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Psychopharmacology > Final > Flashcards

Final Flashcards

1
Q

Fast pain fibers

A

Adelta

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2
Q

Slow pain fibers

A

C fibers

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3
Q

why does rubbing an injured site reduce pain? What is this called?

A

Gate control theory. C fiber inhibits inhibitory interneuron, causing projection neuron to tell brain that youre in pain. If you rub pain site, c fibers will still be activated but a beta fibers will also be activated, stimulating inhibitory interneuron causing it to inhibit projection neuron. ppt 10 slide 11

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4
Q

endogenous opioid that inhibits substance P (Pain) release. what type of inhibition?

A

enkephalin through presynaptic inhibition. opiate receptors are on presynaptic terminals of primary afferent axons with SP. probably how morphine works

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5
Q

what neurotransmitters coming from descending brain pain pathway seem to control enkephalin to inhibit release of substance P

A

5HT and NE

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6
Q

ppt 10 slide 20

A

yes

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7
Q

first peptides discovered linked to endogenous analgesia? what is the other major opioid peptide product?

A

Met-enkephalin and Leu-enkephalin were first to be discovered endogenous opioid peptides, another one is Beta endorphin

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8
Q

cell bodies for beta-endorphine, enkephalin, and dynorpin and their receptors are highly concentrated in what brain region? associated with experience of pain

A

LIMBIC SYSTEM

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9
Q

opioid analgesics exert their effects through (agonist or antagonist) actions on families of receptors

A

agonist- similar structure to endogenous opiates

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10
Q

hallmark sign of opiate use

A

pinpoint pupils- MIOSIS

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11
Q

major opioid antagonist

A

naloxone

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12
Q

what opioid receptor type do morphine and fentanyl act HARD on? Why do we try to shy away from these guys because of it, beginning the development of drugs that bind to other opioid receptor types

A

morphine and fentanyl fuck with mu receptors hard. mu receptor is implicated with respiratory depression symptoms and the development of physical dependence. We are developing mixed opioids to avoid the mu receptor activation and focus on kappa and delta activation

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13
Q

major opioid antagonists- which has longer half life (is more involved in opioid-dependence maintenance)programs)

A

naloxone (fast action antagonist) and naltrexone (LONGER half life. blocks effect of injected heroin for up to 48 hours

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14
Q

three main NON-SELECTIVE COX inhibitors (a branch of NSAIDs)

main selective COX-2 inhibitor (Branch of NSAIDs)

A

aspirin, ibuprofen, indomethacin

Celecoxib (Celebrex)

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15
Q

t or f acetaminophen is not an NSAID

A

t, it has relatively little anti-inflammatory activity

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16
Q

why should COX-2 inhibitors be used with caution

A

COX is made endogenously, a bunch of COX-2 selective inhibitors would cause CV events

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17
Q

two cholinergic hallucinogens. which is agonist which is antagonist

A

muscarine- agonist at muscarinic receptors

scopolamine- antagonist

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18
Q

four catecholamine (NE) like hallucinogens that he wanted us to memorize

A

Mescaline- peyote,

MDA/MDMA- synthetic, mix of catecholamine and 5-HT effects,

Myristin and Elemicin (in nutmeg and mace)

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19
Q

t or f- MDMA works by building up serotonin nerve terminals

A

F- MDMA DESTROYS serotonin nerve terminals

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20
Q

most important indolamine in our body and its most important receptor

A

serotonin,

5-HT 1A

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21
Q

can increase amount of 5-HT in somebody’s body by putting them on what kind of diet

A

high tryptophan diet

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22
Q

important 5-HT1A receptor agonist, reduces 5-HT release

A

8-OH-DPAT

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23
Q

5-HT antagonist

A

methysergide

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24
Q

5-HT storage inhibitor used as a tranquilizer

A

reserpine

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25
Q

5-HT pump inhibitors used as an antidepressant

A

chlorimipramine

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26
Q

5-HT synthesis inhibitor, antisleep, mild aphrodisiac

A

p-Chlorphenylalanine (PCPA)

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27
Q

5-HT MAOI, antidepressant

A

iproniazid

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28
Q

5-HT toxin

A

5,6-Dihydroxytryptamine (5,6DHT)

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29
Q

what nt does this drug act like- psilocybin and psilocin, LAA, DMT

A

5-HT

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30
Q

what nucleus does LSD potentially work on, how

A

raphe nuclei, it inhibits it. raphe nuclei releases its own 5ht, and has 5ht1a receptors. It inhibits itself with too much 5ht so LSD acts as 5ht to inhibit it

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31
Q

Dissociative anaesthetics (2). what kind of trips do they give you bitch

A

PCP- Phencyclidine (Sernyl)
bad trips

Ketamine
less bad trips

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32
Q

where is the PCP binding site? what receptor? does it make it an antagonist or an agonist or what

A

located inside NMDA cation channel, below magnesium binding site, making it an antagonist

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33
Q

PCP like drugs stimulate firing of what neurons

A

VTA dopaminergic neurons

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34
Q

THC receptors CB1 and CB2 are GPCRs or ionotropic, what part of neuron are they located, how do they mostly act

A

GPCRS, CB 1 are located on terminals and axons, act to inhibit release of NT, CB2 are on surface of WBCs

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35
Q

Ring structures that interact with a receptor and mimic the action of an endogenous ligand on CB receptors

A

cannabinoids

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36
Q

most effective brain structure to yield self stimulation in rats? What is the main nt type in this area

A

Medial forebrain bundle MFB. catecholamines. rewarding stimulation causes release of NE into amygdala and hypothalamus (ascending pathway- caudal-rostral). Its stimulation causes dopaminergic neurotrans to be stimulated in the ventral tegmental area to release dopamine in the nucleus accumbens

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37
Q

3 long length dopaminergic systems

A

nigrostriatal mesolimbic mesocortical

38
Q

stimulation of MFB leads to increased stimulation of _____ which causes increased release of DA nts into ______

A

VTA, nucleus accumbens

Drugs of abuse either act to activate system through cell bodies in VTA or to act directly on receptors in nucleus accumbens for reinforcement

39
Q

Dopamine acting on the nucleus accumbens does what for GABA’s action on globus pallidus

A

DA inhibits neurons in the nucleus accumbens, producing locomotion by inhibiting the release of GABA onto globus pallidus

40
Q

slides 50-56 ppt 12

A

yes

41
Q

what would you do in order to avoid death from delirium tremens in alcohol withdrawal if you were trying to wean somebodyoff

A

substitute alcohol with pentobarbital. mild intoxication maintained for 1 to 1.5 days and then you can start withdrawal. immediate withdrawal of a neurodepressant can lead to death

42
Q

most consistent pharmacotherapy to treat amphetamine and cocaine dependence

A

tricyclic antidepressants (desipramine)

43
Q

there is a relationship between behavioral performance and level of arousal. Highly or lowly aroused you perform worse than if you were moderately aroused. what law is this

A

Yerkes-Dodson Law

44
Q

three components of emotion

A

(1) overt behavior, (2) physiological changes (autonomic, endocrine, cardiovascular, respiratory, GI, immune), and (3) subjective (personal) cognitive feelings.

45
Q

Long-term exposure to one stressor or the exposure to a new stressor in the presence of an existing stressor produced exhaustion of resources in dealing with stressors and leads to morbidity/death. what is this called

A

General adaptation syndrome GAS

46
Q

stress: repeated activation of _______ predisposes one toward developing chronic hypertension

A

defense response

47
Q

slide 39-42 ppt 13

A

yes

48
Q

_____ is synthesized in the hypothalamus and secreted to control ACTH release from anterior pituitary, causing glucocorticoid release from adrenal cortex.
In addition, it is also present in brain pathways and activates nuclei with the CNS as a neurotransmitter.

A

corticotropin releasing factor CRF. enhances startle response by interacting with amygdala

49
Q

plasma cortisol concentrations in depressed patients higher or lower than controls on average

A

higher. cortisol peaks in the morning, dips while you sleep. remains pretty high for people who are depressed though

50
Q

what can be administered to lower plasma cortisol concentrations? does it work in people with depression?

A

Dexamethasone (DEX) lowers plasma cortisol. can work with people with depression for a little bit but only for a little bit then the levels skyrocket again

51
Q

does REM sleep start early or late for depressed patient? how about sleep latency (time before they actually fall asleep)? how about deep sleep levels

A

REM starts super early

sleep begins super early. Reduced REM latency and reduced sleep latency. no sleep levels 3 & 4

52
Q

how does sleep deprivation affect some depressed patients the next day

A

their mood increases crazy

53
Q

when is best time to do light box therapy with people who have SAD

A

morning

54
Q

what does the monoamine theory say about neurotransmitters and depression. Is this theory correct? how about the popularity of the treatment used?

A

functionally deficient monoaminergic (NE and 5-HT) transmission in the CNS causes depression.

Theory has no pharmalogical evidence, however monoamine transmission manipulations are still the most successful treatment approaches

55
Q

what drug can you use to cause depression

A

reserpine. inhibits NE and 5-HT storage.

56
Q

how do tricyclic antidepressants work. what theory of depression do they belong tow

A

block reuptake of NE and 5-HT. a part of the monoamine approach

57
Q

what is alpha methyltyrosine used for. what theory of depression does it belong to

A

calming of manic patients by inhibiting synthesis of norepinephrine

58
Q

how does ECT increase mood? what nts are involved

A

increases CNS response to NE and 5-HT

59
Q

What does methyldopa do

A

inhibits NE synthesis, decreases mood

60
Q

slide 27 ppt 14

A

yes

61
Q

does depression increase or decrease your heart rate? how does it affect your heart rate variability

A

increases heart rate, decreases heart rate variability

62
Q

Irreversible MAOI inhibitor? Reversible MAOI inhibitor? if you were prescribing it to test out on a new patient, which one would you use and why

A

Irreversible- Tranlcypromine
Reversible- Moclobemide

you would give them moclobemide because you want to use a reversible inhibitor so you don’t have to wait for new MAO’s to be made in case the medication doesnt work

63
Q

what do MAOI’s do

A

inhibit monoamine oxidase which is an enzyme that regulates the amount of NE and 5-HT in the presynaptic terminal. Inhibiting MAO increases the amount of NE and 5-HT in the presynaptic terminal

64
Q

what kind of people aren’t able to be prescribed tricyclic antidepressants (TCA)

A

people with heart issues

65
Q

how do Tricyclic antidepressants work (TCA)

A

inhibit neuronal reuptake in NE, 5-HT and DA neurons

66
Q

what is an effective treatment drug for bipolar disorder

A

Lithium

67
Q

how does lithium work to treat bipolar disorder

A

increases time between manic episodes, depressive episodes. has a calming effect during manic episodes. proposed to inhibit release of NE

68
Q

postmortem studies of schizophrenia show lower neuron count, larger ventricles, and also an absence of ______

A

gliosis- normally when we lose brain mass, gliosis is a typical response (proliferation of glial cells)

69
Q

schizophrenics show what kind of activity in the frontal cortex

A

hypofrontality

70
Q

schizophrenics show a disorganized (what brain region)

A

hippocampus

71
Q

current theory of schizophrenia with neurons and shit

A

schizophrenia is thought to be produced by excessive activity at D2 receptors. Therapeutic dose for neuroleptics correlates with their affinity for the D2 receptor

72
Q

D1-like receptors are (excitatory or inhibitory) D2-like receptors are (excitatory or inhibitory)

A

D1- excitatory

D2- inhibitory

73
Q

what tract inhibits secretion of prolactin? how?

A

Tuberohypophyseal tract inhibits secretion of prolactin- it is an intermediate length DA tract

74
Q

schizophrenia may develop as an insult to the fetus occurs during the ____ trimester

A

second

75
Q

slide 21 ppt 15 very important

A

yes

76
Q

first drug used to treat schizophrenia in 1950s hint it was a tranquilizer

A

chlorpromazine

77
Q

how do neuroleptics produce an antipsychotic action

A

decrease DA activity by blocking DA receptors

also increase prolactin release (side note)

78
Q

are neuroleptics hydro or lipophilic

A

highly lipophilic

79
Q

what type of drug causes tardive dyskinesia,what do we do to avoid it

A

neuroleptic, use atypical antipsychotics like CLOZAPINE

80
Q

what toxin can be used to model parkinsons in primates after some dumb kids took it cuz they thought it was acid

A

Toxin = N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) can be used to model parkinsons in primates boy

81
Q

physiology of parkinsons NTs

A

reduction in inhibitory DA neurons in basal ganglia

82
Q

slide 38-41 ppt 15

A

yes

83
Q

what drugs do we use for parkinsons treatment

A

L-DOPA because it crosses blood brain barrier and is a precursor to DA which does not cross BBB. We can supplement that with carbidopa which doesnt cross BBB- it is an antagonist of the enzyme that converts L-DOPA to DA so that way DA isn’t made before crossing BBB

84
Q

Knowing thyself: what is this effect called- people remember words from a list well that they previously thought described themselves

A

self-reference effect

85
Q

parts of brain that are more active when you are resting- what is this called and where are they at
(this also includes an area that changes signal when thinking about the self)

A

default network- medial pfc, inferior parietal lobule.

vACC changes signal when we are thinking about ourselves

86
Q

what part of brain is active when we are making positive judgments about OURSELVES

A

vACC ventral anterior cingulate cortex- part of default network. When we are making highly self relevant positive judgments, there is little signal change. When we are making highly self relevant negative judgments, there is a large decrease in signal- default network is deactivated

87
Q

what part of brain is active while you are taking the point of view of others

A

right temporoparietal junction

88
Q

brain area important for interpreting eye gaze- active when we are thinking about the intentions behind someone’s eye movements

A

superior temporal sulcus

89
Q

brain area related to interpretation of the eye gaze of others and how it is affected in autism

A

superior temporal sulcus is smaller in autism

90
Q

While a person is acting, they may have no insight into their behavior at the time of action, but can look back on it later and be like yeah what the fuck that was stupid- this is indicative of damage where

A

orbitofrontal cortex

91
Q

when a person is bad at judging behavior of others in negative social scenarios, this is indicative of damage where

A

frontotemporal lobe

Psychopharmacology (3 decks)

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