Gout/Pseudogout/ RA Flashcards
Hyperuricemia is when uric acid (end product of purine degradation) levels are _____
> 6.8 mg/dl
Hyperuricemia can cause what?
Gouty arthritis = supersaturation of monosodium urate crystals in fluids of joint or tophi (nodular monosodium urate crystal deposts in skin) due to overproduction or under-excretion of uric acid.

What do monosodium urate crystals look like under polarized light?
Needle-shaped, negative birifringence

Who is gout MC?
What can promote gout?
- 90% of gout in M (30-50s)
- Post-menopausal W
- Alcohol or anything high in purines
What is the MC presentation of acute gouty arthritis?
- Acute onset, monoarticular, most often affecting the 1st MTP of the big toe.
- Pain is so bad will wake you up at night.
- Joints are hot, swollen, tender, dusky/red
- Pt will have fever
Chronic gouty arthritis can lead to what?
- Tophi = deposits in ears, forearms and achilles tendon
- Renal insufficiency (urate stones that are radiolucent)
DDX for gouty arthritis
- Infectious arthritis (septic arthritis)
- Reative arthritis
- Pseudogout - CPPD disease (Ca+ pyrophosphate dihydrate)
Treatment for Gout
- Best medication for acute gouty flare?
- Treamtent for asymptomatic hyperuricemia?
- No single best agent
- Do not treat asymptomatic hyperuricemia, EXCEPT in patients about to receive cytotoxic therapy for neoplasm

How do we treat acute gouty flare?
- ASAP within 12- 36 hours with NSAIDS (500mg of Naproxen BID / 50mg of Indomethicin TID).
- Watch bc INC risk of GI bleeding.
What is a reasonable 1st line of treatment for Gout?
Steroids (Prednisone 40 mg PO/day x5-7days -taper)
What drug is effective for gout in the 1st 24 hours of an attack?
Colchicine
When would you use a uric acid lowering agent for gout?
What should you be cautious of?
- Recurrent gouty attacks, tophi, kidney stones or cytotoxic therapy
- Do not start during an acute attack because it cause flares.
How is pseudogout different from gout?
- Deposits of Calcium Pyrophosphate Dehydrate
- Affects larger joints and the knee
- Older patients
- Polyarticular
If chronic pseudogout, what do we see?
- Resembles OA
- Can cause chondrocalcinosis (Ca2+ deposits in articular cartilage)
What do the CPPD crystals in pseudogout look like on polarizing microscopy?
- Short, blunt rods, rhomboids/cuboids
- Weak POSITIVE birefringence

DDx for Pseudogout
- OA
- RA
- Gout
- Septic arthritis
- Aging
- If younger patients => primary hyperparathyroididm and hemochromatosis
Treatment for pseudogout
- NSAID
- Steroids (intra-articular injections)
- Colchicine (variable)
What is Rheumatoid Arthritis?
-
Chronic, inflammatory, systemic AI disease that affects synovial tissues and diarthrodial joints and other organs (lungs and skin)
- __Symmetrical
- Affects SMALL joints
- Polyarthritis
- Extraarticular features

Etiology of RA
Idiopathic, but thought to be have genetic susceptability (HLA-DRB4/DRB1 0401 or 0404) influences that is triggered by an environmental factor.
Rheumatoid Arthritis
- MC in and when?
- How is if affected by pregnancy?
- What is it thought to be associated with?
-
W 20-60 YO
- MC in Yakima & Inuit Native American Tribes
- Improves during pregnancy, but flare ups begin 4-6 weeks after delivery
What do we see in labs for RA?
- Acute phase reactants: ↑↑↑ ESR & ↑↑↑ CRP
- Serology: (+) RF + anti-CCP = 95% pt has RA
What is the purpose of Rheumatoid Factor (RF)?
RF is a IgM Ab made by B-cells in the RA synovium => binds to altered IgG Ab => forms immune complexes that go in synovial fluid => + comlpiment system.
Pathophysiology of Rheumatoid Arthritis
- Genetic + environmental trigger =>
- Modification of our own antigens, like IgG ab, Type 2 Collagen and Vinmentin
- Type 2 collagen and vinmentin under citrullination: Argining => citrilline
- Our bodies immune cells no longer recognize them as self-antigens =>
- Antigens get picked up by APC => presented in LN
- CD4+ T-helper cells are (+) => stimulate B-cells
- B-cells => plasma cells => make autoAB against self-antigens
- T-helper cells & Ab NTR circulation => joints
- T-cells secrete IFN-y and IL-17 => recruit more inflammatory cells, like MO.
- B-cells secrete TNF-a, IL1 and IL6. =>
- => Synovial cells proliferate, creating a pannus (a thick, swollen, synovial membrame with granulation tissue (fibroblasts, myofibroblasts + inflammatory cells)
- Overtime:
- Pannus invades cartilage and bone and synovial cells release proteases, which break down articular cartilage, allowing bones to directly rub against one another.
- Inflammatory cytokines cause T-cells to express RANKL, which binds to RANK on osteoclasts => break down bone
- Rheumatoid factor, an IgM Ab, enters the joint space and binds to fc domain of altered IgG Ab
- Anti-CCP Ab targets citrillinated proteins
- When Ab bind to target, form immune complexes that accumulate in the synovial fluids
- => + compliment system => joint inflammation and injury
- Chronic inflammation =>
- Angiogenesis (new BV), which promotes more inflammatory cells
- As the disease progresses, affects MULTIPLE joints on BOTH sides of body.
- Inflammatory cytokines => mutliple organ systems and cause extraarticular problems.

Rheumatoid synovitis causes:
- 1. Bursitis
- 2. Tendinitis
- 3. Synovitis














