Arthritis Flashcards

1
Q

Components of Synovial Joints

A
  • Each bone is covered in cartilage
  • Ligament attaches the 2 bones to strengthen the joint
  • Fibrous capsule along inside of ligament; followed by synovial membrane (which forms articular capsule to protect synovial fluid); filled w/ synovial fluid
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2
Q

4 General Types of Arthritis

A
  • Mechanical/Degenerative
    • Worse w/ activity
    • <15 min morning stiffness
    • No night pain
    • Minimal swelling
    • Hx trauma
    • Esp weight-bearing joints
  • Inflammatory (non-crystal)
    • > 1 hr morning stiffness
    • Better w/ activity; worse at night and w/ rest
    • Warm, tender, swollen joints
  • Inflammatory Crystal- Induced
    • Gout
    • More localized
    • Severe constant pain, erythema, joint effusion
  • Infectious
    • Severe constant pain, erythema, joint effusion
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3
Q

Synovial Fluid in Types of Arthritis

A

Mechanical

  • Clear, high viscosity which is normal
  • Maybe some WBCs

Inflammatory (non-crystal)

  • Cloudy, opaque w/ less viscosity
  • Many WBCs (5-25,000) and polys

Crystal
Cloudy, opaque w/ less viscosity
-Many WBCs (5-25,000) and polys
-ID monosodium urate crystals

Infectious

  • Very opaque; low viscosity
  • Most WBCs (50.000) and polys
  • Low glucose as microbes consume glucose; and pos gram stain or cx
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4
Q

How does osteoarthritis present?

A
  • Knees (blacks), hips, spines, hands (whites)
  • Joint pain and stiffness –> limited function and loss of motion
  • Pain on passive movement of joints
    • Cartilage has no nerve supply
    • Pain from bone, joint capsule distention and secondary synovitis (can have inflammation in some cases)
  • Crepitus (grinding or cracking) from cartilage loss and incongruity of joint
  • Enlarged joint - do to bony protuberance, synovial inflammation or fluid (effusion)
  • Deformity or subluxation (partial or total dislocation) in later stages
  • HARD AND NODULAR
    • Heberden’s Nodes - DIP joints
    • Bouchard’s Nodes - PIP joints
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5
Q

OA Pathogenesis

A
  • Thinned/lost articular cartilage –> changes in subchondral bone –> osteophytes (bony protuberance)
  • Can also lead to changes in synovium / deformed capsule
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6
Q

OA Risks

A
  • Hx joint damage
  • Obesity
  • Injurious physical activities
  • Vulnerability - age, female, genetics, race, nutrition
  • Knee mal-alignment (as OA evolves there is abnormal stress on cartilage –> bony remodeling)
    • When meniscus removed or damaged there is less distribution of force; all concentrated in one place
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7
Q

OA v. RA Imaging

A

OA - See less and less black space b/n 2 bones as cartilage lost

RA - BONE EROSIONS (as pannus invades bone)

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8
Q

OA Tx

A
  • PT, exercise (strengthen muscles around joints BUT do not run on bad knee joints), wt loss
  • Pharm - acetaminophen, NSAIDs, topical NSAIDs (for pain relief)
  • Joint replacement
    • If surgery cannot be done may need to use opioids for pain reduction
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9
Q

RA Presentation

A
  • Symmetric inflammatory poly-arthritis (most commonly affects small joints of hands and feet)
  • Female > male (approx 1% pop)
  • Prolonged morning stiffness
  • Low grade fever, wt loss, fatigue
  • Local signs of inflammation - erythema, warmth at joint
  • Symmetrical
  • Wrists, MCP, PIP (not DIPs), sometimes feet
  • Boggy, palpable swelling
  • Weak grip and difficulty making fist due to pain
  • Can progress - bone erosion and deformities
  • Systemic feature - can involve vasculitis, lung (interstitial lung disease), anemia, eye inflammation, pericarditis, etc
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10
Q

What is the major risk factor for RA?

A

Smoking

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11
Q

RA Labs

A
  • High RF titer (also prognostic - higher RF = worse disease); not specific
  • Anti -CCPs more specific (directed against citrullinated antigens and inflammatory tissues are citrullinated)
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12
Q

RA Tx

A
  • Methotrexate -
    • Similarly sulfasalazine, hydroxychloroquinolone, leflunomide)
  • Anti-TNF Drugs - adalimumab, etanercept, infliximab
  • Other Bio Drugs - anti-cytokines, anti- T cell, anti-B cell, oral small molecules targeting JAK pathway
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13
Q

Gout and Pseudogout

A
  • Gout = monosodium urate crystals (MSU)
  • Hyperuricemia –> crystals in synovium phagocytosed –> activate inflammasomes w/in myeloid cells –> cytokines and other inflammatory mediators including IL-1
  • Pseudogout = calcium pyrophosphate dihydrate crystals (CPPD)
  • Similar, CPPD deposited in cartilage –> synovium
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14
Q

Definition and Causes of Hyperuricemia

A
  • Hyperuricemia if > 6.8 mg/DL
  • Causes of hyperuricemia include… genetics, drugs, alcohol, diet
  • Usually under-excretion ((kidneys) NOT over-production
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15
Q

Gout Dx (+ how do images and crystals differ from pseudogout?)

A
  • Presentation - podagra (swelling, warmth, red, pain of 1st MTP joint) and tophi under skin
  • SO must r/o septic arthritis (emergency) esp if first time
  • Aspirate joint - remove synovial fluid (arthrocenesis); often not performed b/c so much pain
  • MSU - needle-shaped and neg bifringent (yellow) - yellow when parallel
  • CPPD - rhomboid-shaped and pos bifringent (blue) - blue when parallel
  • Must also do synovial fluid gram stain/cx and cell count
  • Imaging
    • Gout - circular destructive lesions of MTP joints in foot
    • Pseudogout - see calcium deposits b/n bones (chondrocalcinosis)
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16
Q

Short and Long Term Gout Tx

A
  • Short-Term (flares)
    • Remove fluid then inject glucocorticoid (often too painful)
    • NSAIDs
    • Colchicine - concentrates in PMN leuks to dec proliferation and secretion of granule contents (block microtubules); effective early in attack
    • Anakinra (IL-1 antagonist) - newer

**Pseudogout treated similarly; mainly injections and NSAIDs

  • Long-Term (reduce uric acid)
    • Allopurinol, febuxostat - xanthine oxidase inhibitors
    • Probenecid - uricosuric