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Psychopharmacology > Exam 3 - Part 2 > Flashcards

Exam 3 - Part 2 Flashcards

(60 cards)

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1
Q

Cocaine administration

A

cocaine HCL can be taken orally, intranasally, by IV injection; can be smoked by freebasing and crack

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2
Q

Cocaine absorption

A

readily crosses BBB, producing a high; half life of 0.5-1.5 hrs and high lasts about 30 minutes

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3
Q

Benzoylecgonine

A

primary cocaine metabolite

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4
Q

Cocaethylene

A

produced by alcohol interactions with cocaine, has a longer half-life

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5
Q

Cocaine mechanism of action

A

reuptake inhibition that is strongest at DAT but also binds NET, SERT

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6
Q

Cocaine reinforcement without functioning DATs

A

through alpha1 NE receptors and ACh; DA release is also controlled by NE activity which cocaine can increase

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7
Q

Stereotypies

A

as dose increases, behaviors become focused stereotypies

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8
Q

Acute effects of cocaine

A

feelings of exhilaration; sympathomimetic physiological effects that include increased heart rate, vasoconstriction, hypertension, insomnia; mania, paranoia and agitation

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9
Q

Mild vs severe effects of cocaine

A

positive characteristics that contribute to its reinforcing properties become negative with higher dose and duration

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10
Q

Cocaine binges

A

models of self administration show binges followed by periods of exhaustion

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11
Q

Stimulation of core of NAcc with cocaine

A

satiating effects of cocaine and conditioned reinforcement

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12
Q

Stimulation of shell of NAcc with cocaine

A

Cocaine reward

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13
Q

DAT occupancy in humans

A

once a certain minimum level of DAT occupancy is attained the subject may experience a drug-induced high; cocaine reaches brain faster when smoked or IV; DA release is increased in the striatum, amygdala, hippocampus, and PFC when users are presented with cocaine-related stimuli

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14
Q

DA and craving cocaine

A

as striatal DA release increases craving results after exposure to cocaine-related stimuli

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15
Q

Cocaine tolerance

A

decrease in locomotor activity

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16
Q

cocaine sensitization

A

ncrease in stereotypy after chronic administration

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17
Q

How DA markers change in chronic cocaine users

A

after chronic use there is a decrease in DA synthesis, release, DAT binding, and D2/D3 binding

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18
Q

Psychosocial treatment

A

12 step programs, CBT, contingency management

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19
Q

SSRIs for cocaine

A

increased days sober

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20
Q

Disulfiram for cocaine treatment

A

inhibits DBH (altering DA-NE ratio)

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21
Q

Cathinone and ephedrine

A

naturally occurring stimulant compounds

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22
Q

L-amphetamine, D-amphetamine

A

synthetic, structurally related to DA

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23
Q

Methamphetamine

A

synthesized from pseudoephedrine, mostly CNS effects

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24
Q

Methylphenidate

A

treats ADHD

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25
Pipradrol
milder CNS effects, obesity, narcolepsy, ADHD
26
Bath salts
synthetic cathinone
27
Administration of amphetamines
ingested orally, IV, or SC
28
Absorption of amphetamines
a weak base that ionizes in the digestive tract; crosses BBB quickly, concentrates in spleen, kidneys, and brain
29
Excretion
rate of accretion depends on urine pH; if acidic, it is excreted readily in urine; if basic, it reabsorbs and must be metabolized by liver
30
Action of amphetamines
indirect catecholamine agonists; stimulate DA and NE release and block reuptake, also affects 5-HT and E
31
Mechanisms of amphetamines
enter nerve terminal by DAT then stimulates DA release from vesicles and alters DAT to act in reverse direction to release DA into synapse
32
Amphetamine PNS effects
sympathetic arousal (fight or flight)
33
Amphetamine CNS effects (3)
1) increased motor activity (nigro-striatal) 2) euphoria and addiction (meso-limbo-cortical) 3) inhibits pituitary function
34
Amphetamine physiological effects
increased heart rate and blood pressure, vasodilation, brochodilation, reduced sleep time, especially REM
35
Psychosis
continued meth use can transition to a psychotic state that persists long after abstinence; similar to schizophrenia
36
Neurotoxicity
damage or death of DA system neurons
37
Ritalin
activates catecholamine transmission by blocking DAT and NET
38
Modafinil
binds to DAT with low affinity and acts as a weak DA uptake inhibitor; stimulates release of NE and orexin and inhibits GABA release
39
MDD
dysphoria, negative thinking, lack of energy, negative life impact
40
BPD
alternating pattern of depression and mania (or hypomania); mood does not reflect reality
41
Prevalence of affective disorders
15-20% experience MDD at any given time; 1% experience BPD
42
Concordance rates
genetics predispose; 65% concordance for identical twins with MDD. 80% for BPD
43
HPA axis changes in depression
elevated cortisol levels and abnormal circadian rhythm in cortisol secretion; fail to respond to dexamethasone challenge
44
Sleep changes
rouble falling asleep, almost no stage 3 and 4 SWS, more night wakings, rapid onset of first REM bout
45
BDP sleep disturbances
sleep deprivation can trigger an episode of mania
46
Animal models of affective disorders
can only reflect one or a few behavioral symptoms; few models of mania phase or of cycling episodes, several are based on altered circadian rhythms
47
Monoamine theory of depression
reduced level of monoamines in the CNS is responsible for depressed mood
48
Support for monoamine theory of depression
tryptophan depletion challenge leads to depression in individuals with family history or relapse in patients on antidepressant drugs
49
Problems with monoamine theory of depression
cannot explain delay in effects of pharmacology, no solid evidence of abnormal 5-HT in depressed humans, 1/3 of depressed people do not respond to monoamine treatments
50
MAOIs
first gen, iproniazid; increases amount of neurotransmitters available for release; cause insomnia, weight gain, hypertension, drug interactions
51
TCAs
first gen, imipramine; inhibition of reuptake (5-HT and NE); potentially dangerous cardiovascular effects and anticholinergic effects
52
SSRIs
second gen, sertraline, prozac; sexual disfunction, dependence, restlessness, dependence
53
SNRIs
reboxetine
54
Ketamine
third gen, enhances BDNF-stimulated neurogenesis and elaboration of dendritic spine growth
55
ECT
produces up regulation of monoamines and GABA; memory dysfunction and confusion
56
TMS
similar efficacy for most but not all patients, very new
57
DBS
anterior cingulate gyrus
58
Lithium carbonate
eliminates or reduces manic episodes without causing depression, reduces suicide; up regulates 5-HT and down regulates catecholamines
59
valproate
teratogenic, increases GABA levels; for BPD carbamazepine - for BPD - inhibits NE reuptake
60
Light/dark therapy
important in MDD with early morning light, early morning light causes polarity change in BPD patients

Psychopharmacology (2 decks)

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