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[[Image:Synapse_q.jpg|600px]]
[[Image:Synapse_q.jpg|600px]]
|Explanation=Cocaine is a powerful stimulant drug and one of the most commonly abused substances in the world. Acute cocaine toxicity usually presents with hallucinations and paranoid behavior, nausea, vomiting, chest pain, dyspnea, tremors, fever, tachycardia, mydriasis, nystagmus, and seizures. Physical exam usually reveals track marks, skin puncture wounds, and/or eroded nasal mucosa depending on the route of administration. Cocaine acts by inhibiting reuptake of several neurotransmitters, with the most prominent effect on dopamine and norepinephrine reuptake from the synaptic cleft. This causes an increase in neurotransmitter concentration at the synaptic cleft leading to the classic cocaine associated symptoms.  
|Explanation=Clostridium botulinum is a gram positive spore forming bacillus that produces an exotoxin known as the botulinum toxin. Clostridium botulinum thrives in anaerobic conditions and foodborne illness occurs due to the ingestion of preformed botulinum toxin usually found in home canned vegetables prepared without following required methods. Infant botulism is seen in babies less than 12 months that are fed honey that contains the bacteria. Botulinum toxin is inactivated by high temperatures, so boiling home-canned food for 10 minutes prior to eating is preferred.


Educational objective: Cocaine exerts its effect by inhibiting the reuptake of dopamine and norepinephrine from the synaptic cleft.
Botulinum toxin acts by blocking acetylcholine vesicle release from the pre-synaptic cleft leading to flaccid paralysis of all muscles including the diaphragm.
 
Educational objective: Botulinum toxin inhibits acetylcholine vesicles from being release in the pre-synaptic cleft leading to flaccid paralysis. It is produced by Clostridium botulinum an anaerobic gram positive bacillus.


References:
References:
 
Cherington M. Clinical spectrum of botulism. Muscle Nerve. 1998;21(6):701-10.
Gawin FH. Cocaine addiction: psychology and neurophysiology. Science. 1991;251(5001):1580-6.
|AnswerA=A
|AnswerA=A
|AnswerAExp=This refers to neurotransmitter integration into vesicles. Reserpine and vesamicol usually act by inhibiting vesicle formation. Cocaine has a different mechanism of action.
|AnswerAExp=This refers to neurotransmitter integration into vesicles. Reserpine and vesamicol usually act by inhibiting vesicle formation. Botulinum has no effect on vesicle formation.
|AnswerB=B
|AnswerB=B
|AnswerBExp=This refers to vesicle release into the synaptic cleft. The most commonly referred inhibitor of vesicle release is botulinum toxin that prevents the release of acetylcholine containing vesicles leading to flaccid paralysis.
|AnswerBExp=This refers to vesicle release into the synaptic cleft inhibited in botulism. The botulinum toxin prevents the release of acetylcholine containing vesicles leading to flaccid paralysis.
|AnswerC=C
|AnswerC=C
|AnswerCExp=This refers to neurotransmitter binding to specific receptors on the post-synaptic membrane. Neurotransmitter antagonists can exert their effect by this mechanism.
|AnswerCExp=This refers to neurotransmitter binding to specific receptors on the post-synaptic membrane. Neurotransmitter antagonists can exert their effect by this mechanism.
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|AnswerDExp=This refers to neurotransmitter degradation. Acetylcholinersterase inhibitors act by inhibiting the breakdown of acetylcholine at the synaptic cleft. Cocaine has a different mechanism of action.
|AnswerDExp=This refers to neurotransmitter degradation. Acetylcholinersterase inhibitors act by inhibiting the breakdown of acetylcholine at the synaptic cleft. Cocaine has a different mechanism of action.
|AnswerE=E
|AnswerE=E
|AnswerEExp=This refers to the mechasim of action of cocaine which acts by inhibiting reuptake of several neurotransmitters, most importantly dopamine and norepinephrine.
|AnswerEExp=This refers to the reuptake of neurotransmitters, usually inhibited by substances like amphetamines and cocaine. Reuptake inhibition is not seen in botulism.
|RightAnswer=E
|RightAnswer=B
|WBRKeyword=Clostridium botulinum, Botulism, Neurotransmitter,
|WBRKeyword=Clostridium botulinum, Botulism, Neurotransmitter,
|Approved=No
|Approved=No
}}
}}

Revision as of 23:57, 6 October 2013

 
Author [[PageAuthor::Rim Halaby, M.D. [1]]]
Exam Type ExamType::USMLE Step 1
Main Category MainCategory::Microbiology, MainCategory::Pathophysiology
Sub Category SubCategory::Neurology, SubCategory::Infectious Disease
Prompt [[Prompt::A 34 year-old man was brought to the hospital by his son for severe nausea, vomiting and abdominal cramps. The patient had noticeable trouble speaking so his son provided the history. He explained that his father started complaining of blurred vision and difficulty swallowing a short time after he had his dinner. Upon exam, you note generalized weakness, bilateral ptosis, and facial muscle drooping. Vital signs were stable but the patient seems to be hypoventilating. The patient's saturation drops rapidly and he requires emergent intubation. Upon further questioning, the son reports that his father had eaten some canned red peppers his mother had prepared at home. Which of the following steps is likely to be inhibited in this patient?

]]

Answer A AnswerA::A
Answer A Explanation AnswerAExp::This refers to neurotransmitter integration into vesicles. Reserpine and vesamicol usually act by inhibiting vesicle formation. Botulinum has no effect on vesicle formation.
Answer B AnswerB::B
Answer B Explanation AnswerBExp::This refers to vesicle release into the synaptic cleft inhibited in botulism. The botulinum toxin prevents the release of acetylcholine containing vesicles leading to flaccid paralysis.
Answer C AnswerC::C
Answer C Explanation AnswerCExp::This refers to neurotransmitter binding to specific receptors on the post-synaptic membrane. Neurotransmitter antagonists can exert their effect by this mechanism.
Answer D AnswerD::D
Answer D Explanation AnswerDExp::This refers to neurotransmitter degradation. Acetylcholinersterase inhibitors act by inhibiting the breakdown of acetylcholine at the synaptic cleft. Cocaine has a different mechanism of action.
Answer E AnswerE::E
Answer E Explanation AnswerEExp::This refers to the reuptake of neurotransmitters, usually inhibited by substances like amphetamines and cocaine. Reuptake inhibition is not seen in botulism.
Right Answer RightAnswer::B
Explanation [[Explanation::Clostridium botulinum is a gram positive spore forming bacillus that produces an exotoxin known as the botulinum toxin. Clostridium botulinum thrives in anaerobic conditions and foodborne illness occurs due to the ingestion of preformed botulinum toxin usually found in home canned vegetables prepared without following required methods. Infant botulism is seen in babies less than 12 months that are fed honey that contains the bacteria. Botulinum toxin is inactivated by high temperatures, so boiling home-canned food for 10 minutes prior to eating is preferred.

Botulinum toxin acts by blocking acetylcholine vesicle release from the pre-synaptic cleft leading to flaccid paralysis of all muscles including the diaphragm.

Educational objective: Botulinum toxin inhibits acetylcholine vesicles from being release in the pre-synaptic cleft leading to flaccid paralysis. It is produced by Clostridium botulinum an anaerobic gram positive bacillus.

References: Cherington M. Clinical spectrum of botulism. Muscle Nerve. 1998;21(6):701-10.
Educational Objective:
References: ]]

Approved Approved::No
Keyword WBRKeyword::Clostridium botulinum, WBRKeyword::Botulism, WBRKeyword::Neurotransmitter
Linked Question Linked::
Order in Linked Questions LinkedOrder::