Neuro UWorld Flashcards

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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)

A

Cleft 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
Q

Rb tumor suppressor gene function?

A

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
Q

Characteristic abnormality seen in patients with Huntington disease?

A

Bilateral atrophy of caudate nucleus and putamen (striatum)

27
Q

Most characteristic biochemical feature in patients with Huntington disease?

A

Caudate atrophy –> Loss of GABA-containing neurons

28
Q

Neurotransmitter thought to participate in formation of new memories?

A

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
Q

Involuntary perioral movements such as biting, chewing, grimacing, and tongue protrusions

A

Tardive dyskinesia

30
Q

Atypical antipsychotic least likely to cause tardive dyskinesia?

A

Clozapine

31
Q

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?

A

Clozapine is a/w agranulocytosis

32
Q

Subjective feeling of restlessness that compels patient to constantly move around?

A

Akathisia

33
Q

Triad of Wernicke syndrome?

A

Oculomotor dysfunction, ataxia, and confusion

34
Q

Oculomotor dysfunction in Wernicke syndrome is 2/2 damage involving what 3 structures?

A

CN III, CN VI, and vestibular nuclei

35
Q

Ataxia in Wernicke syndrome is 2/2 damage involving what 2 structures?

A

Cerebellar cortex and vestibular nuclei

36
Q

Triad of Korsakoff syndrome?

A

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
Q

Korsakoff syndrome is a/w damage to what 2 structures?

A

Anterior and dorsomedial thalamic nuclei

38
Q

S/p administering thiamine to patient with Wernicke syndrome, what symptom is most likely to persist permanently?

A

Memory impairment is permanent

39
Q

Werknicke-Korsakoff is a/w lesions that commonly involve what brain structure?

A

Mammillary bodies

40
Q

Most common clinical manifestation of primary HSV-1 infection in child aged 1-3 years?

A

Acute gingivostomatitis –> Swollen gums with ulcerative lesions. Oral lesion scrapings demonstrate cells with intranuclear inclusions.