Arthritis

Question 1

Components of Synovial Joints

Answer 1

• 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

Question 2

4 General Types of Arthritis

Answer 2

• 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

Question 3

Synovial Fluid in Types of Arthritis

Answer 3

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

Question 4

How does osteoarthritis present?

Answer 4

• 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

Question 5

OA Pathogenesis

Answer 5

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

Question 6

OA Risks

Answer 6

• 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

Question 7

OA v. RA Imaging

Answer 7

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

RA - BONE EROSIONS (as pannus invades bone)

Question 8

OA Tx

Answer 8

• 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

Question 9

RA Presentation

Answer 9

• 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

Question 10

What is the major risk factor for RA?

Answer 10

Smoking

Question 11

RA Labs

Answer 11

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

Question 12

RA Tx

Answer 12

• 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

Question 13

Gout and Pseudogout

Answer 13

• 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

Question 14

Definition and Causes of Hyperuricemia

Answer 14

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

Question 15

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

Answer 15

• 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)

Question 16

Short and Long Term Gout Tx

Answer 16

• 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