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{{WBRQuestion | {{WBRQuestion | ||
|QuestionAuthor={{Rim}} | |QuestionAuthor={{Rim}}, {{AJL}} {{Alison}} | ||
|ExamType=USMLE Step 1 | |ExamType=USMLE Step 1 | ||
|MainCategory=Microbiology | |MainCategory=Microbiology | ||
Line 20: | Line 20: | ||
|MainCategory=Microbiology | |MainCategory=Microbiology | ||
|SubCategory=Neurology | |SubCategory=Neurology | ||
|Prompt=A 28 year old HIV-positive female | |Prompt=A 28-year-old HIV-positive female presents to the emergency room with a high grade fever, headache, weakness, and tonic-clonic seizures. The patient has a recent history of anorexia. Laboratory work-up reveals CD4 count = 80 cells/µL per year. Head computer tomography (CT) scan demostrates multiple ring enhancing lesions in the frontal lobes. The patient requires treatment with a medication that uses which of the following mechanisms of action? | ||
|Explanation=[[Cerebral toxoplasmosis]] | |Explanation=[[Cerebral toxoplasmosis]], caused by ''[[Toxoplasma gondii]]'', is an opportunistic parasitic infection that frequently infects HIV-positive patients with CD4 counts < 100 cells/µL per year. [[Toxoplasmosis]] manifest with fever, headache, and new-onset seizures. Multiple [[ring-enhancing lesions]] upon cranial CT scan are characteristic. Treatment of [[cerebral toxoplasmosis]] includes [[pyrimethamine]], a [[dihydrofolate reductase inhibitor]], and [[sulfadiazine]], a [[sulfa drug]] that is a [[dihydropteroate synthetase]] inhibitor. | ||
|EducationalObjectives= | |||
Cerebral toxoplasmosis | Cerebral toxoplasmosis, frequently occurring in HIV-positive individuals with CD4 count < 100 cells/µL per year, often manifests with a fever, headache, and new-onset seizures. | ||
Treatment of [[cerebral toxoplasmosis]] includes [[pyrimethamine]], a [[dihydrofolate reductase inhibitor]], and [[sulfadiazine]], a [[sulfa drug]] that is a [[dihydropteroate synthetase]] inhibitor. | |||
|AnswerA=Inhibition of heme polymerase activity | |AnswerA=Inhibition of heme polymerase activity | ||
|AnswerAExp=[[Chloroquine]], an antimalarial drug, is a plasmodium heme polymerase inhibitor. | |AnswerAExp=[[Chloroquine]], an antimalarial drug, is a plasmodium heme polymerase inhibitor. | ||
|AnswerB=Inhibition of dihydrofolate reductase activity | |AnswerB=Inhibition of dihydrofolate reductase activity | ||
|AnswerBExp=[[Pyrimethamine]], a drug used to treat [[toxoplasmosis]], is a dihydrofolate reductase inhibitor. | |AnswerBExp=[[Pyrimethamine]], a drug frequently used to treat [[toxoplasmosis]], is a dihydrofolate reductase inhibitor. | ||
|AnswerC=Free radical toxicity of organism’s DNA | |AnswerC=Free radical toxicity of organism’s DNA | ||
|AnswerCExp=[[Metronidazole]], an [[antibiotic]] and antiprotozoal, forms free radical metabolites that are toxic to bacterial DNA. | |AnswerCExp=[[Metronidazole]], an [[antibiotic]] and antiprotozoal, forms free radical metabolites that are toxic to bacterial DNA. | ||
|AnswerD=Blockade of peptide bond formation at 50S ribosomal subunit | |AnswerD=Blockade of peptide bond formation at 50S ribosomal subunit | ||
|AnswerDExp=Several [[antibiotics]], including [[chloramphenicol]], [[macrolides]], [[clindamycin]], [[streptogramins]], and [[linezolid]], block peptide bond formation at 50S ribosomal subunit. | |AnswerDExp=Several [[antibiotics]], including [[chloramphenicol]], [[macrolides]], [[clindamycin]], [[streptogramins]], and [[linezolid]], block peptide bond formation at the 50S ribosomal subunit. | ||
|AnswerE=Inhibition of DNA polymerase activity | |AnswerE=Inhibition of DNA polymerase activity | ||
|AnswerEExp=Antiviral medications, such as [[acyclovir]], [[ganciclovir]], [[foscarnet]], and [[cidofovir]] are DNA polymerase inhibitors. | |AnswerEExp=Antiviral medications, such as [[acyclovir]], [[ganciclovir]], [[foscarnet]], and [[cidofovir]] are DNA polymerase inhibitors. | ||
|RightAnswer=B | |RightAnswer=B | ||
|WBRKeyword=Toxoplasma gondii, toxomplasmosis, HIV, seizure, ring enhancing lesion, pyrimethamine, dihydrofolate reductase inhibitor | |WBRKeyword=Toxoplasma gondii, toxomplasmosis, HIV, seizure, ring enhancing lesion, pyrimethamine, dihydrofolate reductase inhibitor | ||
|Approved= | |Approved=Yes | ||
}} | }} |
Revision as of 14:44, 22 July 2014
Author | [[PageAuthor::Rim Halaby, M.D. [1], Alison Leibowitz [2] (Reviewed by Alison Leibowitz)]] |
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Exam Type | ExamType::USMLE Step 1 |
Main Category | MainCategory::Microbiology |
Sub Category | SubCategory::Neurology |
Prompt | [[Prompt::A 28-year-old HIV-positive female presents to the emergency room with a high grade fever, headache, weakness, and tonic-clonic seizures. The patient has a recent history of anorexia. Laboratory work-up reveals CD4 count = 80 cells/µL per year. Head computer tomography (CT) scan demostrates multiple ring enhancing lesions in the frontal lobes. The patient requires treatment with a medication that uses which of the following mechanisms of action?]] |
Answer A | AnswerA::Inhibition of heme polymerase activity |
Answer A Explanation | [[AnswerAExp::Chloroquine, an antimalarial drug, is a plasmodium heme polymerase inhibitor.]] |
Answer B | AnswerB::Inhibition of dihydrofolate reductase activity |
Answer B Explanation | [[AnswerBExp::Pyrimethamine, a drug frequently used to treat toxoplasmosis, is a dihydrofolate reductase inhibitor.]] |
Answer C | AnswerC::Free radical toxicity of organism’s DNA |
Answer C Explanation | [[AnswerCExp::Metronidazole, an antibiotic and antiprotozoal, forms free radical metabolites that are toxic to bacterial DNA.]] |
Answer D | AnswerD::Blockade of peptide bond formation at 50S ribosomal subunit |
Answer D Explanation | [[AnswerDExp::Several antibiotics, including chloramphenicol, macrolides, clindamycin, streptogramins, and linezolid, block peptide bond formation at the 50S ribosomal subunit.]] |
Answer E | AnswerE::Inhibition of DNA polymerase activity |
Answer E Explanation | [[AnswerEExp::Antiviral medications, such as acyclovir, ganciclovir, foscarnet, and cidofovir are DNA polymerase inhibitors.]] |
Right Answer | RightAnswer::B |
Explanation | [[Explanation::Cerebral toxoplasmosis, caused by Toxoplasma gondii, is an opportunistic parasitic infection that frequently infects HIV-positive patients with CD4 counts < 100 cells/µL per year. Toxoplasmosis manifest with fever, headache, and new-onset seizures. Multiple ring-enhancing lesions upon cranial CT scan are characteristic. Treatment of cerebral toxoplasmosis includes pyrimethamine, a dihydrofolate reductase inhibitor, and sulfadiazine, a sulfa drug that is a dihydropteroate synthetase inhibitor. Educational Objective: Cerebral toxoplasmosis, frequently occurring in HIV-positive individuals with CD4 count < 100 cells/µL per year, often manifests with a fever, headache, and new-onset seizures.
Treatment of cerebral toxoplasmosis includes pyrimethamine, a dihydrofolate reductase inhibitor, and sulfadiazine, a sulfa drug that is a dihydropteroate synthetase inhibitor. |
Approved | Approved::Yes |
Keyword | WBRKeyword::Toxoplasma gondii, WBRKeyword::toxomplasmosis, WBRKeyword::HIV, WBRKeyword::seizure, WBRKeyword::ring enhancing lesion, WBRKeyword::pyrimethamine, WBRKeyword::dihydrofolate reductase inhibitor |
Linked Question | Linked:: |
Order in Linked Questions | LinkedOrder:: |