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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
Q

Signs of coke ED?

A
  1. Anxiety agitation
  2. Insomnia / hypersomnia
  3. Fatigue / depression
  4. Sweating
  5. Muscle cramps
  6. Hunger
  7. ED
26
Q

Is there treatment of cocaine withdrawal or addiction?

A
  • No long term treatment, treat symptoms
  • Benzos can be used to calm patient
  • Bromocriptine can lessen symptoms: dopamine agonist
27
Q

What is heroin?

A
  • Synthetic opioid synthesized from morphine
28
Q

How do opioids work?

A
  • 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
Q

Heroine pattern of used?

A
  • Lasts 3 - 5 hours
  • Usually taken 2 - 4 hours / day
  • High tolerance and addiction
30
Q

Sign of opioid OD?

A
  1. Unconsciousness
  2. Respiratory depression / pulm edema: kills you
  3. Miosis: pinpoint pupils
  4. Hypotension
  5. Bradycardia
31
Q

Which drug class have cross tolerance?

A
  • Opiods

- Heroin is prodrug metabolized into 6-monoacetylmorphine which becomes morphine = drug effects

32
Q

Characteristics of morphine withdrawal?

A
  • 12 hours to 7 days
  • Can linger for months
  • Extremely painful and possibly life threatening leading to relapse
33
Q

Signs of opioid withdrawal?

A
  1. Lacrimation
  2. Rhinorrhea
  3. Piloerection / gooseflesh
  4. Involuntary movement: “kicking the habit”
34
Q

How to treat opioid OD?

A
  • *Naloxone: Opioid receptor antagonist
  • Very high affinity but short half life
  • Life is lower than heroin so may need many administrations
35
Q

How to treat opioid dependence?

A

Naltrexone: mu antagonist

  • Long 1/2 life
  • Also used with booze
  • Using heroine is no longer rewarding
36
Q

How to treat opioid withdrawal?

A

Methadone: mu agonist
Buprenorphine: partial mu agonist

37
Q

What is methadone?

A
  • 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
Q

How is buprenorphine formulated?

A
  • 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
Q

Active ingredient in marijuana?

A
  • THC
40
Q

MOA of cannabis?

A
  • 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
Q

Acute effects of marijuana?

A
  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
Q

Adverse effects of marijuana?

A
  1. Panic
  2. Tolerance
  3. Gateway drug
  4. Personality changes and loss of short term memory
  5. Amotivation
43
Q

Is alcoholism genetic?`

A

50%

44
Q

What is type A alcoholism?

A
  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
Q

What is type B alcoholism?

A
  1. Early onset:
46
Q

Impact of alcohol in CNS?

A
  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
Q

What happens when suddenly stop taking booze?

A
  • Acute increased glutaminergic activity

- Can lead to death

48
Q

How to treat alcohol withdrawal? Specific drug?

A
  • Benzo with long 1/2 life
  • **Diazepam
  • ***Lorazepam if liver issues
49
Q

Symptoms of alcohol withdrawal?

A
  1. Anxiety, headache, sweating
  2. Anxiety
  3. Hallucinations
  4. Delirium tremens
50
Q

Pharmacotherapy for alcohol dependence?

A

“DNA”

  1. Acamprosate: Restores neuronal excitation / inhibition balance
  2. Naltrexone: Long lasting opioid antagonist
  3. Disulfiram: alcohol aversion therapy
51
Q

How is alcohol metabolized?

A
  • ADH converts to acetaldehyde

- ALDA conversts to acetate

52
Q

How does disulfiram work?

A
  • 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
Q

Asians and alcohol?

A
  • Have ALDH that works more slowly
  • Prevents alcohol dependence
  • **ALDH2
54
Q

How does naltrexone work in alcohol?

A
  1. Antagonist of opioid receptors
    2, Blocks release of dopamine from Nucleus Accumbens
  2. Reduces alcohol cravings
  3. Avoid Naltrexone with Disulfiram together: hepatotoxins
  4. Avoid in opioid dependence: precipitates acute withdrawal
55
Q

How does acamprosate work?

A
  • MOA currently unknown
  • Decreases excitatory glutamate neurotransmission and
    increases GABA-ergic activity
  • Dose adjustment in moderate renal disease
  • 80% success rate
56
Q

MOA of benzos?

A

Indirect agonists of GABA-a receptor

57
Q

Signs of benzo withdrawal?

A

• 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
Q

Nicotine MOA

A

• 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
Q

Treatment of nicotine addiction?

A
  • ** 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
Q

What is Varenicline?

A

Drug used to treat nicotine addiction

61
Q

Target of hallucinogens?

A
  • Serotonin receptors – 5-HT2A in cortex

Pharm: Psych (7 decks)

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