Brainscape's Knowledge GenomeTM

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


See full index

neuro unit IV > drugs of abuse > Flashcards

drugs of abuse Flashcards

1
Q

Opioids examples

A

heroin, oxycodone and hydrocodone

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

CNS depressants examples

A

barbiturates, benzodiazepines, alcohol

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

CNS stimulants examples

A

methamphetamines, cocaine,

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

hallucinogens examples

A

Indoleamines (LSD, DMT, mushrooms), Phenylethylamines (MDMA, mescaline)

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

dissociative anesthetics examples

A

Phencyclidine (PCP), ketamine, dextromethorphan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pharmacologic property of drugs of abuse

A

enhance dopamine activity in the nucleus accumbens

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

levels of drug abuse

A

experimental (one-few trials), circumstantial-recreational (occasional use under certain circumstances), and compulsive (reliance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

pathway of addiction

A

Amygdala learns drug and cues cause pleasure–may signal relief from craving > Drug cues lead to DA release in Nucleus accumbens > triggers output to thalamus and cortex > In absence of activity from reflective reward system (prefrontal cortex) drug-seeking initiated

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

Opioids MOA

A

Agonists at μ-opioid receptors [Gi]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

CNS depressants MOA

A

Enhance GABA - inhibit glutamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

CNS stimulants MOA

A

Block DA reuptake or enhance DA release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

nicotine MOA

A

Agonist at nicotinic neuronal receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

hallucinogens MOA

A

Partial agonist at 5HT2 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

dissociative anesthetics MOA

A

Antagonist at NMDA-Glu receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

cannabinoids MOA

A

Agonist at cannabinoid (CB1-CB2) receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Opioids reinforcing effects

A

Opioids: Euphoria, sedation, anxiolytic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

CNS depressants reinforcing effects

A

CNS Depressants: Euphoria, sedation, loss of inhibition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

CNS stimulants reinforcing effects

A

CNS Stimulants: Euphoria, decreased fatigue, increased arousal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

nicotine reinforcing effects

A

Nicotine: Increased alertness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

hallucinogens reinforcing effects

A

Hallucinogens: Altered sensory perception, enhanced insight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

dissociative anesthetics reinforcing effects

A

Dissociative Anesthetics: Euphoria, heightened emotionality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

cannabinoids reinforcing effects

A

Cannabinoids: Euphoria, “mellowness”, changes in perception

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Opioids acute toxicity and treatment

A

Respiratory depression-pinpoint pupils-coma. Treatment: naloxone

24
Q

CNS depressants acute toxicity and treatment

A

Respiratory depression, coma (extremely rare with BDZs). Treatment- Ethanol: supportive plus fluids-electrolytes-thiamine. Benzodiazepines: flumazenil. Barbiturates: supportive

25
Q

CNS stimulants acute toxicity and treatment

A

SNS overactivity, increased HR-BP-temp, chest pain-MI, psychosis. Treatment: CVS support, vasodilators for BP (phentolamine), BDZs (diazepam) for agitation-seizures, haloperidol for psychotic symptoms

26
Q

nicotine acute toxicity and treatment

A

rare – ingestion of insecticide or cigarettes by children. Nausea-vomiting, diarrhea, CVP collapse, convulsions. Treatment: CVS support, emetics-gastric lavage-charcoal

27
Q

hallucinogens acute toxicity and treatment

A

LSD-Psilocybin: “Bad trip”, severe anxiety. Treatment: “talking down”, BDZs for agitation. MDMA: Agitation, hyperthermia, ADH release causing hyponatremia

28
Q

dissociative anesthetics acute toxicity and treatment

A

PCP and ketamine. Delirium,  RR-HR-BP-temp, agitation, violent behavior. Treatment: supportive for BP-hyperthermia, agitation (BDZs)

29
Q

cannabinoids acute toxicity and treatment

A

Minimal - possible anxiety, impaired coordination-tracking, acute psychosis

30
Q

What is pharmacodynamic tolerance

A

Lessened response at active target site to the same drug concentration. Due to changes in receptor sensitivity or other adaptive changes

31
Q

What is metabolic (dispositional) tolerance

A

Change in pharmacokinetics results in lowered drug Cp at active site, due to increased metabolism

32
Q

What is cross tolerance and give examples

A

•Tolerance develops to one drug – then will be seen to other drugs of the same class - same target. Ie. Heroin and hydrocodone both work at mu opioid receptors, and can develop cross tolerance. Ethanol and benzos work at GABA receptors and can develop cross tolerance

33
Q

What is learned tolerance

A

Reduction in effects of a drug due to learned compensatory mechanisms. Behavioral tolerance and conditioned tolerance

34
Q

What is reverse tolerance

A

Sensitization (increased response) to drug following repeated doses. Sensitization in nucleus accumbens may play a role in drug craving properties

35
Q

Opioids tolerance

A

Develops rapidly (up to 100-fold); not to constipation

36
Q

CNS depressants tolerance

A

Rapid to barbiturates > ethanol, benzodiazepines. Significant to sedation-intoxication, less to lethal dose

37
Q

CNS stimulants tolerance

A

: develops to euphoria-anorexia-hyperthermia, but can see supersensitivity to paranoia

38
Q

nicotine tolerance

A

Develops to subjective effects and nausea

39
Q

hallucinogens tolerance

A

Not common, since repeated use minimal

40
Q

cannabinoids tolerance

A

Rapid to most effects, also disappears rapidly

41
Q

Compare physical and psychological dependence

A

physical: stop use abruptly leads to withdrawal symptoms due to resetting of homeostatic mechanisms. Psychological: perceived need (craving), related to pathologic learning in reward pathway

42
Q

What is cross dependence and give examples

A
  • Ability of one drug to suppress the withdrawal associated with physical dependence on another drug. Related to pharmacological effects at target – not chemical similarities. Ie. Morphine and other opioids. Alcohol, barbiturates and other sedative hypnotics
  • Ability of one drug to suppress the withdrawal associated with physical dependence on another drug. Related to pharmacological effects at target – not chemical similarities. Ie. Morphine and other opioids. Alcohol, barbiturates and other sedative hypnotics
43
Q

opioids dependence

A

develops rapidly (within 1-2 weeks)

44
Q

CNS Depressants dependence

A

Appears within weeks

45
Q

CNS stimulants dependence

A

arguable- strong psychologic dependence

46
Q

nicotine dependence

A

moderate development

47
Q

hallucinogens dependence

A

does not develop

48
Q

dissociative anesthetics dependence

A

probably none

49
Q

cannabinoids dependence

A

accumulating evidence

50
Q

What are the characteristics of withdrawal symptoms

A

•Effects generally opposite of the acute effects of the drug. Ie If a drug relieves fatigue and causes mood elevation, withdrawal is characterized by lethargy and depression

51
Q

Opioids withdrawal symptoms and treatment

A

Rarely life-threatening - insomnia, diarrhea, irritability, cramps, muscle aches, increased BP. Treatment: clonidine (for SNS overactivity), methadone (works via cross tolerance), buprenorphine (partial mu agonist), or naltrexone (blocks reinforcing actions of heroin)

52
Q

CNS depressants withdrawal symptoms and treatment

A

Significant risk of mortality due to seizures (monitor). Treatment: substitution with BDZs - loading dose - then taper to prevent seizures

53
Q

CNS stimulants withdrawal symptoms and treatment

A

sleepiness, fatigue, depression, hyperphagie, craving.. Treatment: behavioral

54
Q

nicotine withdrawal symptoms and treatment

A

Irritability, hostility, anxiety, increased appetite, weight gain. Treatment of relapse: nicotine replacement, bupropion, varenicline (partial nicotine receptor agonist)

55
Q

hallucinogens withdrawal symptoms and treatment

A

Not known, “flashbacks” in some former users [HPPD - hallucinogen persisting perception disorder]

56
Q

dissociative anesthetics withdrawal symptoms and treatment

A

None observed

57
Q

cannabinoids withdrawal symptoms and treatment

A

not clinically significant, no treatment needed

neuro unit IV (25 decks)

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