Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Term 5: Behavioral Science > 6/18- Neurobiology of Addiction 3: Stimulants and Opiates > Flashcards

6/18- Neurobiology of Addiction 3: Stimulants and Opiates Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

__ of physicians known to abuse drugs as known to their colleagues are not reported

A

2/3 of physicians known to abuse drugs as known to their colleagues are not reported

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pharmacotherapy for opiates include?

A
  • Methadone
  • Buprenorphine
  • Naltrexone
  • Lofexidine
  • Clonidine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Pharmacotherapy for alcohol include?

A
  • Naltrexone
  • Disulfiram
  • Acamprosate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Stimulants include what?

A
  • Cocaine
  • Amphetamines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Effects of stimulants (mechanism and disease associations)

A
  • DA and reward
  • Amino acid reuptake carriers
  • Receptor down-regulation (Parkinson’s)
  • Cerebral vasoconstriction (stroke)
  • GABA down-regulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Effects of addictive drugs on NT levels?

Relative amounts? (comparing morphine, cocaine, amphetamine, and nicotine)

A

Increase DA levels

Amphetamine > cocaine > nicotine > morphine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does cocaine alter the brain?

A

Inhibits DA reuptake

- D2 R loss

  • Hypodopaminergic state -> DA damage and Parkinsonism

Chronic stimulants reduce DA receptors and transporters

  • Indirect effect on frontal cortical projection areas of DA neurons
  • DA Rs do not recover; even after 4 mo of abstinence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Parkinsonian (PD) Brain Abnormalities are seen with which drugs of abuse?

A
  • Amphetamine
  • Cocaine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Stimulant abusers can also experience cerebral perfusion deficits.

  • Pathophysiology?
  • Results in what?
A

Stimulant abusers can also experience cerebral perfusion deficits.

Pathophysiology:

  • Abnormally adherent platelets
  • Vasoconstriction

Results:

  • Affective/sensory dysregulation: occipital brain perfusion defects and fMRI abnormalities in occipital and temporal lobes
  • Cognitive impairment: frontal/striatal brain perfusion defects; correlate with degree of neuropsych deficits
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the cardiovascular effects of cocaine?

A
  • Vasoconstriction leads to 30% blood flow reduction during human cocaine administration and cortex flow most reduced
  • Chronic cerebral perfusion defects are evident even after sustained abstinence
  • Platelet adherence and vasoconstriction together may contribute to the sustained perfusion defects
  • Reduced cognitive functioning correlates with defects in perfusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Difference in response to video of sad person for cocaine abusers vs. others?

A
  • Healthy normal people: substantial brain activation when watching video of sad people
  • Cocaine abusers: do not perceive emotions such as sadness in other people; poor blood flow
  • Cocaine abusers pay attention to reminders of cocaine use, but ignore emotions in other people such as sadness (so brain not completely dysfunctional, but very selectively functional)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does cocaine affect GABA and CBF?

A
  • GABA deficiency after chronic cocaine
  • Cortical CBF (cortical blood flow) reflects mostly GABA inter-neuronal activity
  • GABA activity reduced during visual activation to usual cues like sadness compared to normals
  • Cocaine cues lead to over-arousal in users, but are irrelevant to normals, so little visual cortex activity in normals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
  • Brain activation to ____ is reduced by recent cocaine use
  • Brain activation in cocaine abusers is reduced in _______ areas that are used to _________
A
  • Brain activation to visual events is reduced by recent cocaine use
  • Brain activation in cocaine abusers is reduced in visual association areas that are used to understand, judge, and decide about things the cocaine abuser is seeing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does reduced brain activation mean?

A
  • Cocaine abusers cannot understand complex emotional events that they are seeing
  • Cocaine abusers cannot decide quickly to use their relapse prevention cognitive skills when they see cues that stimulate their craving
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Conclusions:

Brain abnormalities in stimulant abusers:

Pathophysiology

  • ___ deficiency - ___
  • _____
  • ___ -> ____

Affective/sensory dysregulation

  • _____
  • fMRI abnormalities: _____
A

Conclusions:

Brain abnormalities in stimulant abusers:

Pathophysiology

  • DA deficiency- Parkinson’s
  • Abnormally adherent platelets
  • Vasoconstriction -> multi-infarct dementia

Affective/sensory dysregulation

  • Occipital brain perfusion defects
  • fMRI abnormalities: occipital and temporal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the different types of opioid receptors mainly distributed in the brain? Functions?

A

Mu:

  • analgesia
  • euphoria
  • respiratory depression
  • addiction

Kappa:

  • analgesia
  • dysphoria
  • diuresis
  • addiction?

Delta

  • analgesia?
  • addiction?
17
Q

Example of and mechanism involved in opiate agonist activity?

A

Ex) Morphine

  • Bind to receptor
  • Activate G protein
  • Affect adenyl cyclase
  • Increase or decrease conversion of ATP -> cAMP
18
Q

Example of and mechanism involved in opiate antagonist activity?

A

Ex) Naltrexone

  • Bind to receptor
  • No activation of G protein
  • Expose “spare or hidden Rs” - traffic effects (Rs transported from ER, vesicles,…); makes them very useful for reversing receptor abnormalities from the use of chronic agonists
19
Q

Example of and mechanism involved in opiate partial agonist activity?

A

Ex) Buprenorphine

  • Bind to receptor
  • Partial coupling to G protein
20
Q

Adventitious properties of Buprenorphine in treatment?

A

Partial agonist, so:

  • High safety profile/ceiling effect
  • Low dependence

Tight receptor binding:

  • Long duration of action
  • Slow onset mild abstinence

[Expose “spare or hidden Rs” - traffic effects (Rs transported from ER, vesicles,…); makes them very useful for reversing receptor abnormalities from the use of chronic agonists]

21
Q

Relative effects of full agonist, partial agonist, and antagonist on opioid receptors (chart)

A
  • Full agonist = Methadone
  • Partial agonist = Buprenorphine
  • Antagonist = Naloxone
22
Q

Mu efficacy and opiate addiction (graph)

A
  • Super agonist = Fentanyl
  • Full agonist = Mophine/heroin, Hydromorphone
  • Partial agonist = Buprenorphine
  • Antagonist = Naltrexone

(With cancer treatments, may get to point where any more would kill them, so must take them off and start over)

23
Q

What is the underlying mechanism of positive opiate effects?

With full agonists (morphine)?

With partial agonists?

A

2nd messenger: cAMP (cyclic adenosine monophosphate)

  • Opiates bind to mu opiate Rs and INHIBIT cAMP formation
  • Chronic opiates up-regulate cAMP, leading to withdrawal symptoms (increased converting enzyme made due to mu opiate R inhibiting cAMP formation)
  • Partial opiate agonists like buprenorphine inhibit cAMP less than full agonists
  • Less inhibition produces milder withdrawal when inhibition is removed by stopping Buprenorphine

Morphine:

  • Morphine binds mu Rs, inhibiting cAMP formation
  • Chronic opiate inhibition of cAMP formation -> more enzymes synthesized to make cAMP
  • When opiate removed, more cAMP than normal is produced due to increased amt of enzyme
  • Increased cAMP levels lead to increased activity in adrenergic neurons and withdrwawal symptoms
24
Q

Buprenorphine inhibits cAMP ____ (more/less) than morphine

A

Buprenorphine inhibits cAMP less than morphine

  • Producing less dependence
  • Milder withdrawal
  • Less effective relief of severe dependence
25
Q

What are the implications of reduced activity of Buprenorphine at mu opiate Rs?

A
  • Buprenorphine reduces cyclic AMP levels less than morphine or methadone
  • Less opiate effects as buprenorphine dose is raised
  • Less compensatory enzyme synthesized to make cyclic AMP - When buprenorphine removed, less cyclic AMP than when methadone removed
  • Less activity in adrenergic neurons and less withdrawal symptoms after stopping buprenorphine than methadone
26
Q

What are some opioid withdrawal symptoms?

A
  • Dysphoric mood
  • Nausea/vomiting
  • Muscle aches/cramps
  • Lacrimation
  • Rhinorrhea
  • Pupillary dilation
  • Sweating, piloerection
  • Diarrhea
  • Yawning
  • Mild fever
  • Insomnia
  • Craving
  • Distress/irritability

“Everything runs”

- Like a bad case of the flu

27
Q

What is used to treat opioid withdrawal?

What characteristics allow it to do so well?

A

Buprenorphine

  • High affinity and slow dissociation from mu opioid receptor
  • Less withdrawal symptoms during detoxification

Equivalent opioid withdrawal severity

28
Q

Summary:

  • Buprenorphine is mu opioid, partial agonist due to action at cyclic AMP second messenger, not poor receptor binding
  • Profile of effects similar to other mu agonist opioids, but less respiratory depression, lower physical dependence, easier withdrawal
A

(:

Term 5: Behavioral Science (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions