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SPP2 substance abuse disorders > final > Flashcards

final Flashcards

1
Q

substances of abuse act ___

A

directly or indirectly on GPCRs
directly - opioids (mu), LSD, mushrooms (5HT), marijuana, K2, spice (CB1), GHB (GABA), caffeine (adenosine)
indirectly -
-Cocaine/ amphetamines: block dopamine transporter = increased dopamine in synapse
-MDMA/ Ecstasy: monoamine transporter: dopamine, serotonin
-Alcohol: Release of endogenous opioids
on ion channels - nicotine (ACh), PCP, ketamine (NMDA), benzos, barbituates (GABA)

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2
Q

dangerous withdrawal symptoms

A

alcohol and tranquilizers

grand mal seizures, heart attacks, strokes, hallucinations, delirium tremens

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3
Q

positive vs. negative reinforcement

A

positive - feels normal, takes drug to feel good

negative - feels bad, takes drug to feel normal

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4
Q

DEA schedules

A

I: no medical use, marijuana, THC, LSD
II: high abuse, cocaine, PCP
III: moderate abuse
IV: low abuse

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5
Q

dopamine

A

drugs or pleasurable events cause a release of dopamine - leads to high and establishes addiction
abuse replaces normal dopamine release that tells our brain what we need to do (eat, sex, school) - instead we only care about getting the drug
dissociation between liking and wanting

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6
Q

incentive salience

A

salience = state or quality of an item that stands out relative to neighboring items
“diving into used toilet for opium suppositories”

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7
Q

synaptic strength

A

increases after long term stimulation

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8
Q

DSM5

A

mild 2-3
moderate 4-5
severe 6+

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9
Q

psychological dependence

A

mental urge to take drug - mind is telling you you want it

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10
Q

physical dependence

A

body needs more drug - tolerance - and withdrawals without the drug
cellular adaptations

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11
Q

emotional withdrawal

A

anxiety, depression, restlessness, insomnia, irritability, HAs, poor concentration

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12
Q

physical withdrawal

A

sweating, racing heart, goose bumps, muscle spasms, tremors, NV, diarrhea

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13
Q

glutamate

A

can increase dopamine activity in NAcc
Destruction of this pathway reduces reward
Rewarding substances cause relative increase in glutamatergic AMPA receptors (NMDA numbers stay relatively the same)
Cellular Memory: all rewards increase AMPA/NMDA ration, but synaptic plasticity endures for unnatural rewards (cocaine, heroin, alcohol)

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14
Q

Describe the therapeutic uses of psychostimulants, which
psychostimulants are used in treatment, and what their
primary target is

A

therapeutic use - ADHD, narcolepsy, suppress appetite, migraine
used in treatment - caffeine, nicotine, amphetamine, methylphenidate, armodafinil (DAT), sodium oxybate, lisdexamphetamine (prodrug), atomoxetine (NET selective), guanfacine, benzphetamine, phentermine, amfepramone
primary targets - DAT, NET

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15
Q

Describe mechanism of action of nicotine. Explain how

nicotine differs from acetylcholine. List smoking cessation drugs and describe MOA

A

MOA - nicotine activates nicotinic acetylcholine receptor (Na/K transporters) = Na enters and K+ leaves = action potential
GABA = inhibitory
First neuron releases more GABA onto GABA receptors = inhibition of second neuron to release GABA
Less GABA release = less inhibition of dopamine release = more dopamine release after nicotine
Nicotine is not degraded by acetylcholinesterase

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16
Q

Describe mechanism of action of cocaine and explain how it

differs from that of amphetamines and ecstasy

A

MOA - blocks dopamine transporters, Da gets trapped in synapse and has longer to bind to receptors, DAT > SERT > NET
amphetamines - do not block the transporter, but are taken up by the transporter, compete with uptake of dopamine, they are MAOi’s which can enter into VMAT and increase Da conc in synapse. They can also bind to TAAR1 which phosphorylates DAT, induces reverse transport function

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17
Q

Explain the health effects associated with psychostimulant
use, psychostimulant withdrawal, risks of dependence and
overdose when used alone or in combination with other drugs
of abuse

A

health effects- increase BP, HR; euphoria; agitation/restlessness/nervousness, Heightened alertness and awareness, increased energy and
motivation, euphoria, Increased sociability and talkativeness, Reduced appetite, Heart palpitations, cardiac arrest, Anxiety, self-destructive behavior, violence, Insomnia, seizures, hyperthermia*, Paranoid delusion, Can last for days, Kidney and liver failure
withdrawal- Anxiety, Depression, Pain and body aches, Exhaustion, Tremors, Increased appetite, Vivid and unpleasant dreams

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18
Q

Explain the legal status ( including scheduling) of natural and synthetic cannabinoids.

A

synthetic cannabinoids are schedule I

marijuana is schedule I, decriminalized for use in many states, legalized in others, federally still illegal

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19
Q

Describe the physical effects associated with marijuana use and summarize the abuse potential of marijuana.

A

Sedation
Red eye (conjunctival injection)ƒ
Tachycardia - Tolerance development
ƒCause angina in patients with Hx of coronary insufficiency
ƒReduction in pulmonary vitality- Deep inhalation, prolonged retention, Chronic bronchial irritation
ƒAnxiety, panic attack with potent marijuana
Low dependence potential, Overdose (non fatal) uncommon, tolerance, Cannabinoid hyperemesis syndrome (NV, relieved by hot shower)

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20
Q

Describe the pharmacology of cannabinoid receptors and the pharmacokinetics of marijuana and other cannabinoids at the CB receptors

A

THC - Quick absorption from lungs into blood, Metabolized in liver (CYP2C9), agonist of cannabinoid receptors - CB1 and CB2, inhibit GABA

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21
Q

stimulants

A

cocaine, amphetamine, meth, bath salts, ecstasy, nicotine

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22
Q

depressants

A

opioids, alcohol, cannabis, GHB, inhalants

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23
Q

psychadelics

A

LSD, psilocybin, PCP, mescaline, ketamine

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24
Q

pathway to addiction

A 
Therapeutic use (opioid being used to relieve pain) -> Positive reinforcement (pain is being relieved = user feels better) -> Negative reinforcement (baseline pain is worse = user takes medication to not feel pain)
Recreational use = positive reinforcement (cocaine feels good) -> negative reinforcement (cocaine prevents bad feelings)
Self Medication = user feels bad so they take heroin (only negative reinforcement) - Need to function (alcohol to mask withdrawal symptoms), Reduce anxiety, mental pain, depression, Escapism
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25
Q

narcolepsy

A

Excessive sleepiness, sudden sleep attack, atypical sleep pattern, cataplexy
Options: amphetamine or methylphenidate
Non-stimulant Options: Armodafinil, Modafinil, Sodium Oxybate (GHB)

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26
Q

ADHD

A

Inattention and/or hyperactivity impulsiveness

Options: amphetamines or methylphenidate

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27
Q

anorectic

A

Stimulate release of NE, DA in lateral hypothalamus
Options: benzphetamine, diethylpropion, phentermine
Weight is often regained when discontinuing drug, chronic use can exacerbate HTN, tolerance, and abuse potential

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28
Q

smoking cessation treatment

A

Replacement: gum, nicotine patch, e-cigarette?
Drugs: Varenicline: partial agonist at nAchR = blocks nicotine effect but less withdrawal incurred; Bupropion: nAchR antagonist = could precipitate withdrawal in heavy smoker

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29
Q

cocaine mechanism

A

Antagonist of amine transporters (DAT > SERT > NET) = prevents dopamine uptake = increased dopamine concentration and duration of action

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30
Q

meth, ecstasy, bath salts MOA

A

Resembles endogenous DA/NE so they compete with reuptake (substrates)

  • Block DA reuptake at VMAT-> push out dopamine from vesicles = increased extra-vesicular dopamine (considered intracellular) and reverses gradient to push dopamine into synapse
  • Activate trace amine-associated receptor (TAAR1) = phosphorylated DAT = reverse transport function = more dopamine in synapse
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31
Q

methamphetamine and amphetamine MOA

A

inhibitors of monoamine oxidase (contraindicated with anti-depressant use d/t risk of serotonin syndrome)

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32
Q

cocaine and crack cocaine

A

Add ammonia to cocaine to get free base precipitate for smoking = crack
Local anesthetic effect
Increase in HR, vasoconstriction, BP

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33
Q

risks of poly drug abuse

A

Stimulant with Depression: mask crash of stimulant with depressant (i.e. benzos and stimulants, alcohol and stimulants, cocaine and heroin)
Dangers: increased risk of overdose, arrhythmias
Treatment: biggest risk first

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34
Q

synthetic cannabinoids

A

K2/spice
Studies suggest higher risk of psychosis
Often originated from scientists academic laboratories and publications
Very potent overdose: panic attacks, convulsions
Physical Effects: anxiety, sedation, red eye, tachycardia, angina
Drug Dependence, OD, Withdrawal:
-Low dependence
-Overdose uncommon: anxiety/panic attacks
-Psychoactive Tolerance: increase strength or use
-Cannabinoid hyperemesis syndrome: N/V
-Withdrawal lasts 1-2 weeks: dysphoria, anxiety, depression, decreased appetite

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35
Q

THC

A

-Agonist to cannabinoid receptors CB1 and CB2 (GPCR)
-Gi = inhibit cAMP , inhibit Ca channels, activate GIRK potassium channels = inhibit release of GABA
Drug Interactions: CNS Depressants (opioids, benzo, barbiturates, alcohol, buprenorphine, GHB)
Brain more CB1 receptors than CB2: Receptors not located in respiratory centers of brainstem = reduced risk of respiratory depression seen with other depressants; CB2 located on glia
Cannabinoid binds to CB receptor on GABA-ergic neuron (neuron #1): THC = inhibit GABA release onto dopaminergic neuron (neuron #2), Less GABA on dopaminergic neuron (neuron #2) = no inhibition on release of dopamine on dopamine receptors = increased dopamine binding
Periphery has more CB2 receptors than CB1: CB2 on lymphocytes, CB1 on liver

36
Q

endogenous cannabinoids

A

Quickly produced near site of action when needed and quick degraded
Anandamide: broken down by fatty acid amide hydrolase
2-arachidonylglycerol
-DAG lipase = synthesis
-MAG lipase = degradation

37
Q

clinical use of cannabinoids

A

inc appetite, chemotherapy induced NV, glaucoma, MS, chronic pain

38
Q

cannabinoid use in increasing appetite

A

Stimulation of POMC neurons in hypothalamus
Increases β-endorphin release over α-MSH (anoreigenic) = increased appetite
Possibly a partial agonist could be use for an anorectic drug

39
Q

cannabinoid use in chemotherapy induced NV

A

Immediate Phase: CB1 presence in GI tract in the submucoasl plexus and myenteric plexus
Delayed Phase: CB1 presence in brain stem in chemoactive trigger zone that controls vomiting

40
Q

cannabinoid use in glaucoma

A

Caused by increased fluid build-up because blocked drainage or increased contraction of ciliary muscles = increase intraocular pressure
Activated CB1 inhibit function of ciliary muscles = relaxed and allow drainage of aqueous humor

41
Q

cannabinoid use in MS

A

Reduction in tremors and spasticity

Endocannabinoids activating shift towards anti-inflammatory T cells (TH2) similar to glatiramer acetate

42
Q

cannabinoid use in chronic pain

A

Substance P increases glutamate signaling and pain signals

CBs inhibit glutamate signaling to decrease central pain sensitization or expression of chronic pain

43
Q

alcohol metabolism

A

Limited by gastric emptying =slowed by food
Men dilute alcohol more due to having more total body water
Zero order kinetics: Above 20-mg/dL due to alcohol dehydrogenase (rate-limiting step), Essentially means that if your BAC doubles, it takes twice as long to metabolize
Metabolism done by alcohol dehydrogenase, microsomal ethanol oxidizing system (MEOS), and aldehyde dehyrogenase - MEOS only at high alcohol concentrations
Molecular Pharmacological Action: alcohol action at nicotinic receptors means varenicline could work for those addicted to smoking and drinking

44
Q

alcohol dehydrogenase

A

Metabolizes alcohol, ethanol, ethylene glycol, etc.
Found in liver, brain, and stomach
Men express higher levels of gastric ADH = start metabolizing sooner
Fomepizole: ADH inhibitor used for ethylene glycol, MeOH poisoning - Alcohol can be used as well to outcompete enzyme, Slow formation of formaldehyde and toxic metabolites and allows more time for the liver to further metabolize toxic metabolites

45
Q

aldehyde dehydrogenase

A

ALDH1B1 and ALDH2
Having less ALDH2 (Asians have 50% less) limits ability to convert acetaldehyde into acetic acid
Genotype for *2 allele:
-Heterozygous: reduced activity, can still consume alcohol
-Homozygous: deficient in ability to metabolize acetaldehyde = essentially intolerant and similar to disulfiram reaction
Disulfiram: inhibitor of aldehyde dehydrogenase = accumulation acetaldehyde = hangover feeling
Treatment with disulfiram is difficult as it requires the patient to choose to take the medication and they likely won’t have great compliance

46
Q

pharmacological actions of alcohol

A

Euphoria, disinhibition: 30-60mg/dL
Analgesia: 60-90mg/dL
CNS stimulation (mood swings aggression): 80-120mg/dL
CNS depression (slurred speech, ataxia, sedation, loss of motor control): 100-120mg/dL
Coma, Death: 300-500mg/dL

47
Q

effects of alcohol

A

Acute: vasodilation (warm, flush), reduce blood pressure, increase HR
Heavy/chronic use: reduce risk of coronary disease; cardiomyopathy, arrhythmias, hypertension, hemostasis
Thermoregulation: hypothermias
GI: Increased HCl secretion -> chronic gastritis, appetite stimulant, depressant
Long-Term
-Liver: cirrhosis, vitamin deficiencies
-Blood: mild anemia, folic acid deficiency
-Cancer: liver, along route of ingestion

48
Q

drug interactions w alcohol

A

CNS Depressants: Opioids antipsychotics, antidepressants, anti-histamines
Aldehyde Dehydrogenase Inhibitors: disulfiram, metronidazole, some cephalosporins, tolbutamide
Acetaminophen: increases toxic metabolite NAPQI; alcohol upregulates this pathway

49
Q

intoxication

A

prevent respiratory depression, aspiration of vomit, metabolic alterations

50
Q

fetal alcohol syndrome

A

facial dysmorphology, low birth weight, decreased brain size, mental retardation

51
Q

alcohol withdrawal

A

anxiety, insomnia; seizures; N/V; hallucination -> delirium tremens
-Treatment: benzos, phenytoin for seizures, electrolytes

52
Q

alcoholism

A

Disulfiram: causes flushing, throbbing, headache N/V, sweating, hypotension, confusion - Patients should be alcohol free for 24 hours
Acamprosate: NMDA receptor antagonist/ GABA agonist - Reduced relapse and prolong abstinence
Naltrexone: opioid receptor antagonist - Prevents relapse
Topiramate: inhibits glutamate signaling and enhances GABA signaling (works more like methadone, not a partial agonist like buprenorphine)
Baclofen: stimulates GABA receptors
Varenicline: weakly activates nicotinic Ach receptors

53
Q

psychadelics

A

psychoactive drugs whose primary function is to alter cognition and perception

  • Hallucinogen: give illusion of perception of sensory cues in external space (LSD)
  • Dissociatives: distort perception of self and environment (PCP)
  • Deliriants: induce delirium (confused state) (salvia)
54
Q

dangers of psychadelics

A

generally non-addicting and typically do not cause excessive CNS stimulation
-Principal danger: psychological changes they can produce and users may injure themselves accidentally

55
Q

MOA of psychadelics

A

action thought to be on the 5HT2c and 5-HT2a serotonin receptors (GPCR)
Mescaline: Increase dopamine and serotonin = more hallucinogenic; cross tolerance to LSD
Dissociatives: NMDA receptor antagonist
-Ketamine: fast and short acting
-Dextromethorphan: serotonin reuptake inhibitor
PCP: NMDA antagonist and dopamine agonist

56
Q

medical use of ketamine

A

Anesthesia: non-depolarizing NMDA antagonist for dissociative anesthesia
Chronic pain analgesia: palliative for opioid tolerant
Anti-depressant: Anti-depressants reduce glutamate transmission, could be useful in treatment resistant patients

57
Q

psychadelics and psychosis

A

Psychosis: abnormal condition of the psyche observed in bipolar disorder, schizophrenia, major depressive disorder treated with anti-psychotics
Psychedelics and certain stimulants can induce short term, drug induced psychosis

58
Q

synthetics/designer drugs

A

o New psychoactive drugs to avoid existing drug laws
Synthetics:
Opioids: Krokodil- codeine derivative -> can cause gangrene, necrosis
Cannabinoids: K2/spice
Stimulants: bath salts, designer steroids
Psychedelics: PCP, NBOMe
-NBOMe: full 5-HT2a agonist
-Reports of lethal overdose (no reported ODs on LSD)

59
Q

inhalant psychadelics

A

Volatile solvents, aerosols, gases, sprays, nitrites, hydrocarbons, ketones
Pharmacology: highly lipophilic = fast entrance to CNS; inhibition of excitatory neurotransmission (NMDA antagonism) and activation of inhibitory neurotransmitters: GABA agonism
Nitrous Oxide: Inhibits NMDA currents, no effect on GABA, release of endogenous opioids = mild analgesia
-Activate dopamine = euphoria

60
Q

heroin

A

cheaper and more available than prescription opioids
Pro-drug
High lipid solubility and rapidly crosses BBB
Active metabolites: 6-monoacetylmorphine, 3-monoacetylmorphine, morphine
Black Tar: incomplete acylation of morphine - Can lead to venous sclerosis: clots form around repeated injected sites = more turbulence and rate of clotting -> eventually clots force vein to collapse

61
Q

Rx opioid dependence

A

Can start in the hospital with opioids to treat pain
Can lead to hyperalgesia -> physical and/or psychological dependence on opioids
Can start at home: pills left over and used for positive reinforcement -> may need to switch to heroin as its cheaper
Opioids can be prescribed with proper awareness, monitoring, communications, with the patient

62
Q

depressants can cause ___ release

A

Depressants can cause dopamine release like stimulants: disinhibition of GABA leads to dopamine in nucleus accumbens
-Stimulants are not identical: stimulants can be used to deal with environment, while depressants, like heroin, may be used in a safer environment

63
Q

opioid withdrawal syndroms and treatments

A

8-12 hours: tearing, sweating, yawning, runny nose
12-14 hours: tossing, restless sleep; awake
24-72 hours: dilated pupils, anorexia, goosebumps, restless, irritability, tremor
48-72 hours: anorexia, irritability, insomnia, sneezing, muscle weakness, depression, N/V, intestinal spasm, diarrhea
Naltrexone, naloxone, buprenorphine may precipitate withdrawal if on opioids

64
Q

diarrhea from opioid withdrawal

A

Opioid agonists: Inhibitory actions on the peristaltic reflex on the intestine
Diphenoxylate with Atropine: Schedule V; atropine to discourage overdose
Loperamide: substrate for PGP = kicked out of CNS; reduced tolerance; OTC

65
Q

opioid tolerance

A

Tolerance: analgesic effects, nausea, urinary retention, respiratory depression, euphoria
No tolerance: constipation, itch, miosis

66
Q

constipation

A

Start management early
Senna (stimulant laxative): cause fluid secretion and colonic contraction
PEG: stool softener; osmotic increase in GI water content
Docusate: stool softener
Mu opioid receptor antagonists: Methylnaltrexone, Nalmefene, Alvimopan, Naloxegol, Naldemedine

67
Q

neonatal abstinence syndrome

A

problems the baby may experience due to maternal drug use
Newborn will not exhibit psychological dependence: requires memories associated with taking the medication; the child is born with physical dependence
Treatment: Non-Pharm: swaddling, hypercaloric formula, frequent feedings, observation, rehydration
Pharmacological: morphine sulfate, methadone, Opium tincture, Phenobarbital, chlorpromazine, diazepam

68
Q

opioid dependence treatment

A

Methadone: full mu receptor agonist; provides relief from withdrawal, Slow pharmacokinetics, Racemic mixture: (+) is NMDA antagonist and can be used for chronic pain, Cross Tolerance, Pro: requires more heroin to overcome, Con: Need more opioid if required for pain
Buprenorphine: mu receptor partial agonist, Blocks full agonist effect by antagonism, Provides some activation by agonism = less withdrawal , Subutex – abuse potential, Suboxone – partially blocks agonist effects (Oral administration = only buprenorphine reaches bloodstream, IV administration = naloxone action = withdrawal), Should not be taken within 24 hours of heroin ingestion
Naltrexone: antagonist, Intramuscular injection once monthly
Naloxone: rapid onset, used for overdose short term

69
Q

DSM 5 criteria applied to

A

alcohol, caffeine, cannabis, hallucinogens, inhalants, opioids, sedative/hypnotics/anxiolytics, stimulants, tobacco, other

70
Q

Problematic patterns of substance use leading to clinically significant impairment or distress, as manifested by two of the following, occurring in a 12 month period

A

Larger amounts than intended
Persistent desire to control use
Great deal of time spent in activities necessary to obtain substance
Craving, strong desire, or urge to use
Recurrent use results in failure to fulfill major obligations
Continued use despite social/interpersonal problems
Important activities are given up or reduced
Recurrent use in situation in which it is physically hazardous
Continued use despite knowledge of having a problem
Tolerance
Withdrawal

71
Q

clinical course of substance use disorders

A

Difficult to determine who will develop substance abuse or dependence
Chronic course with periods of partial or complete remission
Relapse risk: greatest during first years of treatment -> majority will be able to maintain complete or partial remission
Treatment: always recovering, never recovered, patient must be engaged in treatment, includes pharmacotherapy and psychotherapy

72
Q

stages of alcohol withdrawal

A

Stage 1: 6-8 hours: moderate autonomic hyperactivity
Stage 2: 24 hours: autonomic hyperactivity with hallucinations
Stage 3: 1-2 days: can develop seizures
Stage 4: 3-5 days: risk for delirium tremens –> mortality associated with arrhythmias, shock, infection, trauma, aspiration

73
Q

DT risk factors

A

Prior history = top predictor of future DTs
Number of detoxifications
Consumption of 1 pint of whiskey/day for 10 of 14 days prior to admission
Early symptoms of withdrawal
Hepatic dysfunction

74
Q

CIWA

A

validated scale – used clinical settings to assess withdrawal severity

75
Q

treatment of alcohol withdrawal with benzos

A

No liver dysfunction = diazpepam or chlordiazepoxide

Alcoholic Liver Disease =lorazepam

76
Q

other treatments for alcohol withdrawal

A

Thiamine: always recommend if any suspicion of alcohol use
Carbamazepine: may be effective for mild/moderate symptoms
Valproic Acid: may reduce severity of alcohol withdrawal symptoms, including seizures
Phenytoin: not effective for withdrawal seizures

77
Q

wernicke-korsakoff snydrome

A

Wernicke’s encephalopathy
-Result of thiamine deficiency
-Thiamine 100mg IM or slow IV push
-Give before dextrose-containing fluids
-Can switch to oral therapy after 24-48 hours IV
Korsakoff’s psychosis
-Chronic condition -> treat with antipsychotics

78
Q

alcohol use disorders

A

Drug therapy should be accompanied by psychotherapy

79
Q

disulfram

A

Aversive therapy = unpleasant effects if alcohol is used; monitor LFTs; reaction can last for up to 14 days after discontinuation

80
Q

acamprosate

A

Maintenance of abstinence
Suicidality warning
Take regardless of relapse

81
Q

naltrexone for alcoholism

A

Show best response to naltrexone over acamprosate in combination with psychotherapy
Decreases binge drinking, helps to increase time between drinking days
Elevated LFTs common, must monitor

82
Q

treatment for opioid withdrawal

A

Clonidine: reduces autonomic symptoms - Consider if comorbid cardiovascular disorders, Don’t use in patients with sedative withdrawal (alcohol, benzos), Monitor BP
Antidiarrheals, analgesics, antiemetics

83
Q

maintenance treatment for opioid disorders

A

Methadone and buprenorphine are the oral drugs used for maintenance
Methadone must be given in a licensed treatment program
Buprenorphine is usually given in combination with naloxone - Must be written by a prescriber who is certified by DATA 2000

84
Q

methadone

A

Long half-life; once daily dosing is appropriate for use in methadone clinic
Witnessed dosing or may earn take home doses
P450 3A4 substrate
QTc prolongation is a serious concern - EKG recommended

85
Q

bupronorphine

A

Given with naloxone in the same dosage for to decrease abuse; if injected – naloxone will block opiate effect
Should wait at least 4 hours since last opioid use

86
Q

naltrexone in opioid disoders

A

FDA approved to treat opiate dependence disorder

Concern about any pain management that may be required while taking

SPP2 substance abuse disorders (1 decks)

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