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Rim Halaby (talk | contribs) (Created page with "{{WBRQuestion |QuestionAuthor={{Rim}} |ExamType=USMLE Step 1 |MainCategory=Microbiology |SubCategory=Neurology |MainCategory=Microbiology |SubCategory=Neurology |MainCategory=...") |
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Educational Objective: | Educational Objective: | ||
Cerebral toxoplasmosis causes a clinical syndrome of fever, headache, and new-onset seizures typically in an HIV-positive patient with CD4 count < 100 cells/µL per year. Treatment of cerebral toxoplasmosis includes pyrimethamine, a dihydrofolate reductase inhibitor, and sulfadiazine, a sulfa drug that is a dihydropteroate synthetase inhibitor. | Cerebral toxoplasmosis causes a clinical syndrome of fever, headache, and new-onset seizures typically in an HIV-positive patient with CD4 count < 100 cells/µL per year. 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 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 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 | |WBRKeyword=Toxoplasma gondii, toxomplasmosis, HIV, seizure, ring enhancing lesion, pyrimethamine, dihydrofolate reductase inhibitor | ||
|Approved=No | |Approved=No | ||
}} | }} |
Revision as of 12:06, 16 September 2013
Author | [[PageAuthor::Rim Halaby, M.D. [1]]] |
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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 patient presents to the emergency department with high grade fever, headache, and new onset tonic-clonic seizures. The patient also explains she has been anorexic and very weak recently. Laboratory work-up reveals CD4 count = 80 cells/µL per year. Head computer tomography (CT) scan shows multiple ring enhancing lesions in the frontal lobes. The patient requires treatment with a medication that has 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 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 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 is caused by Toxoplasma gondii, an opportunistic parasitic infection that often infects HIV-positive patients with CD4 counts < 100 cells/µL per year. Toxoplasmosis causes a clinical syndrome of fever, headache, and new-onset seizures typically in an HIV-positive patient. Multiple ring-enhancing lesions on head 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 causes a clinical syndrome of fever, headache, and new-onset seizures typically in an HIV-positive patient with CD4 count < 100 cells/µL per year. Treatment of cerebral toxoplasmosis includes pyrimethamine, a dihydrofolate reductase inhibitor, and sulfadiazine, a sulfa drug that is a dihydropteroate synthetase inhibitor. |
Approved | Approved::No |
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:: |