Stimulant Use Disorder Flashcards
What is the prevalence of SUD
Age 18-30 males, increasing use especially in BC and SK
Waht are the three cycles of SUD?
Binge,crash,repeat
Most stimulants are derivative of ___
AMpehtamines
What are considered weak stimulants?
Caffeine, nicotine
What are considered mild stimulants
Ephedrine, pseudoephendrine. dextromethorphan
What are considered moderate stimulants?
Ritalin, dextroamphetamine, vyvanse, modafininl, bupropion
What are considered strong stimulants?
What is the pharmacology/ MOA of stimulabts?
Increases CNS and Autonomic nervous system activity
All effect the reward pathway by increasing ____ at the ___
Dopamine, synapses
What is the duration of stimulants cocaine?
<1hr
What is the duraiton of ampehtamines?
Duration up to 12 hour depending on route and amount
WHat is cocaine?
Powder or rock form
What drug is used world wide and fastest growing drug in youth?
Meth
How is meth used?
Oral (3%)
Nasal 12%
Injecting 25%
Smoking 60%
What effects do stimulants have on the CNS?
Intense euphoria including
What affect do stimulants have on the autonomic nervous system?
What can overdoses of stimulants do?
What are the immediate complications of stimulants? (5)
What are the long term complications of stimulant use?
What are the three pillars of SUD management?
- Acute intoxication
- Acute withdrawal
- Long term pharmacological management
(withdrawal and cravings)
What are the acute intoxication symptoms of SUD?
Psychosis
Mania
Paranoia
Delirium
Increase blood pressure
Chest pain
Agitation
Sweating
Skin picking
What is the management of stimulant intoxication?
Supportive unless delusions or autonomic hyperactivity
Pharmacological agents only if overtly psychotic and agitated or medical crisis
What is the management for SUD agitation?
Lorazepam 2-4mg IM or po PRN q-30min to 6hr
What is the management for psychotic symptoms?
Low dose antipsychotic such as risperidone 0.5-2mg/d, olanzapine 2.5-
7.5mg/d
What are the cardiovascular complications management?
– arrhythmia: administer anti-arrhythmic agents
– Tachycardia (+/- hypertension): administer β-blockers (especially
labetalol/carvedilol), clonidine
What are the seizure risk complications management
– anti-seizure meds if seizing (i.e. diazepam IV, midazolam IM)
– no role as a preventative
What is the 1st stage of withdrawal
The initial crash
When does the crash start?
Begins within hours and lastas 4-7 hours and lasts 4-7 hours
What are the signs and symptoms of stage 1 SUD?
Crash
- agitation
- marked dysphoria
- fatigue
- hypersomnolence
- Hyperphagia or anorexia
What is Stage II withdrawal symptoms of SUD?
Begins after the first week and can last up to 10 weeks
WHat happens during the first week of stage II?
– normal sleep
– euthymia
– little anxiety
– minimal craving
What happens during the subsequent weeks of SUD in stage II?
– anhedonia
– ↑ anxiety & depression
– fatigue
– extreme craving
What is anhedonia?
the inability to feel pleasure
What are the non-pharm managements for SUD?
addictions counselling
support, community supports, rehab options, housing needs
What are the post-acute hyperarousal/anxiety treatments for SUD withdrawal
– Continue benzos a little longer
– Mirtazapine (mixed results)
What are the goals of therapy for long term management of SUD?
- physical dependence? < psychological dependence
Biggest factor leading to relapse and challenge to manage is
craving
What is the rationale for using buproprion in SUD?
Rationale: 5-HT may attenuate reinforcing effects of amphetamine,
and 5-HT/NE counter withdrawal symptoms as depression
If indicated what guidelines should we use the antidepressants in accordance to?
MDD guidelines
What is the role of antipsychotics in SUD?
counterbalance excess DA activity and
restore NT pathways
No difference though
What is the evidence of suing a prescribed stimulant?
Mixed results for long term benefit, may help with cravings.
WHat is the issue with the usage of stimulants?
Our body de-regulates the dopamine receptors and therefore they will never achieve that ‘High”
What is the rationale for dopamine agonists?
Chronic stimulant use leads to DA depletion
What are 2 dopamine agonists?
Amantadine, bromocriptine
What is modafinil?
INdicated for narcolepsy
What evidence is there for modafinil?>
- Mixed evidence of benefit: possibly useful to
reduce cocaine use, but 2 neg trials and risk of
↑ effect of concurrent stimulant use
What is the issue of using buproprion and naltrexone ER
Naltrexone ER not in Canada
What is the non-pharm approach?
1st line = psychosocial approaches (CBT, contingency management,
addictions treatment)
What is the major takeaway from SUD?
No established pharmacotherapy for stimulant use disorder
What may long term users of stimulants appear as?
Traumatic brain injury to the patient. Since there brain has been depleted of dopamine they may appear like a Parkinson disease patient because of this.
What is the issue with AP in SUD?
Increase negative symptoms and relapse possibly
Negative symptoms may increase and clinical sense that this could be promoting cravings
What is the MOA of modafinil?
What is the rationale for using naltrexone in SUD?
Endogenous opioids increase when high, therefore by blocking them we block the high
Why may we use risperidone over olanzapine?
less sedation