Intro / Crystalline Arthritis Flashcards Preview

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Flashcards in Intro / Crystalline Arthritis Deck (21):
1

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

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.

2

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

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.

3

Uric acid is breakdown product of what?

Purines

4

4 drugs that decrease excretion of uric acid

Diuretics, aspirin, cyclosporin, and alcohol

5

2 associated conditions w/ hyperuricemia

Kidney stones an CVD

6

What parts of body does gout usually affect?

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

7

Risk factors for gout
Age / gender
Diet
Diseases
Drugs

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

8

Precipitating events for acute gout flares

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

9

Treating acute gout

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

10

Colchicine
Use
Mechanism
Toxicity

•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

11

Sites of tophi formation

•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.

12

5 indications for chronic gout treatment

•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

13

Goal for treating chronic gout

uric acid less than 6

14

4 meds to treat chronic gout

Allopurinol, probenecid, febuxostat, and pegloticase

15

Allopurinol
What is paired?
Use
Mechanism
Toxicity

•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).

16

Probenecid
Mechanism
Requirements

•Mechanism – increases excretion (uricosuric)
•Requires good kidneys and urate excretion less than 700 mg/day. Not used much.

17

Febuxostat

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

18

Pegloticase
Description
Use
Limitations

•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.

19

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

•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.

20

Presentation of calcium pyrophosphate crystals

•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.

21

Treating pseudogout

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