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Questions and Answers
Which of the following best describes the underlying mechanism of Guillain-Barré Syndrome that leads to demyelination?
Which of the following best describes the underlying mechanism of Guillain-Barré Syndrome that leads to demyelination?
- Type IV hypersensitivity reaction mediated by T-cells targeting myelin.
- Autoimmune targeting and destruction of gangliosides in the peripheral nervous system. (correct)
- Metabolic deficiency impairs the synthesis and maintenance of myelin sheaths.
- Viral reactivation caused by immunosuppression leads to direct infection of oligodendrocytes.
In the context of synaptic transmission, what would be the most immediate consequence of blocking voltage-gated calcium channels on the presynaptic neuron?
In the context of synaptic transmission, what would be the most immediate consequence of blocking voltage-gated calcium channels on the presynaptic neuron?
- Inhibition of neurotransmitter reuptake from the synaptic cleft.
- Enhanced postsynaptic receptor binding and signal transduction.
- Prevention of vesicle docking and neurotransmitter release into the synaptic cleft. (correct)
- Increased neurotransmitter synthesis within the presynaptic neuron.
Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease caused by the reactivation of the JC virus. What condition creates an environment that allows for this reactivation?
Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease caused by the reactivation of the JC virus. What condition creates an environment that allows for this reactivation?
- Hyperglycemia due to diabetes mellitus.
- Severe Vitamin B12 deficiency caused by veganism.
- Chronic infection with Epstein-Barr virus.
- Immunosuppression due to monoclonal antibody treatment. (correct)
In a patient presenting with ascending muscle weakness, loss of reflexes, and a history of a recent infection, which pathological mechanism is most likely contributing to these symptoms?
In a patient presenting with ascending muscle weakness, loss of reflexes, and a history of a recent infection, which pathological mechanism is most likely contributing to these symptoms?
A patient with poorly controlled diabetes mellitus is likely to develop diabetic neuropathy and retinopathy. Which of the following mechanisms is the primary cause of these complications?
A patient with poorly controlled diabetes mellitus is likely to develop diabetic neuropathy and retinopathy. Which of the following mechanisms is the primary cause of these complications?
In the indirect pathway of the striatum, what is the effect of decreased GABA release from the globus pallidus externa (GPe) onto the subthalamic nucleus?
In the indirect pathway of the striatum, what is the effect of decreased GABA release from the globus pallidus externa (GPe) onto the subthalamic nucleus?
How does dopamine binding to D2 receptors in the striatum affect the activity of the globus pallidus externa (GPe)?
How does dopamine binding to D2 receptors in the striatum affect the activity of the globus pallidus externa (GPe)?
What is the primary role of the basal ganglia in motor function?
What is the primary role of the basal ganglia in motor function?
A patient presents with increased motor coordination and fluidity of movement. Based on the indirect pathway of the striatum, which of the following scenarios is most likely occurring in their basal ganglia?
A patient presents with increased motor coordination and fluidity of movement. Based on the indirect pathway of the striatum, which of the following scenarios is most likely occurring in their basal ganglia?
What is the expected motor outcome when the subthalamic nuclei are highly stimulated and releasing large amounts of glutamate onto the globus pallidus interna (GPi)?
What is the expected motor outcome when the subthalamic nuclei are highly stimulated and releasing large amounts of glutamate onto the globus pallidus interna (GPi)?
In the context of the basal ganglia, how does the disruption of dopamine signaling (as seen in Parkinson's disease) primarily manifest in terms of motor control?
In the context of the basal ganglia, how does the disruption of dopamine signaling (as seen in Parkinson's disease) primarily manifest in terms of motor control?
If the striatum is unable to release GABA onto the GPe, what is the resulting effect on the subthalamic nuclei?
If the striatum is unable to release GABA onto the GPe, what is the resulting effect on the subthalamic nuclei?
Damage to the substantia nigra pars compacta, which reduces dopamine production, would have what effect on the GPi, according to the indirect pathway?
Damage to the substantia nigra pars compacta, which reduces dopamine production, would have what effect on the GPi, according to the indirect pathway?
In the direct pathway of the striatum, what is the consequence of dopamine binding to D1 receptors?
In the direct pathway of the striatum, what is the consequence of dopamine binding to D1 receptors?
Which of the following describes the effect of decreased dopamine release in the direct pathway of the striatum?
Which of the following describes the effect of decreased dopamine release in the direct pathway of the striatum?
Which specific area of the substantia nigra experiences the most significant impact from Parkinson's Disease, leading to a reduction in dopamine release?
Which specific area of the substantia nigra experiences the most significant impact from Parkinson's Disease, leading to a reduction in dopamine release?
What motor symptom is most indicative of advanced Parkinson's Disease?
What motor symptom is most indicative of advanced Parkinson's Disease?
Why is carbidopa administered in conjunction with levodopa in the management of Parkinson's Disease?
Why is carbidopa administered in conjunction with levodopa in the management of Parkinson's Disease?
How do MAO-B inhibitors work to alleviate symptoms of Parkinson's Disease?
How do MAO-B inhibitors work to alleviate symptoms of Parkinson's Disease?
Why is bromocriptine, an ergot-based dopaminergic agonist, not typically the first-line treatment for Parkinson's Disease?
Why is bromocriptine, an ergot-based dopaminergic agonist, not typically the first-line treatment for Parkinson's Disease?
What is the enzymatic role of Dopa Decarboxylase in the context of Parkinson's Disease treatment?
What is the enzymatic role of Dopa Decarboxylase in the context of Parkinson's Disease treatment?
A patient in the intensive care unit exhibits repetitive focal motor activity in their right arm, with preserved awareness. EEG confirms localized epileptiform discharges in the contralateral motor cortex. Which of the following is the MOST appropriate initial classification?
A patient in the intensive care unit exhibits repetitive focal motor activity in their right arm, with preserved awareness. EEG confirms localized epileptiform discharges in the contralateral motor cortex. Which of the following is the MOST appropriate initial classification?
A patient is brought to the emergency department in status epilepticus. After initial stabilization with IV benzodiazepines, which of the following medications would be MOST appropriate to administer next for long-term seizure control?
A patient is brought to the emergency department in status epilepticus. After initial stabilization with IV benzodiazepines, which of the following medications would be MOST appropriate to administer next for long-term seizure control?
A patient with a history of COPD presents with altered mental status and new-onset seizures. Lumbar puncture reveals evidence of bacterial meningitis. Which of the following is the MOST likely causative organism?
A patient with a history of COPD presents with altered mental status and new-onset seizures. Lumbar puncture reveals evidence of bacterial meningitis. Which of the following is the MOST likely causative organism?
Which of the following mechanisms BEST explains how hyponatremia contributes to the development of seizures?
Which of the following mechanisms BEST explains how hyponatremia contributes to the development of seizures?
A 22-year-old college student presents with fever, headache, and nuchal rigidity followed by a generalized tonic-clonic seizure. Which of the following is the MOST likely cause of their condition?
A 22-year-old college student presents with fever, headache, and nuchal rigidity followed by a generalized tonic-clonic seizure. Which of the following is the MOST likely cause of their condition?
A patient with a history of HIV/AIDS presents with gradual onset of altered mental status and seizures. An MRI of the brain reveals multiple non-enhancing white matter lesions. Which of the following is the MOST likely infectious etiology?
A patient with a history of HIV/AIDS presents with gradual onset of altered mental status and seizures. An MRI of the brain reveals multiple non-enhancing white matter lesions. Which of the following is the MOST likely infectious etiology?
Which of the following mechanisms BEST explains how hemorrhagic stroke increases the risk of seizures compared to ischemic stroke?
Which of the following mechanisms BEST explains how hemorrhagic stroke increases the risk of seizures compared to ischemic stroke?
A patient returning from a hiking trip presents with a rash, joint pain, and new-onset seizures. Which of the following infectious etiologies is MOST likely?
A patient returning from a hiking trip presents with a rash, joint pain, and new-onset seizures. Which of the following infectious etiologies is MOST likely?
In Huntington's disease, the expansion of CAG trinucleotide repeats leads to an accumulation of Huntingtin protein. What specific effect does this accumulation have on neuronal function within the basal ganglia?
In Huntington's disease, the expansion of CAG trinucleotide repeats leads to an accumulation of Huntingtin protein. What specific effect does this accumulation have on neuronal function within the basal ganglia?
Why does the degeneration of the striatum in the early stages of Huntington's disease lead to hyperkinetic movements such as chorea and athetosis?
Why does the degeneration of the striatum in the early stages of Huntington's disease lead to hyperkinetic movements such as chorea and athetosis?
In the later stages of Huntington's disease, patients often develop bradykinesia and rigidity, similar to Parkinson's disease. What is the primary pathological change that accounts for this transition?
In the later stages of Huntington's disease, patients often develop bradykinesia and rigidity, similar to Parkinson's disease. What is the primary pathological change that accounts for this transition?
How do the visuospatial deficits seen in Huntington's disease manifest, and what specific neural pathway is implicated in these deficits?
How do the visuospatial deficits seen in Huntington's disease manifest, and what specific neural pathway is implicated in these deficits?
What is the primary mechanism by which the accumulation of Huntingtin protein leads to the characteristic enlargement of the lateral ventricles observed in neuroimaging of Huntington's disease patients?
What is the primary mechanism by which the accumulation of Huntingtin protein leads to the characteristic enlargement of the lateral ventricles observed in neuroimaging of Huntington's disease patients?
Why do disruptions of striatal neurons projecting to the frontal cortex in Huntington's disease result in a lack of behavioral and social inhibitions?
Why do disruptions of striatal neurons projecting to the frontal cortex in Huntington's disease result in a lack of behavioral and social inhibitions?
How does the destruction of the striatum affect the release of GABA (gamma-aminobutyric acid) in the basal ganglia circuit during the early stages of Huntington's disease, and what is the consequence of this change?
How does the destruction of the striatum affect the release of GABA (gamma-aminobutyric acid) in the basal ganglia circuit during the early stages of Huntington's disease, and what is the consequence of this change?
What distinguishes the hyperkinetic movement disorder seen in early Huntington's disease in contrast to the hypokinetic movement disorder observed with Parkinson's Disease?
What distinguishes the hyperkinetic movement disorder seen in early Huntington's disease in contrast to the hypokinetic movement disorder observed with Parkinson's Disease?
Which of the following physiological changes is the MOST likely direct consequence of the decreased GABA transmission observed during acute benzodiazepine cessation in a chronically dependent patient?
Which of the following physiological changes is the MOST likely direct consequence of the decreased GABA transmission observed during acute benzodiazepine cessation in a chronically dependent patient?
A patient with a history of chronic benzodiazepine abuse presents with anxiety, tremors, and heart palpitations 12 hours after their last dose. Which benzodiazepine withdrawal characteristic should the physician consider FIRST when determining the appropriate course of treatment?
A patient with a history of chronic benzodiazepine abuse presents with anxiety, tremors, and heart palpitations 12 hours after their last dose. Which benzodiazepine withdrawal characteristic should the physician consider FIRST when determining the appropriate course of treatment?
A patient undergoing alcohol withdrawal develops severe agitation, visual hallucinations, and life-threatening autonomic instability. Which condition is MOST likely indicated by this presentation?
A patient undergoing alcohol withdrawal develops severe agitation, visual hallucinations, and life-threatening autonomic instability. Which condition is MOST likely indicated by this presentation?
Which of the following is the MOST appropriate initial treatment strategy for a patient experiencing severe agitation and aggression during acute alcohol withdrawal?
Which of the following is the MOST appropriate initial treatment strategy for a patient experiencing severe agitation and aggression during acute alcohol withdrawal?
A patient with chronic alcohol use presents with severe nausea and abdominal pain during alcohol withdrawal. What underlying condition should be considered as a PRIMARY contributor to these symptoms?
A patient with chronic alcohol use presents with severe nausea and abdominal pain during alcohol withdrawal. What underlying condition should be considered as a PRIMARY contributor to these symptoms?
A patient in acute benzodiazepine withdrawal is exhibiting paranoia that is escalating into frank aggression. Apart from pharmacological interventions, which immediate step is MOST crucial for ensuring patient and staff safety?
A patient in acute benzodiazepine withdrawal is exhibiting paranoia that is escalating into frank aggression. Apart from pharmacological interventions, which immediate step is MOST crucial for ensuring patient and staff safety?
A patient with a history of chronic alcohol abuse is admitted for detoxification. On the third day, the patient develops visual and tactile hallucinations, severe agitation, and significant autonomic instability. After administering appropriate pharmacological interventions, which of the following should be the NEXT priority in managing this patient?
A patient with a history of chronic alcohol abuse is admitted for detoxification. On the third day, the patient develops visual and tactile hallucinations, severe agitation, and significant autonomic instability. After administering appropriate pharmacological interventions, which of the following should be the NEXT priority in managing this patient?
During which timeframe after the last alcoholic beverage is a patient MOST likely to experience Delirium Tremens?
During which timeframe after the last alcoholic beverage is a patient MOST likely to experience Delirium Tremens?
Flashcards
Saltatory Conduction
Saltatory Conduction
The transmission of electrical signals between nodes of Ranvier along myelinated neurons.
PML
PML
Progressive multifocal leukoencephalopathy, a fatal condition caused by reactivation of the JC virus in immunosuppressed individuals.
Parts of a Synapse
Parts of a Synapse
Consists of presynaptic neuron, synaptic cleft, and postsynaptic neuron.
Role of Calcium
Role of Calcium
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Guillain-Barre Syndrome
Guillain-Barre Syndrome
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Direct Pathway of Striatum
Direct Pathway of Striatum
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Role of Dopamine in Striatum
Role of Dopamine in Striatum
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GPi Function
GPi Function
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Effects of Decreased Dopamine
Effects of Decreased Dopamine
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Symptoms of Parkinson's Disease
Symptoms of Parkinson's Disease
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Levodopa + Carbidopa
Levodopa + Carbidopa
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Dopaminergic Agonists
Dopaminergic Agonists
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MAO-B Inhibitors
MAO-B Inhibitors
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Generalized Convulsive Status Epilepticus
Generalized Convulsive Status Epilepticus
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Non-Convulsive Status Epilepticus
Non-Convulsive Status Epilepticus
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Focal Status Epilepticus
Focal Status Epilepticus
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Management of Status Epilepticus
Management of Status Epilepticus
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Infectious Causes of Seizure
Infectious Causes of Seizure
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Hyponatremia and Seizures
Hyponatremia and Seizures
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Streptococcus Pneumoniae
Streptococcus Pneumoniae
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Herpes Viruses in Encephalitis
Herpes Viruses in Encephalitis
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Basal Ganglia
Basal Ganglia
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Parts of Basal Ganglia
Parts of Basal Ganglia
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Motor Cortex
Motor Cortex
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Role of Dopamine
Role of Dopamine
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GABA
GABA
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Glutamate
Glutamate
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Parkinson's Disease
Parkinson's Disease
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Benzodiazepine Withdrawal Symptoms
Benzodiazepine Withdrawal Symptoms
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Short-acting Benzodiazepines
Short-acting Benzodiazepines
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Long-acting Benzodiazepines
Long-acting Benzodiazepines
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Early Symptoms of Withdrawal
Early Symptoms of Withdrawal
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Late Symptoms of Withdrawal
Late Symptoms of Withdrawal
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Delirium Tremens (DT)
Delirium Tremens (DT)
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Management of Benzodiazepine Withdrawal
Management of Benzodiazepine Withdrawal
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Alcohol Withdrawal Seizures
Alcohol Withdrawal Seizures
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CAG Trinucleotide Repeats
CAG Trinucleotide Repeats
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Striatum
Striatum
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Enlargement of Lateral Ventricles
Enlargement of Lateral Ventricles
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Hyperkinetic Phenotypes
Hyperkinetic Phenotypes
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Chorea
Chorea
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Bradykinesia
Bradykinesia
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Neuropsychiatric Deficits
Neuropsychiatric Deficits
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Dopamine Release
Dopamine Release
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Study Notes
Pathophysiology of Demyelination
- Saltatory conduction is the transmission of neuronal electric current from node of Ranvier to node of Ranvier.
- Causes of demyelination include:
- JC virus (polyomavirus) reactivation, leading to PML (progressive multifocal leukoencephalopathy).
- Cytomegalovirus, often associated with HIV/AIDS (CD4 count < 50).
- Epstein-Barr virus, sometimes linked with multiple sclerosis.
- Guillain-Barré syndrome, an inflammatory demyelinating polyneuropathy characterized by anti-ganglioside autoantibodies.
- Multiple sclerosis, a type IV hypersensitivity syndrome.
- Vitamin B12 deficiency, associated with pernicious anemia.
- Diabetes mellitus, leading to diabetic neuropathy and retinopathy.
Synaptic Structure and Function
- A synapse has three main parts:
- Presynaptic neuron: produces and releases neurotransmitters.
- Synaptic cleft: space containing enzymes (e.g., acetylcholinesterase) that regulate neurotransmitter activity.
- Postsynaptic neuron: contains receptors for neurotransmitters, with effects varying depending on the transmitter.
- Calcium plays a crucial role in neurotransmitter release from the presynaptic neuron by promoting vesicular docking and subsequent release via voltage-gated calcium channels. (Important for synapse functioning)
Basal Ganglia
- The basal ganglia are a key subcortical brain structure for integrating and fine-tuning nerve fiber projections to multiple brain locations.
- Components of the basal ganglia include the globus pallidus (external and internal segments), substantia nigra (compacta and reticulata), striatum (caudate and putamen), and subthalamic nuclei.
- The basal ganglia play a role in modulating motor output to the supplemental motor cortex, but they do not elicit conscious movement. Parkinson's and Huntington's diseases do not result in complete paralysis.
Indirect Pathway of the Striatum
- Without dopamine, the striatum releases GABA onto the globus pallidus external segment (GPe).
- Reduced GABA in GPe leads to increased glutamate release in the subthalamic nucleus.
- This increased glutamate stimulates the globus pallidus internal segment (GPi) to produce more GABA.
- Increased GABA in the thalamus decreases output to the motor cortex, resulting in reduced motor coordination.
Direct Pathway of the Striatum
- With dopamine binding to D1 receptors, the striatum releases less GABA, reducing inhibition of the globus pallidus external segment (GPe).
- This results in more GABA released from the GPe onto the subthalamic nucleus, resulting in reduced glutamate release onto the globus pallidus internal segment (GPi).
- Decreased GABA in the thalamus leads to increased output in the motor cortex, increasing motor coordination.
Parkinson's Disease
- Parkinson's disease primarily affects the substantia nigra pars compacta, decreasing dopamine release.
- Clinical symptoms include bradykinesia, tremors, rigidity, gait abnormalities, and cognitive difficulties.
Huntington's Disease
- Huntington's disease involves an excessive number of CAG trinucleotide repeats on chromosome 4, causing Huntingtin protein accumulation.
- This results in damage to the striatum (caudate and putamen), leading to movement disorders such as chorea and athetosis.
- Associated with neuroimaging findings of enlarged lateral ventricles.
ALS (Amyotrophic Lateral Sclerosis)
- ALS (Amyotrophic Lateral Sclerosis): A progressive neurodegenerative disease.
- Glutamate toxicity plays a part in ALS pathogenesis, leading to increased calcium influx, oxidative stress, and mitochondrial damage.
- ALS commonly causes respiratory failure, contributing to the disease's progression.
Seizure Disorders
- Several factors, including infections (meningitis, encephalitis), stroke (hemorrhagic), and metabolic/electrolyte abnormalities, can trigger seizures.
Neurotransmission
- Neurotransmission involves the release and binding of neurotransmitters at synapses.
- Key neurotransmitters include glutamate, GABA, dopamine, and norepinephrine.
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Description
Overview of demyelination causes like JC virus, CMV, EBV, Guillain-Barré syndrome, multiple sclerosis, B12 deficiency and diabetes. Also, synaptic structure with presynaptic neuron, synaptic cleft, and postsynaptic neuron.