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Psych > Sedation, Epilepsy, Memory (oh my) > Flashcards

Sedation, Epilepsy, Memory (oh my) Flashcards

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1
Q

In classical conditioning, what is a conditioned stimulus?

A

a stimulus that used to be neutral that now provokes a conditioned response after being linked to an unconditioned stimulus

ex. a whistle that is consistently blown while giving a dog food will eventually make the dog drool on its own even without food present

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2
Q

What drug binds at omega receptors on GABA?

A

benzodiazepines (between gamma and alpha subunits)

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3
Q

What benzodiazepine is used for refractory status epilepticus?

A

midazolam (IV infusion)

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4
Q

What are some connections to the limbic system?

A

limbic lobe, olfactory system, amygdaloid connections

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5
Q

What is eszopiclone used for?

A

sleep maintenance insomnia

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6
Q

What seizure disorder can phenobarbital be used for?

A

refractory status epilepticus (IV infusion)

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7
Q

What is the pathway of the paralimbic cortex?

A

cingulate gyrus –> paraolfactory gyrus –> orbitofrontal cortex –> insula –> uncus –> parahippocampal gyrus –> cingulate gyrus

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8
Q

What is a “hypnotic” agent?

A

an agent that causes drowsiness and sleep

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9
Q

What is the main difference between mild and major neurocognitive disorder?

A

modest impairment (not significant)

does not interfere with daily life

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10
Q

What are the downsides of phenytoin?

A

non-linear pharmacokinetics with high protein binding (hard to predict doses)

side effects: sedation, imbalance, diplopia, dizziness, gum hyperplasia, hirsuitism

more serious effects: hepatotoxicity, bone marrow suppression, rash

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11
Q

Which anti-convulsants can also be used for neuropathic pain?

A

gabapentin, carbamazepine, pregabalin

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12
Q

What is the concept of “extinction” in memory?

A

loss of responses to stimuli over time (ex. loss of stimuli conditioning)

failure of extinction may cause PTSD

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13
Q

What is dementia?

A

a generic term for a progressive decline of mental status to the point of interference with daily activities

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14
Q

What are the clinical features of mesial temporal lobe epilepsy?

A

seizures begin in childhood/adolescence

often a predisposing “hit” in the medical history (ex. trauma, infection)

often starts with generalized tonic-clonic seizures followed by typical focal seizures

associated with characteristic auras

usually requires surgery

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15
Q

What is a myoclonus?

A

brief, lightening-like single jerk of a muscle or muscle group

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16
Q

What is the difference between childhood absence epilepsy and juvenile absence epilepsy?

A

juvenile has a later onset (around puberty) and does not always go away (unlike the childhood form)

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17
Q

What is the definition of epilepsy?

A

A set of disease states characterized by a predisposition to unprevoked seizures

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18
Q

What is the metabolism of suvorexant?

A

CYP3A4 followed by glucuronidation

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19
Q

What is the mechanism of valproate?

A

acts on T-type Ca2+ channels and may also act on Na+ channels and increase GABA levels

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20
Q

Which anti-convulsants can also be used for migraines?

A

valproate, topiramate, zonisamide

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21
Q

What is positive reinforcement?

A

providing a reward to increase behavior

ex. pushing a lever to get a treat

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22
Q

In classical conditioning, what is a conditioned response?

A

a response to a conditioned stimulus

ex. salivation by a dog in response to a whistle that has been linked to presentation of food

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23
Q

When is epilepsy onset most common?

A

in childhood or in old age (bimodal peaks)

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24
Q

What are the appropriate pharmacological treatments for alcohol withdrawal?

A

benzodiazepines (diazepam, lorazepam,and oxazepam)

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25
Q

What is zonisamide?

A

a drug that acts on Na+ channels, Ca2+ channels, and carbonic anhydrase inhibition

used for all seizure types

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26
Q

What symptoms are associated with Wernicke-Korsakoff syndrome?

A

Wernicke symptoms: ataxia, eye movement abnormalities, confusional states

Korsakoff symptoms: longer term; anterograde and retrograde amnesia; poor judgment, initiative, impulse control, and sequencing tasks

can cause “spurious answers” to questions

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27
Q

What is C?

A

orbital frontal gyri + insula (not visible)

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28
Q

What are the side effects of topiramate?

A

kidney stones (most common)

paresthesias, sedation, cognitive impairment

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29
Q

What is the metabolism of the long acting ___azepams?

A

phase 1 metabolism by CYP2C19 and CYP3A4 to active intermediates that are hydroxylated (LOTs) and then glucuronidated

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30
Q

What are the side effects of valproate?

A

GI upset, sedation, cognitive impairment

hepatic failure, thrombocytopenia, and pancreatitis

highly teratogenic

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31
Q

What is a “sedative”?

A

a drug that reduces the excitatory responsiveness to external stimuli and produces a calming effect

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32
Q

What is a forgetting curve?

A

A curve that represents the fact that information loss is time dependent

loss decreased by sleep and reviewing

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33
Q

Which type of dementia is associated with inability to look down voluntarily?

A

progressive supranuclear palsy

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34
Q

What is the difference in dose of drug vs. biological effect for benzodiazepines compared to barbituates or propofol?

A

benzodiazepines general saturate at low anaesthetic levels (they function by increasing opening rate of chloride channels, which is self-limiting)

barbituates and propofol continue sedating to the point of coma or death at high doses (they function by increasing the opening duration of chloride channels, which is not self-limiting)

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35
Q

Which benzodiazepines are used for sedation and anaesthesia during medical procedures?

A

midazolam, diazepam

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36
Q

Which type of epilepsy is associated with generalized tonic-clonic seizures that only occur at night and resolve after puberty?

A

benign rolandic epilepsy

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37
Q

What is tigabine? What is it used for?

A

selective GABA reuptake inhibitor

used for partial seizures (but not often)

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38
Q

What are the main functions of the limbic system? What structures are associated with each function?

A

HOME

Homeostatic functions (including autonomic and neuroendocrine control) - hypothalamus

Olfaction - olfactory cortex

Memory - hippocampal formation

Emotions and drives - amygdala

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39
Q

What is the clinical presentation of frontal lobe epilepsy?

A

seizures most often at night

usually not associated with arua or post-ictal confusion

involves bizarre and complex automatisms

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40
Q

What are the steps of the papez circuit?

A

parahippocampal gyrus (entorhinal cortex) –> hippocampus (subiculum) –> fornix mamillary bodies –> anterior thalamic nuclei –> cingulate gyrus –> back to the parahippocampal gyrus

info from the cortex enters this circuit through the perforate pathway and parahippocampal gyrus

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41
Q

What is the cause of absence seizures?

A

abnormal cortico-thalamic interactions with the reticular nucleus of the thalamus acting as the pacemaker for cortical neurons and thalamic relay neurons

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42
Q

What are the spatial patterns of memory consolidation?

A

starts in the hippocampus, spreads out and gets incorporated into the cortex

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43
Q

When is a seizure automatically a medical emergency?

A

when it lasts a long time and becomes status epilepticus

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44
Q

What is levetiracetam?

A

unknown mechanism anti-convulsant

minimalside effect profile, minimal drug interactions

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45
Q

What is the clinical presentation and gross pathology of progressive non-fluent aphasia?

A

clinical presentation: deficits in expressive language, agrammatisms, apraxia of speech

gross pathology: atrophy of interior frontal and insular cortex, associated with both FTD-tau and FTD-TDP

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46
Q

What is A?

A

cingulate gyrus

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47
Q

What is working memory?

A

memory that involves retention of information for brief periods of time that is limited in time and capacity

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48
Q

What condition is associated with temporal lobe epilepsy?

A

mesial temporal sclerosis

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49
Q

What non-benzodiazepine and non-ZAZOLES agents are used to treat insomnia?

A

barbituates, scopolamine (antimuscarinics), diphenhydramine (antihistamines), ethanol

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50
Q

What is the function of the dentate gyrus?

A

thin cortex that acts as the input station for hippocampal information (from the cortex)

cortex –> entorhinal cortex –> dentate gyrus (via perforant pathways) –> hippocampus

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51
Q

What are the two general pathways from the cortex to the hippocampus?

A

alvear pathway (via alveus) and perforant pathway (via dentate)

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52
Q

What are the treatments for frontotemporal lobar degeneration?

A

SSRIs, non-pharmacological interventions (reward based therapy, speech therapy, PT)

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53
Q

What is E?

A

parahippocampal gyrus

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54
Q

What is the treatment for mesial temporal lobe epilepsy?

A

usually requires surgery (anteromesial temporal lobectomy)

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55
Q

What is the utility of topiramate?

A

all seizure types (except absence seizures)

migraines, pain, and essential tremor

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56
Q

What benzodiazepines are used to treat muscle spasms?

A

diazepam and clonazepam

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57
Q

What is the clinical presentation and gross pathology of semantic dementia?

A

clinical presentation: lack of understanding or knowledge of words, objects, faces, and other items; can also have verbal deficits or trouble recognizing faces and behavioral changes

gross pathology: bilateral, frequently asymmetric atrophy of the temporal neocortex, associated with FTD-TDP

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58
Q

What sleep pattern changes are associated with insomnia?

A

longer latency period before sleep, multiple awakenings throughout the night, decreased total sleep tie, reduced slow wave sleep

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59
Q

What are the main side effects of vigabatrin?

A

visual field loss (but maybe not as bad as reported)

headaches, dizziness, depression, etc.

can also cause psychosis or other psychiatric disorders

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60
Q

What benzodiazepines are used for acute seizures?

A

lorazepam, diazepam

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61
Q

What is the clinical presentation of corticobasal syndrome?

A

clinical presentation: asymmetric motor signs and cortical signs

usually associated with FTD-Tau and with FTD-TDP

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62
Q

What are the components of the hippocampal formation?

A

dentate gyrus, hippocampus, subiculum

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63
Q

What is the effect of MT2 agonists?

A

used to treat non-24 hour sleep-wake disorder in patients that are blind

ex. tasimelteon

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64
Q

What is F?

A

fornix

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65
Q

Which anti-convulsants can also be used for bipolar disorder?

A

lamotrogine, valproate

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66
Q

What is the structure of the hippocampus?

A

A structure along the floor of the inferior horn of the lateral ventricle - becomes continuous with the fornix below the splenium of the corpus callosum

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67
Q

What are the side effects of lamotrigine?

A

headache, insomnia, and rash (stevens-johnson syndrome)

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68
Q

What is the effect of GABA antagonists? What are examples of competitive, non-competitive, and uncompetitive inhibitors of GABA-A?

A

they are convulsants

competitive: bicuculline (binds at GABA site)

non-competitive: picrotoxin (binds at the channel region of all subunits)

uncompetitive: penicillin (blocks open channel)

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69
Q

How are ZAZOLES metabolized?

A

With CYP3A4

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70
Q

What are the core features of lewy body disease?

A

1) fluctuations in attention and alertness
2) motor changes of Parkinsonism
3) recurrent visual hallucinations
* must have at least 2/3*

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71
Q

What types of seizures is carbamazepine used for?

A

partial and generalized tonic-clonic seizures

can make absence, atonic, and myoclonic seizures worse

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72
Q

What is the effect of HSV1 on the limbic cortex?

A

HSV1 has a tropism for the limbic cortex and can cause encephalitis of the limbic areas

leads to profound anterograde amnesia

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73
Q

What is the main indication for clobazam?

A

to treat drop attacks in children

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74
Q

Which type of dementia is associated with asymmetric vision, balance, speech, and swallowing problems?

A

corticobasal degeneration

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75
Q

What are the side effects of barbituates?

A

sedation, respiratory depression, cognitive impairment, hepatotoxicity, allergic rashes

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76
Q

What is the mechanism of eslicarbazepine?

A

potent inhibition of sodium channel activity

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77
Q

What is zaleplon used for?

A

good for sleep onset insomnia

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78
Q

What anti-convulsants are selective CYP3A inducers?

A

felbamate, topiramate, oxcarbazepine

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79
Q

What is the metabolism of ___azolam drugs?

A

metabolized by CYP3A4 before glucuronidation

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80
Q

What are the clinical features of lennox-gastaut syndrome?

A

mental retardation (usually severe)

multiple seizure types (GTC, myoclonic, atypical absence, atonic, focal)

seizures are not controllable

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81
Q

What is the effect of MT1 agonists?

A

reduce sleep latency (but do not alter the number of times waking up) in patients with insomnia

ex. ramelteon

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82
Q

What is positive punishment?

A

utilizing an aversive stimulus to decrease behavior

ex. shock delivered every time lever is pressed

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83
Q

What types of auras are associated with mesial temporal lobe epilepsy?

A

aura caused by limbic system malfunction

rising epigastric sensation (insular cortex)

deja vu (temporal neocortex)

olfactory hallucination (uncus)

sudden emotion (amygdala)

perceptual distortions (temporo-parieto-occipital association areas)

autonomic symptoms (insular cortex)

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84
Q

Where is the insula/insular cortex?

A

underneath the frontal lobe laterally

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85
Q

Where do benzodiazepines bind on the GABA-A receptor?

A

at the junction of the alpha and gamma subunits

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86
Q

What is the general mechanism of benzodiazepines?

A

allosteric modulation of the GABA-A receptor, which leads to increased fequency of Cl- channel opening and membrane hyperpolarization

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87
Q

What is zolpidem used for?

A

normalizes sleep without producing drowsiness

used for sleep onset insomnia and in patients who awaken frequently during the night

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88
Q

What structures are linked to explicit/episodic memories?

A

hippocampus and limbic system

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89
Q

What are the clinical features of neocortical epilepsy?

A

seizures that have a focal onset anywhere in the cortex (except mesial temporal lobe)

can have auras or can spread quickly and become generalized tonic-clonic seizures

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90
Q

What conditions can make benzodiazepines dangerous?

A

if patients have obstructive sleep apnea or COPD

when used in combination with opioids or ethanol

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91
Q

What are the criteria of major neurocognitive disorder?

A

1) evidence of significant cognitive decline
2) cognitive deficits interfere with daily activities
3) cognitive deficits do not occur specifically within the context of delirium
4) cognitive deficits are not better explained by another mental disorder

92
Q

Which seizure syndrome is associated with mental retardation and uncontrollable seizures?

A

lennox-gastaut syndrome

93
Q

What are the downsides of gabapentin?

A

only mildly effective for partial seizures

limited absorption (GI)

mild sedation, weight gain side effects

renal-only elimination

94
Q

What is the difference between the neocortex, mesocortex, and archicortex?

A

archicortex = oldest cortex; 3 layers; hippocampus and dentate gyrus

mesocortex = 3-5 layers; parahippocampal gyrus, cingulate gyrus, subcallosal gyrus

neocortex = newest cortex; 5+ layers; primary motor cortex, primary sensory cortex, association cortex

95
Q

What is the cause of juvenile myoclinc epilepsy and childhood absence epilepsy?

A

genetic - mutations found in GABA receptor, chloride channel, and calcium channel

96
Q

What is 1?

A

uncus

97
Q

What networks are responsible for encoding memories?

A

frontal networks

98
Q

What is C?

A

mammillary body

99
Q

What are the clinical uses of benzodiazepines?

A

to treat anxiety and insomnia, to produce sedation and amnesia for medical procedures, as anticonvulsants, and to treat muscle spasms and ethanol withdrawal

100
Q

What are the clinical features of juvenile myoclonic epilepsy?

A

onset age 12-18

always occur upon awakening in AM

myoclonic seizures can culminate in a generalized tonic-clonic seizure

probably lifelong, but responds well to appropriate meds

101
Q

What is A?

A

anterior thalamic nucleus

102
Q

Which benzodiazepines are best to use in elderly patients and why?

A

lorazepam, oxazepam, temazepam

all three are intermediate-acting benzodiazepines that do not require CYPs for inactivation and do not have active intermediates

older patients have reduced CYP function with age

103
Q

What are the consequences of chronic epilepsy?

A

self-injury

memory impairment

more seizures

psychiatric conditions

psychosocial maladjustment

discrimination

(rarely) sudden death

104
Q

What side effects are associated with tigabine?

A

sedation, cognitive impairment, depression

105
Q

Where is the entorhinal cortex?

A

anterior portion of parahippocampal cortex

106
Q

In classical conditioning, what is an unconditioned response?

A

a reflexive response to an unconditioned stimulus

ex. when a dog drools after being presented with food

107
Q

What are the components of neurofibrillary tangles?

A

hyperphosphorylated form of the tau protein

108
Q

Where specifically do mesial temporal lobe epilepsy seizures originate?

A

hippocampus and/or amygdala

109
Q

What is the general anatomical cause of dementia?

A

progressive disruption or damage to various brain circuits

110
Q

What is the difference between seizures and epilepsy?

A

seizures are a symptom (can be caused by epilepsy or another trigger)

epilepsy is a disorder that involves seizures

111
Q

What is the post-ictal period?

A

a period of confusion or lethargy that can follow seizures

112
Q

What gross pathology and brain scan changes are associated with behavioral variant frontotemporal dementia?

A

relatively symmetric bilateral atrophy of the frontal and temporal lobes

113
Q

What are the side effects of ZAZOLES?

A

sleep-related eating, driving, and amnesia

114
Q

Which anti-convulsant is associated with Steven-Johnson Syndrome?

A

lamotrigine

115
Q

What is the most common target for depressant drugs?

A

GABA-A receptor

116
Q

What is a generalized tonic-clonic seizure?

A

also called a grand mal seizure

characterized by initial stiffening followed by back-and-forth shaking

can also be just tonic (stiffening) or just clonic (shaking)

117
Q

What was learned from the case of H.M.?

A

formation of new memories involves structures in the mesial temporal lobes

118
Q

What are some structural and metabolic causes of epilepsy?

A

hippocampal sclerosis

neoplasms

vascular malformations

cortical malformations

traumatic brain injury

ischemic stroke/hemorrhage

anoxic injury

tuberous sclerosis

cysticercosis

119
Q

What is status epilepticus?

A

a state of continual seizure activity

120
Q

What is the function of the papez circuit?

A

ties the cerebral cortex to the hypothalamus, provides an anatomic substrate for the convergence of cognitive activities, emotional experiences, expressions

121
Q

What is the mechanism of carbamazepine and oxcarbazepine?

A

it blocks voltage-sensitive Na+ channels (like phenytoin)

122
Q

What aspects of insomnia are remedied by benzodiazepines?

A

shorter latency, increased overall sleep duration (via increased duration of stage 1 and 2 sleep)

does NOT improve deep sleep (slow wave and REM) - makes it worse

123
Q

What are three important examples of drugs that may exacerbate epileptic seizures?

A

tramadol, venflaxine (antidepression), and bupropion

124
Q

What is the main pathway of the arousal circuitry?

A

light –> retina –> suprachiasmatic nucleus –> subparaventricular zone –> dorsomedial hypothalamic nucleus –> inhibition of the VLPO (sleep switch) and stimulation of orexin neurons (leads to release of arousal amines)

125
Q

What is an example of a benzodiazepine antagonist?

A

flumazenil

126
Q

What benzodiazepines are used to treat anxiety or aggression?

A

diazepam (and most of the ___azepams)

targets the limbic system

127
Q

What networks are responsible for retention of memories?

A

limbic memory networks

128
Q

What are the treatments for Alzheimer’s disease?

A

cholinesterase inhibitors (increases cerebral acetylcholine levels) and memantine (blocks overexcited NMDA glutamate receptors)

129
Q

What is the function of the “ZAZOLES” drugs? Where do they bind?

A

a group of drugs that produce hypnosis (and normalize sleep architecture) but not anxiolytic effects or muscle relaxation

they bind at the junction of alpha1 and gamma subunits on the GABA-A receptor

130
Q

What is the clinical presentation of behavioral variant frontotemporal dementia?

A

presents with significant changes in personality and behavior including deficits in attention, loss of personal and social awareness, disinhibition, hyperorality, stereotyped/compulsive behaviors, apathy, and abulia

131
Q

What are the steps of the perforant pathway?

A

information goes from the cortex to the dentate –> mossy fibers goto the CA3 area of the hippocampus –> fibers bend above the thalamus and project to the fornix –> axons of the fornix terminate in the mammillary body of the hypothalamus or the septal area and and anterior thalamus

132
Q

What structures are linked to working memory?

A

front-parietal cortices

133
Q

What are the benefits and downsides of variable schedule reinforcement?

A

more reliable response rates and resistant to extinction

slower time to conditioning

134
Q

A 32-year-old female is diagnosed with panic disorder and agoraphobia. A drug is prescribed that acts as an agonist at both omega1 and omega2 benzodiazepine binding sites on GABA-A receptors possessing both alpha1 and alpha2 subunits. Which one of the following agents was prescribed?

a) flumazenil
b) alprazolam
c) zolpidem
d) zaleplon
e) ramelteon

A

b) alprazolam

135
Q

What networks are responsible for retrieval of memories?

A

frontal networks

136
Q

What is D?

A

uncus

137
Q

What imaging findings are associated with Wernicke-Korsakoff syndrome?

A

markedly increased signal intensity in the periaqueductal gray matter, mammillary bodies, and dorsomedial thalami

138
Q

Which type of dementia is associated with muscle weakness, shrinkage, and jerking?

A

FTD-MND

139
Q

How are all benzodiazepines inactivated?

A

glucuronidation

140
Q

What is negative punishment?

A

removal of a positive stimulus to decrease a behavior

ex. pushing a lever means food is not dispensed

141
Q

What is Todd’s paresis/paralysis?

A

a focal weakness in part of the body after a seizure

142
Q

What are the three categories of focal seizures?

A
  • focal seizure without impairment of consciousness/awareness
  • focal seizure with impairment of consciousness/awareness
  • focal seizure evolving into a bilateral, convulsive seizure
143
Q

What are the unwanted pharmacological effects of benzodiazepines?

A

anterograde amnesia, breakthrough panic attacks, tolerance (after months), withdrawal symptoms

144
Q

What is the effect of penicillin on GABA?

A

at high doses (or in people with reduced renal function), it acts as an uncompetive inhibitor of the GABA-A receptor (only works when it is opened by GABA)

145
Q

What is the clinical presentation of childhood absence epilepsy?

A

onset between ages 4-8

may be provoked by hyperventilation and occur dozens of times per day

normal intellectual function

responds easily to medicines

resolves by puberty

can rarely also have some generalized tonic-clonic seizures

146
Q

What is 2?

A

amygdala

147
Q

Where does GABA bind on the GABA-A receptor?

A

binds at the junction of the alpha and beta subunits

148
Q

What is G?

A

cingulate gyrus

149
Q

Which type of GABA receptor targeting sedative require GABA to be present at all doses?

A

benzodiazepines

150
Q

What are the routine tests for determining diagnosis and treatability of dementia?

A

history and physical exam (with mental status exam)

brain imaging

laborator tests (including TSH, vitamin B12, electrolytes, and CBC)

neuropsychological testing

151
Q

What is the proposed mechanism of gabapentin?

A

increases GABA concentration at the synapse, possibly byreversing the direction of the GABA pump on neurons

152
Q

What sectors of the hippocampal formation are most susceptible to ischemia?

A

Sommer sector (CA1 and 2)

153
Q

What is variable interval reinforcement?

A

unpredictable reinforcement schedule based on an average time-period

154
Q

What two diseases are associated with damage to the papez circuit generally?

A

Alzheimer’s disease

transient global amnesia

155
Q

What are the five major neurocognitive networks?

A

spatial attention (right)

face and object recognition (bilateral)

working memory/executive/comportment (bilateral)

memory/emotion (bilateral)

language (left)

156
Q

Which benzodiazepines are used as anticonvulsants?

A

diazepam, lorazepam, or clonazepam

157
Q

What is the mechanism of topiramate?

A

1) phenytoin-like effects on Na+ channels
2) inhibitionof voltage-sensitive Ca2+ channels
3) benzodiazepine-like effects on GABA-induced Cl- currents
4) inhibition of AMPA/kainate type glutamate receptors
5) inhibition of carbonic anhydrase

158
Q

What is autoimmune limbic encephalitis?

A

inflammatory process that is localized to structures of the limbic system

produces cognitive impairment along with disordered perception, mood changes, and sleep disturbances (HOME-related symptoms)

seizures

may be paraneoplastic

159
Q

What benzodiazepines are used for treating ethanol withdrawal?

A

lorazepam and oxazepam - will not accumulate in patients with liver dizease or the elderly

160
Q

What is B?

A

paraolfactory gyrus (paraterminal gyrus on top of subcallosal gyrus)

161
Q

What are the benefits and downsides of fixed schedule reinforcement?

A

faster response rate/conditioning

variable response rates (may decrease immediately after getting reinforcement)

162
Q

What are the side effects of benzodiazepines?

A

sedation and respiratory depression (especially if combined with other sedatives/depressants)

163
Q

What is D?

A

entorhinal cortex

164
Q

What are automatisms? What type of epilepsy are they most associated with?

A

repetitive quasi-purposeful movements (ex. lip-smacking, swallowing, fumbling, etc)

associated with mesial temporal lobe epilepsy

165
Q

What are risk factors for vascular dementia?

A

age

also: hypertension, cigarette smoking, MI, AFib, diabetes mellitus, hypercholesterolemia, hyperhomocysteinemia

166
Q

What are the adverse effects of ramelteon?

A

metabolized by CYP1A2 (can have adverse effects if people have altered CYP1A2 function)

dizziness, fatigue, endocrine disorders

167
Q

A 28-year-old actor was found unconscious in his hotel room from a multiple drug overdose. The drugs included alprazolam, diazepam, and temazepam, two opioids, and a sedative antihistamine. With respect to the benzodiazepines, which one of the following is a long-acting active metabolite that is the most likely to have contributed to prolonged respiratory depression seen with this multiple drug overdose?

a) the glucuronide derivative of temazepam
b) the hydroxylated derivative of alprazolam
c) the product of oxidative dealkylation of diazepam (nordazepam)
d) the glucuronide derivative of oxazepam

A

c) the product of oxidative dealkylation of diazepam (nordazepam)

168
Q

What is the difference between unimodal and multimodal association areas?

A

unimodal = processing of one type of information

multimodal = integration of multiple types of information

169
Q

In classical conditioning, what is a neutral stimulus?

A

a stimulus that does not evoke any response

ex. blowing a whistle at a dog (no food present)

170
Q

What is seizure semiology?

A

signs and symptoms of epileptic seizrues

171
Q

What are the indications for gabapentin?

A

partial seizures (mildly effective)

neuropathic pain (more common use)

172
Q

What anti-convulsants are hepatic enzyme inhibitors?

A

valproate (UDP glucuronosyltransferase, CYP2C19)

topiramate and oxcarbazepine (CYP2C19)

felbamate (CYP2C19)

173
Q

What is the difference between MT1 and MT2 receptors?

A

MT1 receptors - mediate sleepiness

MT2 receptors - alter phase shift of the circadian rhythm

174
Q

What is E?

A

subiculum

175
Q

What limbic system changes are associated with Alzheimer’s disease?

A

degeneration of parts of the papez circuit

176
Q

What is the mechanism of ethosuximide? What is it used for?

A

blocks T-type Ca2+ channels in a voltage-dependent manner

used to treat absence seizures

177
Q

What structures are linked to implicit/priming/procedural memory?

A

basal ganglia and cerebellum

178
Q

Which epilepsy syndromes are associated with generalized 3Hz spike and wave patterns on EEG?

A

absence epilepsy (childhood or juvenile)

179
Q

What are the four categories of seizure semiology?

A

subjective sensory or autonomic symptoms (aura)

objective motor symptoms

autonomic effects

cognitive effects

180
Q

What is the difference betweencarbamazepine and oxcarbazepine?

A

oxcarbazepine is better tolerated, does not induce hepatic enzymes as much, and does not cause hepatic toxicity

181
Q

How is vascular dementia diagnosed?

A

must have the clinical presence of dementia and a temporal relationship between the occurence of stroke and dementia

182
Q

What is fixed interval reinforcement?

A

reinforcement delivered after a set time-period

ex. a paycheck delivered every 2 weeks

183
Q

What is B?

A

mammillothalamic tract

184
Q

What is the definition of an epileptic seizure?

A

clinical manifestation of epilepsy that is presumed to result from abnormal or excessive discharge of a set of neurons in the brain

it is characterized by a sudden, rhythmic change in cortical electrical activity and is accompanied by a change in behavior (either outwardly or subjectively)

185
Q

What is negative reinforcement?

A

remove an averse stimulus to increase a behavior

ex. pushing a lever makes the shock generator stop shocking you

186
Q

What are the intermediate acting benzodiazepines?

A

LOT

Lorazepam

Oxazepam

Temazepam

187
Q

What is the clinical presentation of progressive supranuclear palsy?

A

starts with falls, changes in executive functions and subtle changes in personality

also can be associated with progressive oculomotr dysfunction

associated with FTD-Tau

188
Q

What types of memory are limbic-dependent vs. limbic-independent?

A

limbic-dependent: explicit memory (episodic or semantic)

limbic-independent: previously consolidated explicit memories, implicit memory (priming, skills/habits, conditioning)

189
Q

What is the clinical presentation and gross pathology associated with logopenic progressive aphasia?

A

clinical presentation: slow speech, anomia, impaired repetition

gross pathology: atrophy of the left posterior temporal cortex and inferior parietal lobule, associated with FTD-TDP and AD

190
Q

What aspects of insomnia are remedied by ZAZOLES?

A

they restore normal sleep patterns (decreased latency and awakenings, increased duration, and improved deep sleep)

191
Q

What is the function of the GABA-A receptor?

A

it is a chloride ion channel that, when activated, causes membrane hyperpolarization and impairs membrane excitation

192
Q

What is the characteristic EEG pattern associated with childhood absence epilepsy?

A

generalized (all leads) 3Hz spike and wave pattern

193
Q

Where are the most likely locations of neocortical epilepsy?

A

temporal neocortex and frontal lobe

parietal and occipital lobe less common

194
Q

What is the mechanism of lamotrigine?

A

a Na+ channel blocker that enhances the slow inactivated state of the channel

also inhibits glutamate release and acts on calcium channels

195
Q

What would be a likely effect of mesial temporal lobe damage?

A

anterograde amnesia (bilateral hippocampal damage)

196
Q

Which anti-convulsant is associated with kidney stones?

A

zonisamide

197
Q

What benzodiazpines can be used to treat insomnia?

A

flurazepam, temazepam,clonazepam

they are targeted to the “sleep switch” in the hypothalamus

198
Q

What is fixed ratio reinforcement?

A

reinforcement that occurs after a set number of correct responses

ex. getting $1 for every $10 in sales

199
Q

What are these? What disease are they associated with?

A

amyloid plaques (left) and Tau protein tangles (right)

cause of Alzheimer’s disease

200
Q

What is continuous reinforcement?

A

reinforcement that is provided with every correct action

201
Q

What is the most common neurodegenerative cause of dementia?

A

Alzheimer’s disease

202
Q

What is the cause of Wernicke-Korsakoff syndrome?

A

thiamine/B1 deficiency, most common in alcoholics or with bilateral necrosis of mammillary bodies (or of medial diencephalic or other periventricular nuclei)

203
Q

What are the components of the limbic lobe?

A

parahippocampal gyrus, cingulate gyrus, subcallosal gyri

204
Q

What is variable ratio reinforcement?

A

unpredictable reinforcement schedule based on an average ratio of correct responses

ex. slot machines

205
Q

What is the effect of bilateral damage to the hippocampus?

A

loss of ability to establish new memories (anterograde amnesia) and loss of spatial memory

206
Q

What is the function of orexin receptors? Orexin antagonists?

A

receptors: mediate wakefulness
antagonists: inactivates wakefulness to treat insomnia

207
Q

A well-established sleep center at a major research university just received funding from the NIH to perform a comprehensive re-evaluation of the effects of selected pharmacological agents on the stages of sleep in patients with insomnia. Which one of the following results is the most likely to emerge from these studies?

a) ramelteon decreases sleep latency and decreases number of awakenings
b) scopolamine does not alter sleep latency but decreases the number of awakenings
c) diphenhydramine decreases sleep latency but does not change the number of awakenings
d) flurazepam decreases sleep latency, decreases the number of awakenings and increases both slow wave and REM sleep
e) eszopiclone decreases sleep latency, decreases the number of awakenings and can normalize REM and slow wave sleep architecture

A

e) eszopiclone decreases sleep latency, decreases the number of awakenings and can normalize REM and slow wave sleep architecture

208
Q

What is an absence seizure?

A

“petit mal” seizure

characterized by an abrupt loss of awareness that lasts only seconds, sometimes associated with eye fluttering or automatisms

209
Q

Which anti-convulsants are broad spectrum hepatic inducers?

A

carbamazepine, phenytoin, phenobarbital/primidone

inducers = increase clearance and decrease steady-state concentrations of other drugs

210
Q

What is 3?

A

hippocampus

211
Q

What is the spinal fluid protein profile associated with Alzheimer’s disease?

A

low amyloid, high P-Tau

212
Q

What is atonia?

A

a “drop attack” characterized by brief loss of muscle tone (can have devastating consequences)

213
Q

In classical conditioning, what is an unconditioned stimulus?

A

a stimulus that produces a reflexive response

ex. food produces a reflexive drooling response in dogs

214
Q

The emergency room attending physician wishes to reverse the respiratory depressant effects of the multiple benzodiazepines and their active metabolites in the overdose described in question 2. Which one of the followingagents should be employed?

a) suvorexant
b) flumazenil
c) flunitrazepam
d) esopliclone

A

b) flumazenil

215
Q

What gene is associated with increased risk for alzheimer’s disease?

A

E4 allele of apolipoprotein E

216
Q

What is the mechanism of vigabatrin?

A

inhibits the catabolism of GABA by irreversibly inhibiting GABA transaminase

217
Q

What is the most disruptive side effect of levetiracetam?

A

irritability and psychological effects

218
Q

What are the two pathological hallmarks of Alzheimer’s disease?

A

beta-amyloid plaques (between neurons) and neurofibrillary tangles (within neurons)

219
Q

What is lacosamide? What are the side effects?

A

sodium channel-active agent that extends the slow-depolarization phase of sodium channel closure

side effects: significant ataxia

220
Q

What are the side effects of carbamazepine?

A

hepatotoxicity, bone marrow suppression, and rash

hyponatremia

decreases in WBC count

major hepatic inducer

221
Q

What are the long acting benzodiazepines?

A

diazepam, flurazepam

222
Q

What benzodiazepines are useful for panic attacks?

A

alprazolam or clonazepam - provides immediate relief

acts on limbic system

223
Q

What are the clinical features of benign rolandic epilepsy?

A

onset age 5-9

generalized tonic-clonic seizures occuring only at night

normal cognitive function, normal MRI

seizures always resolve by puberty and do not require treatment

224
Q

Which form of epilepsy is associated with seizures upon waking up in the morning?

A

juvenile myoclonic epilepsy

225
Q

What is the mechanism of phenytoin?

A

it produces voltage- and frequency-dependent block of Na+ channels, which prevents high-frequency firing of action potentials (associated with seizures)

226
Q

What is the duration of each of the ZAZOLES?

A

ZAleplon - ultrashort

ZOLpidem - short/intermediate half life

ESzopiclone - intermediate duration

Psych (6 decks)

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