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Preventative and addiction medicine > Addiction medicine > Flashcards

Addiction medicine Flashcards

1
Q

define

  • dependence
  • addiction
  • abuse
  • misuse
  • use
  • habit vs any of the above
A
  • dependence = medicalised view, BUT you may be dependent on things which may not be a problem
  • addiction = STIGMA, DO NOT EVER CALL SOMEONE AN ADDICT
  • abuse = negative connotations
  • misuse = preferred
  • use = preferred but does not acknowledge the problem
  • habit very different to above
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2
Q

how do we know whats being used

A
  • monitoring schemes (IDRS, EDRS, household drug use surveys)
  • needle syringe program reporting
  • hospitalisations, coronial inquiry
  • forensic capture
  • sewage monitoring
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3
Q

what drugs are being used locally?

A
  • alcohol and tobacco
  • steroids
  • IVDU
  • opiate use (90%+ prescription)
  • amphetamines
  • benzodiazepines (major issue in 1% of pop -> drug using community 30-40% uses)
  • OTC misuse
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4
Q

why do people misuse substances?

A
  • social, environmental, biomedical/neurochemical + genetic factors
  • ALSO personality types, exposure, societal attitudes
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5
Q

is there a genetic predisposition to substance misuse?

A
  • yes
  • genetic predisposition to some drugs that may enhance/ alter their addictive ability
  • EG1
    10% of community does not convert codeine to morphine (so you dont feel the effects) AND 10% of the community hypermetabolises (so you get around 2x the effects and are at high risk for dependence)
  • EG2
    have a core expression of alcohol dehydrogenase but do not have secondary metabolism (can get accumulation of early products which means you get flushing + feel unwell)
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6
Q

what are some social and environmental risk factors for substance misuse?

A
  • SES
  • education
  • Fam Hx
  • social acceptability
  • incarceration
  • exposure
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7
Q

explain the biomedical/neurochemical risk factors for substance misuse?

A
  • reward pathway -> food, water, sex, nurturing

- the reward pathway of users gets hijacked by the drug and tops the list

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8
Q

what is the National Drug Strategy

A
  • an integrated strategy focusing on
    1) demand reduction
    2) supply reduction
    3) harm reduction
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9
Q

what are the acute effects of substance use?

A

1) acute effects
- use (saliva drug test for driving, urine drug screening in athletes etc.)
- intoxication (BAL in driving/consent)
- adverse effects (acute harms EG. injection injury, OD, accident/ other injury, social harms etc)
- overdose: special subcategory of harm

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10
Q

what are the majority of drug deaths attributed to?

A
  • accidental
  • many acute
  • around same as MVA
  • approx 50% opioid
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11
Q

what are some routes of administration?

A

1) oral - drop it
2) IV - boot it
3) inhalation/smoke - chase it
4) rectal - shaft it

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12
Q

what are the patterns of drug use?

A

starts out experimental -> occasional-> recreational-> regular-> dependent

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13
Q

what are some harms associated with acute use?

A

1) social harms
- forensic, child safety issues, unplanned pregnancy, broken relationships, depletion of finances, employment issues

2) mental health
- psychosis, aggression, anxiety
3) physical harms
- IVDU related, OD, injury while intoxicated, LOC

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14
Q

what are some IVDU related harms?

A
  • injection injury
    (embolic events, foreign body, vasospasm, thromboembolism, vessel rupture, vessel damage, ischaemic/necrotic limb, nerve damage)
  • secondary disease
    (septicaemia, endocarditis, distant infective/body embolus, abscesses, organ failure)
  • BBV
    (hep C, hep B, HIV)
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15
Q

list some physical harms of stimulant and depressant intoxication

A

stimulants

  • rhabdomyolysis
  • renal failure
  • stroke
  • MI
  • seizures
  • cardiac failure

depressants

  • seizures
  • hypoxic brain injury
  • respiratory failure
  • aspiration
  • cardiac failure
  • leukoencephalitis
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16
Q

what are the harms associated with chronic substance use?

A

1) related to loss of function
2) social harms
forensic, incarceration, child safety issues, fertility issues, homelessness, relationship issues, prostitution, financial harms

3) mental health
- dependence, depression, anxiety, PTSD, psychosis

4) physical harms
- physiological dependence, organ damage, BBV, IVDU related harms, rapid ageing, STIs, repeated exposures to acute harms, malnutrition

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17
Q

outline dependence

A
  • requires time and use
  • context dependent
  • substance needs to be able to activate reward pathway
  • physiological and psychological aspects work together
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18
Q

what are the physiological steps to dependence?

A

1) exposed to substance with abuse potential (cross BBB)
2) +ve aspects > -ve aspects
3) environment conducive to repeated use
4) repeated use = receptor adaptation
5) downstream neurological functioning alters to adjust for receptor change (HOMEOSTASIS)
6) tolerance = when same amount of drug produces less of a physiological response
7) tolerance fuels desire to use more of substance
8) dependence= normal function now requires increased levels of binding
9) withdrawal= removal prod adverse effects

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19
Q

what are the psychological aspects of dependence?”

A

1) involved in likelihood of trying drug
2) involved in resistance to social forces
3) people with poor coping strategies tend to seek out dissociation from reality (internal locus = resilience, sense of control, identity VS external locus = supports, role models, opportunities)
4) psychological factors in the resistance to adverse experiences in stopping if desired

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20
Q

what is the DSM V criteria for substance use disorder?

A
  • problematic pattern of use
  • leads to clinically significant impairment
  • 2-3 mild; 4-5 moderate: 6+ severe
  • in 1 year incl at least 2 of:
  1. larger amounts/ longer period of substance use than intended
  2. persistent desire/ unsuccessful efforts to cut down/ control use
  3. lots of time spent in obtaining, using + recovering from substance
  4. Craving/strong desire to use substance
  5. Recurrent use resulting in a failure to fulfil major obligations
  6. Continued use despite persistent/recurrent social/interpersonal problems caused or exacerbated by use
  7. Important social, occupational/recreational activities given up or reduced due to use
  8. Recurrent use in situations that may be hazardous
  9. Use is continued despite knowledge of harm
  10. Tolerance
  11. Withdrawal syndrome on cessation or reduction
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21
Q

when does substance withdrawal occur?

A
  • only occurs when there is physiological adaptation
  • some types can be fatal

(context

  • Anticipation/ Expectation - Environment
  • Co-morbidity/Risk Factors - Extent of dependence)
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22
Q

what are some general features of withdrawals of CNS stimulants/ depressants

A
  • sweating
  • nausea, vomiting, appetite disturbances
  • restlessness, irritability, cranky, angry, violent reactions
  • loss of self- control
  • anxiety, panic attack
  • depression
  • headaches
  • muscle/ ab cramps, aches and pains
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23
Q

outline the pharmacology of alcohol intoxication

A

1) allosteric inhibition of NMDA receptors + facilitates of GABA-A mediated chloride flux
2) reward response via DA release in mesolimbic pathways increases post-synaptic D1 response
3) bilateral signalling btw pre-frontal cortex + mesolimbic pathway (VTA- nucleus accumbens)

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24
Q

what are the current guidelines for alcohol consumption?

A
  • no more than 2 std drinks daily to reduce lifetime risk of death/ injury due to alcohol
  • no more than 4 on any one occasion to decrease risk of injury/ harm that occasion
  • U18 NO alcohol because of increased risk of dependence associated with age of onset
  • NO alcohol during pregnancy/ breastfeeding
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25
Q

what is a standard drink?

A

drink containing 10g of pure alcohol

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26
Q

how many standard drinks are found in some common alcoholic beverages?

A

BEER

  • 285ml full strength (4,8%) = 1.1 std drinks
  • 425ml full strength (4,8%) = 1.6 std drinks
  • 375ml (bottle + can) full strength (4,8%) = 1.4 std drinks

WINE

  • 150ml sparkling wine (12%) = 1.4 std drinks
  • 150ml red wine (12%) = 1.6 std drinks
  • 150ml white wine (11,5%) = 1.4 std drinks
  • 750ml (bottle) red wine (12%) = 8 std drinks

SPIRITS

  • 330ml full strength ready to drink (5%) = 1.2 std drinks
  • 375ml (can) full strength premix (5%) = 1.5 std drinks
  • 300ml (can) high strength premix (7%) = 1.6 std drinks
  • 30ml high strength spirit nip (40%) = 1 std drink
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27
Q

how are standard drinks calculated?

A

NUMBER OF STANDARD DRINKS = vol of container (litres) x % alcohol in vol (ml/100ml) x 0.789 (specific gravity of alcohol)

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28
Q

what percentage of deaths are attributable to excessive alcohol use?

A
  • 10% all cancers
  • 20% intentional injuries
  • 7% deaths
  • GLOBALLY KILLS MORE THAN HIV/AIDS
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29
Q

what are the physical effects of alcohol?

A
  • affects almost every organ
  • KEY: liver, brain, GIT, heart
  • NB -> Wernickes/Korsakoffs Syndrome; liver failure, pancreatitis (+- secondary DM), gastritis (& gastric bleeding), neurological effects
    + ACUTE effects of intoxication
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30
Q

what are the psychological effects of alcohol?

A
  • insomnia, fatigue, anxiety disorders, depression, suicide, suicidal ideation, exacerbation of existing mental disorders
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31
Q

what are the social effects of alcohol?

A
  • disinhibition, unplanned sex, violence, trauma, STI, use of drugs, marital problems, workplace absenteeism, child abuse and neglect, road safety issues etc.
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32
Q

what are the potential consequences of consuming alcohol in pregnancy?

A
  • FAS (a lot unDx -> think it’s ADHD)
  • DISCRIMINATING FEATURES: short palpebral fissures, flat mid face, short nose, indistinct philtrum, thin upper lip
  • ASSOCIATED FEATURES: epicanthal folds, low nasal bridge, minor ear abnormalities, micrognathia
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33
Q

what are the harms of alcohol consumption to others?

A

AUS STAT

  • around 400 people dead + 14000 hospitalised due to drinking of others
  • 70000+ DV
  • 20000+ child abuse
  • 10million experienced some negative effect of a stranger’s drinking (1yr)
  • 70% affected in some way by another’s drinking
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34
Q

what is the cost of alcohol consumption?

A
  • around $20.6 billion
  • tangible costs $14.3 billion
  • intangible costs $6.4 billion
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35
Q

what are some barriers to seeking help for excessive alcohol consumption?

A

PATIENT

1) lack of concern
2) do not perceive risks to be significant
3) sensitive to subject (get defensive)
4) underestimate difficulty of changing
5) reluctance to seek help
6) use to cope with stress
7) stigma
8) lack of self-efficacy

DOCTOR

1) unwillingness to ask
2) lack of knowledge of guidelines
3) attitudes + beliefs
4) skills + referral practices
5) lack of time, remuneration + infrastructure

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36
Q

what are the alcohol screening tools?

A

C.A.G.E (2+)

1) have you ever felt the need to CUT down on your drinking?
2) have people ANNOYED you by criticising your drinking?
3) have you ever felt bad/ GUILTY about your drinking?
4) have you ever had a morning first thing in the morning to steady your nerves/ get rid of a hangover (EYE-opener)

AUDIT C (4+ men; 3+ women)
1) how often did you have an drink containing alcohol in the past year?
(0 never, 1 monthly, 2 two-four x month, 3 two-three x week, 4 four+ week)

2) how many drinks did you have on a typical day when you were drinking in the past year?
(0= 0-2; 1 =3-4; 2= 5-6; 3= 7-9; 4=10+)

3) how often did you have 6+ drinks on one occasion in the past year?
(0=never; 1

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37
Q

are brief interventions effective in people who have an excessive alcohol intake?

A
  • level A evidence = yes, reduce alcohol in people with risky drinking problems/ non dependent people who experience alcohol related harm
  • implement in GP+ ED
  • not recommended for severe alcohol related problems/ dependence
  • FLAGS = feedback, listening, advice, goals, strategies
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38
Q

when is screening with indirect biological markers used (alcohol)

A
  • LFT (high)

- used as adjunct to AUDIT C-> less Sn+Sp

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39
Q

what are some psychosocial interventions that can be used in people who partake in excessive alcohol consumption?

A

1) motivational interviewing
2) behavioural self-management (if no/low dependence)
3) coping skills training
4) cue exposure with other skills
5) behaviour couples therapy
6) relapse prevention strategies for mod-severely dependent

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40
Q

what does the evidence say regarding self help in people who consume excessive amounts of alcohol?

A
  • level A evidence that referral to AA improves outcomes
  • level B evidence that effective for maintenance of abstinence in some pt
  • GOV POLICY IS HARM MINIMISATION NOT ABSTINENCE
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41
Q

what are the relevant pharmacotherapies that aid in relapse prevention for dependent drinkers?

A

1) Acamprosate
- block GLUTAMATE receptor
- activate GABA A
- fewer side effects
- need normal renal function
2) Naltrexone
- oral opiate antagonist
- not suitable if taking other opiate medication
- need normal liver function
3) Disulfiram
- aversive drug
- close supervision, no Cl

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42
Q

what is Wernickes encephalopathy and Korsakoff’s psychosis?

A
  • preventable BUT potentially irreversible CONFUSIONAL/ AMNESIC state
  • can be fatal
  • caused by thiamine deficiency

ALWAYS GIVE THIAMINE + ALWAYS LOOK FOR NYSTAGMUS

WE

  • physiological component
  • usually early in presentation
  • confusion, ophthalmological changes (nystagmus>opthalmoplegia)

KP

  • psychological/ behavioural
  • often later at irreversible stage
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43
Q

what are some causes of thiamine deficiency?

A

alcohol more likely to progress to KP; non alcohol related causes more likely to be fatal

  • Alcohol (most common)
  • Malnutrition
  • Anorexia nervosa
  • Psychotic Disorders
  • Renal disease,PD
  • Bariatric Surgery
  • Diabetes/KA
  • Diuretic Drugs
  • Hyperemesis Gravidarum
  • Metastatic disease
  • Parenteral nutrition
  • IBD eg Chrohns
  • Amphetamine use
44
Q

when is alcohol withdrawal likely?

A

• >30yo
• >8sd males OR >6sd females
•

45
Q

what are some key Mx points in caring for someone going through alcohol withdrawal?

A
  • can be fatal
  • diazepam (if liver is impaired use oxazepam -> short acting)
  • tailor to withdrawal scale
  • THIAMINE
  • manage electrolytes
  • 1-2 days = seizures

if seizure Hx/ previous severe or complicated withdrawal/ significant co-morbidities -> undertake in residential setting

46
Q

what are some effective tobacco control measures?

A

1) tax
2) restrictions (indoor smoking)
3) well funded antismoking campaigns + adult focused tobacco control programs

NOTE adult focused tobacco control programs DECREASE adolescent smoking

1) decrease adolescents who see their parents/ adults smoke
2) when parents quit it reduces the likelihood their kids will smoke
3) many anti-smoking programs directly influence adolescents themselves

47
Q

at what age do you start screening for tobacco?

A
  • 10yo +
48
Q

what are some questions to ask when screening for tobacco use?

A
  • regardless of amount they smoke:
    1) ask about interest in quitting
    2) assess whether they are nicotine dependent:
  • min after waking to ciggy? (30min)
  • number per day (15+)
  • cravings/ withdrawals in previous quit attempts? (yes)
    3) advised to stop smoking
    4) offered referral (QUITLINE)

+ brief intervention (motivational interviewing, pharmacotherapy, 5As, Quitline, prevention of relapse-> follow up)

49
Q

what are some nicotine withdrawal symptoms?

A
  • dysphoria/depression
  • insomnia
  • irritability
  • frustration/ anger
  • anxiety
  • difficulty concentrating
  • decreased HR
  • increased appetite/ weight gain
50
Q

what is NRT? explain when it is used, how long it is used for + some side effects

A

NRT = nicotine replacement therapy

  • used in ALL groups of smokers (safe in pregnancy, children, adolescents + CVD)
  • available OTC (less side effects + can be used in pregnancy)
  • side effects = skin irritation and sleep disturbance
  • use for at least 10 weeks
  • follow up GP visits
  • encourage support services
51
Q

what are the pharmacotherapy options given to smokers?

A

1) NRT
2) bupropion
- Indications: smoker -> give for 2 weeks (7 weeks of therapy)

  • contraindications: pregancy, seizures, drugs that lower seizure threshold, concurrent MOA inhibitors
  • Benefits: PBS, non nicotine oral preparation, helps in chronic disease + depression
  • Side effects: allergic responses (skin rashes) and insomnia

3) varenicline
- indications: smoker -> give for 4weeks initially (should be 24 weeks of therapy)

  • Contraindications: renal impairment, child, pregnancy, existing psychological/psychiatric disorder
  • Side effects: nausea (30%) and strange dreams (monitor for neuropsychiatric symptoms)
  • Benefits: on PBS (only gets approval with follow ups), lack severe side effects and drug interactions , most effective pharmacotherapy
  • Arrange regular follow ups
52
Q

what are the steps to quitting for nicotine dependent people?

A
  • NRT will not relieve dependence
  • 90% smokers are dependent
    (for smokers who are non-dependent offer non pharmacological strategies such as: counselling, written info, Quitline, follow up + coping strategies)
  • Fagerstorm questionnaire
  • 4Ds (not useful at high end of dependence) -> delay, drink water, deep breathe and do something else
53
Q

what are the major concerns of cannabis?

A

USE

  • heavy in U16 yo
  • Increased risk of mental health problems (6 x schizophrenia + earlier onset of psychosis
  • 3yrs); dropping out, becoming dependent, using other drugs, attempting suicide, reduced life opportunities
  • A&TSI = 19% lifetime use + 1 in 4 indigenous Aus had used in last year

LONG TERM RESP HARMS (exacerbation/causation):

  • Primarily smoked (‘mull’ tobacco + cannabis-> harms additive)
  • Contains 3x tar and 5x carbon monoxide (1 joint = 3-5 ciggys in lung damage)
  • Inhale deeper= stays in lungs 4x longer (reaches more SA)
  • Higher combustion temp and burns hotter on throat and mouth

Confusion about potency
Dependence and withdrawal (fat soluble so fat people have amounts leaching into blood stream = easier withdrawal)
Cannabis and mental health
Impaired healing = impairs NK cell activity

54
Q

what are the statistics around cannabis usage?

A
  • most widely used illicit substance
  • average age 18
  • 1 in 5 aus have smoked
  • more in a+tsi -> lower SES and mental health conditions
55
Q

what are the consequences of smoking cannabis using a bong?

A
  • may present with atypical lung infections (fungi + bacteria)
  • many people use bongs as they are: economical, provides a bigger hit, smoother inhalation
  • research shows: no reduction of tar/ CO exposure + results in exposure to byproducts + petro chemicals
56
Q

why is there a variation in cannabis potency?

A
  • stronger potency due to genetics (selected seed varieties + cultivation of female plants); variation in cannabinoids + concentration of THC, CBN etc; environmental factors (cultivation techniques, prevention of fertilisation and seed products); freshness (storage degradation of THC less likely); now smoking the stronger part of the plant (head/buds)
57
Q

what are the withdrawal symptoms for cannabis?

A

1) lasts 1-7 days: anger, aggression, irritability, decreased appetite, anxiety, nervousness, restlessness, sleep difficulties + strange dreams
2) less common -> stomach pain, chills, night sweats, shaking, depressed mood

58
Q

what is cannabis induced psychosis?

A
  • short lived psychotic disorder that usually results from heavy/prolonged use
  • responds well to treatment
  • lasts couple of days
  • characterised by hallucinations, memory loss, delusions + confusion
59
Q

what are the medical uses of cannabis?

A
  • efficacy in MS
  • some evidence in other centrally mediated pain disorders
  • some improvement in AIDS cachexia
  • some evidence of effectiveness in cancer chemotherapy induced vomiting (against old drugs)
  • NO ROLE FOR SMOKED MARIJUANA
    (use CBD not whole cannabis/ THC)
60
Q

what are the stats for opiate usage?

A
  • heroin 0.2% pop
  • prescription opiates 3.6%
  • commonly injected/ smoked/ inhaled/ oral intake
61
Q

what is the MOA of heroin?

A
  • heroin = opiate

1) bind to opiate receptor resulting in:
- GABA activation (which indirectly results in DA release)
2) NOTE: delta and kappa receptors responsible for PHYSIOlogical effects + mu responsible for PSYCHOlogical effects

62
Q

what are the risks for opiate use?

A
  • main: OD (mostly accidental)
  • mix with other CNS depressants (alcohol/ benzos) -> death
  • highly dependence forming
  • respiratory threshold (can occur suddenly -> stop breathing)
  • IVDU related
  • miscarriage
  • leukoencephalopathy
63
Q

what are the immediate effects of opiates??

A

1) CNS depressant
- slows breathing/ decreases HR, low BP, dry mouth + pinpoint pupils

2) pain relief, heightened sense of well being, intense pleasure, warm, sleepy, impaired balance and coordination
3) reduced appetite and sexual urges
4) N+V (opiate induced vomiting more common in newer users)

64
Q

how do you manage opiate OD?

A

1) DRSABCD
2) recovery position
3) ambo
4) O2
5) IV/IM naloxone (opioid antagonist -> people wake up very angry)

65
Q

what is the difference between long vs short acting opiates?

A
  • depends on how its used
    EG. long acting opioid meant to be absorbed by gut but injected instead -> 1/2 life irrelevant
OPIOID POTENCY 
100mg of morphine:
- 100mg hydrocodone
- 65mg oxycodone
- 25mg hydromorphine 
- >37mcg/hr fentanyl
66
Q

what do high doses of opiates cause?

A

high doses:

  • nausea and vomiting
  • impaired concentration + drowsiness
  • sweating, itching, increased urinary output/ retention
  • respiratory depression (breathe slow + shallow)
  • hypotension + bradycardia
  • coma, death
67
Q

outline opiate withdrawal

A
  • short acting (10days), long acting (20 days), methadone (couple of months)
  • looks like sudden onset of flu + sense of doom
  • safe UNLESS severe med, psychiatric comorbidities/ pregnancy (fatal to pregnancy)
  • use COWS/SOWS (clinical/subjective opiate withdrawal scale)
  • can either stop it, swap it with another then taper/ taper dose
  • CLONIDINE can be used but drops BP (narrow therapeutic window)
  • can also use METHADONE (long acting and more addictive)/ BUPRENORPHINE
68
Q

what meds are used in opiate withdrawal?

A

1) methadone = long acting opiate agonist
2) buprenorphine = long acting, partial opiate agonist (no drowsiness)
3) buprenorphine + naloxone (4:1)
- naloxone is IV so does nothing when taken orally
- if you tried to inject combo, naloxone will block opioid receptors + buprenorphine will not give an effect

69
Q

what is the mechanism of dependence and withdrawal?

A

1) increased mu opioid receptor internalisation and degradation
2) decreased efficacy of mu signalling transduction
3) hyper activation of adenylyl cyclase signalling -> enhanced GABA release + increased gene transcription

70
Q

what are the aims of the opiate substitution public health program?

A
  • reduce BBV
  • reduce injury from injections
  • reduce crime
  • increase engagement in treatment

requirements:
- 18+ yo
- need to be opiate dependent
- PRIORITY to forensic discharge, pregnant and have BBV

71
Q

what are BENZODIAZEPINES?

A
  • dissociative and sedative hypnotic
  • CNS depressant
  • basically mimic alcohol
    EG. DIAZEPAM, OXAZEPAM, TEMAZEPAM
  • induce hypnotic state that mimics sleep (become more sleep deprived over time); dissociative state, sense of well being + euphoria
  • ONLY drug class that kills easily in withdrawal and intoxication (effects worse if you add another CNS depressant)
72
Q

what is the MOA of benzodiazepines?

A
  • reacts with booster site on GABA which enhances inhibitory effects of GABA (nerve impulse may be blocked)
  • ADDICTIVE because of increased DA release
73
Q

outline bento withdrawa

A
  • similar to alcohol withdrawal (starts later + more prolonged)
  • seizures can be fatal
  • CIWA B (clinical institute withdrawal assessment - benzos)
  • taper dose to minimise severe withdrawals
74
Q

what are reasonable uses for benzodiazepines?

A
  • alcohol withdrawal (7 days max)
  • maybe acute grief/ psychological distress (<3days + no other CNS depressants)
  • short acting procedures
  • acute inpatient <3 days
75
Q

what are the effects of benzodiazepines?

A
  • memory impairment
  • Falls (sedation, low BP, dizziness)
  • Mimic BPD, mimic ADHD
  • Suicide risk increase
  • Ataxia
  • Cognitive impairment
  • Reflex tachy
  • Seizures -> hard to treat
76
Q

what are the risks of benzodiazepines?

A
  • cause resp depression (worsened with another CNS depressant)
  • Increase change of death (no back up resp drive)
  • Used by any route
  • Acute harms similar to opiates
  • Intoxication = may get paradoxical aggressions and seizures (benzos used for seizures, drop seizure threshold)
77
Q

list the stimulants and depressants

A

Stimulants

1) amphetamines
2) Cocaine
3) Caffeine
4) Nicotine
5) Amyl nitrate
6) Ecstasy

Depressants

1) Benzodiazepines
2) Alcohol
3) Cannabis
4) Opiates

78
Q

what are some general CNS depressant/ stimulant withdrawal symptoms?

A

1) sweating
2) Nausea and vomiting, appetite disturbances
3) restlessness, irritability, cranky, angry, violent
reactions
4) Loss of self-control
5) Anxiety, panic attack
6) Depression
7) Headaches
8) Muscles/ abdominal cramps, aches and
pains

79
Q

what are some specific features of CNS stimulant withdrawal?

A
  • poor concentration
  • Mood instability
  • Hypersomnia
  • Lowering of BP, HR, RR, temperature
  • AIR HUNGER = amphetamines -> trouble
    breathing but sats are fine (gasps)
80
Q

what is the MOA, mechanism of dependence/ withdrawal of cocaine?

A

MOA : increases DA via DA reuptake inhibition

Mechanism of dependence/ withdrawal 
1) DAT expression increases
2) number of postsynaptic DA receptors
decrease
3) presynaptic DA is depleted
  • increase DA transmission via reuptake inhibition
  • Similar to amphetamines
  • More prominent: hyperthermia, pulmonary
    oedema, seizures and muscle rigidity
  • Snorting leads to -> chronic nose running/ sniffing, nose bleeds, septal erosion

Withdrawal
- onset= 2-4 days, duration 10 weeks
- DO NOT get full restoration of normal mood
regulation after heavy use

81
Q

outline ecstasy as a drug?

A
  • technically refers to MDMA
  • In practice refers to stimulant party drugs that may not
    contain MDMA
  • Like amphetamines with more prominent HYPERTHERMIA
    and HYPONATRAEMIA
  • Possible liver toxicity and neurotoxicity
  • Usually acute effects that are problematic, high level/
    chronic use = similar to cocaine/amphetamine
  • Releases 5HT (blocks reuptake) + DA (to lesser extent)
82
Q

what is GHB?

A
  • gamma hydroxybutyrate
  • Contaminates ecstasy -> Hypnotic + narrow therapeutic window = OD common (N&V, seizures, aggression, resp depression, coma)
83
Q

explain the effects of caffeine? (safe levels, max addition etc)

A 
RARE but could have cardiac effects in:
- Caffeine sensitive
- Preexisting cardiac disease
- Psychiatric patients
- Increase due to high energy
drinks and tablet use
- Max addition is 145mg/L
- Max addition incl natural extracts
= 320mg/L
- Safe level <400mg/day (preg
<200mg/day)
84
Q

what is the MOA of amphetamines?

A

1) Structurally analogous to catecholamine neurotransmitters
2) Monamine oxidase (MAO)
analogues -> inhibits MAO reuptake resulting in increased DA release (do not affect mt bound MAO much)
3) Methamphetamine more of an impact on dopaminergic release than any other drug = HIGH ABUSE POTENTIAL

85
Q

what happens in amphetamine withdrawal?

A

1) key risks: predominantly left from intoxication -> heart complications, stroke, rhabdomyolysis, renal failure, psychosis, self harm, treatment resistant severe depression
2) Approach: symptomatic relief + psychotherapy (use SLOW approach)
3) Withdrawal scale: Amphetamine Withdrawal Scale

86
Q

what are specific features of CNS stimulant withdrawal?

A
  • poor concentration
  • Mood instability
  • Hypersomnia
  • Lowering of BP, HR, RR, temperature
  • AIR HUNGER = amphetamines -> trouble breathing
    but sats are fine (gasps)
87
Q

what are amphetamine harms?

A 
Physical harms
OVERDOSE (speeds up adrenaline response)
1) Rhabdomyolysis
2) Renal failure
3) MI (esp young people)
4) Malnutrition
5) Cardiac failure
6) Seizures
7) Stroke

LONG TERM

  • chronic insomnia, HTN, rapid and irregular heartbeat, MI/ HF
  • Self medicate with depressants (benzos -> to sleep…)
  • Increased sex drive (masturbation injuries + unsafe sex)
  • Brain damage = reduced memory, impaired thinking, cognitive and motor impairment (can improve over time)
  • BBV, malnutrition = increased risk for infections
  • Psychosis, anxiety + depression
  • Violent, paranoid + aggressive
88
Q

outline effects of amphetamine use during pregnancy

A
  • bleeding, premature labour, miscarriage
  • Increased HR-> less O2 to baby -> low birth
  • weight and slow growth & development
    Overactive and agitated at birth = baby goes into
    withdrawal
  • Breast feed -> feed poorly and irritable
89
Q

what does imaging show with amphetamine induced psychosis?

A
  • more likely with ice (than cannabis)
  • Recovery takes around 2 weeks and can
    be incomplete
  • Imaging shows:
    1) Bleeding
    2) Ischaemia
    3) Brain infarct
    4) Significant changes in blood flow = permanent cognitive impairment such as memory loss
90
Q

what are some amphetamine related harms?

A

1) acquisition
- not enough money, stigma, poor relationships, dealing, supplying, alienation, secrecy, ripped off by dealers, unknown drug quality
2) administration
- vein abscesses and scarring, thrombosis, contaminants, BBV, nasal infections, needle sharing
3) Intoxication
- agitation, teeth grinding, weight loss, tachycardia, CV problems, dehydration, hyperthermia, poor immunity, paranoia, delusions, hallucinations, restlessness, sleeplessness, teeth grinding, death, stroke, seizures
4) intoxicated behaviour
- risk taking behaviours
- Other drug use, unsafe sex, relationship
problems, aggression etc.
5) withdrawal/ crash
- depression, restlessness, cravings, suicidal
ideation, job issues, flat mood, dependence, poor social function

91
Q

what are the phases in using and stopping amphetamines?

A

Using and stopping amphetamines

1) “run” phase = intoxication 2) “crash” = like VERY bad hangover
3) Each crash can lead to decreasing function, withdrawal can take from 2,5 weeks - 1 month

92
Q

in the crash phase for amphetamines what is the time since last stimulant use + common signs and symptoms?

A

time since last stimulant use

  • Onset: 12-24 hrs after last use
  • Subsides: day 2-4

common signs and symptoms
-Exhaustion, fatigue, sleep disturbances (typically
- increased);
low cravings (generalised
- aches and pains),
mood disturbances (euphoria and flat mood)

93
Q

in the withdrawal phase for amphetamines what is the time since last stimulant use + common signs and symptoms?

A

time since last stimulant use

  • Onset: 2-4 days after last use
  • Subsides: over 2-4 weeks (peaks in severity at 7-10 days)

common signs and symptoms
- strong cravings
- Fluctuating mood and
energy levels (irritability, restlessness and agitation; fatigue, anhedonia
- Disturbed sleep (insomnia, vivid dreams
- General aches and pains, headaches, muscle tension
- Poor concentration and attention
- Increased appetite

94
Q

in the extinction phase for amphetamines what is the time since last stimulant use + common signs and symptoms?

A

time since last stimulant use
- Weeks to months

common signs and symptoms

  • gradual resumption of normal mood with fluctuations in mood and energy levels
  • Disturbed sleep
  • Episodic cravings
95
Q

what are the stats for gambling + compulsive disorder?

A

1) economic mismatch (1% in high income; 10% household income in low SES)
2) Heterogenous population (mental health comorbidity, education level strongest link)
3) Increasing due to online gambling

96
Q

what are the Australian guidelines for gambling + compulsive disorder?

A
  • problem gambling
  • Difficulty limiting money/ time on gambling, leads to adverse consequences for gambler/others in community
  • Pathological gambling = Persistent and recurrent maladaptive gambling behaviour that disrupts
    personal, family/ vocation pursuits
  • Disordered gambling = Moving between the two above
97
Q

what are the recommendations, screening tools + treatment for gambling + compulsive disorder?

A

Recommendations
1) screening with 3 item screening tool -> refer to
trained specialist if positive
2) Adults, adolescents and children with mental
health problems or at risk be screened with validated tools
3) Those at high risk should be screened (anxiety, depression, family violence, alcohol and drug abuse, impulse control issues, personality disorders)

SCREENING TOOLS
1) BBGS (brief biosocial gambling screen)
= during past 12 months have you become anxious when trying to stop/cut down on gambling (withdrawal) ; have you tried to keep your family or friends from knowing how much you gambled (deceive); did you have such financial trouble that you had to get help with living expenses? (need money)

TREATMENT
- reduce gambling behaviour
- CBT and motivational interviewing
- Naltrexone but not PBS listed
- DO NOT USE ANTIDEPRESSANTS UNLESS
DRIVEN BY DEPRESSION; SELF HELP INEFFECTIVE
  • motivational interviewing -> 12 weeks (motivational enhancement therapy) -> comprehensive assessment and feedback in two sessions; follow up in week 6 and 12
  • GAMBLING HELPLINE
  • Set budget, limit time, diary to record
98
Q

what are hallucinogens?

A
  • disparate group of drugs -> hallucinations primary aim
    (LSD, mushrooms angel trumpets, synthetics)
  • usually acute use -> harms (OD - potency variable; bad trips, accidental harms + flashbacks)
  • management: supportive therapy + treatment of injuries
99
Q

what is LSD?

A
  • archetype hallucinogen
  • MOA:
    1) Activates serotonin receptors
    2) Mechanism for hallucinations and flashbacks uncertain -> reduced activity in R middle temporal gyrus, frontal gyrus, anterior cingulate cortex, L superior frontal and post central gyrus and cerebellum)
    -> Use in therapy (controversial)
    -> Harms = accidents while intoxicated/ crimes committed while under the influence (either worsening psychiatric diseases/
    think they can fly and jump off)
100
Q

what are mushrooms + what are their potential harms?

A
  • mushroom subspecies containing PSILOCYBIN/ similar
  • ID may be difficult -> look similar to poisonous mushrooms
  • ingested/smoked (with cannabis/tobacco)
  • Harms=
  • > Relatively rare
  • > Accidental poisoning
  • > Muscle weakness
  • > Anxiety and paranoia
  • > Seizures (for people with low seizure threshold)
  • > Flashbacks
  • > accidents/ forensic harms
101
Q

what is ketamine + what is the MOA of ketamine?

A
  • dissociative anaesthetic
  • Rapid onset, short duration (narrow
    therapeutic window)
  • MOA: DIRTY DRUG
    1) NMDA receptor antagonist
    2) (also opiate receptors, monoaminergic
    receptors, muscarinic receptors and VG
    Ca2+ channels)

Mixed with MDMA -> increased risk of
harm

102
Q

what is mephedrone (+ derivatives?)

A
  • 4-methylmethcathinone
  • Stimulant (psychoactive)
  • “bath salts”
  • Indirect adrenaline booster, narrow
    therapeutic windows
  • Snorted
103
Q

outline the following for inhalants and volatile substances:

1) acute effects
2) harms
3) management - acute and chronic

A

GENERAL INFO
- broad group EG. Petrol, varnish, thinner, glues, nail polish remover
- Used in adolescents (males)
- Administered by:
1) Sniffing (from container)
2) Huffing (saturated material over/ in mouth/ nose)
3) Bagging (contents in paper bags/ plastic bags over
mouth/nose)
- short duration of action, cheap and accessible
- RAPID TOLERANCE DEVELOPMENT

ACUTE EFFECTS

  • euphoria, excitation
  • N&V, headaches, diarrhoea, ab pain
  • AT HIGHER DOSES = slurred speech, disorientation, delusions, weakness, tremor, visual disturbance, ataxia, decrease level of consciousness, seizures, loss of consciousness, cardiac arrest, death

HARMS
- Volatile substances are lipid soluble and damage cell membranes in the CNS
1) Damages brain = cerebellar damage, white matter destruction, cortical atrophy, peripheral neuropathy, optic atrophy, hearing loss
2) IN PREGNANCY= crosses the placenta -> oral
clefts, microencephaly, miscarriage, foetal growth
retardation, prematurity and developmental delay
3) Asphyxia, suffocation, hypoxia
4) BM suppression
5) Forensic hams and accidents

MANAGEMENT
ACUTE
-> Recognize (smell, paint/substance on clothing, eye oscillation, sneezing, salivation, conjunctival injection)
-> Be alert (often combative); be aware (used in combo); monitor (sats and ECG); O2 where indicated,
decontamination (clothing, skin) … wait it out

CHRONIC

  • > Underlying reasons (kids unsupervised, distractions, educational attainment, safety)
  • > Physical assessment of needs (neurological impairment???)
  • > Harm minimisation
  • > Psychosocial needs -> psychotherapy, life skills etc.
104
Q

outline the vaccine schedule

A

birth

  • Hep B (IM, 24hrs - 7 days after)
  • TB (A&TSI intra dermal)

2 months AND 4 months

  • DTPa-hepB-IPV-Hib
  • pneumococcal
  • rotavirus (oral admin: 1st dose <15 weeks and 2nd dose <25 weeks)

6months

  • DTPa-hepB-IPV-Hib
  • pneumococcal (A&TSI), children with risk factors/ premature infants born <28weeks)

6 months to <5years
- influenza (two doses required with min 1 month in between doses)

12months

  • MMR
  • Meningococcal ACWY
  • pneumococcal
  • hep a (A&TSI)
  • hep b (prem baby <32 weeks gestation OR <2000g birthweight)

18months

  • MMR- varicella
  • haemophilius influenzae type b
  • DTPa
  • hep A (A&TSI)

4 years

  • DTPa-IPV
  • pneumococcal (children with risk factors)
105
Q

how do vaccines work and what are their effects?

A

WORK
Stimulate the immune system to create antibodies/memory cells in the absence of disease symptoms.

EFFECTS
1) individual protection

2) herd immunity
- resistance of a group to invasion + spread of an infectious agent based on the immunity of a high proportion of individual members of the group

3) reduction in morbidity and mortality from vaccine preventable infectious diseases + eventually certain cancers (cervical and liver)

Preventative and addiction medicine (5 decks)

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