MSEM146.pdf

11/27/23, 4:57 AM Realizeit for Student Metabolic and Endocrine Diseases Associated with Rheumatic Disorders Pathophysiology Gout is caused by hyperuricemia (increased serum uric acid). Uric acid is a by-product of purine metabolism; purines are basic chemical compounds found in high concentration...

11/27/23, 4:57 AM Realizeit for Student Metabolic and Endocrine Diseases Associated with Rheumatic Disorders Pathophysiology Gout is caused by hyperuricemia (increased serum uric acid). Uric acid is a by-product of purine metabolism; purines are basic chemical compounds found in high concentrations in meat products. Urate levels are affected by diet, medications, overproduction in the body, and inadequate excretion by the kidneys. Hyperuricemia (serum concentration greater than 6.8 mg/dL) can, but does not always, cause urate crystal deposition. However, as uric acid levels increase, the risk becomes greater. The initial cause for the gout attack occurs when macrophages in the joint space phagocytize urate crystals. Through a series of immunologic steps, interleukin-1β is secreted, increasing the inflammation. This process is exacerbated by the presence of free fatty acids. Both alcohol and consumption of a large meal, especially with red meat, can lead to increases in free fatty acid concentrations; they also are implicated as triggers to acute gout attacks (Norris, 2019). With repeated attacks, accumulations of sodium urate crystals, called tophi, are deposited in peripheral areas of the body, such as the great toe, the hands, and the ear. Renal uratelithiasis (kidney stones), with chronic kidney disease secondary to urate deposition, may develop. Primary hyperuricemia may be caused by severe dieting or starvation, excessive intake of foods that are high in purines (shellfish, organ meats), or heredity. In secondary hyperuricemia, gout is a clinical feature secondary to any of a number of genetic or acquired processes, including conditions in which there is an increase in cell turnover (leukemia, multiple myeloma, some types of anemias, psoriasis) and an increase in cell breakdown. Altered renal tubular function, either as a major action or as an unintended side effect of certain pharmacologic agents (e.g., diuretics such as thiazides and furosemide), low-dose salicylates, or ethanol can contribute to uric acid underexcretion (Klippel et al., 2008). The finding of urate crystals in the synovial fluid of asymptomatic joints suggests that factors other than crystals may be related to the inflammatory reaction. Recovered monosodium urate crystals are coated with immunoglobulins that are mainly IgG. IgG enhances crystal phagocytosis, thereby demonstrating immunologic activity (Klippel et al., 2008). Clinical Manifestations Manifestations of the gout syndrome include acute gouty arthritis (recurrent attacks of severe articular and periarticular inflammation), tophi (crystalline deposits accumulating in articular tissue, osseous tissue, soft tissue, and cartilage), gouty nephropathy (renal impairment), and uric acid urinary calculi. Four stages of gout can be identified: asymptomatic hyperuricemia, acute https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=0Dn26kXyU%2f6F5gOCz4%2f2IT%2f2%2bt0zmWpgA%2fttBl%2bYliu9txYeiNyhjGIrXvrN… 1/3 11/27/23, 4:57 AM Realizeit for Student gouty arthritis, intercritical gout, and chronic tophaceous gout (Neoai, Jansen, Dalbeth, et al., 2015). The subsequent development of gout is directly related to the duration and magnitude of the hyperuricemia. Therefore, the commitment to lifelong pharmacologic treatment of hyperuricemia is deferred until there is an initial attack of gout. Acute arthritis is the most common early clinical manifestation. The metatarsophalangeal joint of the big toe is a commonly affected joint. The tarsal area, ankle, or knee may also be affected. Less commonly, the wrists, fingers, and elbows may be affected. Trauma, alcohol ingestion, dieting, medications, surgical stress, or illness may trigger the acute attack. The abrupt onset often occurs at night, awakening the patient with severe pain, redness, swelling, and warmth of the affected joint. Early attacks tend to subside spontaneously over 3 to 10 days without treatment. The attack is followed by a symptom-free period (the intercritical stage) until the next attack, which may not come for months or years. However, with time, attacks tend to occur more frequently, involve more joints, and last longer (Becker & Gaffo, 2019). Tophi (seen in chronic tophaceous gout) are generally associated with more frequent and severe inflammatory episodes. Higher serum concentrations of uric acid are also associated with more extensive tophus formation. Tophi most commonly occur in the synovium, olecranon bursa, subchondral bone (bony plate that supports the articular cartilage), infrapatellar and Achilles tendons, and subcutaneous tissue on the extensor surface of the forearms and overlying joints. They have also been found in the aortic walls, heart valves, nasal and ear cartilage, eyelids, cornea, and sclera. Joint enlargement may cause a loss of joint motion. Uric acid deposits may cause renal stones and kidney damage. Medical Management Given that the incidence of gout increases with age, its management can be complicated by other medical conditions, medications, and age-related changes. A definitive diagnosis of gouty arthritis is established by polarized light microscopy of the synovial fluid of the involved joint. Uric acid crystals are seen within the polymorphonuclear leukocytes in the fluid during a disease flare up (CDC, 2019). Acute attacks are managed with colchicine (oral or parenteral), an NSAID such as indomethacin, or a corticosteroid. Management of hyperuricemia, tophi, joint destruction, and renal disorders is usually initiated after the acute inflammatory process has subsided. Once the acute attack has subsided, uric acid lowering therapy should be considered. Xanthine oxidase inhibitors, such as allopurinol and febuxostat, are the agents of choice. Given the role of IL-1 in the pathogenesis of gout, some experts suggest that there may be a role for anakinra, an IL-1 receptor antagonist in the management of acute gout (Becker & Perez-Ruiz, 2019). https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=0Dn26kXyU%2f6F5gOCz4%2f2IT%2f2%2bt0zmWpgA%2fttBl%2bYliu9txYeiNyhjGIrXvrN… 2/3 11/27/23, 4:57 AM Realizeit for Student Management between gout attacks needs to include lifestyle changes such as avoiding purinerich foods, weight loss, decreasing alcohol consumption, and avoiding certain medications. Uricosuric agents, such as probenecid, may be indicated in patients with frequent acute attacks. Uricosuric medications correct hyperuricemia and dissolve deposited urate. Corticosteroids may also be used in patients who have no response to other therapy. In patients with refractory chronic gout who are not controlled with the regimens mentioned earlier, pegloticase, a newer agent, has been shown to be effective in lowering uric acid levels (Becker & Perez-Ruiz, 2019). Specific treatment is based on the serum uric acid level, 24-hour urinary uric acid excretion, and renal function. Nursing Management Research indicates that providers overestimate patient knowledge of gout and that patients prefer the use of both written and verbal materials (Abhishek & Doherty, 2018). Therefore, the nurse takes every opportunity to educate and reinforce knowledge of gout verbally and in writing. Severe dietary restriction is not necessary; however, the nurse encourages the patient to restrict consumption of foods high in purines, especially organ meats, and to limit alcohol intake. Maintenance of normal body weight should be encouraged. In an acute episode of gouty arthritis, pain management with prescribed medications is essential, along with avoidance of factors that increase pain and inflammation, such as trauma, stress, and alcohol. Medication adherence is critical but poor among patients prescribed urate lowering therapies (Scheepers, van Onna, Stehouwer, et al., 2018). The nurse reinforces the importance of taking prescribed medications. Between acute episodes, the patient feels well and may abandon medications and preventive behaviors, which may result in an acute attack. Acute attacks are most effectively treated if therapy begins early. https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=0Dn26kXyU%2f6F5gOCz4%2f2IT%2f2%2bt0zmWpgA%2fttBl%2bYliu9txYeiNyhjGIrXvrN… 3/3