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USMLE® Step 1 questions

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A 53-year-old man comes to the physician complaining of a painless nodule on the back of the left heel. He has had several episodes of joint pain in the last 2 years, involving the toes and knees, that would often resolve after taking ibuprofen. He has not had any fevers, recent joint trauma, or weight loss. Past medical history is significant for hypertension and hyperlipidemia. He is currently on hydrochlorothiazide and pravastatin. He has been drinking 5-6 beers daily for the last 13 years. He denies tobacco or illicit substance use. Temperature is 37.0°C (98.6°F), pulse is 88/min, respirations are 12/min, and blood pressure is 138/95 mmHg. Physical examination reveals a nontender, hard, chalky nodule on the left Achilles tendon, as seen in the image below:

Image reproduced from Wikimedia Commons

Similar nodules are present on the left elbow and right external pinna of the ear. Further evaluation of this patient will most likely reveal which of the following?

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Alcohol use

gout and p. 477


for gout p. 477, 500

gout p. 726

Chronic gout

treatment p. 726


acute gout attack p. 726

gout p. 477, 500


gout p. 251


gout exacerbation p. 477


in gout p. 500


gout p. 477, 500, 726

Furosemide p. 253, 632

gout with p. 251


acute gout attack p. 726

gout p. 477, 500

Gout p. 477

as drug reaction p. 251

drug therapy for p. 499

kidney stones and p. 628

lab findings p. 722

Lesch-Nyhan syndrome p. 35

loop diuretics and p. 632

presentation p. 718

treatment p. 726

Von Gierke disease p. 85

Indomethacin p. 499

gout p. 477

Metatarsophalangeal (MTP) joints

gout p. 477

Naproxen p. 499

acute gout drugs p. 501


gout p. 251

Nonsteroidal anti-inflammatory drugs (NSAIDs) p. 499

acute gout attack p. 726

gout p. 477, 501


gout p. 477

presentation p. 718

Probenecid p. 253

for gout p. 500, 726

Pyrazinamide p. 194

gout p. 251

Thiazides p. 633

gout p. 251

Tophi in gout p. 718

Uric acid

gout p. 500



Gout is an inflammatory disease in which monosodium urate crystals deposit into a joint, making it red, hot, tender and swollen within hours.

When this happens, it’s called a gouty attack.

The underlying cause is hyperuricemia—too much uric acid in the blood, which results in the formation of sharp, needle-like crystals, in areas with slow blood flow like the joints and the kidney tubules.

Over time, repeated gouty attacks can cause destruction of the joint tissue which results in arthritis.

To understand where the uric acid comes from, let’s start with purines, which, together with pyrimidines, are nature’s most common nitrogen-containing heterocycles.

A heterocycle being any molecular ring or cycle with different types of atoms.

Purines, as well as pyrimidines, are key components of nucleic acids like DNA and RNA, and when cells, along with the nucleic acids in those cells, are broken down throughout the body, those purines are converted into uric acid—a molecule that can be filtered out of the blood and excreted in the urine.

Uric acid has limited solubility in body fluids, though. Hyperuricemia occurs when levels of uric acid exceed the rate of its solubility, which is about 6.8mg/dL.

At a physiologic pH of about 7.4, uric acid loses a proton and becomes a urate ion, which then binds sodium and forms monosodium urate crystals.

These crystals can form as a result of increased consumption of purines, like from consuming purine-rich foods like shellfish, anchovies, red meat or organ meat.

Also, though, they can result from increased production of purines, for example high-fructose corn syrup containing beverages could contribute to the formation of uric acid by increasing purine synthesis.

Another way crystals could form is from decreased clearance of uric acid, which can result from dehydration from not drinking enough water or from consumption of alcoholic beverages, both of allowing uric acid to precipitate out.

Regularly eating these kinds of foods can also lead to obesity and diabetes, both of which are risk-factors for gout.

Hyperuricemia can also develop as a result of chemotherapy or radiation treatment, since cells die at a faster-than-normal rate.


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  3. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  4. "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
  5. "Gout" The Lancet (2016)
  6. "Update on gout: new therapeutic strategies and options" Nature Reviews Rheumatology (2010)
  7. "Diagnosis of Acute Gout: A Clinical Practice Guideline From the American College of Physicians" Annals of Internal Medicine (2016)

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