Substance Abuse Disorders - Cooley Flashcards
a primary, chronic disease of brain reward, motivation, memory and related circuitry
- seeking pain relief, seeking drugs for euphoric effects
- pathologically pursuing reward and/or relief by substance use and other behaviors
addiction
result of DA-system malfunction
- malfunction is complicit in vulnerability to addiction
- helps us understand the compulsive use that characterizes addiction vs physical dependency
reward deficiency syndrome
- most well-known evidence that supports an addiction syndrome
- the neurobiological circuitry of the central nervous system is the ultimate common pathway for addictive behaviors
what do genetic studies show regarding reward deficiency syndrome?
common molecular mechanisms for drug addiction and compulsive running behavior
strictly conceptual model used for risk assessment and treatment planning
genetic hx of:
- addictive disorders
- intractable mood disorders
- personality disorder or habitual criminal behavior
personal/family hx of:
- polysubstance use
- trauma
- chronic psychosocial stressors starting at young age
addictophrenia spectrum
what are common comorbidities seen with substance abuse?
- antisocial PD
- depression
- suicide
- using larger amounts of substances, or for longer time than intended
- persistent desire or unsuccessful attempts to cut down/control use
- great deal of time obtaining, using, or recovering
- craving
- fail to fulfil major roles (work, school, home)
- persistent social or interpersonal problems caused by substance use
- important social, occupational, recreational activities given up/reduced
- use in physical or psychological problems caused by use
- tolerance
- withdrawal
substance use disorder KNOW this
what is considered mild substance use disorder?
2-3 symptoms
what is considered moderate substance use disorder?
4-5 symptoms
what is considered severe substance use disorder?
6+ symptoms
what is considered early remission for substance use disorder?
no criteria (except craving) for >3 months but <12 months
what is considered sustained remission for substance use disorder?
no criteria (except craving) for >12 months
the disorder represents a clinically significant symptomatic presentation of a relevant mental disorder
there is evidence from the hx, PE, or lab findings of both of the following:
- the disorder developed during or within 1 month of a substance intoxication or withdrawal or taking a medication
- the involved substance/medication is capable of producing the mental disorder
substance-induced mental disorder
the disorder is not better explained by an independent mental disorder
- the disorder preceded the onset of severe intoxication/withdrawal or exposure to the medication
- the full mental disorder persisted for a substantial period of time after the cessation of acute withdrawal or severe intoxication
the disorder does not occur exclusively during the course of a delirium
the disorder causes clinically significant distress or impairment in social, occupational, or other important areas of functioning
substance-induced mental disorders
reversible substance-specific syndrome d/t recent ingestion of a substance
- behavioral/psychological changes d/t effects on CNS after ingestion
- not d/t another medical condition/mental disorder
- does not apply to tobacco
intoxication
substance-specific syndrome problematic behavioral change d/t stopping or reducing prolonged use
- physiological and cognitive components
- significant distress in social, occupational or other important areas of functioning
- not d/t another medical condition or mental disorder
withdrawal
refers to underlying CNS changes that occur following repeated use such that person develops tolerance and/or withdrawal
neuroadaptation
what is pharmacokinetic neuroadaptation?
adaptation of metabolizing system
what is pharmacodynamic neuroadaptation?
ability of CNS to function despite high blood levels
need to use an increased amount of a substance in order to achieve the desired effect
OR
markedly diminished effect with continued use of the same amount of the substance
tolerance
what treatment option for substance abuse did Cooley stress?
motivational interviewing in the primary care setting
- twelve step facilitation (AA, NA, etc)
- also treat co-occurring psychiatric disorders (50% will have another psychiatric disorder)
what is the legal intoxication level of alcohol?
blood alcohol 0.08 g/dL
what are the signs of early alcohol withdrawal?
anxiety, irritability, tremor, HA, insomnia, nausea, tachycardia, HTN, hyperthermia, hyperactive reflexes
- seizures (generally seen 24-48 hours)
what is withdrawal delirium?
altered mental status, hallucinations, marked autonomic instability
- life threatening
- generally seen between 48-72 hours
the most severe manifestation of alcohol withdrawal, occurs 3-10 days following the last drink
- agitation, profound global confusion, disorientation, hallucinations, fever, HTN, diaphoresis, autonomic hyperactivity (tachycardia)
Delirium Tremens (DT) - medical emergency with high mortality rate
chronic alcohol use causes increased release of which NT?
GABA - the inhibitory NT, which leads to up-regulation of NMDA receptor
- during withdrawal, loss of GABA stimulation is associated with tremors, diaphoresis, tachycardia, anxiety
what is the CIWA?
clinical institute withdrawal assessment for alcohol
- assigns numerical values to orientation, N/V, tremor, sweating, anxiety, agitation, tactile/auditory/visual disturbances and HA
- total score of >10 indicates more severe withdrawal
- based on severity of withdrawal or hx of previous withdrawal seizures or DT’s, med therapy can be scheduled or symptom triggered
what is the med tx for alcohol withdrawal?
benzo’s:
- GABA-agonist, reduce risk of seizure
anticonvulsants: (carbamazepine or valproic acid) - reduce risk of seizure, helpful for protracted withdrawal
- *thiamine supplementation**
- risk of thiamine deficiency (wernicke/korsakoff)
when would Naltrexone be appropriate to give?
alcohol use disorder (also for eating disorders)
- is an opioid antagonist, thought to block mu receptors reducing intoxication, euphoria and cravings
NOTE: acamprosate can also be given. unknown mech but thought to stabilize neuron excitation and inhibition (may interact with GABA)
what meds?
- similar to alcohol but less cognitive/motor impairment
- variable rate of absorption (lipophilia) and onset of action and duration in CNS
- the more lipophilic and shorter the duration of action, the more addicting
benzo’s and barbiturates
what is the withdrawal of benzo’s like?
similar to alcohol with anxiety, irritability insomnia, fatigue, HA, tremor, sweating, poor concentration
- common detox mistake is tapering too fast, sx worse at end of taper
- convert short elimination of benzo’s to longer elimination half life drug then taper slowly (decrease doese every 1-2 weeks)
what is the half life of alprazolam?
6-20 hrs
what is the half life of oxazepram?
8-12 hrs
what is the half life of temazepam?
8-20 hrs
what is the half life of clonazepam?
18-50 hrs
what is the half life of lorazepam?
10-20 hrs
what is the half life of chlordiazepoxide?
30-100 hrs
what is the half life of diazepam?
30-100 hrs
what drug class binds to the mu receptors in the CNS to modulate pain?
opioids
- intoxication: pinpoint pupils, sedation, constipation, bradycardia, hypotension, decreased RR
- withdrawal: not life threatening unless severe medical illness, but extremely uncomfortable. dilated pupils, lacrimation, goosebumps, N/V, diarrhea, arthralgia, dysphoria/agitation
what meds can be used for opiate use disorder?
- methadone (opioid substitution)
- naltrexone
- buprenorphine (opioid substitution)
what medication is considered HIGH RISK
- can be deadly when used with a benzo
- frequently causes QTC prolongation - sometimes fatal
- dangers increase when used with another 3A4 substrate
- is a mu agonist, oral solution only
methadone
NOTE: do NOT use with benzo’s or other 3A4 substrates
what med:
- partial mu agonist with a ceiling effect
- any physician can Rx after taking certified ASAM course
- helpful for highly motivated people who do not need high doses
buprenorphine
what drug class causes:
- euphoria, enhanced vigor, gregariousness, hyperactivity, restlessness, interpersonal sensitivity, anxiety, tension, anger, impaired judgement, paranoia
- tachycardia, papillary dilation, HTN, N/V, diaphoresis, chills, weight loss, chest pain, cardiac arrhythmias, confusion, seizures, coma, hyperthermia
stimulants
affective blunting (narrowed range of emotional responses), fatigue, sadness, social withdrawal, hypotension, bradycardia, muscle weakness
chronic intoxication of stimulants
which drug:
- has vasoconstrictive effects that may outlast use and increase risk of CVA and MI
- can get rhabdomyolisis with compartment syndrome from hypermetabolic state
- can see psychosis associated with intoxication
cocaine
cocaine mainly prevents the reuptake of which NT?
dopamine
what drug type:
- chronic use results in neurotoxicity possibly from glutamate and aonal degeneration
- can be fatal at lower doses in setting of Brugada syndrome
- tx similar as for cocaine but no known substances to reduce cravings
amphetamines
amphetamines inhibit reuptake of which NT’s?
DA (mainly), NE, 5HT
what are the main drug interactions with tobacco?
induces CYP1A2
- watch for interactions when starting or stopping (Olanzapine)
nicotine interacts with which NT receptors?
Ach receptors on DA neurons in ventral tegmental area
- release DA in nucleus accumbens
what meds can be given for tobacco use disorder?
- bupropion (150mg bid)
- varenicline (1mg po)
which drug:
- tachycardia, sweating, muscle spasms, EXTREMELY HIGH FEVER
- in severe toxicity, high fever can progress to rhabdomyolysis, renal failure, seizures, disseminated intravascular coagulopathy, cardiac arrhythmias and death
MDMA
MDMA interacts with which NTs?
5HT (mainly), DA, NE
what is the half life of cannabis?
50 hours
- lipid soluble molecule, reaches peak effectiveness 10-30min
cannabis interacts with which receptors in brain/body?
CB1, CB2
- coupled with G proteins and adenylate cyclase to Ca-channels, inhibiting Ca influx
- decreases uptake of GABA and DA
what drug:
- dissociative anesthetic
- similar to ketamine
- severe dissociative reactions: paranoid delusions, hallucinations, can become very agitated/violent with decreased awareness of pain
- NYSTAGMUS, ataxia, dysarthria
- with severe overdose: mute, catatonic, muscle rigidity, HTN, hyperthermia, rhabdomyolysis, seizures, coma, death
phenacyclidine (PCP), aka Angel Dust
what is the tx for PCP?
- antipsychotic drugs or benzo’s
- low stimulation environment
- acidify urine if severe toxicity/come
PCP interactions with which receptor type?
- opioid receptors
- allosteric modulator of glutamate NMDA receptor
