Intro / Crystalline Arthritis

Question 1

Inflammatory vs Non-Inflammatory arthritis
Morning stiffness
Swelling / warmth
Activity response
Distribution

Answer 1

Inflammatory: morning stiffness > 30 min, has swelling / warmth, improves w/ activity. Found in PIP, MCP, wrist, MPT, and small joints.

Non-inflammatory: morning stiffness less than 30 min, no swelling / warmth, activity makes pain worse. Found in large weight bearing joints or DIPs.

Question 2

Differentiating joint aspirations: category, appearance / cellularity, Diff Dx
Noninflammatory
Inflammatory
Septic
Hemorrhagic

Answer 2

Non-inflammatory: straw clear and viscous. Cell count below 1500. Diff Dx includes OA, trauma, neuropathic joint.

Inflammatory: cloudy and thin. Cell count 1500-100,000. Diff Dx includes RA, spondyloarthritis, crystalline, viral / fungal infection.

Septic: purulent. Cell count >100k. Caused by bacterial infection.

Hemorrhagic: bloody w/ variable cell count. Diff Dx includes fracture, tumor, or coagulopathy.

Question 3

Uric acid is breakdown product of what?

Answer 3

Purines

Question 4

4 drugs that decrease excretion of uric acid

Answer 4

Diuretics, aspirin, cyclosporin, and alcohol

Question 5

2 associated conditions w/ hyperuricemia

Answer 5

Kidney stones an CVD

Question 6

What parts of body does gout usually affect?

Answer 6

1st MTP (podagra) > midfoot > ankle > knee

Question 7

Risk factors for gout
Age / gender
Diet
Diseases
Drugs

Answer 7

• Men >40 y/o, postmenopausal women
• Obesity, high protein diet, alcohol
• Hyperuricemia
• Diseases: Renal failure, illness, tumor
• Drugs: cyclosporine HCTZ, diuretics

Question 8

Precipitating events for acute gout flares

Answer 8

Surgery, trauma, illness, dehydration, alcohol, and diet change.

Question 9

Treating acute gout

Answer 9

Avoid meat, alcohol, and dehydration
Colchicine
NSAIDs
Corticosteroids - 1 week oral taper or injected if monoarticular. Good for polyarticular gout if renally impaired.

Question 10

Colchicine
Use
Mechanism
Toxicity

Answer 10

• Used for acute gout flares less than 48 hours after onset.
• Mechanism: antimicrotubule → suppressed cell proliferation, chemotaxis, and activation of white cells. Suppresses caspase-1 and IL-1 activation.
• Toxicity: diarrhea, risk of marrow suppression, myopathy

Question 11

Sites of tophi formation

Answer 11

• Tophi usually occur on fingers, wrists, ears, knees, olecranon bursa (weenis), and pressure points such as ulnar forearm / Achilles.
• Tophi may also occur in connective tissue of kidney, heart valves, sclerae, and ears.

Question 12

5 indications for chronic gout treatment

Answer 12

• 3 episodes / yr or 5 lifetime episodes
• Hyperuricemia serum level > 13
• Tophi / erosive gout changes on radiograph
• Uric acid nephropathy / nephrocalculi
• Prophylaxis w/ cytolytic chemo treatments

Question 13

Goal for treating chronic gout

Answer 13

uric acid less than 6

Question 14

4 meds to treat chronic gout

Answer 14

Allopurinol, probenecid, febuxostat, and pegloticase

Question 15

Allopurinol
What is paired?
Use
Mechanism
Toxicity

Answer 15

• Colchicine is paired daily for the 1st 6 months to prevent flares.
• Used for both gout and uric acid kidney stones. Don’t use until 2 weeks after resolution of 1st acute flare due to possibility of worsening the flare.
• Mechanism – xanthine oxidase inhibitor. Doesn’t help in the middle of an acute gout flare, due to increased crystallization at the start of decreased levels.
• Toxicity – cytopenias, rash, drug fever, hypersensitivity including Stevens Johnson (never rechallenge if rash appears).

Question 16

Probenecid
Mechanism
Requirements

Answer 16

• Mechanism – increases excretion (uricosuric)

* Requires good kidneys and urate excretion less than 700 mg/day. Not used much.

Question 17

Febuxostat

Answer 17

New oral non-purine selective xanthine oxidase inhibitor. Only use if allergic to allopurinol.

Question 18

Pegloticase
Description
Use
Limitations

Answer 18

• New IV recombinant uricase. Enzyme found in non-human vertebrates that breaks down uric acid into allantoin by urate oxidase.
• Used w/ severe, refractory tophaceous arthritis and tumors that have high cell turnover.
• Limited by high cost, IV, and anaphylaxis.

Question 19

Calcium pyrophosphate crystals
Population
Cause
Precipitating factors (3)
Pathophysiology
Involved sites
Associated conditions (5)
Crystals
Imaging

Answer 19

• Most common in old age
• Occurs when calcium pyrophosphate crystals are released from cartilage and phagocytosed by PMNs → mono / polyarthritis w/ pain and swelling.
• Precipitating factors include surgery, trauma, and severe illness, but NOT alcohol (diff than gout).
• Calcium pyrophosphate dihydrate apatites may stimulate the release of metalloproteases → cartilage degradation.
• Knee > wrist > hand (esp 2nd-3rd MCP) > ankle > hip. Does NOT involve the 1st MTP
• Associated w/ hypothyroidism, hyperparathyroidism, hemochromatosis, hypomagnesia, and hypophosphatemia. May be involved in pathogenesis of OA.
• Rhomboid crystals appear blue when parallel. Much smaller than RBCs.
• Radiology shows chondrocalcinosis (articular / meniscal cartilage calcification) of capsule, tendon, or ligament. May see degenerative changes w/ large “dripping” osteophytes.

Question 20

Presentation of calcium pyrophosphate crystals

Answer 20

• Acute episodes last 5-14 days, w/ or w/o treatment. Present similar to gout (pseudogout) w/ sudden onset pain, swelling, warmth, and redness in 1+ joints. May involve systemic sxs such as fever, sweats, and leukocytosis.
• May cause “boxer glove” dorsal hand swelling
• Chondrocalcinosis may be asymptomatic.

Question 21

Treating pseudogout

Answer 21

NSAIDs, steroids, and chochicine (if less than 48 hrs)