A female client with rheumatoid arthritis (RA) comes to the clinic with swelling of her wrists after she braced herself against a fall in the bathroom. Which pathophysiological mechanism should the nurse explain to the client regarding RA?
Bone reabsorption exceeds bone formation which leads to an increase in bone fragility.
Repetitive stress initiates a cascade leading to protease destruction of joints’ cartilage surfaces.
T-cells generate cytokine production and antigen-antibody reactions that trigger inflammatory responses.
Imbalance of uric acid metabolism deposits urate crystals in joint tissues which leads to inflammation.
The Correct Answer is C
Choice A reason: Bone reabsorption exceeding formation describes osteoporosis, not rheumatoid arthritis. RA involves autoimmune inflammation of synovial joints, driven by cytokines and T-cells, not primary bone fragility. This choice is incorrect, as it misrepresents RA’s immune-mediated synovial pathology with a bone density disorder.
Choice B reason: Repetitive stress may cause osteoarthritis, not RA. RA is an autoimmune condition where T-cells and cytokines attack synovium, causing inflammation and cartilage damage. Stress may exacerbate symptoms, but it is not the primary mechanism, making this incorrect for RA’s pathophysiological explanation.
Choice C reason: RA’s pathophysiology involves T-cells producing cytokines (e.g., TNF-α) and antigen-antibody reactions, triggering synovial inflammation. This autoimmune process causes wrist swelling and joint damage, as seen in the client. This mechanism accurately explains RA’s inflammatory nature, per rheumatology evidence, and is appropriate for client education.
Choice D reason: Uric acid imbalance and urate crystal deposition cause gout, not RA. RA is driven by autoimmune T-cell and cytokine activity, not crystal-induced inflammation. This choice is incorrect, as it describes a different arthritic condition unrelated to the client’s autoimmune rheumatoid arthritis pathology.
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Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is B
Explanation
Choice A reason: Failure of angiotensin I to convert to angiotensin II would reduce blood pressure, as angiotensin II is a potent vasoconstrictor. Primary hypertension involves increased angiotensin II, driving vasoconstriction and sodium retention. This failure is not a cause, making it incorrect for the mechanism of hypertension.
Choice B reason: Increased angiotensin II levels in the bloodstream cause vasoconstriction and aldosterone-mediated sodium retention, elevating blood pressure in primary hypertension. This is a key mechanism in the renin-angiotensin-aldosterone system (RAAS), driving chronic hypertension. This aligns with cardiovascular pathophysiology, making it the correct mechanism for the nurse to recognize.
Choice C reason: Excess sodium and water retention is a consequence of RAAS activation in hypertension, not the primary cause. Angiotensin II drives this retention via aldosterone. While important, sodium/water release is secondary to angiotensin’s vasoconstrictive effects, making this less precise than increased angiotensin levels.
Choice D reason: Juxtaglomerular cells release renin, initiating RAAS, but the systemic effect is mediated by angiotensin II, not renin alone. Hypertension results from angiotensin’s vasoconstriction and sodium retention. This choice is less specific, as angiotensin II’s actions are the direct cause, making it incorrect.
Correct Answer is D
Explanation
Choice A reason: Artificial sweeteners do not directly contribute to diabetic nephropathy. Nephropathy results from chronic hyperglycemia damaging glomerular vessels. Sweeteners may affect diet but lack evidence linking them to renal damage, making this incorrect compared to elevated HbA1c, the primary driver of diabetic complications.
Choice B reason: Frequent hypoglycemia may cause acute symptoms but does not directly cause nephropathy. Chronic hyperglycemia, reflected by high HbA1c, damages renal glomeruli, leading to nephropathy. Hypoglycemia is a treatment complication, not a risk factor for renal damage, making this an incorrect choice.
Choice C reason: Moderate alcohol consumption may affect overall health but is not a primary risk factor for diabetic nephropathy. Chronic hyperglycemia, indicated by elevated HbA1c, drives glomerular damage. Alcohol’s impact is less direct, making this incorrect compared to the established link between poor glycemic control and nephropathy.
Choice D reason: Consistently elevated HbA1c reflects chronic hyperglycemia, the primary cause of diabetic nephropathy. High glucose levels damage glomerular capillaries, leading to proteinuria and renal decline. This is a well-established risk factor, supported by endocrinology evidence, making it the correct choice for increased nephropathy risk.
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