Neuro UWorld Flashcards

(40 cards)

1
Q

Kinesin?

A

Microtubule-associated, ATP-powered motor protein that facilitates anterograde transport of intracellular vesicles and organelles toward plus (rapidly growing) ends of microtubulesNeurons: Kinesin transports neurotransmitter-containing secretory vesicles away from cell body, down axons, toward synaptic nerve terminals

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2
Q

Nissl substance = ?

A

rER in neurons

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3
Q

Postulated mechanism for acute opioid tolerance?

A

Phosphorylation of opioid receptors by protein kinase

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4
Q

Postulated mechanism(s) for chronic opioid tolerance?

A

Increased adenylyl cyclase activity or increased nitric oxide (NO) levels

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5
Q

Neurotransmitter shown to interact with opioid pathways to modulate morphine tolerance?

A

Glutamate

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6
Q

Mechanism by which ketamine blocks tolerance development to morphine?

A

Glutamate is an excitatory neurotransmitter that binds and activates NMDA receptorsNMDA receptor activation –> Increased phosphorylation of opioid receptors and increased NO levels –> opioid toleranceKetamine = NMDA receptor antagonist –> Blocks action of glutamate on NMDA receptor and effectively blocks morphine tolerance

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7
Q

Glycine function re: glutamate and NMDA receptors?

A

Glycine is a co-agonist for glutamate and is required for binding of glutamate to NMDA receptorsBinding of both glycine and glutamate is necessary for NMDA receptor activation

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8
Q

Progressively weakening diaphragmatic contractions during maximal voluntary ventilation with intact phrenic nerve stimulation indicates what 2 possible disturbances?

A

Neuromuscular junction pathology –> Myasthenia gravisAbnormally rapid diaphragmatic muscle fatigue –> Restrictive lung disease, chest wall disease

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9
Q

Cellular receptor for cytomegalovirus (CMV)?

A

Cellular integrins

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10
Q

Cellular receptor for Epstein-Barr virus (EBV)?

A

CD21

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11
Q

Cellular receptor for HIV?

A

CD4 and CXCR4/CCR5

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12
Q

Cellular receptor for rabies virus?

A

Nicotinic ACh receptor

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13
Q

Cellular receptor for rhinovirus?

A

ICAM-1 = CD54

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14
Q

Agitation, disorientation, pharyngospasn, and photophobia leading to coma and death?

A

Rabies encephalitisPharyngeal muscle spasm cause dysphagia, which can lead to avoidance of food and water (hydrophobia)

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15
Q

Rabies virus is a single-stranded RNA virus enveloped by a capsule with what unique shape?

A

Bullet-shaped capsule, which is studded by glycoprotein spikes that bind to nicotinic AChRs

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16
Q

Mechanism by which rabies virus travels to CNS?

A

Bind AChRs on peripheral nerve axons and travel via retrograde transport to CNS

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17
Q

Post-exposure prophylaxis for rabies virus is no longer effective when?

A

Symptoms of rabies encephalitis appear

18
Q

Improper fusion of maxillary prominence with medial nasal prominence?

A

Cleft lip1) Fusion of 2 medial nasal prominences to form midline intermaxillary segment2) Left and right maxillary prominences fuse with midline intermaxillary segment to form upper lip

19
Q

Improper fusion of palatine shelves, or improper fusion of palatine shelf with intermaxillary segment (primary palate)

20
Q

Intracranial calcified cystic mass filled with thick brownish fluid that is rich in cholesterol?

A

Craniopharyngioma

21
Q

White pupillary reflex is indicative of?

A

Retinoblastoma

22
Q

Sporadic retinoblastoma:Associated malignancy?Unilateral/bilateral?

A

Associated malignancy –> None! Children with sporadic retinoblastoma are not at risk for other malignancies Sporadic retinoblastoma is usually unilateral

23
Q

Familial retinoblastoma:Associated malignancy?Unilateral/bilateral?

A

Associated malignancy –> OsteosarcomaFamilial retinoblastoma is usually bilateral

24
Q

Familial retinoblastoma: Gene?Chromosome?

A

Gene –> Rb tumor suppressor geneChromosome 13

25
Rb tumor suppressor gene function?
Rb protein --> Active and inactive statesActive (dephosphorylated) Rb protein does not allow cell to proceed from G1 to S stage of cell cycle When cell is stimulated by a growth factor, Rb protein is converted to inactive state (phosphorylated), which permits cell divisionCells with 2 inactive Rb genes divide uncontrollably and give rise to malignancy
26
Characteristic abnormality seen in patients with Huntington disease?
Bilateral atrophy of caudate nucleus and putamen (striatum)
27
Most characteristic biochemical feature in patients with Huntington disease?
Caudate atrophy --> Loss of GABA-containing neurons
28
Neurotransmitter thought to participate in formation of new memories?
Nitric oxide NO is a unique neurotransmitter in that it freely diffuses across cell membranes and does not need to interact with other neurons via a synapse
29
Involuntary perioral movements such as biting, chewing, grimacing, and tongue protrusions
Tardive dyskinesia
30
Atypical antipsychotic least likely to cause tardive dyskinesia?
Clozapine
31
Tardive dyskinesia is best managed by decreasing dose of offending antipsychotic OR discontinuing offending antipsychotic and replacing with clozapine. Why is clozapine a medication of last resort?
Clozapine is a/w agranulocytosis
32
Subjective feeling of restlessness that compels patient to constantly move around?
Akathisia
33
Triad of Wernicke syndrome?
Oculomotor dysfunction, ataxia, and confusion
34
Oculomotor dysfunction in Wernicke syndrome is 2/2 damage involving what 3 structures?
CN III, CN VI, and vestibular nuclei
35
Ataxia in Wernicke syndrome is 2/2 damage involving what 2 structures?
Cerebellar cortex and vestibular nuclei
36
Triad of Korsakoff syndrome?
Memory loss, confabulation, anterograde amnesia Confabulation = When unsure of a fact, patient fills in memory gap with fabricated story he/she believes to be trueAnterograde amnesia = Inability to form new memories Korsakoff syndrome = Complication of Wernicke syndrome
37
Korsakoff syndrome is a/w damage to what 2 structures?
Anterior and dorsomedial thalamic nuclei
38
S/p administering thiamine to patient with Wernicke syndrome, what symptom is most likely to persist permanently?
Memory impairment is permanent
39
Werknicke-Korsakoff is a/w lesions that commonly involve what brain structure?
Mammillary bodies
40
Most common clinical manifestation of primary HSV-1 infection in child aged 1-3 years?
Acute gingivostomatitis --> Swollen gums with ulcerative lesions. Oral lesion scrapings demonstrate cells with intranuclear inclusions.