Gout Flash Cards
What is gout?
A form of inflammatory arthritis caused by monosodium urate crystal deposition in joints.
What causes gout?
Elevated uric acid levels (hyperuricemia) leading to crystal deposition in joints.
What are the common risk factors for gout?
Male gender, obesity, alcohol consumption, high purine diet, and diuretic use.
What is the most commonly affected joint in gout?
The first metatarsophalangeal (MTP) joint, known as podagra.
What are the clinical features of acute gout?
Severe joint pain, redness, swelling, and warmth, often involving one joint.
What is chronic tophaceous gout?
Advanced gout with tophi (deposits of urate crystals) in soft tissues and joints.
What dietary factors increase the risk of gout?
High-purine foods like red meat, seafood, and alcohol (especially beer).
What is the gold standard for diagnosing gout?
Synovial fluid analysis showing needle-shaped negatively birefringent crystals.
What is the typical serum uric acid level in gout?
Greater than 6.8 mg/dL, but not all patients with hyperuricemia develop gout.
What is pseudogout?
Calcium pyrophosphate deposition disease (CPPD), which mimics gout but involves calcium crystals.
What are the common triggers for acute gout attacks?
Alcohol intake, high-purine meals, dehydration, and sudden changes in uric acid levels.
What is the first-line treatment for acute gout?
Nonsteroidal anti-inflammatory drugs (NSAIDs) like indomethacin or naproxen.
What medication is used for gout patients who cannot tolerate NSAIDs?
Colchicine or corticosteroids (oral or intra-articular).
What is the mechanism of action of colchicine?
Inhibits microtubule formation, reducing inflammation caused by urate crystals.
What are the common side effects of colchicine?
Gastrointestinal symptoms like diarrhea, nausea, and abdominal pain.
What is the role of corticosteroids in gout?
Used to reduce inflammation in patients who cannot take NSAIDs or colchicine.
What are xanthine oxidase inhibitors?
Medications like allopurinol and febuxostat that reduce uric acid production.
What is the target serum uric acid level in gout management?
Less than 6 mg/dL to prevent gout flares and crystal deposition.
What is the role of probenecid in gout treatment?
Increases uric acid excretion by inhibiting renal tubular reabsorption.
What are tophi?
Deposits of monosodium urate crystals in soft tissues, often seen in chronic gout.
What imaging finding is characteristic of chronic gout?
Erosions with overhanging edges, known as ‘rat bite’ lesions.
What is the recommended dietary modification for gout patients?
Low-purine diet, reducing alcohol intake, and increasing hydration.
What is the association between gout and kidney disease?
Hyperuricemia can lead to uric acid nephropathy and chronic kidney disease (CKD).
What is uric acid nephrolithiasis?
Kidney stones composed of uric acid, commonly seen in gout patients.
What is the role of uricosuric agents?
They increase renal excretion of uric acid, used in underexcretors of uric acid.
What is the relationship between diuretics and gout?
Diuretics like thiazides can increase uric acid levels and trigger gout.
What are the contraindications for allopurinol?
Severe renal impairment and hypersensitivity to the drug.
What is the genetic association with gout?
Variants in the SLC2A9 and ABCG2 genes affecting urate transport.
What is the mechanism of action of febuxostat?
Inhibits xanthine oxidase, reducing uric acid synthesis.
What is the treatment for refractory chronic gout?
Pegloticase, a recombinant uricase enzyme that breaks down uric acid.
What lifestyle changes can reduce gout flares?
Weight loss, regular exercise, avoiding alcohol, and staying hydrated.
What is the role of aspirin in gout?
Low-dose aspirin can increase uric acid levels and is generally avoided.
What is the relationship between metabolic syndrome and gout?
Metabolic syndrome increases the risk of hyperuricemia and gout.
What are the complications of untreated gout?
Chronic joint damage, tophi formation, kidney stones, and nephropathy.
What is the first step in managing a patient with suspected gout?
Synovial fluid aspiration and analysis to confirm crystal presence.
What are the long-term medications for gout management?
Allopurinol, febuxostat, and uricosuric agents like probenecid.
What is the risk of starting urate-lowering therapy during an acute gout attack?
It can exacerbate the attack; therapy should be started after inflammation subsides.
What is the role of lifestyle modification in gout prevention?
Reduces uric acid levels and decreases the frequency of gout attacks.
What are the indications for initiating urate-lowering therapy?
Frequent gout attacks, tophi, joint damage, or kidney stones.
What is the recommended hydration level for gout patients?
At least 2-3 liters of water per day to prevent uric acid crystallization.
What is the primary cause of hyperuricemia in gout?
Impaired renal excretion of uric acid or overproduction of uric acid.
What is the difference between primary and secondary gout?
Primary gout is idiopathic; secondary gout is due to underlying conditions like CKD or malignancies.
What is the role of vitamin C in gout prevention?
May reduce uric acid levels and lower gout risk.
What is the duration of an acute gout attack?
Typically resolves within 3-10 days with appropriate treatment.
What is the effect of alcohol on gout?
Increases uric acid levels by reducing renal excretion and increasing purine metabolism.
What foods should gout patients avoid?
Organ meats, shellfish, red meat, and high-fructose corn syrup.
What is the role of dairy products in gout?
Low-fat dairy products may reduce uric acid levels and lower gout risk.
What is the relationship between gout and cardiovascular disease?
Gout is associated with an increased risk of hypertension, MI, and stroke.
What is podagra?
Acute gout affecting the first metatarsophalangeal joint.
What is the role of losartan in gout management?
It lowers uric acid levels and can be used in hypertensive gout patients.
What are the features of intercritical gout?
Asymptomatic periods between acute gout attacks.
What is the effect of obesity on gout?
Increases uric acid production and decreases renal excretion.
What is the role of NSAIDs in chronic gout management?
Used for acute attacks but not recommended for long-term urate-lowering therapy.
What is the mechanism of urate crystal formation?
Occurs when serum uric acid exceeds its solubility threshold (6.8 mg/dL).
What is the importance of patient education in gout management?
Helps patients adhere to lifestyle changes and medication regimens.
What is monosodium urate?
The type of crystal responsible for gout.
What is calcium pyrophosphate dihydrate (CPPD)?
The type of crystal responsible for pseudogout.
