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Psychopharmacology > Exam 3 - Part 2 > Flashcards

Exam 3 - Part 2 Flashcards

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
Q

Pipradrol

A

milder CNS effects, obesity, narcolepsy, ADHD

26
Q

Bath salts

A

synthetic cathinone

27
Q

Administration of amphetamines

A

ingested orally, IV, or SC

28
Q

Absorption of amphetamines

A

a weak base that ionizes in the digestive tract; crosses BBB quickly, concentrates in spleen, kidneys, and brain

29
Q

Excretion

A

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
Q

Action of amphetamines

A

indirect catecholamine agonists; stimulate DA and NE release and block reuptake, also affects 5-HT and E

31
Q

Mechanisms of amphetamines

A

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
Q

Amphetamine PNS effects

A

sympathetic arousal (fight or flight)

33
Q

Amphetamine CNS effects (3)

A

1) increased motor activity (nigro-striatal) 2) euphoria and addiction (meso-limbo-cortical) 3) inhibits pituitary function

34
Q

Amphetamine physiological effects

A

increased heart rate and blood pressure, vasodilation, brochodilation, reduced sleep time, especially REM

35
Q

Psychosis

A

continued meth use can transition to a psychotic state that persists long after abstinence; similar to schizophrenia

36
Q

Neurotoxicity

A

damage or death of DA system neurons

37
Q

Ritalin

A

activates catecholamine transmission by blocking DAT and NET

38
Q

Modafinil

A

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
Q

MDD

A

dysphoria, negative thinking, lack of energy, negative life impact

40
Q

BPD

A

alternating pattern of depression and mania (or hypomania); mood does not reflect reality

41
Q

Prevalence of affective disorders

A

15-20% experience MDD at any given time; 1% experience BPD

42
Q

Concordance rates

A

genetics predispose; 65% concordance for identical twins with MDD. 80% for BPD

43
Q

HPA axis changes in depression

A

elevated cortisol levels and abnormal circadian rhythm in cortisol secretion; fail to respond to dexamethasone challenge

44
Q

Sleep changes

A

rouble falling asleep, almost no stage 3 and 4 SWS, more night wakings, rapid onset of first REM bout

45
Q

BDP sleep disturbances

A

sleep deprivation can trigger an episode of mania

46
Q

Animal models of affective disorders

A

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
Q

Monoamine theory of depression

A

reduced level of monoamines in the CNS is responsible for depressed mood

48
Q

Support for monoamine theory of depression

A

tryptophan depletion challenge leads to depression in individuals with family history or relapse in patients on antidepressant drugs

49
Q

Problems with monoamine theory of depression

A

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
Q

MAOIs

A

first gen, iproniazid; increases amount of neurotransmitters available for release; cause insomnia, weight gain, hypertension, drug interactions

51
Q

TCAs

A

first gen, imipramine; inhibition of reuptake (5-HT and NE); potentially dangerous cardiovascular effects and anticholinergic effects

52
Q

SSRIs

A

second gen, sertraline, prozac; sexual disfunction, dependence, restlessness, dependence

53
Q

SNRIs

A

reboxetine

54
Q

Ketamine

A

third gen, enhances BDNF-stimulated neurogenesis and elaboration of dendritic spine growth

55
Q

ECT

A

produces up regulation of monoamines and GABA; memory dysfunction and confusion

56
Q

TMS

A

similar efficacy for most but not all patients, very new

57
Q

DBS

A

anterior cingulate gyrus

58
Q

Lithium carbonate

A

eliminates or reduces manic episodes without causing depression, reduces suicide; up regulates 5-HT and down regulates catecholamines

59
Q

valproate

A

teratogenic, increases GABA levels; for BPD
carbamazepine - for BPD - inhibits NE reuptake

60
Q

Light/dark therapy

A

important in MDD with early morning light, early morning light causes polarity change in BPD patients

Psychopharmacology (2 decks)

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