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{{WBRQuestion | {{WBRQuestion | ||
|QuestionAuthor={{Rim | |QuestionAuthor={{Rim}} | ||
|ExamType=USMLE Step 1 | |ExamType=USMLE Step 1 | ||
|MainCategory=Pathophysiology | |MainCategory=Pathophysiology | ||
Line 20: | Line 20: | ||
|MainCategory=Pathophysiology | |MainCategory=Pathophysiology | ||
|SubCategory=Musculoskeletal/Rheumatology | |SubCategory=Musculoskeletal/Rheumatology | ||
|Prompt= | |Prompt=A 63 year-old male obese patient with history of dyslipidemia on statin and hypertension treated with thiazide diuretics complains of rapidly progressive pain in his big toe. The pain started in the morning and became much worse within the last 6 hours. Upon physical exam, the toe is erythematous, swollen and tender upon palpation. The patient reports that this is not the first time it happens with him; in fact, he has had two previous similar episodes which were less painful and resolved spontaneously within a few days. Synovial analysis reveals strongly birefringent needle-shaped crystals. Deposition in the joint of which of the following most likely explains the symptoms of the patient? | ||
|Explanation=[[Gout]] is an inflammatory disease of the joint | |Explanation=[[Gout]] is an inflammatory disease of the joint characterized by deposition of monosodium urate crystals. Gout is associated with hyperuricemia resulting from either overproduction or underexcretion of [[uric acid]]. It is characterized by an initial phase of intermittent self-resolvable monoarticular attacks and a chronic tophaceous phase characterized by attacks involving more than one joint and crystal deposition not only in the joints but also in soft tissues. Triggers of gout include recent surgery, [[trauma]], treatment with [[thiazide]] diuretics, high protein diet and [[alcohol]] intake. The first line treatment for acute gout is either [[NSAID]]s or [[colchicine]]. Long-term treatment of gout includes dietary modification in addition to medications such as xanthine oxidase inhibitors in case of overproduction of uric acid and uricosuric agents in case of underexcretion. | ||
Educational objective: [[Gout]] is an inflammatory disease of the joint characterized by deposition of monosodium urate crystals. | |||
Reference: Tuhina N (2011). Gout. NEJM. 2011; 364:443-452 | |||
|AnswerA=Uric acid | |AnswerA=Uric acid | ||
|AnswerAExp=The presentation of this patient is consistent with gouty arthritis. Hyperproduction or underexcretion of uric acid | |AnswerAExp=The presentation of this patient is consistent with gouty arthritis. Hyperproduction or underexcretion of uric acid leads to hyperuricemia predisposing to gout. However, the crystal deposits in gouty arthritis are monosodium urate. | ||
|AnswerB=Monosodium urate | |AnswerB=Monosodium urate | ||
|AnswerBExp=The presentation of this patient is consistent with gouty arthritis, a condition characterized by deposition of monosodium urate crystals. | |AnswerBExp=The presentation of this patient is consistent with gouty arthritis, a condition characterized by deposition of monosodium urate crystals. | ||
|AnswerC=Calcium pyrophosphate dehydrate | |AnswerC=Calcium pyrophosphate dehydrate | ||
|AnswerCExp=Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease, also known as chondrocalcinosis, pseudogout | |AnswerCExp=Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease, also known as chondrocalcinosis, pseudogout and pyrophosphate arthropathy is a rheumatologic disorder with varied symptoms and signs arising from the accumulation of crystals of calcium pyrophosphate dihydrate in the connective tissues. [[Pseudogout]] usually involves larger joints but can present similarly to [[gout]]. The presence of needle shape crystals which are strongly birefringent is diagnostic for gout and not pseudogout. | ||
|AnswerD=Phosphoribosylpyrophosphate | |AnswerD=Phosphoribosylpyrophosphate | ||
|AnswerDExp=Increased levels of phosphpribosylpyrophosphate ([[PRPP]]) | |AnswerDExp=Increased levels of phosphpribosylpyrophosphate ([[PRPP]]) leads to the overproduction and accumulation of uric acid leading to hyperuricemia and hyperuricosuria. Increased levels of PRPP are present in Lesch-Nyhan Syndrome. Decreased levels of hypoxanthine guanine phosphoribosyl transferase (HGPRT) causes this accumulation, as PRPP is a substrate used by HGPRT during purine salvage. Elevated PRPP predisposes to gout which is characterized by deposition of monosodium urate crystals. | ||
|AnswerE= | |AnswerE=Calcium | ||
|AnswerEExp=The presentation of this patient is consistent with gouty arthritis. Gout is not characterized by | |AnswerEExp=The presentation of this patient is consistent with gouty arthritis. Gout is not characterized by calcium deposition in the joint. | ||
|RightAnswer=B | |RightAnswer=B | ||
|WBRKeyword=Gout, Arthritis | |WBRKeyword=Gout, Arthritis | ||
|Approved= | |Approved=No | ||
}} | }} |
Revision as of 18:17, 9 March 2015
Author | [[PageAuthor::Rim Halaby, M.D. [1]]] |
---|---|
Exam Type | ExamType::USMLE Step 1 |
Main Category | MainCategory::Pathophysiology |
Sub Category | SubCategory::Musculoskeletal/Rheumatology |
Prompt | [[Prompt::A 63 year-old male obese patient with history of dyslipidemia on statin and hypertension treated with thiazide diuretics complains of rapidly progressive pain in his big toe. The pain started in the morning and became much worse within the last 6 hours. Upon physical exam, the toe is erythematous, swollen and tender upon palpation. The patient reports that this is not the first time it happens with him; in fact, he has had two previous similar episodes which were less painful and resolved spontaneously within a few days. Synovial analysis reveals strongly birefringent needle-shaped crystals. Deposition in the joint of which of the following most likely explains the symptoms of the patient?]] |
Answer A | AnswerA::Uric acid |
Answer A Explanation | AnswerAExp::The presentation of this patient is consistent with gouty arthritis. Hyperproduction or underexcretion of uric acid leads to hyperuricemia predisposing to gout. However, the crystal deposits in gouty arthritis are monosodium urate. |
Answer B | AnswerB::Monosodium urate |
Answer B Explanation | AnswerBExp::The presentation of this patient is consistent with gouty arthritis, a condition characterized by deposition of monosodium urate crystals. |
Answer C | AnswerC::Calcium pyrophosphate dehydrate |
Answer C Explanation | [[AnswerCExp::Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease, also known as chondrocalcinosis, pseudogout and pyrophosphate arthropathy is a rheumatologic disorder with varied symptoms and signs arising from the accumulation of crystals of calcium pyrophosphate dihydrate in the connective tissues. Pseudogout usually involves larger joints but can present similarly to gout. The presence of needle shape crystals which are strongly birefringent is diagnostic for gout and not pseudogout.]] |
Answer D | AnswerD::Phosphoribosylpyrophosphate |
Answer D Explanation | [[AnswerDExp::Increased levels of phosphpribosylpyrophosphate (PRPP) leads to the overproduction and accumulation of uric acid leading to hyperuricemia and hyperuricosuria. Increased levels of PRPP are present in Lesch-Nyhan Syndrome. Decreased levels of hypoxanthine guanine phosphoribosyl transferase (HGPRT) causes this accumulation, as PRPP is a substrate used by HGPRT during purine salvage. Elevated PRPP predisposes to gout which is characterized by deposition of monosodium urate crystals.]] |
Answer E | AnswerE::Calcium |
Answer E Explanation | AnswerEExp::The presentation of this patient is consistent with gouty arthritis. Gout is not characterized by calcium deposition in the joint. |
Right Answer | RightAnswer::B |
Explanation | [[Explanation::Gout is an inflammatory disease of the joint characterized by deposition of monosodium urate crystals. Gout is associated with hyperuricemia resulting from either overproduction or underexcretion of uric acid. It is characterized by an initial phase of intermittent self-resolvable monoarticular attacks and a chronic tophaceous phase characterized by attacks involving more than one joint and crystal deposition not only in the joints but also in soft tissues. Triggers of gout include recent surgery, trauma, treatment with thiazide diuretics, high protein diet and alcohol intake. The first line treatment for acute gout is either NSAIDs or colchicine. Long-term treatment of gout includes dietary modification in addition to medications such as xanthine oxidase inhibitors in case of overproduction of uric acid and uricosuric agents in case of underexcretion.
Educational objective: Gout is an inflammatory disease of the joint characterized by deposition of monosodium urate crystals. Reference: Tuhina N (2011). Gout. NEJM. 2011; 364:443-452 |
Approved | Approved::No |
Keyword | WBRKeyword::Gout, WBRKeyword::Arthritis |
Linked Question | Linked:: |
Order in Linked Questions | LinkedOrder:: |