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Brain and Behavior Part 2 > Week 5 Lectures > Flashcards

Week 5 Lectures Flashcards

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1
Q

4a’s

A

abnormal associations, autistic thinking/behavior, abnormal affect, ambivalence

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2
Q

first rank symptoms

A

auditory hallucinations, thought insertion/withdrawal/broadcasting, made feelings/behaviors/impulses, delusional perception

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3
Q

Schizophrenics die sooner/later

A

sooner

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4
Q

T/F Men have a higher incidence of schizophrenia than women.

A

T

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5
Q

T/F Men have a higher prevalence of schizophrenia than women.

A

F –> only incidence

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6
Q

Prodromal psychosis

A

attenuated psychotic symptoms before the onset of overt psychosis –> visual and auditory illusions, mild paranoid ideas or ideas of reference, functional decline and evidence of negative symptoms, cognitive difficulty

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7
Q

T/F for a diagnosis of schizophrenia must affect life/occupation.

A

T

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8
Q

What kind of hallucinations are most common with schizophrenia?

A

Auditory but also visual, olfactory, gustatory, somatic/tactile

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9
Q

disorder of salience

A

hypothesis that hyperdopaminergic mesolimbic pathways led to aberrant salience being attributed to random stimuli leading to delusions in schizophrenia

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10
Q

delusions

A

persecutory and delusions of reference most common: grandiose, somatic, religious, nihilistic

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11
Q

Tx of catatonia

A

benzodiazepines

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12
Q

Negative symptoms of schizophrenia

A

alogia, flat affect, anhedonia, avolition, asociality

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13
Q

Deficit syndrome

A

in 25% of schizophrenics, severe persistent negative symptoms are most prominent problem

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14
Q

Mood symptoms of schizophrenia

A

25-33% depression, related to suicide rate, anxiety, social phobia, ocd

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15
Q

___% of schizophrenics complete suicide

A

5

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16
Q

Schizoaffective disorder

A

period of psychosis that persists beyond mood symptoms, major depressive episode, or mixed episode while also meeting criteria for schizophrenia

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17
Q

Cognitive deficits of schizophrenia

A

global deficit is 1-2 standards below population norms –> verbal/visual learning and memory, attention, speed of processing, executive function

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18
Q

When is schizophrenia related cognitive deficits first detectable?

A

age 6-7 first testing w/dramatic decline between 12-17

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19
Q

Phases of schizophrenia

A

premorbid, prodromal, psychotic, stable

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20
Q

Tx of schizophrenia

A

antipsychotics (1st and 2nd generation)

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21
Q

___ generation antipsychotics occupy what receptors?

A

D2

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22
Q

Best antipsychotic

A

clozapine (atypical) –> improves cognition, improves negative symptoms but causes agranulocytosis

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23
Q

receptors targeted by atypical antipsychotics

A

D2 and serotonin

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24
Q

effectiveness differences between 1st and 2nd generation

A

none except clozapine

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25
Q

side effect profile of antipsychotics

A

1st gen = tardive dyskinesia and eps, 2nd gen = metabolic syndrome

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26
Q

Rule of thirds for schizophrenia

A

1/3 - treatment refractory, episodic relpase, good response with prolonged remission

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27
Q

good outcome prognostic factors

A

later/acute onset, shorter illness duration, better premorbid functioning, greater support, affective symptoms, female gender, paucity of negative symptoms

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28
Q

T/F schizophrenia is associated with grossly enlarged ventricles

A

T

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29
Q

T/F schizophrenia is associated with less gray matter

A

T

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30
Q

T/F schizophrenia is associated with normal white matter tracts

A

F –> reduction in organization

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31
Q

T/F schizophrenia is associated with normal rate of gray matter loss

A

F –> faster rate

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32
Q

neurodevelopmental model of schizophrenia

A

deleterious events in utero disrupt brain development, coupled with genetic vulnerability and later environmental factors (substances, stress) can lead to schizophrenia

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33
Q

4 leading genes in schizophrenia

A

disc1, dysbindin, neuregulin, comt

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34
Q

behaviors or laboratory measures that represent the activity of something that is disrupted by the function of a gene, short of overt symptomatology

A

endophenotypes (e.g. high cholesterol in one family)

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35
Q

Pre pulse inhibition

A

how much can suppress startle response –> schizophrenics cannot as well (Neuregulin1)

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36
Q

VGlut1

A

schizophrenics tend to have higher Vglut1 which results in increased glutamine levels coupled with dysbindin reduction which may lead to hyperexcitability

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37
Q

When in the year do schizophrenics tend to be born?

A

winter (also cities)

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38
Q

Neuronal migration and schizophrenia

A

not all neurons end up where they are supposed to end up in neuroembryonic development (Disc1 plays a role in this process)

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39
Q

Schizophrenics tend to have higher/lower expression of genes involved in presynaptic expression and an over/underexpression of genes involved in nt expression.

A

under and under

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40
Q

dopamine hypothesis of schizophrenia

A

hyper dopamine activity results in schizophrenia (cocaine and amphetamines mimic it and antipsychotics target D2 receptor and reduce symptoms)

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41
Q

Pts with higher/lower dopamine levels do better on antipsychotics.

A

higher

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42
Q

Glutamate hypothesis of schizophrenia

A

NMDA glutamate receptor antagonists (ketamine, PCP) mimic schizophrenia and receptor blockade can lead to hyperactive glutamergic activity in pyramidal cells –> neurotoxicity, secondary hyperdopaminergia

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43
Q

There is reduction/increase in NMDA receptor expression in schizophrenia

A

reduced

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44
Q

T/F schizophrenics have lower mismatch negativity

A

T

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45
Q

polygenic

A

hundreds of thousands of genes may contribute to risk for a nosologic entity

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46
Q

T/F most addicts report making annual attempts to quit but relapse most often follows after brief interval

A

T

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47
Q

Polydrug addiction

A

some alleles predispose to drug addiction without regard to pharmacologic class (but there are also specific alleles for specific drugs too)

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48
Q

which ions are regulated by nicotine receptors (NachRs)

A

calcium and sodium

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49
Q

Which subunit of nicotine receptors cannot form pentamers on their own

A

alpha 5

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50
Q

consequence of alpha5 variant on nicotine addiction

A

nicotine addiction risk allele becomes desensitized and fluxes calcium less well than the wild type–> hypofunctional –> if can develop positive allosteric regulators for this allele, might be able to reduce nicotine addiction

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51
Q

hypoactive alpha5 allele increases/reduces aversive consequences of nicotine

A

reduces –> therefore increases risk of addiction

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52
Q

The Lys allele for ALDH2 frequency in asians is ____% and conveys risk for _____

A

30 –> toxicity risk from acetaldehyde accumulation –> reduces risk of alcoholism

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53
Q

Alcohol’s euphoric properties are mediated by what receptor?

A

Gaba A (along with with barbituates, benzos, and neurosteroids)

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54
Q

Which GABA subunit has a variation that conveys risk for alcohol addiction?

A

alpha2

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55
Q

pretreatment with neurosteroid has what effect on alcohol consumption

A

reduced euphoria

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56
Q

schizophrenia cognitive endophenotypes

A

failure to activate dorsolateral frontal cortex, large lateral ventricles, impaired gamma oscillations and delayed latency in eeg

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57
Q

disc1

A

translocation in scottish kindred associated with schizophrenia and uni/bipolar illness

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58
Q

ank3

A

associates with voltage gated sodium and potassium channels at nodes of ranvier and orients these channels –> null mutant develops tremor and ataxia –> bipolar risk gene

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59
Q

l type calcium channel cacna1c

A

mutations that increase calcium flux (GOF) cause timothy syndrome including autistic features and prolonged QT –> bipolar risk gene

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60
Q

Anorexia nervosa

A

Restriction of food intake relative to caloric requirements leading to the maintenance of body weight less than 85% of that expected; or failure to make expected weight gain during period of growth, leading to body weight less than 85% of that expected, intense fear of gaining weight, disturbance in way experience body weight or shape, absence of 3 consecutive menstrual cycles due to underweight status

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61
Q

Anorexia subtypes

A

restricting: during the last three months, the person has not engaged in recurrent episodes of binge eating or purging behavior, and bingeating/purging: during the last three months, recurrent binge/purge episodes

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62
Q

When does AN onset?

A

often after crisis in family, school, sexuality

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63
Q

Which nt is implicated in AN and bulimia?

A

serotonin –> positive response to antideprx in bulimia

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64
Q

Tx of AN

A

inpatient medical treatment, maybe atypical antipsychotics in tx resistant AN

65
Q

Maudsley family therapy

A

20 sessions over 6-12 months for adolescents (NOT ADULTS –> independent counseling) –> 3 phases: 1. parents control refeeding, 2. return to independent eating, 3. focus on general issues

66
Q

% Full recovery from AN

A

1/3- 1/2

67
Q

Bulimia

A

recurrent episodes of binge eating during 2hour period, lack of control over eating, compensatory behavior –> 1/ week for 3 months & not during episode of AN –>AN binge subtype (need below weight for dx)

68
Q

BN fail to activate _____ circuits to the same degree as healthy controls in right/left inferolateral prefrontal cortex indicating _____

A

frontostriatal on left cortex meaning less self-regulation

69
Q

T/F first binge usually in response to severe caloric deprivation during dieting

A

t

70
Q

Complications of bulimia

A

hypokalemia, erosion of enamel, electrolyte imbalance, parotid gland enlargement from elevated serum amylase

71
Q

Tx of bulimia

A

behavior therapy, antidepressants (desipramine, fluoxetien), interpersonal psychotherapy, cognitive therapy

72
Q

Firstline tx of bulimia

A

cbt

73
Q

Binge eating disorder

A

recurrent episodes of binging with lack of self control –> 1/week for three months

74
Q

Tx of choice for binge eating

A

CBT –> but no weight loss so + Behavioral weight loss–> structure eating, etc. + ssri

75
Q

Purging disorder

A

regular occurrence of inappropriate compensatory behaviors + normal body weight + no binging

76
Q

Atypical anorexia

A

all criteria for AN except significantly low weight such as bariatric surgery pts

77
Q

Subthreshold bulimia

A

all criteria for BN but not as many purges as required

78
Q

LSD/acid

A

hallucinations with micropsia or macropsia, synesthesia, derealization, depersonalization–> unknown dosage on the street –> 45 minute onset with 4-12 hours experience

79
Q

Clinical manifestations of lsd

A

euphoria/lability and ego fragmentation –> expanded consciousness, unlocking secrets of universe

80
Q

Mx of lsd

A

involves post-synaptic serotonin-2 receptor

81
Q

Chronic consequences of lsd

A

no permanent damage, unmasks psychiatric vulnerabilities, state of panic due to fear of imminent insanity

82
Q

Tx of lsd bad trips

A

ride the wave, reassurance benzodiazepines

83
Q

PCP (wet, angel dust, peace, hog)

A

detachment from reality/dissociative, analgesia with alertness, staring gaze, flat faces, rigid muscles –> smoked or snorted

84
Q

onset of pcp

A

5 minutes….4-6 hours effect with plateau at 45 minutes –> 24-48 hours for recovery

85
Q

clinical manifestations of pcp

A

euphoria, disconnection, flat affect, uncommunicative –> vertical nystagmus, slurred speech, rolling gate, numbness, depersonalization of body

86
Q

are large doses of pcp lethal?

A

yes w/high dose–> hyperacusis, amnesia, hostility, muscle rigidity, excess salivation/no gag, increased bp/pulse, coma/convulsions

87
Q

Mx of pcp

A

nmda receptor antagonist (like ketamine) –> blocks activity of excitatory gluatmate + also other receptors

88
Q

chronic consequences of pcp

A

no permanent damage, 2-3 weeks of dysfunction after abstinence –> dulled thinking, dulled reflexes, loss of impulses

89
Q

Tx of pcp

A

NO REASSURANCE –> benzodiazepines prophylactic against seizures, antipsychotics, acidification of urine, gastric suction

90
Q

Metamphetamine/ecstasy/molly/MDMA

A

club drug –> elation and freedom //adjunct in psychotherapy to increase empathy –> pills/wafers

91
Q

Clinical manifestations of ectasy

A

loss of boundaries, disinhibition, promotes intimacy, cognitive distortions (slower, apathy), perceptual distortions (hallucinations, spatial relations altered), increased anxiety, tachycardia, dehydration, clenched jaw/bruxism, dry mouth

92
Q

Mx of ecstasy

A

dopamine and serotonin release

93
Q

Chronic consequences of ecstasy

A

long lasting/permanent destruction of serotonergic pathways –> depression

94
Q

Tx of ecstasy

A

dehydration, reassurance, support, education

95
Q

Anticholinergics

A

usually due to polypharmacy –> atropine, benadryl, tcas, sleep ais

96
Q

anticholinergic delirium

A

wax and waning consciousness, impulsivity, impaired judgement, hallucinations

97
Q

Clinical manifestations of anticholinergics

A

fever, warm/dry skin, fixed dilated pupils, tachycardia, decreased peristalsis, atonic bladder

98
Q

Tx of anticholinergic delirium

A

discontinue offending agent, protect pt against harm, gastric lavage, parenteral physostigmine

99
Q

Drug of choice in controlling anticholinergic delirium

A

haldol

100
Q

Inhalants

A

volatile hydrocarbons –> toluene, gasoline, kerosene, nitrous oxide, amyl/butyl nitrates/poppers –> GABA a

101
Q

Clinical manifestations of inhalants

A

stimulation, disinhibition, nystagmus, muscular incoordination, perceptual distortions, misperceptions

102
Q

Long term consequences of inhalants

A

CNS damage –> demyelination and cerebellar atrophy –> impairments in memory, attention, concentration, intelligence

103
Q

Which part of the brain is active in alterations of unpleasantness of pain?

A

anterior cingulate cortex

104
Q

which part of the brain is active in perception of pain itself?

A

primary somatosensory cortex

105
Q

T/F Need specific hypnotic suggestions to change perception of unpleasantness.

A

T

106
Q

Which side of the brain is specifically related to verbal mediation of hypnotic suggestions, working memory functions, and reinterpretation of the sensory experience?

A

Left

107
Q

treatments that promote welllness, those used alongside conventional care, and those used to replace conventional treatments

A

complementary and alternative medicine

108
Q

T/F most patients who take cam do not bring it up with their doctor.

A

T

109
Q

T/F Patients with DSM IV diagnoses have a significantly higher use of CAM

A

T

110
Q

What % of pts with depression or anxiety who treat with CAM also take traditional meds?

A

67%

111
Q

Omega 3

A

may play a role in pro-inflammatory state in body –> reduction in western society (EPA and DHA are efficacious in treating psychiatric conditions)

112
Q

Which omega 3 fatty acids may help in tx of mood disorders?

A

DHA and EPA

113
Q

T/F omega 3 supplementation can help with bipolar mania

A

F –> only in treating depressive symptoms

114
Q

Major side effects of omega 3 augmentation.

A

bleeding risk, high doses can increase risk of mood cycling in bipolar, GI upset

115
Q

Which B vitamins are relevant to mood enhancement?

A

B9 and B12 aka folate and cobalamin

116
Q

Which B vitamin deficiency is strongly associated with depression?

A

folate/b9

117
Q

Which B vitamin deficiency is strongly associated with peripheral neuropathy?

A

cobalamin/b12

118
Q

Which b vitamin might be viable as a depression prophylactic

A

b12/cobalamin

119
Q

Which B vitamin might have value as an adjunct in tx of depression?

A

B9/folate

120
Q

Which B vitamin might help slow cognitive decline in MCI

A

both b9 and b12

121
Q

SAMe

A

universal methyl group donor which helps in DNA construction, nt, etc –> aberrant methylation associated with CNS and psychiatric disorders

122
Q

Effect of SAMe on brain

A

increased serotonin availability –> as good as traditional antidepressants

123
Q

____ depletes SAMe stores in brain

A

levodopa for parkinsons

124
Q

Contraindication for SAMe

A

avoid in bipolar disorder–> risk of inducing mania

125
Q

Suboptimal levels what vitamin may increase risk for depression?

A

D3

126
Q

N-acetylcysteine

A

replenishes anti-oxidants for anti-inflammation –> maybe useful in bipolar as adjuvant

127
Q

Tryptophan supplementation

A

limited evidence for deprx but reduces serotonin syndrome with SSRI combined use

128
Q

St. John’s Wort

A

mimics traditional pharmacologics in tx of deprx –> equal efficacy to TCA with fewer side effects than TCAs//equivalent to SSRIs –> mild/moderate depression

129
Q

Contraindications for st johns wort

A

bipolar, in combo with ssri (serotonin syndrome), CYP3a induction (need low hyperforin formulation)

130
Q

Kava

A

ceremonial drink that is relaxing due to increase GABA transmission; reduces anxiety

131
Q

Side effects of kava

A

gi upset, fatigue, facial swelling, liver damage, platelet response

132
Q

Kava drug interactions

A

coma with alcohol, benzos, muscle relaxants; may inhibit p450

133
Q

Chamomile

A

inhibits gaba metabolizing enzymes –> mild use for anxiety

134
Q

Gingko biloba

A

exerts anti oxidant and anti-inflammatory effects via anti PAF; increases cerebral bloodflow –> no good evidence for clinical value

135
Q

Risks of gingko biloba

A

bleeding risk when consumed with antiplatelet or anticoagulants

136
Q

acupuncture and depression

A

not very good evidence

137
Q

yoga and depression

A

no good studies but yoga breathing does stimulate vagus nerve–> increases alertness, focus, integration, calm, decreases worry, fear, and cortisol

138
Q

Which parts of the brain are activated with mindfulness meditation?

A

prefrontal cortex and anterior cingulate cortex, dorsalmedial prefrontal cortex

139
Q

half life of nicotine

A

1.5 hours

140
Q

main metabolism of nicotine

A

liver CYP2A6

141
Q

T/F after brief nicotine exposure, receptors become desensitized

A

T

142
Q

T/F route of administration affects speed of access of nicotine to brain

A

T –> smoking is fast, gum is not

143
Q

risk of addiction from tobacco

A

> 30%

144
Q

nicotinic effects on dopamine

A

direct via nAChRs and indirect via GABA and Glu receptors –> increases phasic dopamine and inhibits tonic firing of dopamine –> creates a larger difference between basal dopamine and phasic/burst dopamine –> greater feeling of good

145
Q

most widely used measure of nicotine addiction

A

fagerstrom test

146
Q

Tx of nicotine addiction

A

cold turkey, cessation counseling, NRT, Bupropion, varenicline

147
Q

Cold turkey effectiveness

A

high relapse rate; only 5% long-term abstinence

148
Q

most effective non pharmacologic tx of nicotine addiction

A

behavior therapy > brief advice > no therapy

149
Q

contraindications for nicotine pharmacotherapy

A

smokers < 10/day, pregnant/breastfeeding, adolescents

150
Q

which nicotine replacement has the best abstinence at 6 months?

A

spray –> but NRT works generally 2x better than placebo

151
Q

contraindications for nicotine gum

A

TMJ or dental problems –> fixed dosage for 12 weeks

152
Q

nicotine inhaler

A

vaporizes –> 80puffs/20 minutes vs 10 puffs for cigarette –> Rx only

153
Q

nicotine nasal spray

A

8 doses/day for 12 weeks –> nasal irritation and Rx only

154
Q

Contraindication for nicotine patch

A

skin disorders

155
Q

Bupropion

A

antideprx that was repurposed for smoking cessation –> consistent abstinence over time//dose proportional

156
Q

T/F combination therapy with NRT and/or pharmacologics like bupropion is moe effective than a simple titrative approach

A

T

157
Q

Varenicline

A

partial agonist at alpha4beta2 nAChR -> reduces craving and withdrawal symptoms –> antagonist effect, blocks satisfaction and rewarding effects of nicotine

158
Q

adverse effects of varenicline

A

nausea, vomiting, abdominal symptoms, effects on depression and suicide, serious cardiovascular effects

Brain and Behavior Part 2 (6 decks)

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