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Psych Week 2 > ICL 8.7: Psychopharmacology of Substance Use Disorders > Flashcards

ICL 8.7: Psychopharmacology of Substance Use Disorders Flashcards

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1
Q

what are the 3 broad objectives of pharmacological agents used for withdrawal?

A
  1. detoxification: management of acute withdrawal syndromes through detoxification

benzodiazepines in alcohol use disorders and benzodiazepine use disorders

methadone or buprenorphine in opioid use disorders

  1. initial recovery: attenuation of cravings and urges to use illicit drugs
  2. prevention of relapse to compulsive drug use
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2
Q

which 3 medications are FDA approved for alcohol withdrawal disorder treatment?

A
  1. disulfiram (antabuse)
  2. naltrexone (revia, vivitrol)
  3. acamprosate (campral)
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3
Q

what is the MOA of disulfiram?

A

antabuse blocks aldehyde dehydrogenase in the liver

it’s used to treat alcohol withdrawal

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4
Q

what is disulfiram used for?

A

it’s used to treat alcohol withdrawal

it causes an aversion to alcohol by causing flushing, nausea/vomiting, headache, palpitation, SOB –> this is because it blocks aldehyde dehydrogenase in the liver so alcohol doesn’t get broken down and the person essentially gets a hangover

best used in highly motivated patients; the goal is complete abstinence*!

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5
Q

what are the side effects of disulfiram?

A

it’s contraindicated in severe cardiac disease, pregnancy and psychosis

↑ acetylaldehyde buildup leads to nausea, vomiting, hypertension, death), can be triggered by small amounts of alcohol present in household products

you should also monitor liver function; check LFTs before and yearly

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6
Q

what is the MOA of naltrexone?

A

revia/vivitrol is a opiate mu receptor antagonist (OPRM1 gene)

this interrupts the reward pathway and the goal is relapse prevention

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7
Q

what is naltrexone used for?

A

treatment of alcohol withdraw by interrupting the reward pathway and decreasing the desire/craving

the goal is relapse prevention = reduce drinking, prevent cravings

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8
Q

what are the side effects of naltrexone?

A

revia/vivitrol can cause:

  1. GI upset
  2. headaches
  3. fatigue

be careful giving it to patients with chronic pain on opioid therapy

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9
Q

what are the precautions you have to take with naltrexone?

A

ensure OK LFTs (GGT, AST, ALT, bili)

IM vivitrol bypasses first pass metabolism; so you must have zero opioids for 7-10 days prior to injection otherwise will precipitate withdrawal

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10
Q

what is the MOA of acamprosate?

A

campral is a glutamate antagonists so so it modulates the overactive glutamatergic brain activity that happens after stopping heavy chronic alcohol use

it’s used to treat alcohol withdrawal and the goal is relapse prevention

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11
Q

what is acamprosate used for?

A

alcohol withdrawal with the goal of relapse prevention = reduce drinking, prevent cravings

continue this medication even if there is a relapse on alcohol!

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12
Q

what are the side effects of acamprosate?

A
  1. diarrhea
  2. fatigue
  3. depression

also ensure that there are no hepatic issues

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13
Q

which off label medications are used for alcohol withdrawal disorder?

A
  1. topiramate (topamax)
  2. baclofen (lioresel)
  3. gabapentin (neurontin)
  4. ondansetron (zofran)
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14
Q

what are the characteristics of topiramate? what’s its MOA?

A

GABA mediated neuronal inhibition and antagonizes certain glutamate receptor subtypes

indicated for migraines, seizures (also binge eating disorder, alcohol use disorder, and a strategy to mitigate psych-med induced weight gain) –> used off label to treat alcohol withdrawal

reduces cravings

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15
Q

what are the side effects of topiramate?

A
  1. impaired memory/concentration
  2. paresthesia
  3. decreased appetite/weight loss
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16
Q

what is the MOA of baclofen? what’s it used for?

A

GABA-b receptor agonist approved for treating spasticity –> used off label to treat alcohol withdrawal

helps with obsessive cravings, anxiety

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17
Q

what are the side effects of baclofen?

A
  1. nausea
  2. fatigue
  3. sleepiness
  4. vertigo
  5. abdominal pain

it’s eliminated by kidneys so do baseline labs prior to starting

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18
Q

what is the MOA of gabapentin? what’s it used for?

A

structurally similar to GABA thus inhibiting glutamate, and reducing NE and DA release

approved for epilepsy and postherpetic neuralgia

used off label for alcohol withdrawal and also sleep, anxiety and cravings

19
Q

what is the MOA of ondansetron? what’s it used for?

A

serotonin receptor type 3 antagonist

used off label for alcohol withdrawal

20
Q

what are the side effects of ondansetron?

A
  1. constipation
  2. diarrhea
  3. LFTs
  4. tachycardia
  5. headache

contraindicated in long QT syndrome, QTc prolongation risk, hepatic impairment

21
Q

what are the 3 ways you can treat opioid use disorder?

A
  1. methadone –> full agonist
  2. medication assisted treatment (MAT) –> buprenorphine is a partial agonist
  3. opioid antagonists (naltrexone) –> antagonist
22
Q

what is MAT?

A
  1. buprenorphine products
  2. buprenorphine + naloxone products
  3. sublingual, implantable, patch long acting injectable
23
Q

what is methadone including its MOA?

A

it’s a long acting opioid receptor agonist

once day dosing; used to treat opioid withdrawal

significantly reduces morbidity and mortality

restricted to federally licensed substance use treatment programs

24
Q

what are the risks associated with methadone?

A

↑ QTc prolongation

screen EKG in high risk patients

25
Q

what is the MOA of buprenorphine?

A

partial opioid receptor agonist

26
Q

what is buprenorphine?

A

partial opioid receptor agonist used to treat opioid withdrawal

can precipitate withdrawal if used too soon after full opioid agonists like methadone

SL (sublingual) formulation is safer than methadone because effects reach plateau and overdose is unlikely

only available by prescription from specially licensed office-based physician

27
Q

what is the MOA of naltrexone?

A

competitive opioid antagonist

precipitated withdrawal if used within 7 days of heroin use

28
Q

what is naltrexone?

A

competitive opioid antagonist used to treat opioid withdrawal

useful in motivated patients

oral preparation or monthly injection

29
Q

what is the MOA of naloxone?

A

high affinity µ opioid receptor antagonist

30
Q

what is naloxone?

A

high affinity µ opioid receptor antagonist used to treat opioid withdrawal

aka narcan!!

has high bioavailability when injected

in combination with Buprenorphine it prevents diversion and overdose –> IV/IM formulations are used in opioid overdose

31
Q

which stimulants do not have FDA approved medications to treat?

A
  1. cocaine
  2. methamphetamine
  3. cannabis
32
Q

what is the MOA of caffeine?

A

adenosine antagonist = increases excitatory neurotransmitters

↑cAMP

33
Q

what are the effects of more than 2 cups of coffee (250 mg)?

A
  1. anxiety
  2. insomnia
  3. muscle twitching
  4. rambling speech
  5. flushed face
  6. diuresis
  7. GI symptoms
  8. excitement and tachycardia

if you drink more than 1 g of coffee you can get tinnitus, severe agitation, visual light flashes and cardiac arrhythmias

more than 10 g can cause death secondary to seizures and respiratory failure

34
Q

what is a toxic dose of caffeine?

A

3 grams in kids

5-10 grams in adults

35
Q

what are the potential negative effects of caffeine?

A
  1. diuretic & dehydration
  2. stimulates cardiac muscles
  3. relaxes esophageal sphincter and increases GI motility
  4. increase blood glucose levels in diabetics
  5. osteoporosis
  6. seizures
  7. worsening anxiety disorders, bipolar disorder, and schizophrenia
  8. caffeine withdrawal
  9. insomnia
36
Q

what drug-drug interactions does caffeine have?

A
  1. caffeine can decrease thyroid medicine Synthroid (if taken within 1 hour)
  2. caffeine can increase the level of other meds (that are also substrates at 1A2) – duloxetine
37
Q

which medications can effect caffeine levels?

A
  1. caffeine is increased by certain antibiotic cipro, tagamet for heartburn
  2. caffeine is increased in pregnancy & women on oral contraceptives or estrogen replacement
38
Q

what enzyme is caffeine metabolized by

A

CYP1A2

the same enzyme that tobacco is metabolized by

39
Q

how does smoking effect caffeine?

A

caffeine and tobacco are both metabolized by CYP1A2

excessive smoking increases the activity of CYP1A2 enzyme overall so it will also metabolize other compounds that go through that system more resulting in decreased levels of that compound up to 50% – like coffee

when someone stops smoking cigarettes = liver recovers, and the increased activity goes back to normal, which means that suddenly the caffeine isn’t being metabolized at double time and having its levels halved anymore = caffeine levels skyrocket

so if someone is stopping smoking, warn them to also decrease their caffeine intake because of this

40
Q

which drugs are FDA approved to treat nicotine withdrawal?

A
  1. varenicline (chantix)
  2. bupropion (zyban)
  3. nicotine replacement therapy; patch, gum, nasal spray
  4. behavioral support/counseling
41
Q

what is the MOA and use for varenicline?

A

_4b2 nicotinic cholinergic receptor( nAChR) partial agonist

reduces reward and prevents withdrawal symptoms from nicotine

42
Q

what is the MOA and use for bupropion?

A

inhibitor of DA and NE reuptake

Reduces craving and withdrawal symptoms of nicotine

43
Q

how is smoking and mental illness related?

A

smoking is very prevalent in people who have mental illness, more than in populations without mental illness

this isn’t good because smoking effects a lot of the medications used to treat mental illnesses!!

44
Q

which medications are effected by smoking?

A
  1. antipsychotics
  2. antidepressants
  3. mood stabilizers
  4. anxiolytics

people with mental health conditions smoke about 2x the rate of the general population (41% versus 22%)

Psych Week 2 (18 decks)

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