A nurse is conversing with a client who has a new diagnosis of gout.
When the client asks the nurse how she got the disorder, the nurse should explain that gout develops when?
Deposits of uric acid crystals cause inflammation, pain, and redness in the affected joints.
Uric acid levels drop significantly below the normal reference range.
Tophi forms in the kidneys and impairs the excretion of uric acid.
Articular cartilage thins leading to splitting and fragmentation.
The Correct Answer is A
Choice A rationale
Gout is a form of inflammatory arthritis triggered by hyperuricemia, which is an excess of uric acid in the blood. When the concentration exceeds the solubility limit, monosodium urate crystals precipitate in the joints. This triggers an immune response where white blood cells engulf the crystals, releasing inflammatory mediators. This process causes the classic signs of heat, redness, and extreme pain. Normal serum uric acid levels are generally 3.5 to 7.2 mg/dL.
Choice B rationale
The development of gout is associated with high levels of uric acid, not low levels. Uric acid is a byproduct of purine metabolism. When levels drop significantly below the normal range, it does not cause crystal deposition or joint inflammation. The pathology of the disease relies entirely on the saturation of the blood and synovial fluid with urate, leading to crystallization. Therefore, a decrease in uric acid would actually reduce the risk of an attack.
Choice C rationale
Tophi are large, visible deposits of urate crystals that typically form in the skin, cartilage, or joints after years of uncontrolled hyperuricemia. While urate crystals can deposit in the kidneys and lead to renal stones or urate nephropathy, the tophi themselves are a result of the disease rather than the initial cause of it. The primary cause is the underlying metabolic imbalance or decreased renal excretion of uric acid that leads to the initial crystallization.
Choice D rationale
The thinning, splitting, and fragmentation of articular cartilage are the primary pathophysiological hallmarks of osteoarthritis, which is a degenerative joint disease. Gout is distinct from osteoarthritis because it is an inflammatory process caused by chemical crystals rather than mechanical wear and tear. While chronic gout can eventually lead to secondary joint damage and cartilage destruction, the initial development of the disorder is specifically defined by the presence and reaction to uric acid crystals.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is D
Explanation
Choice A rationale
Otitis externa is an inflammation or infection of the external auditory canal, often referred to as swimmer ear. It is typically caused by bacterial or fungal overgrowth in the outer ear canal due to moisture or trauma. Aspirin use does not have a known physiological mechanism that would cause infection of the external ear structure. The symptoms mentioned, like hearing disturbances, originate in the inner ear or nerve pathways rather than the external canal.
Choice B rationale
Vertigo is a sensation of spinning or dizziness often associated with inner ear imbalances or vestibular nerve issues. While aspirin can sometimes cause dizziness as a side effect, the specific report of hearing disturbances is more indicative of damage to the cochlear system rather than just a balance issue. Vertigo alone does not capture the full scope of potential sensory damage to the cranial nerve VIII that high doses of acetylsalicylic acid can cause over time.
Choice C rationale
Nystagmus involves involuntary, rapid, and repetitive eye movements that can be horizontal, vertical, or rotary. It is often a sign of vestibular dysfunction or central nervous system pathology. Although aspirin toxicity can affect the neurological system, nystagmus is not the primary or most common indicator of salicylate-induced sensory damage. Hearing loss and tinnitus are the classic early warning signs of aspirin reaching toxic levels in the blood, which requires immediate dose adjustment.
Choice D rationale
Ototoxicity refers to the toxic effect that certain medications, including high-dose aspirin, have on the inner ear or the vestibulocochlear nerve. Salicylates can disrupt the electrochemical balance in the cochlea, leading to tinnitus and hearing impairment. Monitoring for these symptoms is crucial because the damage can sometimes become irreversible if the dose is not reduced. By decreasing the aspirin dosage, the nurse helps protect the delicate sensory hair cells from further chemical-induced injury.
Correct Answer is ["B","C","D"]
Explanation
Choice A rationale
Amiodarone is a class III antiarrhythmic medication primarily utilized for ventricular and supraventricular tachycardias. Its common side effect profile includes pulmonary toxicity, thyroid dysfunction, and corneal microdeposits. Unlike certain other cardiac medications, it is not traditionally classified as a primary ototoxic agent. It does not typically cause significant damage to the hair cells of the cochlea or the vestibulocochlear nerve during standard therapeutic use.
Choice B rationale
Loop diuretics, such as furosemide, are well-documented ototoxic agents. These medications inhibit the sodium-potassium-chloride symporter in the thick ascending limb of the loop of Henle and can also alter the electrolyte balance in the stria vascularis of the inner ear. This disruption in endolymph composition can lead to temporary or permanent hearing loss and tinnitus, particularly when administered rapidly or at high doses via intravenous routes.
Choice C rationale
Nonsteroidal anti-inflammatory drugs, or NSAIDs, including aspirin and ibuprofen, can cause ototoxicity when taken in high doses. These agents inhibit prostaglandin synthesis and can decrease blood flow to the cochlea, leading to cellular metabolic stress. Patients frequently report tinnitus, which is often reversible once the medication is discontinued. Monitoring is essential as chronic high-dose therapy can result in a more persistent sensorineural hearing impairment.
Choice D rationale
Vancomycin is a potent glycopeptide antibiotic used for serious gram-positive infections. It is recognized for its potential to cause nephrotoxicity and ototoxicity, especially when serum trough levels exceed the normal range of 15 to 20 mcg/mL. The mechanism involves direct damage to the auditory nerve or the cochlear hair cells. Risk increases significantly when combined with other ototoxic drugs, requiring close monitoring of hearing and renal function.
Choice E rationale
Cimetidine is a histamine H2-receptor antagonist used to reduce gastric acid secretion in conditions like peptic ulcer disease and GERD. While it has several systemic side effects and drug interactions due to cytochrome P450 inhibition, it is not classified as an ototoxic medication. It does not typically interfere with the delicate neurosensory structures of the ear or the fluid dynamics necessary for normal auditory processing.
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