NURS 6501 NEUROLOGICAL AND MUSCULOSKELETAL DISORDERS MODULE 4

Gout refers to chronic inflammatory arthritis characterized by the deposition of monosodium urate monohydrate crystals in tissues. Gout is relatively common with an estimated global prevalence of 1 to 4% (Dehlin et al., 2020). In the United States, gout affects more than 2 million adults (Dehlin et al., 2020). The incidence of gout increases with age as well as a family history of gout. Additionally, gout is slightly male preponderance with up to 2 to 6 times higher in males than females. The pathophysiology of gout is considered complex and multifactorial. Factors implicated in the development of gout include alcohol, medications, hypertension, hyperlipidemia, obesity, diabetes mellitus, cardiovascular disease, diet, chronic kidney disease, advanced age, ethnicity, family history, and male gender (Dehlin et al., 2020). Gout is contemplated as a disorder of metabolism resulting in the accumulation of urate and uric acid in blood and tissues. Consequently, tissues become supersaturated leading to the precipitation of urate salts forming monosodium urate crystals. The deposition of these crystals occurs in an array of tissues although the synovium, kidney, bone, ligament, skin, tendon, and cartilage are among the most common sites. Uric acid is less soluble under low temperatures and acidic conditions. Finally, microcrystals may be shed from preexisting tophi initiating an inflammatory response.

Explain why a patient with gout is more likely to develop renal calculi

Individuals with gout have high levels of urate and uric acid in their plasma. Uric acid is a weak organic acid. It exists in a less soluble non-ionized form in acid conditions such as in urine. Physiologically, uric acid production is from purine metabolism in the liver with a slight contribution from the small intestines. Similarly,  the glomerulus filters almost all the urate. As a result, the entire pool of urate is managed by renal excretion in steady-state conditions. Hyperuricemia increases the urate pool which causes supersaturation and precipitation of uric acid and the formation of uric acid calculi. According to Cicerello (2018),  hyperuricemia,  diminished fractional excretion of uric acid, and constantly low urinary pH levels are common in patients with gout which leads to uric acid nephrolithiasis. For instance, a reduction in pH induces alterations in uric acid dissolution and acid-base status while a reduction in urine output leads to highly concentrated urinary solutes resulting in precipitation (Cicerello, 2018). Finally, individuals with gout may also develop renal calculi due to hyperuricosuria and a decrease in crystallization inhibitors such as urinary glycosaminoglycans.

Discuss what is osteoporosis and how it develops pathologically

Osteoporosis refers to low bone mineral density as a result of altered bone microstructure. Osteoporosis predisposes patients to fragility and low-impact fractures. Globally, osteoporosis affects over 200 million individuals with its incidence increasing with age. Generally, women are more affected. Osteoporosis can be primary or secondary. According to Pouresmaeili et al. (2018), primary osteoporosis is a consequence of aging and a reduction in sex hormones while other disease processes cause secondary osteoporosis. Osteoporosis develops from an imbalance between bone formation and resorption. An interplay of several factors including genetic, lifestyle, intrinsic and exogenous factors interact to cause an imbalance between bone resorption and formation leading to decreased skeletal mass (Pouresmaeili et al., 2018). For instance, with aging, bone resorption exceeds bone formation. Physiologically, bone mass peaks in the third decade. Consequently, factors that cause osteoporosis result in failure to achieve a normal peak bone mass as well as an acceleration of bone loss.

The pt. had various symptoms, explain how these factors are associated with RA and what is the difference between RA and OA