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{{WBRQuestion
{{WBRQuestion
|QuestionAuthor={{Rim}} {{Alison}}
|QuestionAuthor= {{SSK}} (Reviewed by Serge Korjian)
|ExamType=USMLE Step 1
|ExamType=USMLE Step 1
|MainCategory=Pathophysiology
|MainCategory=Pathophysiology
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|MainCategory=Pathophysiology
|MainCategory=Pathophysiology
|SubCategory=Musculoskeletal/Rheumatology
|SubCategory=Musculoskeletal/Rheumatology
|MainCategory=Pathophysiology
|MainCategory=Pathophysiology
|MainCategory=Pathophysiology
|MainCategory=Pathophysiology
|MainCategory=Pathophysiology
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|MainCategory=Pathophysiology
|MainCategory=Pathophysiology
|SubCategory=Musculoskeletal/Rheumatology
|SubCategory=Musculoskeletal/Rheumatology
|Prompt=An obese 63-year-old male with history of dyslipidemia on statin and hypertension, treated with thiazide diuretics, presents with rapidly increasing pain in his big toe. The pain began in the morning and became progressively worse within the last 6 hours. Upon physical examination, the toe is observed to be erythematous, swollen, and tender upon palpation. The patient experienced two previous similar episodes, which resolved without treatment within a few days. Synovial fluid analysis reveals strongly birefringent needle-shaped crystals. Which of the following substances most likely composes the crystals?
|Prompt=A 63-year-old obese man with history of hypertension treated with thiazide diuretics complains of rapidly progressive pain in his big toe. The pain began in the morning and has become much worse in the last 6 hours. On physical exam, the toe is erythematous, swollen and tender to palpation. The patient reports two similar prior episodes that were less painful and resolved spontaneously. Synovial analysis reveals strongly birefringent needle-shaped crystals on polarized light microscopy. Deposition of which of the following most likely explains the symptoms in the patient?
|Explanation=[[Gout]] is an inflammatory disease of the joint, characterized by the deposition of monosodium urate crystals. [[Gout]] is associated with hyperuricemia, resulting from either overproduction or underexcretion of [[uric acid]]. Triggers of gout include recent surgery, [[trauma]], treatment with [[thiazide]] diuretics, high protein diet, and excessive [[alcohol]] intake. Often, acute symptoms associated with gout are treated with [[NSAID]]s or [[colchicine]]. In addition to dietary modifications, long-term treatments of gout include medications such as xanthine oxidase inhibitors, in case of overproduction of uric acid, and uricosuric agents, in case of underexcretion.
|Explanation=[[Gout]] is an inflammatory disease of the joints characterized by deposition of monosodium urate (MSU) crystals. Gout is associated with hyperuricemia resulting from either overproduction (most-common) 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 the 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.


|EducationalObjectives= [[Gouty arthritis]] is an inflammatory disease of the joint characterized by deposition of monosodium urate crystals.
[[File:MSUandCPPD.png]]
|References= 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 often leads to hyperuricemia predisposing gout. However, the crystal deposits in gouty arthritis are composed of monosodium urate.
|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, and pyrophosphate arthropathy, is a rheumatic 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 characteristic of gout but not pseudogout.
|AnswerCExp=Calcium pyrophosphate dihydrate (CPPD) has a similar presentation to gout but it is caused by the accumulation of crystals of calcium pyrophosphate dihydrate in the connective tissues. Pseudogout usually involves larger joints than gout. The presence of rhombus-shaped crystals which are weakly birefringent on polarized light microscopy is diagnostic for pseudogout.
|AnswerD=Phosphoribosylpyrophosphate
|AnswerD=Phosphoribosylpyrophosphate
|AnswerDExp=Increased levels of phosphpribosylpyrophosphate ([[PRPP]]), frequently leads to the overproduction and accumulation of uric acid, resulting in hyperuricemia and hyperuricosuria. Increased levels of PRPP are often present in [[Lesch-Nyhan syndrome]], which is characterized by decreased levels of hypoxanthine guanine phosphoribosyl transferase (HGPRT), responsible for purine salvage.
|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.
|AnswerE=Basic calcium phosphate
|AnswerE=Calcium
|AnswerEExp=The presentation of this patient is consistent with gouty arthritis. Gout is not characterized by basic calcium phosphate deposition in the joint.
|AnswerEExp=The presentation of this patient is consistent with gouty arthritis. Gout is not characterized by calcium deposition in the joint.
|EducationalObjectives=Gout is an inflammatory disease of the joint characterized by deposition of monosodium urate crystals.
|References=Tuhina N (2011). Gout. NEJM.  2011; 364:443-452
|RightAnswer=B
|RightAnswer=B
|WBRKeyword=Gout, Arthritis
|WBRKeyword=Gout, Arthritis, Monosodium urate, CPPD, Pseudogout, Hyperuricemia, Thiazide diuretics
|Approved=Yes
|Approved=Yes
}}
}}

Latest revision as of 02:01, 28 October 2020

 
Author [[PageAuthor::Serge Korjian M.D. (Reviewed by Serge Korjian)]]
Exam Type ExamType::USMLE Step 1
Main Category MainCategory::Pathophysiology
Sub Category SubCategory::Musculoskeletal/Rheumatology
Prompt [[Prompt::A 63-year-old obese man with history of hypertension treated with thiazide diuretics complains of rapidly progressive pain in his big toe. The pain began in the morning and has become much worse in the last 6 hours. On physical exam, the toe is erythematous, swollen and tender to palpation. The patient reports two similar prior episodes that were less painful and resolved spontaneously. Synovial analysis reveals strongly birefringent needle-shaped crystals on polarized light microscopy. Deposition of which of the following most likely explains the symptoms in 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) has a similar presentation to gout but it is caused by the accumulation of crystals of calcium pyrophosphate dihydrate in the connective tissues. Pseudogout usually involves larger joints than gout. The presence of rhombus-shaped crystals which are weakly birefringent on polarized light microscopy is diagnostic for 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.]]
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 joints characterized by deposition of monosodium urate (MSU) crystals. Gout is associated with hyperuricemia resulting from either overproduction (most-common) 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 the 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.
References: Tuhina N (2011). Gout. NEJM. 2011; 364:443-452]]

Approved Approved::Yes
Keyword WBRKeyword::Gout, WBRKeyword::Arthritis, WBRKeyword::Monosodium urate, WBRKeyword::CPPD, WBRKeyword::Pseudogout, WBRKeyword::Hyperuricemia, WBRKeyword::Thiazide diuretics
Linked Question Linked::
Order in Linked Questions LinkedOrder::