02c: Gout Flashcards
Gout is a(n) (X) resulting from (Y) deposition in joints/soft tissues.
X = inflammatory arthritis Y = monosodium urate crystals
(X)% of gout occurs due to under-excretion of urate. Typically, how much urate is synthesized and then secreted daily?
X = 90
450/750 mg secreted by kidneys and 300/750 mg secreted by GI tract
When serum urate concentration exceeds (X), crystals precipitate out and deposit in soft tissue/joints.
X = 6.8 mg/dL
T/F: Hyperuricemia typically preceeds the first attack by a few months.
False - by 5-10 years
T/F: Knee is involved in gout, pseudogout, and septic joint arthritis.
True
Joint pattern in Gout v Pseudogout.
Gout: small/peripheral
Pseudogout: large/axial
T/F: Tophi are commonly involved in gout, pseudogout, and septic joint arthritis.
False - common in gout, VERY rare in pseudogout, and never occur in septic joint
Patient presents with fever, leukocytosis, and inflammed knee. He claims it’s been getting progressively worse over the past few days. Which part of history makes you think this is (gout/pseudogout/septic arthritis)?
Septic arthritis;
Onset timing: severe within days (not hours)
Initial gout attack is (mono/poly)-articular most of the time and involves 1st MTP (X)% of the time.
Mono;
X = 50
List the triggers for an acute gouty attack.
- Minor joint trauma
- EtOH
- Purine-rich food
- Acute illness
- Diuretic use
- Dehydration
T/F: Untreated acute gouty attacks will resolve on their own in a few hours.
False in 3-10 days
Aspiration of joint affected by gout will reveal:
- Leukocytosis (50,000-100,000!)
2. Monosodium urate crystals (neg birefringent, needle-like), usually engulfed by PMNs
T/F: Tissue biopsy is gold standard for gout diagnosis.
False - joint aspiration (with visualization of urate crystals)
T/F: Hyperuricemia is mandatory for precipitation of gout.
True
30% of patients have normal serum uric acid during acute gout attack. This may be due to the (X) effect of (Y).
X = uricosuric Y = IL-6
Also more free water reabsorption in kidney (ADH release)
T/F: Gouty arthritis risk is strictly environmental, not genetic.
False - large portion of urate metabolism is inherited
Tophi are masses of (X). Where are they frequently seen?
X = uric acid crystals
Olecranon bursa, top of ears, over extensor surfaces of joints
What does the development of tophi in gouty arthritis depend on?
Duration and severity of hyperuricemia (decrease in incidence since anti-hyperuricemic agents have been available)
T/F: Decision to administer chronic treatment for gout is determined partly by magnitude of hyperuricemia.
False
Long-term therapy for gout recommended in which scenarios?
- Over 2 attacks/yr
- Tophi
- Uric acid kidney stones
- Renal insufficiency
Goal of chronic gout therapy is to reduce serum urate to (X)
X = under 6 mg/dL
Unless tophi present, then under 5 mg/dL
Gout: How would you counsel your patient on lifestyle?
Exercise/weight management; avoid purine-rich food, EtOH, fructose-rich/sugary drinks; drink water!
60 y.o. male patient with history of IV drug use and hypertension continues to have gouty attacks, despite having lost weight and altered diet. What could be going on?
May be on thiazide diuretic for HT (which is a hyperuricemic drug)
List treatment options for acute gout attack.
- NSAIDs
- Injection glucocorticoids
- Systemic glucocorticoids
- Colchicine (low dose)
Allopurinol mechanism of action.
Inhibits xanthine oxidase (precursors of urate more quickly excreted and don’t cause gout)
(X) gout drug and its major metabolite are converted into riboNT by HGPT, thus inhibiting (Y).
X = allopurinol Y = de novo purine synthesis
Patient put on chronic therapy for gout (allopurinol). Which other medication should be started for initial (X) months of therapy? Why?
Colchicine
X = 4-6
Lowering serum urate paradoxically increase risk of acute flare
T/F: Patients on allopurinolmay be on various doses, depending on amount of urate produced/excreted.
True
Max dose of allopurinol given.
800 mg/day
List allopurinol’s most common side effect. And its most dangerous.
Hypersensitivity rash (2%); severe hypersensitivity (life-threatening)
Allopurinol causes significant drug interactions with drugs that are (X). Give an example.
X = cleared by xanthing oxidase (purine analogues)
Azathioprine (immunosuppressant)
Provenecid is a(n) (X) agent that has which mechanism of action?
X = uricosuric (anti-hyperuricemic)
Increases renal clearance of urate by blocking PCT reabsorption (via URAT1 urate transporter)
Patient on treatment for acute gout has developed uric acid kidney stones. Which drug has he likely been prescribed? What can be done to reduce the reoccurrence?
Probenecid (uricosuric agent);
Increase fluid intake and alkalinization of urine
Probenecid is only indicated for gout patients that are (undersecretors/overproducers) of uric acid.
Undersecretors