DOMAIN 1A- NEUROBIOLOGY QUESTION AND ANSWER Flashcards
Which brain structure is primarily responsible for regulating emotions such as fear and aggression, and plays a significant role in post-traumatic stress disorder (PTSD)?
- Hippocampus
- Amygdala
- Prefrontal cortex
- Basal ganglia
Answer: Amygdala
Rationale:
The amygdala is central to fear, aggression, and emotional responses. In PTSD, hyperactivity of the amygdala is linked to heightened fear and emotional reactivity.
Hippocampus: While involved in memory consolidation, hippocampal atrophy in PTSD contributes to difficulties distinguishing past from present, not emotion regulation.
Prefrontal cortex: Hypoactivity in the prefrontal cortex contributes to impaired emotional regulation in PTSD, but it is not the primary structure regulating fear.
Basal ganglia: The basal ganglia are involved in motor control and habit formation, not emotion processing.
A 50-year-old patient with difficulty initiating movement, resting tremors, and bradykinesia most likely has a dysfunction in which brain structure?
- Cerebellum
- Basal ganglia
- Hypothalamus
- Thalamus
Answer: Basal ganglia
Rationale:
Correct: The basal ganglia, particularly the degeneration of dopaminergic neurons in the substantia nigra, lead to motor symptoms seen in Parkinson’s disease.
Cerebellum: The cerebellum is involved in coordination and balance, not initiating movement or tremors.
Hypothalamus: This structure regulates autonomic and homeostatic functions, not motor control.
Thalamus: The thalamus relays sensory and motor signals but is not the primary site of pathology in Parkinson’s disease.
Which brain region is most affected in Alzheimer’s disease, leading to memory impairment and cognitive decline?
- Occipital lobe
- Parietal lobe
- Hippocampus
- Amygdala
Answer: Hippocampus
Rationale:
Correct: The hippocampus, critical for memory consolidation, is the first region to show significant atrophy in Alzheimer’s disease, resulting in memory loss.
Occipital lobe: This area processes visual information, and dysfunction here would result in visual disturbances, not memory loss.
Parietal lobe: The parietal lobe is responsible for spatial and sensory processing, which are not primarily affected in early Alzheimer’s disease.
Amygdala: While the amygdala contributes to emotional memory, its dysfunction does not primarily cause cognitive decline in Alzheimer’s.
Which part of the brain is primarily responsible for executive functions such as planning, decision-making, and impulse control, and is hypoactive in individuals with schizophrenia?
- Occipital lobe
- Prefrontal cortex
- Temporal lobe
- Thalamus
Answer: Prefrontal cortex
Rationale:
Correct: Hypoactivity in the prefrontal cortex is linked to executive dysfunction in schizophrenia, such as poor planning and decision-making.
Occipital lobe: This lobe processes visual input and is not implicated in executive dysfunction.
Temporal lobe: The temporal lobe is involved in auditory processing and memory, not executive functions.
Thalamus: The thalamus relays sensory signals but does not play a major role in executive functioning.
A stroke affecting the left frontal lobe of the brain is most likely to result in which of the following deficits?
- Impaired language production
- Loss of coordination
- Inability to recognize faces
- Memory loss
Answer: Impaired language production
Rationale:
Correct: Damage to Broca’s area in the left frontal lobe causes expressive aphasia, resulting in impaired language production.
** Loss of coordination**: This is associated with cerebellar dysfunction, not the frontal lobe.
Inability to recognize faces: This results from damage to the fusiform gyrus in the temporal lobe, not the frontal lobe.
Memory loss: Memory is primarily governed by the hippocampus, not the frontal lobe.
Which brain region is associated with reward processing and is implicated in substance use disorders?
- Amygdala
- Nucleus accumbens
- Hypothalamus
- Parietal lobe
Answer: Nucleus accumbens
Rationale:
Correct: The nucleus accumbens is a key component of the brain’s reward system, involved in the reinforcing effects of addictive substances.
Amygdala: While involved in emotional regulation, it does not directly mediate reward processing.
Hypothalamus: The hypothalamus regulates homeostasis, not reward processing.
Parietal lobe: This lobe processes spatial and sensory information, not reward or addiction.
Damage to the parietal lobe is most likely to result in:
- Loss of motor coordination
- Inability to understand spatial relationships
- Loss of vision
- Impaired impulse control
Answer: Inability to understand spatial relationships
Rationale:
Correct: The parietal lobe is essential for spatial processing and awareness. Damage can cause deficits in spatial perception and navigation.
Loss of motor coordination: This is linked to cerebellar damage, not the parietal lobe.
Loss of vision: The occipital lobe processes visual input, and damage there causes visual deficits.
Impaired impulse control: This is associated with the prefrontal cortex, not the parietal lobe.
Which brain structure is critical for maintaining homeostasis and is involved in regulating hunger, thirst, and the sleep-wake cycle?
- Thalamus
- Hypothalamus
- Brainstem
- Cerebellum
Answer: Hypothalamus
Rationale:
Correct: The hypothalamus regulates homeostasis, including hunger, thirst, and circadian rhythms.
Thalamus: The thalamus relays sensory and motor signals but does not regulate homeostasis.
Brainstem: The brainstem controls basic autonomic functions such as respiration and heart rate but not hunger or thirst.
Cerebellum: The cerebellum governs motor coordination and balance, not homeostasis.
A 32-year-old patient with schizophrenia is started on a dopamine D2 receptor antagonist. Two weeks later, she develops muscle rigidity and tremors. Which dopamine pathway is most likely responsible for these symptoms?
- Mesolimbic pathway
- Mesocortical pathway
- Nigrostriatal pathway
- Tuberoinfundibular pathway
Answer: Nigrostriatal pathway
Rationale:
Correct: The nigrostriatal pathway regulates motor function. Dopamine blockade in this pathway leads to extrapyramidal symptoms (EPS), such as rigidity, tremors, and bradykinesia.
Mesolimbic pathway: Dopamine blockade here reduces positive symptoms of schizophrenia, such as hallucinations, but does not cause motor symptoms.
Mesocortical pathway: Dysfunction in this pathway contributes to negative and cognitive symptoms, not motor symptoms.
Tuberoinfundibular pathway: Dopamine blockade here results in hyperprolactinemia, not motor dysfunction.
A patient with Parkinson’s disease is treated with a dopamine precursor. While motor symptoms improve, they develop compulsive gambling behavior. Which dopamine pathway is most likely responsible for this side effect?
- Mesolimbic pathway
- Nigrostriatal pathway
- Tuberoinfundibular pathway
- Mesocortical pathway
Answer: Mesolimbic pathway
Rationale:
Correct: The mesolimbic pathway mediates reward and motivation. Excess dopamine in this pathway can lead to impulse control disorders, such as compulsive gambling, a known side effect of dopaminergic therapy in Parkinson’s disease.
Nigrostriatal pathway: This pathway regulates motor function and is targeted for Parkinson’s symptoms, but it does not cause compulsive behaviors.
Tuberoinfundibular pathway: Dopaminergic therapy reduces prolactin levels but does not affect impulse control.
Mesocortical pathway: This pathway is associated with cognition and emotion, not compulsive behavior.
A patient taking a dopamine D2 receptor antagonist develops galactorrhea and menstrual irregularities. Which dopamine pathway is most likely involved?
- Nigrostriatal pathway
- Mesolimbic pathway
- Mesocortical pathway
- Tuberoinfundibular pathway
Answer: Tuberoinfundibular pathway
Rationale:
Correct: The tuberoinfundibular pathway inhibits prolactin release. Dopamine antagonists block this inhibition, leading to hyperprolactinemia and symptoms such as galactorrhea and menstrual irregularities.
Nigrostriatal pathway: Blockade here causes motor side effects, not endocrine dysfunction.
Mesolimbic pathway: Blockade here alleviates positive symptoms of schizophrenia but does not affect prolactin.
Mesocortical pathway: Dysfunction in this pathway is associated with negative and cognitive symptoms, not prolactin regulation.
A 40-year-old patient with a history of methamphetamine use disorder reports intense cravings when exposed to environments associated with prior drug use. Which dopamine pathway is primarily responsible for this phenomenon?
- Mesolimbic pathway
- Nigrostriatal pathway
- Mesocortical pathway
- Tuberoinfundibular pathway
Answer: Mesolimbic pathway
Rationale:
Correct: The mesolimbic pathway is central to the brain’s reward system and is hyperactivated in addiction. Environmental cues trigger dopamine release, reinforcing cravings.
Nigrostriatal pathway: This pathway governs motor function and is not involved in cravings.
Mesocortical pathway: This pathway is related to cognitive and emotional regulation, not drug-seeking behavior.
Tuberoinfundibular pathway: This pathway regulates prolactin, not reward or craving
A patient presents with anhedonia and poor motivation after prolonged treatment with an antipsychotic medication. Which dopamine pathway is most likely affected?
- Mesolimbic pathway
- Nigrostriatal pathway
- Tuberoinfundibular pathway
- Mesocortical pathway
Answer: Mesolimbic pathway
Rationale:
Correct: The mesolimbic pathway is responsible for pleasure and reward. Dopamine blockade in this pathway can lead to anhedonia and lack of motivation, which are side effects of antipsychotic treatment.
Nigrostriatal pathway: Blockade here causes motor side effects, not anhedonia.
Tuberoinfundibular pathway: Blockade affects prolactin levels but does not influence motivation or pleasure.
Mesocortical pathway: Hypoactivity in this pathway contributes to negative symptoms of schizophrenia, but it is not the direct target of most antipsychotic side effects.
A 55-year-old patient with schizophrenia treated with a high-potency antipsychotic develops severe restlessness and an inability to sit still. What is the most likely explanation for this condition?
- Hyperprolactinemia due to tuberoinfundibular pathway blockade.
- Dopamine blockade in the mesocortical pathway.
- Dopamine blockade in the nigrostriatal pathway.
- Excess dopamine in the mesolimbic pathway
Answer: Dopamine blockade in the nigrostriatal pathway
Rationale:
Correct: Restlessness and motor agitation (akathisia) are extrapyramidal side effects caused by dopamine blockade in the nigrostriatal pathway.
Hyperprolactinemia: This would cause endocrine symptoms, not motor restlessness.
Dopamine blockade in the mesocortical pathway: This contributes to cognitive and emotional symptoms but does not cause akathisia.
Excess dopamine in the mesolimbic pathway: This is associated with psychosis, not akathisia.
A patient with schizophrenia experiences resolution of hallucinations but develops severe apathy and social withdrawal on a dopamine-blocking medication. Which pathway is most likely involved in these new symptoms?
- Mesolimbic pathway
- Nigrostriatal pathway
- Mesocortical pathway
- Tuberoinfundibular pathway
Answer: Mesocortical pathway
Rationale:
Correct: Dopamine hypoactivity in the mesocortical pathway is linked to negative symptoms, such as apathy and social withdrawal. Dopamine antagonists can worsen these symptoms in some patients.
Mesolimbic pathway: Blockade here reduces positive symptoms but does not cause negative symptoms.
Nigrostriatal pathway: Blockade causes motor side effects, not apathy.
Tuberoinfundibular pathway: Blockade leads to hyperprolactinemia, not apathy or social withdrawal.
A 45-year-old male presents with memory impairment, difficulty planning tasks, and recent personality changes. He has a family history of neurodegenerative disease. MRI shows frontal and temporal lobe atrophy. Which condition is the most likely diagnosis?
- Alzheimer’s Disease
- Frontotemporal Dementia (FTD)
- Lewy Body Dementia
- Normal Pressure Hydrocephalus (NPH)
Answer: Frontotemporal Dementia (FTD)
Rationale:
Correct: FTD primarily affects the frontal and temporal lobes, leading to early personality changes, executive dysfunction, and behavioral symptoms.
Alzheimer’s Disease: Memory impairment is the hallmark symptom in early Alzheimer’s, but personality changes and frontal atrophy are less typical.
Lewy Body Dementia: Associated with visual hallucinations, fluctuating cognition, and parkinsonism, which are absent here.
Normal Pressure Hydrocephalus: The classic triad includes gait disturbance, urinary incontinence, and cognitive impairment, which are not described in this case.
A patient with a history of bipolar I disorder is prescribed lithium. During a follow-up, she reports increased tremors and difficulty concentrating. Her lab results show a lithium level of 2.0 mEq/L. What is the most appropriate next step?
- Increase hydration and recheck levels in 24 hours.
- Discontinue lithium and begin hemodialysis.
- Administer activated charcoal.
- Hold lithium and initiate supportive treatment
Answer: Hold lithium and initiate supportive treatment
Rationale:
Correct: A lithium level of 2.0 mEq/L indicates moderate toxicity. Holding the medication and providing supportive treatment, such as hydration, is the first step.
Increase hydration and recheck levels in 24 hours: Hydration is necessary, but the medication must be held immediately.
Discontinue lithium and begin hemodialysis: Hemodialysis is only indicated for severe toxicity (e.g., levels >4.0 mEq/L or life-threatening symptoms).
Administer activated charcoal: Lithium is not adsorbed by activated charcoal, so this intervention is ineffective.
Which of the following neurotransmitter abnormalities is most consistently associated with generalized anxiety disorder (GAD)?
- Increased glutamate activity.
- Reduced gamma-aminobutyric acid (GABA) levels.
- Excess serotonin activity.
- Reduced dopamine transmission
Answer: Reduced gamma-aminobutyric acid (GABA) levels
Rationale:
Correct: GAD is linked to reduced GABA activity, resulting in heightened excitability and anxiety.
Increased glutamate activity: May lead to excitotoxicity but is not specific to GAD.
Excess serotonin activity: Serotonin is implicated in anxiety but is not typically overactive in GAD.
Reduced dopamine transmission: Dopamine is less directly involved in GAD.
A 32-year-old patient reports feeling “numb and disconnected” after surviving a traumatic car accident 3 months ago. They describe intrusive flashbacks and difficulty sleeping. Which pharmacologic treatment has the strongest evidence for managing this condition?
- Benzodiazepines
- Selective serotonin reuptake inhibitors (SSRIs)
- Atypical antipsychotics
- Beta-blockers
Answer: Selective serotonin reuptake inhibitors (SSRIs)
Rationale:
Correct: SSRIs are first-line treatments for PTSD, as they effectively target core symptoms such as flashbacks and hyperarousal.
Benzodiazepines: Not recommended due to dependency risk and lack of evidence for efficacy in PTSD.
Atypical antipsychotics: Can be used adjunctively for severe symptoms but are not first-line treatments.
Beta-blockers: May reduce hyperarousal but do not address the core symptoms of PTSD.
Which of the following medications is contraindicated in a patient with a history of traumatic brain injury (TBI) and epilepsy?
- Carbamazepine
- Lamotrigine
- Valproic Acid
- Bupropion
Answer: Bupropion
Rationale:
Correct: Bupropion lowers the seizure threshold, making it contraindicated in patients with TBI or epilepsy.
Carbamazepine: An effective anticonvulsant used in epilepsy and mood stabilization.
Lamotrigine: Commonly used for epilepsy and mood stabilization, safe for TBI patients.
Valproic Acid: Safe and effective for epilepsy and mood disorders, commonly used in this population.
A patient with Parkinson’s disease presents with vivid hallucinations but no evidence of delirium. His current medications include carbidopa/levodopa and a COMT inhibitor. Which intervention is most appropriate?
- Add risperidone
- Reduce carbidopa/levodopa dose
- Initiate quetiapine
- Discontinue COMT inhibitor
Answer: Initiate quetiapine
Rationale:
Correct: Quetiapine is a second-generation antipsychotic with minimal dopaminergic blockade, making it suitable for managing hallucinations in Parkinson’s disease without worsening motor symptoms.
Risperidone: Strong dopamine blockade may exacerbate Parkinsonian motor symptoms.
Reduce carbidopa/levodopa dose: This could worsen motor symptoms, reducing the patient’s quality of life.
Discontinue COMT inhibitor: May help, but it could also compromise motor symptom control.
A 60-year-old patient presents with symptoms of depression, weight loss, and psychomotor slowing. Neurological examination reveals resting tremor, bradykinesia, and masked facies. Which is the most likely diagnosis?
- Parkinson’s Disease with Depression.
- Major Depressive Disorder.
- Dementia with Lewy Bodies.
- Multiple System Atrophy
Answer: Parkinson’s Disease with Depression
Rationale:
Correct: Depression is a common non-motor symptom of Parkinson’s disease and may precede its motor symptoms. Resting tremor, bradykinesia, and masked facies are hallmark motor symptoms of Parkinson’s.
Major Depressive Disorder: Depression does not typically present with motor symptoms like bradykinesia or masked facies.
Dementia with Lewy Bodies: Visual hallucinations and fluctuating cognition are key features, which are not present here.
Multiple System Atrophy: While it involves Parkinsonian symptoms, autonomic dysfunction is a more prominent feature, which is not described here.
A 65-year-old patient presents with progressive memory loss, disorientation, and difficulty performing daily tasks. Which neurotransmitter imbalance is most likely involved in their condition?
- Decreased dopamine
- Increased glutamate
- Decreased acetylcholine
- Decreased norepinephrine
Answer: Decreased acetylcholine
Rationale:
Correct: Alzheimer’s disease is characterized by decreased acetylcholine levels, which significantly impair memory and cognitive function.
Decreased dopamine: Primarily associated with movement disorders like Parkinson’s disease.
Increased glutamate: Linked to excitotoxicity but not specific to Alzheimer’s disease.
Decreased norepinephrine: While involved in mood regulation, it is not a hallmark neurotransmitter imbalance in Alzheimer’s.
A patient with schizophrenia is most likely to exhibit which neurotransmitter imbalance?
- Decreased serotonin and decreased norepinephrine.
- Increased dopamine and increased glutamate.
- Decreased acetylcholine and increased GABA.
- Increased norepinephrine and decreased dopamine
Answer: Increased dopamine and increased glutamate
Rationale:
Correct: Schizophrenia is strongly associated with increased dopamine activity (positive symptoms like psychosis) and glutamate dysregulation (cognitive symptoms and excitotoxicity).
Decreased serotonin and norepinephrine: Characteristic of depression, not schizophrenia.
Decreased acetylcholine and increased GABA: This combination is not typical of schizophrenia.
Increased norepinephrine and decreased dopamine: Not a relevant imbalance in schizophrenia.
Which neurotransmitter imbalance is most likely associated with the negative symptoms of schizophrenia, such as flat affect and social withdrawal?
- Decreased glutamate
- Increased norepinephrine
- Increased dopamine
- Decreased GABA
Answer: Decreased glutamate
Rationale:
Correct: Negative symptoms of schizophrenia are associated with decreased glutamate activity, especially in the cortical areas.
Increased norepinephrine: Not a known contributor to schizophrenia’s negative symptoms.
Increased dopamine: Linked to positive symptoms, not negative ones.
Decreased GABA: More related to anxiety disorders than schizophrenia.
A 40-year-old patient presents with feelings of worthlessness, difficulty concentrating, and hypersomnia for the past month. Which neurotransmitter changes are most consistent with their presentation?
- Decreased norepinephrine and serotonin.
- Increased glutamate and acetylcholine.
- Decreased dopamine and increased GABA.
- Increased serotonin and norepinephrine
Answer: Decreased norepinephrine and serotonin
Rationale:
Correct: Depression is strongly associated with decreased levels of serotonin and norepinephrine, both critical for mood and energy regulation.
Increased glutamate and acetylcholine: These changes are not characteristic of depression.
Decreased dopamine and increased GABA: Dopamine may decrease in depression, but GABA levels are not typically increased.
Increased serotonin and norepinephrine: Opposite of what occurs in depression.