The pathophysiology of gout

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A 68-year-old obese male presents to the clinic with a 3-day history of fever with chills, and Lt. great toe pain that has gotten progressively worse. Patient states this is the first time that this has happened, and nothing has made it better and walking on his right foot makes it worse. He has tried acetaminophen, but it did not help. He took several ibuprofen tablets last night which did give him a bit of relief.
HPI: hypertension treated with Lisinopril/HCTZ .
SH: Denies smoking. Drinking: “a fair amount of red wine” every week. General appearance: Ill appearing male who sits with his right foot elevated.
PE: remarkable for a temp of 100.2, pulse 106, respirations 20 and BP 158/92. Right great toe (first metatarsal phalangeal [MTP]) noticeably swollen and red. Unable to palpate to assess range of motion due to extreme pain. CBC and Complete metabolic profile revealed WBC 15,000 mm3 and uric acid 9.0 mg/dl.
Diagnoses the patient with acute gout.
Question: Explain the pathophysiology of gout.

 

 

Sample Solution

Gout is a disease that occurs in response to the presence of monosodium urate (MSU) crystals in joints, bones, and soft issues. It may result in one or a combination of acute arthritis (a gout flare), chronic arthritis (chronic gouty arthritis), and tophi (tophaceous gout). Hyperuricemia is a common and necessary pathogenic factor in the development of gout, but it is insufficient to explain clinical expression of either self-limited gout flares, chronic gouty arthritis, or tophaceous gout. A number of complex interacting processes are responsible for the pathophysiology of gout. These include: metabolic, genetic, and other factors that result in hyperuricemia.

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