ic16 OA and RA Flashcards
what are the differentials of joint pain
- inflamm
i) RA
ii) psoriatic arthritis
iii) gout
iv) pseudogout
v) spondyloarthritis - infection
i) septic arthritis
ii) osteomyelitis - degenerative
i) OA - soft tissue rheumatism
i) tendonitis
ii) bursitis - trauma
i) fracture
ii) dislocation
iii) ligamentous injury
iv) patella problems - tumor
how to differentiate between gout, RA, septic arthritis, gout and pseudogout
- hematological tests
- erythrocyte sedimentation rate (ESR) (an inflamm marker)
- C-reactive protein (CRP) (an inflamm marker)
- rheumatoid factor (RF) (present in pts w RA)
- anti-citrullinated protein Ab (ACPA/ anti-CCP) (present in pts w RA)
- joint aspiration (to look for presence of crystals in joint fluid for gout or WBC in joint fluid for septic)
- xray/ MRI (to look at extent of damage)
differentiate between OA, RA and gout based on key features and presentation (no. of joints, location, symmetry, pain characteristics, assoc s/sx, deformities for adv disease, diagnostic labs)
OA
i) number of joints: polyarthritis
ii) location: usually weight bearing joints (knees, hip, cervical, possibly fingers)
iii) symmetry: asymmetrical
iv) pain characteristics: gradual onset, pain on movement, worse at end of day, no nocturnal pain, relieved with rest
v) assoc s/sx: joint swelling possibly, erythema possibly, early morning stiffness <30min, crepitus (noisy knee)
vi) deformities: enlarged joints due to osteophytes (heberden’s/ bouchard’s nodes on fingers)
vii) labs: usually not done, imaging show presence of joint space narrowing and osteophytes
RA
i) number of joints: polyarthritis
ii) location: wrist, fingers, elbows, shoulders, hips, knees, ankles
iii) symmetry: asymmetrical
iv) pain characteristics: worse after rest, worse in morning, nocturnal pain, relieved with exercise, chronic w acute/ subacute flares/ sx
v) assoc s/sx: joint swelling, erythema early morning stiffness >30min, systemic sx
vi) deformities: fingers = swan neck, boutonneire; elbow = rheumatoid nodules; back of knees = popliteal cysts; toes = MTP subluxation
vii) labs: RF and anti-CCP pos, incr ESR, incr CRP, decr hematocrit, incr WBC, incr PLT
GOUT
i) number of joints: usually monoarthritis
ii) location: usually MTP of big toe, possibly mid foot/ ankle/ knee/ hand/ wrist/ elbow
iii) symmetry: asymmetrical
iv) pain characteristics: excruciating pain, rapid onset (usually overnight), acute/ subacute flares
v) assoc s/sx: alot of tenderness and joint swelling and erythema
vi) deformities: gout tophi
vii) labs: incr serum uric acid, uric acid crystals seen in joint aspirate, incr WBC
what are the risk factors for OA
i) genetic predisposition: rare mutations in collagen types II, IX, XI; gene GDF5
(collagen is an impt component that makes up the cartilage so mutations would affect cartilage repair after an injury)
ii) anatomic factors: varus alignment (bow legged), vagus alignment (knocked knee)
iii) joint injury
iv) obesity: incr load on weight bearing joints
v) ageing: leads to changes in ECM (thinning, decr hydration, incr brittleness)
vi) gender: <50yo M>W but once W reach postmenopausal will catch up; also affects the type of activity pt engages in
vii) occupation: affects the type of activity pt engages in
what is the pathophysiology of OA
factors (injury, aging, incr load etc) -> articular cartilage damage -> incr chondrocyte activity to remove or repair damage -> aberrant chondrocyte func results in greater cartilage breakdown instead -> cartilage loss and apoptosis of chondrocyte (also caused by subchondral bone release of vasoactive peptides and matrix metalloproteinases which incr break down of collagen) -> formation of fibrillations in cartilage and cartilage shards* -> subchondral bones rub against each other, become dense and smooth and more brittle and stiffer w decr weight bearing ability + development of sclerosis, microfractures and osteophytes (a compensatory structure to stabilise osteoarthritic joints)
*cartilage shards also causes inflamm and pathologic changes in joint capsule and synovium (mediated by TNFalpha, IL1, PGE2, NO) -> effusion and synovium thickening
how does pain arise as a result of OA
pain arises from:
i) activation of nociceptive nerve endings within the joint by mechanical and chemical irritants
ii) distension of synovial capsule from incr joint fluid, microfracture, periosteal irritation or damage to ligament, synovium or meniscus
what is the compensatory response of joint and surrounding tissues to the failed repair in OA
- cartilage degradation: articular cartilage damage cause chondrocytes to proliferate but also undergo phenotypic switch thus producing improperly mineralised collagen leading to weakening and degradation of collagen matrix in synovium
- bone remodelling and osteophyte formation: weakened collagen matrix causes thickening of the subchondral bone resulting in sclerosis and formation of bone spurs aka osteophytes and osteophytes cause widening of joints that was intended to stabilise the joint in response to abnormal mechanical loads
- synovial inflamm: weakening and degradation of the collagen matrix causes cartilage to flake off as shards thus the synovial membrane recruits lymphocytes and macrophages to remove debris which further lead to production of pro inflamm cytokines causing synovitis and contribute to disease progression via more pro inflamm cytokines and damage assoc molecular patterns (DAMPs)
what is the clinical presentation of OA (info that can be gathered from hx taking, physical examination, radiographic findings and lab findings)
i) inflamm: pain (deep, aching, on motion), swelling (from joint effusion), erythematous (redness), warm
ii) morning stiffness <30min
iii) limited joint movement
iv) functional limitation or instability
v) asymmetrical polyarthritis (typically on weight bearing joints)
HX TAKING: impacts negatively on ADL, instability, falls
PHYSICAL EXAMINATION: asymmetric monoarticular, crepitus on motion, reduced range of motion, transient joint effusion, palpable warmth, bone tenderness, bone enlargement
RADIOGRAPHIC FINDINGS: joint space narrowing, marginal osteophytes, subchondral bone sclerosis, abnormal alignment of joint
LAB FINDINGS: ESR <20mm/h
what are the three progressive stages relating to the pain from OA
stage 1: predictable sharp pain with mechanical insult -> limits high impact activities and modest effect on func
stage 2: pain becomes more constant, with unpredictable episodes of stiffness -> ADL starts getting affected
stage 3: constant dull/ aching pain punctuated by episodes of often unpredictable intense, exhausting pain -> severe limitations in func
how can the diagnosis of OA be made
w/o radiography and/or labs in presence of typical s/sx in at risk age group
i) 45yo and older
ii) activity related joint pain in one or a few joints
iii) morning stiffness less than 30mins
additional testings considered for
i) younger
ii) presence of atypical s/sx that suggests alternative or additional diagnosis (eg. hx of recent trauma, rapidly worsening sx or deformity, concerns of infection or malignancy)
what are the goals of tx for OA
i) relieve pain (and inflamm if any) through pharmacotx
ii) improve or preserve range of motion and joint func through non pharmacotx
iii) improve QoL
what is the tx approach for OA
non pharmacotx:
*firstline
i) exercise to reduce pain and improve physical func (strengthening, neuromuscular training, low impact aerobic) approx 30 mins 3x/w
ii) consider referral to PT for supervised exercise
iii) weight management can improve QoL and physical func and reduce pain by reducing the load on weight bearing joints
iv) engage and empower pts with information and support (cannot rely on analgesics to relieve pain forever but do exercises to strengthen func of joint and prevent further deterioration)
pharmacotx:
*start with least systemic exposure or toxicity, use lowest effective dose for shortest possible period
i) TOP NSAIDs (less feasible for OA on hands bc freq hand washing, also not for hips bc of the depth of joint beneath skin surface)
ii) PO NSAIDs/ coxibs
iii) PO paracetamol/ tramadol (only if c/i to NSAIDs)
iv) IA GC inj for short term sx relief but effects v shortlived (6w to a few months) and cannot be given to regularly (3-4inj/yr)
v) duloxetine (for moderate to severe sx w c/i or inadequate resp to NSAIDs; will have SNRI s/e)
vi) TOP capsaicin
referral for surgical tx (total joint arthroplasty)
i) considered for pts with QoL substantially affected or non surgical tx ineffective or unsuitable
ii) postoperative rehabilitation essential for successful outcome (mainly PT, while pharmacotx is helpful in becoming pain free to start PT to use new joints and strengthen muscles and periarticular structures)
iii) c/i for active infection, chronic lower extremity ischemia, skeletal immaturity
what are the s/e of NSAIDs
- GI s/e
i) N/V, dyspepsia, abdominal pain
ii) risk of mouth and GI ulcer if use for >5d and if high risk (risk factors incl: >65yo, hx of ulcer, high dose or chronic NSAIDs, concom GC or antiPLT or anticoag *considered high risk if 3 or more or hx of complicated ulcer) switch to coxib or add PPI - CV s/e
i) MI, stroke, vascular death
*limit celecoxib dose to <400mg/d, if using high dose diclofenac (usual 150mg/d) for >4w, lower to 100mg/d or less for c/i pts (pts w established CVD or uncontrolled HTN) - renal s/e
i) PGE2: Na and H2O retention, HTN, peripheral edema
ii) PGI2: suppression of aldosterone and renin secretion, hypoK, AKI (risk factors incl: CKD, vol depletion, effective arterial vol depletion, severe hyperCa or renal artery stenosis, hypoNa or hyperK, >65yo, drugs (amphotericin B, AG, ACEi/ARB, diuretics, radiocontrast material))
*for CKD eGFR<60 can use NSAID for <5-7d but avoid NSAID and coxibs if eGFR<15 - pseudoallergy (non immunogenic) and true allergy (IgE mediated)
i) pseudoallergy: aspirin exacerbated respiratory disease (AERP) eg. bronchospasm in hx of urticaria, angioedema and asthma
*avoid non selective NSAIDs, can use coxibs w caution
ii) true allergy: urticaria, angioedema, anaphylaxis
*avoid all NSAIDs and coxibs if rxn is anaphylaxis - others
i) elevation in BP *monitor
ii) skin rxn (photosensitivity)
iii) hematologic (inhibition of PLT)
iv) CNS (dizziness, HA)
when might NSAID induced GI complication be suspected
when pt presents with
i) fatigue
ii) severe dyspepsia
iii) sx of GI bleed
iv) unexplained blood loss
v) Fe deficiency
*refer!
compare the safety concerns between non selective NSAIDs and coxibs
CROSS SENSITIVITY
i) for NSAIDs, avoid across all NSAIDs incl aspirin if anaphylaxis
ii) for coxibs, avoid across all NSAIDs, coxibs, aspirin (+ sulfonamides for celecoxib) if anaphylaxis
NSAID-EXACERBATED RESPIRATORY DISEASE
i) for NSAIDs, avoid in asthma
ii) for coxibs, caution in asthma
TERATOGENICITY
i) for NSAIDs, avoid in third trimester of pregnancy (24-40w)
ii) for coxibs, avoid in third trimester of pregnancy
INCR RISK FOR GI BLEED
i) for NSAIDs, avoid in concom antiPLT or anticoags or NSAIDs, avoid in active PUD or GI bleed
ii) for coxibs, avoid in concom NSAIDs or baby aspirin, caution in active PUD or GI bleed
RENAL S/E
i) for NSAIDs, avoid in severe renal impairment, triple whammy
ii) for coxibs, avoid in severe renal impairment, triple whammy
CV S/E
i) for NSAIDs, avoid in HF/ IHD/ PAD/ uncontrolled HTN
ii) for coxibs, avoid in HF/ IHD/ PAD/ uncontrolled HTN, but can consider low dose celecoxib at 200mg/d if necessary
