MODULE 5 KNOWLEDGE CHECK
• Question 1
1 out of 1 points
A 52-year-old obese Caucasian male presents to the clinic with a 2-day history of fever,
... [Show More] chills, and right great toe pain that has gotten 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. Past medical history positive or hypertension treated with hydrochlorothiazide and kidney stones. Social history negative for tobacco use but admits to drinking “a fair amount of red wine” every week. General appearance: Ill appearing male who sits with his right foot elevated. Physical exam remarkable for a temp of 101.2, pulse 108, respirations 18 and BP 160/88. 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 14,000 mm3 and uric acid 8.9 mg/dl. The APRN diagnoses the patient with acute gout.
Question 1 of 2:
Describe the pathophysiology of gout.
Selected Answer: At the cellular level, purines are synthesizes to purine nucleotides, which are used in the synthesis of nucleic acids, adenosine triphosphate, cyclic adenosone monophosphate(cAMP),and cyclic guanosine triphosphate monophosphate(cGMP). Uric acid is a breakdown product of purine nucleotides. A defeciency of the enzyme HGPRT can lead to an increased production of uric acid. A complete absence of HGPRT can occur in the X-linked Lesch-Nyhan syndrome, with males at risk for hyperuricemia, neurologic alterations, and sometimes gouty arthritis.
Correct Answer:
Gout is an inflammatory response to excessive quantities of uric acid in the blood and other body fluids including synovial fluid. The elevated level of uric acid lea to the formation of monosodium urate crystals in and around joints. When the uric acid levels exceed approximately 6.8 mg/dl, it crystalizes and forms an insoluble precipitate that are deposited into connective tissue through the body. When crystallization occurs in synovial fluid, it triggers Tumor Necrosis Factor (TNF)-α, which causes the release of inflammatory cytokines and interleukins. The result is an acute inflammatory response within the joint.
Gout is caused by a defect in purine metabolism and kidney function. Uric acid is a byproduct of purine nucleotides. People with gout may have an elevated level of purine synthesis accompanied by a rise in uric acid level.
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