Gout/Pseudogout Flashcards
Gout
general
Metabolic disorder caused by hyperuricemia that results in the precipitation of monosodium urate crystals in and around joints, most often causing recurrent acute or chronic arthritis
Prevalence is approximately 3% in the United States
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Most common in middle-aged men and postmenopausal women
Presentation before age 30 → severe disease
Risk increases with higher body mass index (BMI)
Condition often runs in families
Gout
Hyperuricemia
Plasma urate level >6.8 mg/dL
Increased intake, overproduction, and/or underexcretion of uric acid
Relationship between hyperuricemia and gout is unclear
The majority (90%) of people with hyperuricemia do not have gout
Normal or low serum UA levels do not rule out gout
The greater the degree and duration → the greater the likelihood that gout develops
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Increased intake of UA
Consumption of purine-rich foods/drinks contribute to hyperuricemia (30%)
Red meat, liver, tuna, scallops, mussels, shrimp, asparagus, mushrooms, carbonated beverages
Ethanol (beer)
Strict low-purine diet lowers serum urate by ~1 mg/dL
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UA Overproduction
Causes of overproduction:
Hereditary
Ethanol is believed to stimulate urate synthesis in the liver
Hematological conditions (leukemia, lymphoma, hemolytic anemia)
Conditions with increased rates of cellular proliferation (psoriasis)
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UA Underexcretion
Most common cause of hyperuricemia
Uric acid is excreted mainly through the kidneys
Causes of decreased renal excretion:
Hereditary
Receiving diuretics or aspirin
High doses of cyclosporine (transplant patients)
Diseases that ↓ glomerular filtration rate (GFR)
Gout
patho
Hyperuricemia→ supersaturation → needle-shaped monosodium urate (MSU) crystals deposition into soft tissue and synovial joints
Can erode the bone and damage other tissues such as tendons and cartilage
Causerecurrent monoarticular arthritis and chronic deforming arthritis
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Risk Factors for Hyperuricemia
Diet:
High purine diet
Beverages containing fructose, alcohol
Obesity
Medical conditions: untreated hypertension, diabetes, metabolic syndrome, heart and kidney diseases
Medications:
Thiazide & furosemide diuretics
Low-dose aspirin
Anti-rejection/immunosuppressive drugs used in organ transplantation (cyclosporine)
Family history of gout
Age and sex:
Middle-aged and older men
Post-menopausal women
Dehydration
Acute Gouty Arthritis
general
Sudden onset of pain (often nocturnal)
Typically monoarticular
Commonly occurs in the lower extremities,most often at the base of the great toe (1st metatarsophalangeal joint) or the knee
Other sites: ankle, wrist, and elbow
Podagra = gouty attack at the 1st MTP joint
Acute gouty arthritis
Pain
Intensely inflammation, causing severe pain, “burning”, redness, warmth, swelling, and disability
Pain peaks within 12–24 hours and resolving within 3–10 days even without treatment
Nocturnal pain
Pain is often described as the joint on fire; weight of a sheet over the area can produce significant pain
Pain is the result of cytokines released from WBCs that enter the joint to remove uric acid
Acute gout flare
Clinical Course
Subsequent flares
Upon resolution of an acute gout flare, patients enter an intercritical (between-flares) period
Most often entirely asymptomatic
Variable in duration
Most patients left untreated will develop a recurrent flare within 2 years
Subsequent flare-ups
Shorter symptom-free intervals between flares
Higher likelihood of being polyarticular
Persist up to 3 weeks if untreated
Chronic Tophaceous Gout
general
Form of gout resulting from chronic inflammation
Palpable tophi develop
Firm yellow or white papules or nodules
Single or multiple
Locations:
Fingers, hands, feet, and around the olecranon or Achilles tendon
Kidneys
Can erupt through the skin, discharging chalky masses of urate crystals
Cause deformities and secondary osteoarthritis
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Dx
Suspected in patients with acute monoarticular arthritis
Diagnosis is established via microscopic analysis of thejoint aspirate, which shows:
Crystals of MSU,which arenegatively birefringent(yellow when parallel to polarizing light) andneedle-shaped
WBC > 2,000/μL with > 50% neutrophils (an acute inflammatory synovial fluid)
X-ray:
Shows no changes early in the disease
Punched-out erosions with an overhanging rim of cortical bone develop with progressive disease
Arthrocentesis and synovial fluid analysis should be done at the initial presentation
Yellow crystals when parallel to the polarizing light and blue when perpendicular
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Blood work may show:
Hyperuricemia (may be normal or low during a flare; best to measure 2 weeks after flare)
Elevated WBC
Elevated erythrocyte sedimentation rate (ESR)
Arthrocentesis
Also referred to as joint aspiration
Clinical procedure of using a syringe to collect synovial fluid from a joint capsule
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