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Neuropsychiatry and Psychopharmacology > L11 - Substance Use > Flashcards

L11 - Substance Use Flashcards

1
Q

What are the two groups of substance disorders?

A

Substance Use Disorders

Substance induced disorders

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2
Q

What are the classes of drugs

A
  • Alcohol
  • Caffeine
  • Cannabis
  • Hallucinogens
  • Inhalants
  • Opioids
  • Sedatives
  • Anxiolytics
  • Stimulants
  • Tobacco
  • Other
  • Gambling….
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3
Q

Severity of disorder?

A

Depends on number of symptoms endorsed

mild - 2-3 symps
mod - 4-5
severe 6 or +

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4
Q

Intoxication?

A

Reversible substnace-specific syndrome, due to recent ingestion of a substance.

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5
Q

What does the clinical picture of intoxication depend on?

A
  • substance
  • dose
  • route of administration
  • duration/chronicity
  • individual degree of tolerance
  • time since last dose
  • person’s expectaitons of substance effect
  • contextual variables.
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6
Q

What is withdrawal?

A

substance specific syndrome problematic behavioural change due to stopping or reducing prolonged use.

physiological and cognitive components.

PCP, hallucinogens and inhalants dont have withdrawal.

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7
Q

substance induced mental disorder?

A
  • potentially severe, usually temporary but sometimes persisting CNS syndromes
  • occurs during or within 1 month of use.
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8
Q

Neuroadaptation?

A

underlying CNS changes that occur following repeated use such that person develops tolerance and/or withdrawal.

pharmacokinetic and pharmacodynamic

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9
Q

Name some stimulants

A 
cocaine
amphetamine 
methylphenidate
rispiridone
Caffeine
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10
Q

Generally, what do CNS stimlants do?

A

increase motor behaviour and elevate a person’s mood and level of alertness.

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11
Q

Cocaine?

A

derived from coca leaves/plant.

  • potent local anaesthetic, constrictor of blood vessels and psychostimulant.

Blocks dopamine re-uptake

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12
Q

What is the mode of action for cocaine

A

 Blocks dopamine reuptake
 Cocaine decreases the discharge of neurons in ventral tegmental area and the nucleus acumbens
 Cocaine potentiates the dopamine-induced decrease in discharge rate
 D2 sites induce positive behavioural effects, reinforcement and movement effects
 D1 permissive effect in behavioural expression

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13
Q

Effects of cocaine?

A 
 intense euphoria
 enhanced vigour
 gregariousness
 hypervigilance
 interpersonal sensitivity/ increased sexual responsivity 
 alertness
 Talkativeness, anxiety, grandiosity
 increased tension
 anger
 stereotyped and repetitive behaviour  impaired judgement

motor twitches due to facilitation of dopamine circuitry - parkinson-like

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14
Q

Some psychological effects of acute intoxication of cocaine?

A 
 confusion
 rambling speech
 headache
 transient ideas of reference
 tinnitus
 paranoid ideation
 auditory hallucinations in a clear sensorium
 tactile hallucinations
 extreme anger with threats or acting out of aggressive behaviour can occur.
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15
Q

What is the usage of cocaine usually like?

A

short half life = frequent dosing necessary

usage can be chronic or episodic (binges)

tolerance develops quickly.

most effective is injection

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16
Q

what is cocaine withdrawal like?

A

 Intense and unpleasant feelings of lassitude and depression, often increased suicidal ideation or behaviour.
 Mood changes, with depression, suicidal ideation, emotional lability, anhedonia, disturbance of attention and concentration
 During sustained use weight loss, malnutrition, and impaired personal hygiene

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17
Q

Mode of action for amphetamine?

A

Dopamine agonist: releases dopamine and NA into the synapse and blocks the reuptake of dopamine, as well

(similar to cocaine in that it blocks reuptake)

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18
Q

Uses for amphetamine?

A

Some Uses:
Initially an asthma treatment
Study aid
Improvement of alertness and productivity Weight-loss aid

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19
Q

Why would increasing dopamine in ADHD be better?

A

adhd is associated with high levels of dopamine. flooding the synapse will desensitise the post synaptic receptor.

effectively decreases dopamine receptor function.

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20
Q

Side effects of amphetamine/dextroamphetamine?

A

 Side effects: dry mouth, metallic taste, can pass thought the placenta, also in breast milk
 Paradoxical effect: both increases attention span and has a calming effect

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21
Q

Mode of action for methylphenidate?

A

Increases release of noradrenaline and dopamine in the CNS and reticular activating system
Onset 30-60 mins, duration 4-6 hrs, metabolised by liver, excreted by kidneys
Paradoxical effect: both increases attention span and has a calming effect

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22
Q

Mode of action for respiridone?

A

Unclear, but probably related to its antagonism of dopamine and serotonin receptors
Peak plasma level in 1-2 hours, metabolism by the liver
Side effects: Dry mouth, stomatitis (infection of the mouth), taste alteration (but rare).

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23
Q

What is a ‘general stimulant’?

A

CAFFEINE!

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24
Q

Mode of action for caffeine?

A

 Inhibits the enzyme the normally breaks down the second messenger cyclic AMP
 Increase in cAMP leads to an increase in glucose production within cells, which makes more energy available and allows for higher rates of cellular activity

Antagonizes activity of adenosine
Produces behavioural sedation
inhibit the release of many neurotransmitters i.e. NA, DA, Ach, Glu, and GABA: thus increasing NT turnover

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25
Q

What systems does adenosine affect?

A 
SYSTEM
 CNS
 Cardiovascular  Renal
 Respiratory
 Gastrointestinal  Metabolic
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26
Q

What effects does adensoine have?

A 
 Sedation
 Dilation of vessels
 Anti-diuresis
 Broncho-constriction 
 Inhibition of acid
 Inhibition of lipolysis
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27
Q

What are some direct and desired effects of caffeine

A

 relaxes smooth muscle; dilates vessels in body, constricts in
brain
  alertness, speeds thought, decreases fatigue

 withdrawal: headache, drowsiness, fatigue, negative mood
after placebo

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28
Q

What are some harmful effects of caffeine

A

 caffeinism: anxiety, insomnia, mood change: tachycardia, hypertension
 panic attacks may be exacerbated (4-5 cups)
 may be harmful in pregnancy

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29
Q

Long term effects of caffeine?

A 
 No nutritional value
 Harmful to health including
Cardiovascular system
 Osteoporosis
 Lower birth weights
 Adverse effects upon other medications  Malaise
 No beneficial effects of habitual use
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30
Q

mode of action for nicotine?

A

Tobacco stimulates the cholinergic neurons in the CNS thus increasing heart rate, blood pressure, concentration, memory, and improving mood

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31
Q

medications to stop using tobacco?

A

 bupropion (Zyban) 150mg po bid,

 varenicline (Chantix) 1mg po bid

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32
Q

What are some CNS depressants?

A

Benzodiazepines
barbiturates
alcohol
z drugs

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33
Q

Barbiturates?

A
  • produces sedation and sleep

- can also produce anaesthesia, coma and death

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34
Q

Mode of action for CNS depressants?

A

Activates the two cites on the GABA-a receptor

  • sedative hypnotic site - alcohol & barbiturates (Cl- influx)
  • antianxiety site - benzodiazepines (enhances binding effects of GABA)

harder to overdose on benzos as it depends on how much GABA is present - if you mix with alcohol, then easy to overdose.

in general, when the GABA receptor is excited, an influx of Cl- ions flow through to hyperpolarise the neuron

  • there is a good picture on the slide*
35
Q

What are CNS depressants also called

A

antianxiety agents and sedative hypnotics

36
Q

What is the cumulative effect of hypnotic use?

A

Ref to page 455 of stahl text.

The half-lives of hypnotics can have an important impact on their tolerability and efficacy profiles.
(A) Hypnotics
with ultra-long half-lives (greater than
24 hours: for example, flurazepam and quazepam) can cause drug accumulation with chronic use. This can cause impairment that has been associated with increased risk of falls, particularly
in the elderly.
(B) Hypnotics with moderate half-lives (15–30 hours: estazolam, temazepam, most tricyclic antidepressants, mirtazapine, olanzapine) may not wear off until after the individual needs to awaken and thus may have “hangover” effects (sedation, memory problems).
(C) Hypnotics with ultra-short half-lives (1–3 hours: triazolam, zaleplon, zolpidem, melatonin, ramelteon) can wear off before the individual needs
to awaken and thus cause loss of
sleep maintenance.
(D) Hypnotics with half-lives that are short but not ultra-short (approximately 6 hours: zolpidem CR and perhaps low doses of trazodone or doxepin) may provide rapid onset of action and plasma levels above the minimally effective concentration only for the duration of a normal night’s sleep.

37
Q

Adverse effect of benzo use?

A

 Cognitive impairment, decreased motor skills, daytime sedation
 Additive CNS depression (with ethanol, antihistamines, opioids)
 Dependence
 Behavioural disinhibition (paradoxical)
 Anterograde amnesia
 Abrupt withdrawal can result in panic attacks, rebound anxiety
 Risk of foetal deformation (1st trimester)

38
Q

Cog effects of long term benzo use?

A
  • global cognitive impairment
  • improvement after long term benzo users discontinued

benzos much worse than z drugs…

39
Q

Solvent abuse?

A

Inhaling of aliphatic and aromatic hydrocarbons found in substances such as petrol, glue, paint thinners and spray paints.
 Less common is inhaling halogenated hydrocarbons (found in cleaners, correction fluid and aerosol propellants) and other volatile compounds containing esters, keytones and glycols.

40
Q

What are common inhalants

A

toluene, chroming, butane and petrol

May be a cumulative effect which does not manifest until 10 or more years following abuse

41
Q

Mech of action for inhalants/solvents?

A
  • thought to work in a similar way to alcohol, being that they are not mediated by a single transmitter.
  • thought to dissolve myelin sheath surrounding neurons resulting in cell death
42
Q

Toxicity of solvents?

A
  • acute - cardiac arrhythmia, depression, delirium, respiratory failure
  • chronic - damage to vital organs such as heart, lungs, brain, liver and kidneys.
43
Q

What are psychotomimetics

A

these are another name for hallucinogens, as they mimic psychosis.

44
Q

What are the main types of hallucinogen

A

 Acetylcholine psychedelics
 Norepinephrine (catecholaminergic) psychedelics (e.g.,
mescaline)
 Serotonin psychedelics (e.g., lysergic acid diethylamide)
 Psychedelic anaesthetics (e.g., PCP, ketamine)
 Tetrahydrocannabinol (THC): active ingredient in marijuana

45
Q

Anticholinergic agents?

A
  • Hallucinogens
     Scopolamine and atropine
     obtained from belladonna, datura, and
    mandrake
46
Q

Mode of action for anticholinergic agents?

A

acts on PNS

47
Q

What are the effects of anticholinergic agents?

A

act on pNS causing…

decreased sweating and salivation, increased body temperature, dilation of the pupils, blurring of vision, increasing the heart rate
at higher doses causes CNS effects including, delirium, confusion, sedation and amnesia

48
Q

Catecholaminergic agents?

A

Mescaline, STP, MDA, MDMA (ecstasy), MMDA, DMA, myristin and elimicin

49
Q

How do catecholaminergic drugs work

A

Psychedelic action probably as a consequence of their agonistic effect on post synaptic 5-HT2 receptors

50
Q

Effects of catecholaminergic drugs?

A

time distortion, altered perception of colour, sound, and shapes, complex hallucinations, synaesthesia, dreaminess, depersonalisation, altered affect and somatic effects

51
Q

What are designer drugs?

A

Chemical analogues of psychoactive substances
 Have slightly different and often even more
powerful effects than the model drug
 Not identical in structure to illegal substances so not covered by drug laws

52
Q

mode of action for MDMA?

A

 Releases reservoirs of serotonin in brain
 More serotonin induces feelings of happiness
 Effects begins in 20 min – 1 hour, Lasts 3 - 4 more hours
 Takes 1 - 2 weeks to produce sufficient amount of serotonin to re-experience same feelings
 Death by overdose is rare, but possible
 Down Regulation-Serotonin receptor “retreat” into the cell membrane to avoid damage after excessive stimulation
 Thus fewer receptors to respond to serotonin

53
Q

What is MDMA?

A

Ecstasy

54
Q

What are the side effects of mdma?

A 
 Increased heart rate
 Increased blood pressure
 Pupil dilation
 Muscular tension- jaw clenching  Exhaustion
 Dry mouth & throat
 Nervousness
 Anti-fatigue effects
 Profuse sweating
 Numbness
 Dehydration
 Increased body temperature
55
Q

How do most deaths from MDMA occur?

A

Dehydration and overheating

56
Q

Long term effects of MDMA?

A

 Anxiety/paranoia/depression especially in people with pre-existing mental disorders
 Possible liver damage
 Possible brain damage
 Heart problems especially if one has pre-existing conditions
 Some combination of dosage, frequency, & duration will destroy serotonin receptors
 Does not cause Parkinson’s
 Need more research on long-term effects

57
Q

PATTERN of action for MDMA?

A

usually users are depressed due to serotonin depletion after use.

not physically dependent.

nerve damage can cause memory problems and increase depression

58
Q

serotonergic drugs?

A

LSD, psilocybin, psilocin, DMT, bufotenine, ololiuqui, harmine

Effect can be divided into three phases: somatic, sensory and psychic

59
Q

Physical effects of LSD?

A

Rise in heart rate & blood pressure Higher body temperature
 Dizziness
Dilated pupils
Some sweating like amphetamines

60
Q

Mental effects of LSD?

A

 Intensified sensations
 Synaesthesia (crossed sensations: seeing sound, hearing
colour, smelling shape)
 Illusions
 Delusions
 Hallucinations (usually visual)
 Altered mood
 Impaired motivation, concentration and judgment
 Distorted reasoning including increased gullibility
 Flash backs
 “Bad trips” (acute anxiety reactions) if in an unstable environment or mental state

61
Q

What are the active ingreidents in magic mushrooms

A

psilocybin & psilocin

Effects:
 Nausea before psychedelic effects
 Visceral sensations
 Changes in sight, hearing, taste, and touch  Altered state of consciousness

62
Q

Psychedlic anaesthetics?

A

PCP and ketamine

63
Q

ketamine effects?

A 
 Effects:
 Mellow, colourful dreamlike intoxication  Slurred speech
 Impaired muscular coordination
 Dizziness
 Hallucinations
64
Q

marijuana effects?

A

Sedative, euphoriant and hallucinogenic properties

has its own receptor with its own agonist, anandamide

65
Q

acute effects of marijuana?

A

 physical lethargy
 euphoria
 stimulates appetite i.e. the ”munchies”
 In some cases can cause
 anhedonia
 mild depression
 anxiety or irritability (about one third of chronic users)
 Usually one of the first drugs which young people experiment with

66
Q

Higher doses of marijuana can do what?

A
  • mimics other hallucinogens… causing bad trips etc..

- correlationally related to onset of psychotic disorders.

67
Q

Adverse effects of marijuana

A

 Interferes with cognitive function including short-term memory
 Interferes with the operation of machinery (e.g. an automobile)
 Contributes to psychological problems in adulthood
 Elevates heart rate
 Impairs lung structure and function

68
Q

Therapetic actions of marijuana?

A

 Reduces the nausea and loss of appetite associated with chemotherapy
 Can reduce pain signaling (via THC)
 Can be used to treat the discomfort of
AIDS
 Can reduce the pressure increases in the eye associated with glaucoma

69
Q

Cognitive effects of marijuana?

A
  • temporary effects associated with withdrawal symptoms
  • not clear whether there are long term irreversible effects.

regular use = poor functioning, though.

70
Q

In which drugs are opiates usually found?

A

analgesics, anaesthetics, antidiarrheal drugs, and cough suppressants

71
Q

What are some opioid analgeics?

A

heroine, morphine, naloxone, nalorphine, endorphin

72
Q

What are opioid analgeics’ mode of action

A

Action mediated by the opiate receptors which have three types: mew, kappa and delta.

73
Q

Nalorphin and naloxone?

A

NARCOTIC ANALGESIC

opiate antagonists that block the effects of morphine

74
Q

Heroin?

A

NARCOTIC ANALGESIC

synthesised from morphine

penetrates BBB faster than morphine therefore producing rapid pain relief.

75
Q

Endorphin

A

NARCOTIC ANALGESIC

peptide hormone that acts as a neurotransmitter and may be associated with feelings of pain and pleasure

mimicked by opioid drugs such as morphine, heroine, opium and codeine.

76
Q

Morphine?

A

NARCOTIC ANALGESIC

acts on 3 opioid receptor classes - mu, delta, kappa

77
Q

effects of long term opioid use?

A

Chronic users suffer no ill effects, provided they have continuing access to sufficient quantities.
With those users who experience chronic intoxication, there can appear bouts of depression.
Often associated with criminal behaviour, other drug offences and taking of other substances.

78
Q

Effects of opioid withdrawal?

A

 Euphoria, followed by drowsiness, slowed breathing, and often profound analgesia
 At high doses respiration is completely suppressed and death follows
 Withdrawal syndrome:
 Can be extremely unpleasant: yawning, chills, muscle aches, vomiting, nausea, diarrhoea and insomnia (1-3 days)

79
Q

Treatment of opiate use disorder?

A

CD treatment
support, education, skills building, psychiatric and
psychological treatment, NA

Medications
Methadone (opioid substitution)
Naltrexone
Buprenorphine (opioid substitution)

80
Q

what are the drugs used to help with opiate use disorder?

A

Methadone (opioid substitution) - opioid blocker
Naltrexone - mu agonist
Buprenorphine (opioid substitution) - partial mu agonist with a ceiling effect - good for people who are highly motivated and do not need high doses

81
Q

What drugs have been associated with brain damage or cog impairment

A

 Amphetamines
MDMA (“ecstasy”): Serotonin neurons Methamphetamine: Dopamine neurons
 Cocaine:
Blocks cerebral blood flow
Phencyclidine (PCP or “angel dust”): Blocks NMDA receptors
 Alcohol
 Benzodiazepines

82
Q

What drugs have not be associated with long lasting brain damage?

A

 LSD
 Marijuana
 Opiates

83
Q

Prevention of substance use disorders?

A

Often aimed at adolescents
Utilize some or all of the following elements:
 Enhancing self-esteem
 Social skills training
 Peer pressure resistance training
 Parental involvement in school programs
 Warning labels on alcohol bottles
 Education regarding alcohol impairment
 Testing for drugs and alcohol at school or work  Correction of beliefs and expectations
 Inoculation against mass media messages
 Peer leadership

Neuropsychiatry and Psychopharmacology (12 decks)

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