A client with a sudden onset of big toe joint pain and swelling is diagnosed with gout. Which pathophysiologic process is producing the symptoms of gout?
Deposition of crystals in the synovial space of the joints produces inflammation and irritation.
Chondrocyte injury destroys joint cartilage, producing osteophytes and joint inflammation.
An immune complex and autoantibody deposition in connective tissue results in inflammation.
An autoimmune inflammation involving IgG response to an antigen causes joint destruction.
The Correct Answer is A
Gout is a type of inflammatory arthritis caused by the deposition of monosodium urate crystals in the joints and surrounding tissues. Here's an explanation of the pathophysiological process producing the symptoms of gout:
A) Deposition of crystals in the synovial space of the joints produces inflammation and irritation:
Correct. In gout, elevated levels of uric acid in the blood lead to the formation and deposition of monosodium urate crystals in the synovial fluid of joints, particularly in the big toe joint (first metatarsophalangeal joint) in many cases. These crystals trigger an inflammatory response, activating immune cells and causing swelling, redness, warmth, and severe pain in the affected joint. The inflammation and irritation result from the body's immune response to the presence of these crystals.
B) Chondrocyte injury destroys joint cartilage, producing osteophytes and joint inflammation:
This option describes a process more characteristic of osteoarthritis, where degeneration of joint cartilage leads to the formation of osteophytes (bone spurs) and joint inflammation. Gout involves the deposition of urate crystals rather than direct chondrocyte injury.
C) An immune complex and autoantibody deposition in connective tissue results in inflammation:
This process describes the pathophysiology of autoimmune diseases such as rheumatoid arthritis, where immune complexes and autoantibodies contribute to inflammation and tissue damage. In gout, the inflammation is primarily triggered by the deposition of urate crystals rather than immune complex deposition.
D) An autoimmune inflammation involving IgG response to an antigen causes joint destruction:
This option describes the autoimmune process seen in diseases like rheumatoid arthritis, where antibodies target specific antigens, leading to joint destruction. Gout is not an autoimmune disease, and joint destruction in gout is primarily due to inflammation caused by urate crystal deposition rather than autoimmune mechanisms.
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Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is D
Explanation
The loop of Henle, a critical structure within the nephron of the kidney, plays a key role in the concentration of urine through the process of countercurrent multiplication. Here's why option D is the correct choice:
A) Calyx:
The calyx is a structure in the kidney that collects urine from the renal papillae and channels it into the renal pelvis. It does not directly participate in the concentration of urine.
B) Proximal convoluted tubule:
The proximal convoluted tubule primarily reabsorbs water, electrolytes, and nutrients from the glomerular filtrate, but it does not contribute significantly to the concentration of urine.
C) Renal pelvis:
The renal pelvis is a funnel-shaped structure that collects urine from the calyces and funnels it into the ureter. It is not directly involved in the concentration of urine.
D) The loop of Henle:
Correct. The loop of Henle is the nephron segment responsible for generating a hypertonic medullary interstitium, which creates the osmotic gradient necessary for urine concentration. The loop of Henle achieves this through countercurrent multiplication, where the descending limb allows passive reabsorption of water, while the ascending limb actively pumps out sodium and chloride ions. This creates an osmotic gradient that allows for further water reabsorption in the collecting ducts, leading to concentrated urine.
Correct Answer is C
Explanation
A. Myocardial infarction one year ago:
A myocardial infarction (MI) that occurred one year ago is not directly related to the current acid-base imbalance described in the scenario. While a history of MI may have implications for the client's overall cardiovascular health and management, it is not the most likely cause of the acid-base imbalance indicated by the laboratory results.
B. Occasional use of antacids:
Occasional use of antacids is unlikely to cause the acid-base imbalance described in the scenario. Antacids primarily work by neutralizing gastric acid and are not typically associated with significant alterations in acid-base status, especially when used intermittently.
C. Chronic renal insufficiency:
Chronic renal insufficiency is the most likely cause of the acid-base imbalance indicated by the laboratory results. A low hemoglobin level suggests anemia, which can occur in chronic kidney disease due to decreased erythropoietin production. An elevated creatinine clearance indicates impaired kidney function, as the kidneys are clearing creatinine at a faster rate than normal. Decreased urine specific gravity suggests the kidneys' inability to concentrate urine properly, which is a common finding in renal insufficiency. Renal insufficiency can lead to metabolic acidosis due to the kidneys' decreased ability to excrete acid and regulate bicarbonate levels.
D. Shortness of breath with exertion:
Shortness of breath with exertion, a symptom commonly seen in COPD exacerbations, is unlikely to directly cause the acid-base imbalance described in the scenario. While respiratory distress can lead to respiratory acidosis, which is characterized by elevated carbon dioxide levels and decreased pH, the laboratory results indicate metabolic rather than respiratory acidosis.
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