Drugs of Abuse Flashcards
(106 cards)
1
Q
Psychomotor stimulants
A
Cocaine, amphetamines
2
Q
Opiates and opioids
A
Heroin, morphine, codeine, oxycodone, hydromorphone
3
Q
Cannabinoids
A
Marijuana
4
Q
Sedatives
A
Barbituates, benzodiazepines
5
Q
Hallucinogens
A
LSD, mescaline “club drugs”
6
Q
Three signs of dependence
A
Abuse
Craving
Legal Problems
7
Q
Criteria (within 12 months) for Substance Use Disorder by DSM-V
A
Tolerance Withdrawal Use of larger amounts than intended Persistent desire Inability to control use Excessive time spent Normal activities given up Use despite knowledge of problems drug cause
8
Q
Mild Substance Use Disorder
A
2-3 symptoms
9
Q
Moderate Substance use disorder
A
4-5 symptoms
10
Q
Severe substance use disorder
A
5+ symptoms
11
Q
Withdrawal
A
A marker of physiological dependence
Signs and symptoms emerge when use of the drug is stopped, or are reversed when drug is administered again
12
Q
Drug Tolerance
A
Decreased effect with repeated use of the drug
Need to use more drug to have the same effect
13
Q
Where does the mesolimbic dopamine system originate
A
The VTA
14
Q
Where does the mesolimbic dopmaine system project to
A
The nucleus accumbens
The amygdala
The prefrontal cortex
15
Q
what happens when the VTA nucleus accumbens is activated by drugs of dependence
A
Release of dopamine
16
Q
The shorter amount of time between injection of drug and delivery of the compound to brain, the ___ “high” somebody feels
A
more
17
Q
What are the two ways to get withdrawal?
A
1) Give an antagonist
2) Let the drug naturally decay
No longer binding the receptor
18
Q
What are some medical uses of cocaine?
A
1) stimulant of CNS
2) Freud used to treat depression
3) appetite suppressant (obesity)
4) topical anesthetic (historically- eye/nasal surgery, currently nasal/lacrimal duct surgery)
19
Q
Cocaine MOA
A
Cocaine inhibits the dopamine transporter on the presynaptic terminal > causes levels of dopamine in the synaptic cleft to increase (particularly in the nucleus accumbens)
20
Q
Amphetamine MOA
A
Amphetamines inhibit the VMAT2 (vesicular monoamine transporter 2)
DA not placed in presynaptic vesicles, high levels of dopamine in cell, travel reversely through the dopamine transporter (DAT) > causes increased levels of dopamine in the presynaptic cleft (particularly nucleus accumbens)
21
Q
Historical uses for amphetamines
A
Treat asthma, narcolepsy, obesity
22
Q
What is amphetamine?
A
synthetic phenylethylamine
23
Q
Acute effects of psychostimulants (cocaine, amphetamines)
A
Rush Euphoria and arousal Increased energy Feelings of competency Decreased feelings of fatigue/boredom Decreases appetite Increased HR, BP, temp
24
Q
Onset, magnitude (potency), and duration depend on____
A
route of administration (smoked, injected, inhaled)
25
If taken IV, cocaine reaches peak in ___
15 seconds
26
What is the half-life of cocaine?
40-80 mins
27
Where is cocaine metabolized?
Liver (cholinesterases)
28
What is cocaine metabolized into?
Benzoylecgonine
| can be monitored in biological fluids
29
How long can you detect cocaine in the urine?
up to 8 days after use
30
Cocaine in the presence of ethanol makes what compound
Cocaethylene
31
What are the characteristics of cocaethlyene?
Produces more euphoria
| Long duration of action than cocaine
32
What is the risk of cocaetylene?
More cardiotoxic
| Can cause cardiac arrest
33
What are the consequences of long term use of psychostimulants?
Sensitization
Tolerance
Impairment of neurocognitive functions
Increased risk of autoimmune/connective tissue diseases (lupus, goodpasture, SJS)
34
Overdose signs and symptoms of psychostimulants
```
Hyperactivity
Sweating
Dilated pupils
Agitation/tremor
Tachycardia/chest pain
Cardiac Arrhythmia*******
Hypertension
Hyperpyrexia
Stereotypical behavior
Seizures/coma
Paranoia/tactiel hallucinations
```
35
Withdrawal signs and symptoms of psychostimulants
```
Anxiety and agitation
Insomnia and hypersomnia
Fatigue and depression
Sweating
Muscle cramps
Hunger
Erectile dysfunction
```
36
Treatment of cocaine withdrawal (acute withdrawal=symptomatic treatment)
Bromocriptine (dopamine agonist)
| Benzodiazepines (in pts with severe agitation and sleep disturbance)
37
Treatment of long term cocaine addiction
No FDA approved pharma Rx
Cognitive Behavioral Therapes (functional analysis, skills training)
Development of vaccine against cocaine?
38
What is opium derived from?
Extracts of juice of the opium poppy, Papaver somniferum
39
Opioid MOA
Inhibit the GABAergic interneurons by binding u receptors > double inhibition > elevated DA levels in nucleus accumbens
40
Opioid potential routes of adminitration
```
Oral
IV
Snorting
Smoking
Subcutaneous ("skin popping")
```
41
How long do Heroin's effects last?
3-5 hours
42
Average addict uses ___ times/day?
2-4
43
Signs of Opioid Overdose
```
Unconsciouness
Miosis
Hypotension
Bradycardia
Respiratory depression***
Pulmonary edema****
```
44
Opioid cross tolerance
Tolerance to one opioid is usually associated with tolerance to other opioids
45
Metabolism of Heroin (why it is so addictive!)
Metabolized to 6-monoacetylmorphine > metabolized to morphine (2 drugs in one!)
46
When does Heroin withdrawal begin?
12 hours after last dose
47
When does Heroin withdrawal peak?
1 1/2 - 3 days
48
When does Heroin withdrawal finish?
Usually over by 5-7 days
49
Heroin and protract abstinence syndrome
Lingering symptoms of withdrawal can persist for months and are associated with relapse
50
Can Heroin withdrawal be life threatening?
YES! also very painful
51
Opioid withdrawal symptoms
```
Anxiety and dysphoria
Craving and drug-seeking
Sleep disturbance
Nausea, vomiting, diarrhea
Lacrimation*
Rhinorrhea*
Yawning*
Piloerection*
Sweating
Mydriasis
Cramps
Hyperpyrexia (high fever)
Involuntary movement*
```
*specific to heroin withdrawal
52
Treatment of opioid addiction
```
Self-help groups
Inpatient detox
Individual therapy
Prescription opioids
Pharmacotherapy
```
53
Goals of pharmacotherapy
Cure of withdrawal or overdose
| Create window of opportunity for pt to receive psycho-social intervention
54
Treatment of Opioid Overdose
Naloxone
55
MOA of Nalaxone
u-opioid competitive antagonist with very high affinity but short half-life
56
Individuals treated for overdose with Nalaxone must be____-
Kept under observation for duration of the opioids drug's effects
57
Treatment of Opioid Dependence
Naltrexone
58
MOA of Naltrexone
u-opioid antagonist with long half-life
| heroin self-administration no longer rewarding
59
What is Naltrexone FDA approved for?
Opioid dependence
| Alcohol dependence
60
Contraindication for Naltrexone
Avoid in pts with liver failure
61
Treatment with Methadone
| for opioid
Prevents withdrawal symptoms and cravings, has a cross tolerance with other opioids
Only dispensed in federally licensed clinics (daily visits)
62
MOA of methadone
u-opioid receptor agonist with long half life
63
Treatment with Buprenorphine (for opioid)
Given in formulation with nalaxone, has high affinity for receptors and dissociates slowly
Take Sublingually
64
What happens when Buprenorphine is misused intravenously
Will result in withdrawal symptoms (due to presence of Naloxone)
65
What happens if buprenorphine is initiated prior to onset of acute withdrawal signs
Can leads to abrupt withdrawal syndrome
66
Active constituent of marijuana
THD (delta-9-tetrahydrocannabinol)
67
MOA of THC
Inhibits GABAergic interneurons by binding the CB1 receptors >stimulation of DA release in nucleus accumbens
68
Acute effects of marijuana
```
sedation, relaxation
Mood alteration
Altered perception and time estimation
impaired judgement, memory, and concentration
Increase heart rate, dry mouth
Increased appetite
Injection of the conjunctiva
```
69
Adverse effects of marijuana use
Panic, delirium, paranoia, poor judgement, tolerance, personality chances, gateway to other drug abuse
70
Treatment of marijuana abuse is symptomatic
Anxiolytics
Antipsychotics
Cognitive behavioral therapy
71
Characteristics of Type A Alcohol Dependence
```
Late onset (>25)
Few familial
Milder form
Environmental influence
Minimal criminality
```
72
Characteristics of Type B Alcohol Dependence
Early onset (
73
Primary diseases associated with chronic alcohol use
```
Alcohol poisoning
Alcoholic heart disease
Alcoholic gastritis
Alcoholic liver cirrhosis
Alcoholic nerve disease
Alcoholic psychoses
```
74
Secondary diseases associated with chronic alcohol us
```
Cancer (lip, mouth, pharynx, esophagus, larynx, liver, stomach)
Diabetes
GI disease
Heart disease
Liver disease
Pancreatitis
```
75
Effects of alcohol on neural circuits
Indirectly increasing dopamine levels in mesocorticolimbic system
Indirect activation of opioid receptors
Increases effect of GABA > (decreased GABA receptors)
Inhibits the effects of glutamate (>upregulation of NMDA receptors)
76
Treatment stages of alcohol dependence
1. identification (CAGE)
2. detoxication/withdrawal
3. Rehab
4. Aftercare
77
Treating symptoms of alcohol withdrawal
Benzidiazepines (indirect agonist of GABA)
Diazepams (long half-life)
Lorazepam (shorter half-life)
78
Which drug is preferable to treat alcohol withdrawal in a patient with cirrhosis?
Lorazepam
79
Minor alcohol withdrawal symptoms
6-36 hrs after
CNS hyperactivity
anxiety, headache, sweating, palpitations, GI upset, insomnia, nausea
80
Seizures from alcohol withdrawal
6-48 hours after
tonic-clonic seizures (3%)
status epilecticus
life threatening
81
Alcoholic hallucinations
12-48 hours after
| Visual, auditory, tactile
82
Delirium tremens
49-96 hours after (can last 5 days)
| Withdrawal from long-term alcohol consumption or benzodiazepine withdrawal
83
Symptoms of delirium tremens
Confusion, hallucinations, tremors of extremities, fever, tachycardia, HTN, diaphoresis
84
Treatment of delirium tremens
Benzodiazepines with long half-life (diazepam, lorazepam)
85
FDA approved therapies for alcohol dependence
Disulfiram
Naltrexone
Acamprosate
86
Disulfiram
Alcohol aversion therapy
| inhibit ALDH > increased levels of acetaldehyde > nausea, dizziness, headache, hypotension, vomiting
87
Risk of disulfiram
Hepatotoxicity
| Does not increase abstinence
88
Which genetic variant of the ALDH enzyme to asians have which protects against alcohol dependence?
ALDH2*2
89
Naltrexone
Long acting opioid antagonist
Blocks release of dopamine from nucleus accumbens
Reduces alcohol cravings
90
Avoid naltrexone in which types of patients?
pts taking disulfiram
| pts dependent on opioids
91
Acamprosate
Restores balance between neuronal excitation and inhibition (mechanism unknown)
-decreases glutamate, increases GABA
92
Side effects of acamprosate
Diarrhea, allergic reactions, irregular heart beats
93
Contraindication of acamprosate
Severe renal disease
| dose adjust in patients with moderate renal disease
94
What is the BEST drug on the market for treating alcohol dependence?
Acamprosate (80% success)
95
Therapeutic use of benzodiazepines
severe anxiety, panic attacks, phobias
| insomnia, muscular disorders, alcohol withdrawal, epilepsy
96
MOA of benzodiazepines
indirect agonist of GABA receptor
97
Benzodiazepine Withdrawal symptoms
```
anxiety, agitation
Increased sensitivity to light/sound
Muscle cramps
sleep disturbance
dizziness
Myoclonic jerks
```
98
Treatment of benzodiazepine withdrawal
diazepam
| long half-life--gradually taper off the drug
99
Nicotine
selective agonist of the nicotinic acetylcholine receptor > stimulates dopaminergic neurons in VTA, increases DA release in nucleus accumbens
100
Treatment of nicotine addiction
Nicotine patches, nasal spray, nicotine lozengem varenicline (chantix)
101
Varenicline (Chantix)
Non-nicotine medication
Partial agonist that binds subunits of nicotine Ach receptors
Relieves cravings and withdrawal symptoms
Binds with greater affinity than nicotine
102
Symptoms of hallucinogens
Changes of sensation, illusions, hallucinations, create fantasies, living nightmares
103
Do hallucinogens induce dependence or addiction?
NO!
104
Molecular target of hallucinogens
Serotonin receptors (5-HT2A in cortex)
105
Treatment for non-psychotic agitation (due to hallucinogens)
anti-anxiety drugs (diazepam)
106
Treatment for severe agitation (due to hallucinogens)
Anti-psychotic drugs
