosions: MCP, wrists, PIP
- NO acral osteolysis
PsA:
- Periostitis
- Ankylosis
- Erosions: MCPs, PIPs, DIPs,
- Dactylitis
- Acral Osteolysis , Arthritis mutilans
- Pencil in cup
- Axial and SI involvement
- Syndesmophytes
2 diseases w/ MCP subluxation but NO erosions
SLE - Jaccoud’s
Rheumatic fever
Neurologic: cerebral palsy, post CVA
Direct/indirect societal costs of RA
Direct
- Treatment costs eg meds
- Hospital costs
- Cost of transport, aids
Indirect
- Lost productivity (to employer)
- Home care
- Intangible costs on self esteem, well being
Das 28 components
SJC, TJC, ESR, Pt global
10 methods used in the literature to measure the response on meds in RA?
Das 28, CDAI, SDAI, RAPID 3
EULAR response, ACR response,
ACR 20, ACR 50, ACR70
Patient activity scale
3 combination tx w/ MTX that is superior to MTX alone
MTX+SSZ+HCQ
MTX+LFN
MTX+IFX
MTX+ADA
MTX+ETN
What is rate of radiographic progression in RA when using antiTNF?
Total sharp score
- Mean annual progression 2.1/year w/ DMARD and 0.7/year by TNF
Fertility vs Obstetric outcomes in RA vs healthy
Fertility/preg outcomes worse if active disease
Obstetric outcomes increased: HTN, IUGR, C-section, preterm birth,
** Change of child developing RA or SARDs if mother has RA**
3x more likely to develop RA
Increased likelihood of thyroid disease
Risk factors for RA flare during pregnancy
TNFi discontinuation early in pregnancy
High disease activity
** Vaughan-Jackson deformity DDX **
- Extensor tendon subluxation at MCP (ie not ruptured, but just dysfunctional)
- Volar subluxation of metacarpal heads preventing finger extension (active and passive)
- Ulnar nerve palsy affecting 4th and 5th lumbricals, with unopposed MCP extension and unopposed IP flexion
- Trigger fingers stuck in flexion
