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Pharm: Psych > 2.18: Abuse > Flashcards

2.18: Abuse Flashcards

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1
Q

What are the psychomotor stimulants of abuse?

A
  1. Cocaine

2. Amphetamines

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2
Q

What are the opiates of abuse?

A
  1. Heroin
  2. Morphine
  3. Codeine,
  4. Oxycodone
  5. Hydromorphone
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3
Q

What are the sedatives of abuse?

A
  1. Benzos

2. Barbituates

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4
Q

Components of substance abuse?

A
  1. Abuse
  2. Cravings
  3. Dependence
    * **Used to be legal problems but not longer
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5
Q

What is withdrawal?

A
  1. Signs surface with substance is stopped

2. Symptoms reverse with substance readministered

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6
Q

What is tolerance?

A
  1. Decreased effect with repeated use of drug

2. Need to use more drug to have same effect

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7
Q

Which pathway is activated by drugs of dependence?

A
  • VTA to the Nucleus accumbens pathway resulting in release of dopamine
  • VTA also projects to frontal cortex and amygdala
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8
Q

Where does inhibitory onto dopamine neurons come from?

A
  • GABAergic neurons present within the VTA or as feedback loop from accumbens
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9
Q

Where will increased dopamine be seen in addiction?

A

Nucleus accumbens

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10
Q

What characteristic of a drug makes you feel extremely high?

A
  • Short time between drugs delivery and its arrival at the receptors in the brain
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11
Q

What does withdrawal mean?

A
  • Drug no longer in the system and is unable to occupy the receptors in the brain
  • Also, receptors could be occupied by antagonist in presence of the drug: antagonist needs higher affinity for this to work
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12
Q

What does cocaine stimulant?

A
  • Sympathetic system of CNS

- Has been used as appetite suppressant, and topical anesthetic for lacrimal duct therapy

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13
Q

Characteristics of amphetamines?

A
  • Synthetic phenylethylamines originally used to treat asthma, narcolepsy, and obesity
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14
Q

Mechanism of cocaine?

A
  • Cocaine blocks DAT (dopamine reuptake transporter) in presynaptic terminal
  • {dopamine} increases in presynaptic cleft
  • This primarily occurs in nucleus accumbens
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15
Q

Mechanism of amphetamines?

A
  • Inhibits VMAT2 in presynaptic neurons preventing placement of dopamine in presynaptic vesicles
  • Leads to increased [free dopamine] in presynaptic neuron that floods (direction opposite of normal) through DAT into cleft
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16
Q

Effects of psychostimulants?

A
  1. Rush (orgasmic)
  2. Euphoria / arousal
  3. Increased energy
  4. Feelings of competency
  5. Decreased feelings of fatigue/boredom
  6. Decreased appetite
  7. Increased HR, BP, temperature
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17
Q

How to feel highest on cocaine?

A

IV - 15 seconds before high

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18
Q

Where is cocaine metabolized?

A
  • In liver by cholinesterases into benzoylecgonine

- This is what is measured in urine for up to 8 days

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19
Q

What happens to cocaine in presence of ethanol?

A
  • Transesterified into cocaethylene
  • Leads to more euphoria and longer duration
  • More cardiotoxic
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20
Q

What is cocaethylene?

A
  • What cocaine is metabolized into when taken with booze

- Leads to greater high, longer duration, and greater cardiotoxicity

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21
Q

Which are the psychostimulants?

A
  1. Cocaine

2. Methamphetamines

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22
Q

Long term effects of psychostimulants?

A
  1. Sensitization: increased response
  2. Tolerance
  3. Increased risk of autoimmune connective tissue disease
  4. Impaired neurocognition: visuomotor, attention, memory
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23
Q

Signs of psychostimulant OD?

A
  1. Hyperactivity
  2. Sweating
  3. Dilated pupils
  4. Tachy / chest pain
  5. Arrhythmias
  6. Htn.
  7. Tactile hallucination
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24
Q

How does coke kill you?

A
  • Cardiac arrhythmia
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25
Signs of coke ED?
1. Anxiety agitation 2. Insomnia / hypersomnia 3. Fatigue / depression 4. Sweating 5. Muscle cramps 6. Hunger 7. ED
26
Is there treatment of cocaine withdrawal or addiction?
- No long term treatment, treat symptoms - Benzos can be used to calm patient - Bromocriptine can lessen symptoms: dopamine agonist
27
What is heroin?
- Synthetic opioid synthesized from morphine
28
How do opioids work?
- Inhibition of GABAergic neurons by binding mu receptors in VTA - GABAergic neurons are inhibitory: opioids act as agonists inhibiting inhibitory action of GABA neurons leading to disinhibition of dopamine system
29
Heroine pattern of used?
- Lasts 3 - 5 hours - Usually taken 2 - 4 hours / day - High tolerance and addiction
30
Sign of opioid OD?
1. Unconsciousness 2. Respiratory depression / pulm edema: kills you 3. Miosis: pinpoint pupils 4. Hypotension 5. Bradycardia
31
Which drug class have cross tolerance?
- Opiods | - Heroin is prodrug metabolized into 6-monoacetylmorphine which becomes morphine = drug effects
32
Characteristics of morphine withdrawal?
- 12 hours to 7 days - Can linger for months - Extremely painful and possibly life threatening leading to relapse
33
Signs of opioid withdrawal?
1. Lacrimation 2. Rhinorrhea 3. Piloerection / gooseflesh 4. Involuntary movement: "kicking the habit"
34
How to treat opioid OD?
* *Naloxone: Opioid receptor antagonist - Very high affinity but short half life - Life is lower than heroin so may need many administrations
35
How to treat opioid dependence?
Naltrexone: mu antagonist - Long 1/2 life - Also used with booze - Using heroine is no longer rewarding
36
How to treat opioid withdrawal?
Methadone: mu agonist Buprenorphine: partial mu agonist
37
What is methadone?
- Mu agonist: same as heroin - 1/2 life is 15 - 60 hours preventing cravings / withdrawal - Requires daily visit to clinic - WIll also get you hooked
38
How is buprenorphine formulated?
- Formulated with naloxone (antagonist) - Thus if someone tries to crush and inject they cant abuse - If used before withdrawal can cause abrupt withdrawal by displacing morphine
39
Active ingredient in marijuana?
- THC
40
MOA of cannabis?
- THC inhibits GABAergic interneurons - Causes disinhibition of mesolimbic DA system - Leads to DA release in accumbens * **Work on CB1 receptor unlike opioids which work on mu
41
Acute effects of marijuana?
1. Increased HR 2. Munchies: drops blood sugar 3. Red eyes: "Injection of conjunctiva" decreases BP 4. Dry mouth 5. Sedation 6. Altered time perception 7. Impaired judgement
42
Adverse effects of marijuana?
1. Panic 2. Tolerance 3. Gateway drug 4. Personality changes and loss of short term memory 5. Amotivation
43
Is alcoholism genetic?`
50%
44
What is type A alcoholism?
1. Late onset: >25 years old 2. Few familial alcohol dependence 3. Slower progression 4. Milder form of alcohol dependence 5. Important environmental influence
45
What is type B alcoholism?
1. Early onset:
46
Impact of alcohol in CNS?
1. Increases effect of GABA: inhibitory NT 2. Inhibits effect of glutamate: Excitatory NT * **Chronic use leads to: 3. Reduced GABAergic receptors 4. Upregulation of NMDA receptors
47
What happens when suddenly stop taking booze?
- Acute increased glutaminergic activity | - Can lead to death
48
How to treat alcohol withdrawal? Specific drug?
- Benzo with long 1/2 life * **Diazepam * ***Lorazepam if liver issues
49
Symptoms of alcohol withdrawal?
1. Anxiety, headache, sweating 2. Anxiety 3. Hallucinations 4. Delirium tremens
50
Pharmacotherapy for alcohol dependence?
"DNA" 1. Acamprosate: Restores neuronal excitation / inhibition balance 2. Naltrexone: Long lasting opioid antagonist 3. Disulfiram: alcohol aversion therapy
51
How is alcohol metabolized?
- ADH converts to acetaldehyde | - ALDA conversts to acetate
52
How does disulfiram work?
- Inhibits ALDH increasing acetaldehyde when you drink - Causes nausea, dizziness, headache, hypotension, vomiting - Decreases desire to drink but not dependence * ***Leads to increased hepatotoxicity * ***Person will just stop taking drug as it does not stop craving
53
Asians and alcohol?
- Have ALDH that works more slowly - Prevents alcohol dependence * **ALDH2
54
How does naltrexone work in alcohol?
1. Antagonist of opioid receptors 2, Blocks release of dopamine from Nucleus Accumbens 3. Reduces alcohol cravings 4. Avoid Naltrexone with Disulfiram together: hepatotoxins 5. Avoid in opioid dependence: precipitates acute withdrawal
55
How does acamprosate work?
- MOA currently unknown - Decreases excitatory glutamate neurotransmission and increases GABA-ergic activity - Dose adjustment in moderate renal disease - 80% success rate
56
MOA of benzos?
Indirect agonists of GABA-a receptor
57
Signs of benzo withdrawal?
• Anxiety, agitation • Increased sensitivity to light and sound • Muscle cramps • Sleep disturbance • Dizziness • Myoclonic jerks ****Must be treated with benzo that has long half life: Diazepam
58
Nicotine MOA
• Selective agonist of nicotinic ACH receptor (nAChR) • Nicotine acts on nAChR receptors, stimulates DA neurons in VTA and increases release of DA in nucleus accumbens
59
Treatment of nicotine addiction?
* ** Varenicline: partial agonist binds subunits of nAChR - Because stimulates the receptors, relieves cravings and withdrawal during abstinence - Binds with greater affinity than nicotine: reduces pharmacologic reward from smoking
60
What is Varenicline?
Drug used to treat nicotine addiction
61
Target of hallucinogens?
- Serotonin receptors – 5-HT2A in cortex

Pharm: Psych (7 decks)

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