Flashcards in week 8- MSk 3 Deck (66)
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1
• Osteoarthritis:
o Aka Degenerative Joint Disease
o Mc type of joint dz
o Dt breakdown of articular (hyaline) cartilage in synovial joints (actually entire joint organ)
o Mostly dt ↑wear and tear, or 2nd nonspecific inflammatory changes
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• Prevalence of OA
o ↑ w age
o 20M in US; ↓45 M > F; >55 F > M
o using x-rays, >50% >65
o 80-90% >65 have evidence of OA
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• OA etio:
o Multifactorial
o Local inflame
o Hx jt trauma
o Systemic hormones: esp E
o ↓proprioception
o Genetics
o Obesity: ↑mechanical stress
o Mineral def
o Biomechanical: post trauma; squatting, climbing stairs, excessive kneeling
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• Pathology of OA:
o Metalloproteases: collagenase, stromelysin, gelatinase
o Cytokines: IL-2, IL-6, TNFa
o NO
o ↓ proteoglycans → cartilage softens, ↓elasticity
o ↓jt surface integrity → loss of jt space
o Proliferation of new bone & cartilage at jt margins (spurs or osteophytes)
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• Subsets of OA:
o 1st or 2nd
o Local or general
o Hypertrophic or atrophic
o +/- diffuse idiopathic skeletal hyperostosis (DISH)
o +/- overt inflame
o +/- chondrocalcinosis
o Rate of progression
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• 1st OA:
o Dt aging, idiopathic
o in previously intact joints, no apparent initiating factor
o usu C and L spine, PIPs, DIPs, base of thumb, hips, knees, 1st MTP
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• 2nd OA:
o Predisposing: Trauma Congenital or developmental dos, CPPD,
o Osteonecrosis, RA, gouty arthritis, septic arthritis, Paget dz of bone
o DM, acromegaly, hypothyroid, neuropathic (Charcot) arthropathy, frostbite
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• OA ssx:
o related pain, deep achy
o ↓ROM
o Crepitus
o Stiffness during rest (gelling)
o AM jt stiffness, usu ↓30 mins
9
• PE for OA:
o Heberden’s and Bouchard’s nodes
o Mild-mod firm jt swelling
o Crepitus
o ↓ROM
o Tender jt line, mb warm, effusion
o Wasting of mm assoc w jt
o Periarticular tenderness
o Deformities or instability in advanced dz
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• Labs for OA:
o Not useful in dx
o CRP/ESR
o RF (-)
o Eval synovial fluid
o xray
o cartilage degradation products
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• Pt archetypes of OA:
o Menopausal/Erosive
o DISH
o Charcot
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• Menopausal/Erosive OA:
o Aka erosive or inflam OA
o Usu F beginning in menopause
o Pain, swelling, inflame, redness in hand IP’s
o Erythema subsides → enlarged, stiff, st deformed jt
o Boney erosions and cystic swellings
o DMARDs don’t help, settles down on its own in a few yrs
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• DISH OA:
o Bridging enthesophytes in spine
o Osteophytes in peripheral jts
o ↓ ROM
o Metabolic syndrome, usu older obese M or DM
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• Charcot OA:
o Dt denervation of jts
o Destructive form of OA
o Extensive new bone formation around jts
o Found in diabetic neuropathy
15
• Radiographs of OA:
o Jt space narrowing
o Osteophytes
o Sclerosis
o Deformity
o Gull wing/saw tooth
o Spurring
o Subchondral cysts
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• OA ddx:
o PsA: dacylitis
o Onychodystrophy
o AS
o ReA
o EA
o RA- DIP unaffected, systemic ssx
o CPPD: crystals in jt fluid, calcification of cartilage, knee, brief attacks
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• Crystal induced coditions:
o Gout
o Calcium Pyrophosphate Deposition (CPPD)
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• Gout:
o deposition of monosodium urate crystal in and around jt
o M:F 9:1, most F post menopausal
o 40-60
o 3 clinical stages: asx hyperuricemia, acute intermittent, advanced (Chronic Tophaceous)
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• Gout etio:
o Metabolic:
o 1st: ↑uric acid dt specific enzyme defects, def, overactivity
o 2nd: ↑uric acid dt ↑nucleic acid turnover: myelo-proliferative dos, chronic hemolytic anemia, psoriasis
o ↑intake dietary purines: rich foods, esp w alcohol
o Renal: ↓excretion dt Pb nephropathy, acute ethanol ingestion, toxemia of pg, drugs (salicylates, diuretics)
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• Asx Hyperuricemia:
o Most ppl w ↑uric acid never → gout, tophi, KD stone
o ULN serum urate: 8.0-8.5mg/dL
o > 6.8mg/mL is > soluble concentration of monosodium urate in body
o =physiologically hyperuricemia
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• Acute Intermittent Gout:
o Mc in primary care
o Rapid development of warmth, swelling, erythema and PAIN
o Pain escalates over 8-12 hrs
o Initial attack usu monoarticular, 1st MTP
o Other: midfoot, ankle, heel, knee
o → Walking difficult to impossible
o Lc: wrist, finger, elbow
o mb systemic sx (fever, malaise)
o Erythema may extend beyond involved jt , resemble bacterial cellulitis
o Attacks hrs-2 wks, gradual ↑ duration, freq; feel normal bw
o Synovial fluid has crystals even if asx
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• Chronic Tophaceous Gout
o Usu after >10 yrs acute intermittent gout
o intercritical periods are no longer pain free
o Less painful then acute intermittent gout attacks bw attacks
o exquisite pain, more often, st every few wks
o mb diffuse, symmetrical involvement in hands, like RA
o Tophi around jts or other areas, fingers, wrists, ears, knees, olecranon bursa, Achilles tendon
o Microtophi inside synovial fluid, w MRI
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• Dx of gout:
o ONLY WITH JOINT ASPIRATION
o ↑Serum uric acid
o Synovial fluid shows needle or rod shaped crystals, yellow one direction, blue the other
o WBCs 5000-80,000/mm3
o also culture to r/o infx
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• Calcium Pyrophosphate Deposition (CPPD)
o Aka pseudogout: acute attacks of CPPD crystal-induced synovitis
o Aka Chondrocalcinosis: radiographic calcification in hyaline/fibrocartilage
o Aka Pyrophosphate arthropathy
o 1.3/ 1000, ~50% pop have xray changes of CPPD by 80
o M>F 1.5:1
o Assoc metabolic dos: hemochromatosis, hyperparathyroid, hypomagnesemia, hypophosphatasia, hypothyroid
25
• Clinical Manifestations of CPPD (sub-types):
o Asx (will have radiographic changes) may be found incidentally
o Pseudogout
o Pseudo-rheumatoid arthritis
o Pseudo-osteoarthritis
o Pseudo-neuropathic joint disease
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• Pseudogout:
o = self-limited acute or subacute attacks of arthritis (mono or pauci) in extremities
o Provoked: Trauma, surgery, severe medical illness
o St both urate and CPPD crystals in a single inflammatory effusion
o Systemic: fever, leukocytosis w left shift, ESR
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• Pseudo-rheumatoid arthritis
o nonerosive, asynchronous, inflame
o CPPD crystals in jt fluid
o Rarely mimics sepsis
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• Pseudo-osteoarthritis
o 50% w sx CPPD show progressive jt degeneration
o knees, wrists, MCP’s, hips, shoulders, elbows, spine
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• Pseudo-neuropathic joint dz:
o severe jt degeneration and disruption w of neuro do → jt denervation
o Charcot jt
o Underlying dos: DM (mc), tabes dorsalis, syringomyelia
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