Substance-related disorders Flashcards
∆ btwn substance-induced mood symptoms vs primary mood symptoms?
substance-induced mood symptoms - improve during abstinence
primary mood symptoms - persist
DSM criteria of ABUSE
pattern of substance use that leads to IMPAIRMENT OR DISTRESS for at least 1 year
- failure to fulfill obligations
- use in dangerous situations (driving)
- legal problems
- social/interpersonal problems related to use
DSM criteria of DEPENDENCE
pattern of substance use that leads to IMPAIRMENT OR DISTRESS for at least 1 year
- TOLERANCE
- WITHDRAWAL effects
- using more than originally intended with persistent desire or unsuccessful efforts to cut down
- significant time in getting, using, or recovering from substance
- decrease social, occupational, or recreational activities
continued use despite subsequent or psychological problem
definition of withdrawal
development of substance-specific symptoms due to abrupt cessation of use that has been heavy and prolonged
definition of tolerance
need for increasing amounts of substance to achieve the desired effect (or diminished effect if using the same amount of the substance)
MoA of alcohol (what R does it act on) and its net effects
activates GABA-R and serotonin-R in the CNS
inhibits glutamate R and VG Ca channels
net: depressant
how does alcohol affect body’s pH and the anion gap?
what other substances cause the same effects?
metabolic acidosis + increased AG
methanol
ethylene glycol
What should you always give an alcoholic and why?
Thiamine - prevents/treat Wernicke’s encephalopathy
Folate
treatment of immediate alcohol withdrawal (anxious, diaphoretic, and tachycardic) and justification
What should you give in a patient whose liver function is compromised?
benzodiazepine taper (chlordiazepoxide/Librium, diazepam, lorazepam) to minimize risk of ASH: arrhythmias, seizures, HTN
Lorazepam = Liver Low
what do you worry about in chronic alcoholics?
withdrawal - potentially lethal due to compensatory hyperactivity (ASH = arrhythmias, seizures, HTN)
when do signs of OH withdrawal first manifest?
6-24 hours
when do generalized tonic-clonic seizures of OH withdrawal manifest?
6-48 hours, with peak around 13-24 hrs
signs of OH wtihdrawal
Tremors, irritability, GI ∆s
diphoresis, HTN, tachycarida, FEVER, disorientation
tonic clonic seizures, DTs, hallucinations
What is delirium tremens/DT?
When does it begin?
Signs?
Treatment? 2
48-72 hours
delirium, tremors, visual hallucinations, autonomic instability
Dilantin (phenytoin) and benzodiazepines (chlordiazepoxide/Librium, diazepam, lorazepam)
Thiamine, folic acid, and multivitamin (banana bag)
how can you tell someone is an alcoholic based on their LFTs?
AST:ALT ratio is > 2:1
elevated GGT
how can you tell someone is an alcoholic based MCV?
macrocytosis
4 Rx to treat alcohol dependence
1) disulfiram (antabuse) - blocks aldehyde dehydrogenase
2) naltrexone (revia, IM-vivitrol)
3) acamprosate (campral)
4) Topiramate (Topomax)
disulfiram (antabuse) MoA
blocks aldehyde DH and causes an adverse rxn to the alcohol (flushing, HA, N/V, palpitations, SOB)
naltrexone (revia, IM-vivitrol) MoA
blocks opioid receptors, thereby blocking dopaminergic (reward) pathways and reduces desire/craving and the high associated with OH use
what happens if you give thiamine before glucose to a patient with altered mental status from OH abuse?
prevents Wernicke’s Korsakoff’s syndrome from occurring
If glucose was given before thiamine, it will exacerbate the rate of cell death and worsen the condition
Acamprosate (campral) MoA
when is it started?
who can it be used in? not used in?
GABA-like mimetic that inhibits glutamatergic system
started in patients with liver disease
contraindicated in patients with severe renal disease
Topiramate (Topomax) MoA
anticonvulsant that can reduce alcohol cravings; potentiates GABA and inhibits glutamate receptors
2 long-term complications of OH abuse
Wernicke's encephalopathy (ACUTE) Korsakoff syndrome (CHRONIC)
Wernicke’s encephalopathy
- features?
- cause?
- how to reverse?
broad-based/stumbling ataxia, confusion, nystagmus, gaze palsies
B1 deficiency
reverse with thiamine followed by glucose
Korsakoff syndrome
- features?
retrograde/anterograde amnesia with compensatory confabulation
What is confabulation?
unconsciously making up answers when memory has failed
Cocaine MoA
blocks dopamine reuptake from synaptic cleft, causing a stimulant effect as well as behavioral reinforcement “reward”
How can cocaine OD cause death and why? 4
cocaine has severe vasoconstrictive effects :
cardiac arrhythmias/chest pain cardiomyopathies MI stroke TIAs seizures (status epilpeticus) respiratory depression tactile hallucinations
What type of hallucinations do cocaine cause?
tactile hallucinations
Cocaine intoxication effects
cocaine is an indirect sympathomimentic, therefore intoxication mimics the flight/fight response:
euphoria heightened self-esteem autonomic instability (tachycardia, HTN) DILATED pupils weight loss psychomotor ∆s chills sweating nausea
treatment of cocaine mild-moderate intoxication? severe?
mild-moderate agitation/anxiety: benzos
severe agitation/psychosis: antipsychotics (haloperidol)
why is it that cocaine is often accompanied by other substance use d/o (ie opiates, OH)?
because these are often used to temper the irritability and hyper-vigilance that can follow cocaine intoxication and withdrawal
cocaine withdrawal effects
CRASH (post-intoxication depression)
- malaise, fatigue,
- hypersomnolence
- depression
- hunger
- constricted PUPILS
- vivid dreams
- psychomotor ∆s
- dysphoric
- suicidal
how long does it take for cocaine withdrawal symptoms to resolve? how long does it take to clear from the body?
within 18 hours
clears within 3 days
Classic Amphetamines MoA
Designer Amphetamines MoA
clinical use for both
Classic: blocks reuptake/facilitates release of DA and NE –> stimulant
Clinical use: ADHD, narcolepsy, depressive d/o
Designer: release DA, NE, 5HT
Use: dance clubs, raves
classic amphetamines?
dextroamphetamine
methylphenidate
methamphetamine
designer amphetamines?
MDMA (Ecstasy)
MDEA (Eve)
signs of amphetamine abuse
dilated pupils INCREASED libido perspiration respiratory depression chest pain
chronic amphetamine use can result in these 2 things
Acne
Accelerated tooth decay (“meth mouth”) - due to decreased saliva production in conjunction with increased cravings for sugar
signs of amphetamine intoxication
similar to that of cocaine intoxication:
- tachycardia, arrhythmias
- HTN
- pupil DILATION
- diaphoresis
- chills
- N/V
- CP
- respiratory depression
- muscle weakness/dystonia/dyskinesia
- weight loss due to decreased appetite
- confusion
- seizures/coma
signs of amphetamine withdrawal
prolonged depression/dysphoria
fatigue /increased need for sleep
psychomotor slowing
INCREASED appetite
3 signs of amphetamine overdose
hyperthermia
dehydration
rhabdomyolysis (renal failure)
Phencyclidine (PCP) MoA
antagonizes NMDA receptors + activates dopaminergic neurons
Ketamine is similar to what other drug? what kind of effects does it produce?
PCP, but less potent
produces tachycardia, tachypnea, hallucinations, amnesia
What is the PCP triad of intoxication? (earliest signs)
early signs: nystagmus, muscle rigidity, numbness
Other signs of PCP intoxication
early signs: nystagmus, muscle rigidity, numbness
agitation, impaired judgement, assaultiveness, high tolerance to pain, ataxia, depersonalization, tactile and visual hallucinations, synesthesia, impaired speech, HTN, tachycardia
Lab signs of PCP intoxication
elevated creatine phosphokinase + AST
treatment for PCP intoxication
benzodizepines (lorazepam) - agitation, anxiety, muscle spasms, seizures
antipsychotics (haloperidol) - severe agitation or psychotic sx
PCP withdrawal effects
flashbacks
what do cocaine and PCP intoxication both have in common
tactile + visual hallucinations
what is the problem with using typical antipsychotics in PCP intoxication? 4
increased risk of PCP-induced hyperthermia, dystonia, anti-cholinergic reactions, and decreased seizure threshold
-> use atypicals instead
2 sedative hypnotics that are commonly abused
what is their MoA and common clinical use?
benzodiazepines (BDZ) - increase frequency of Cl channel opening
-> anxiety d/o
barbiturates - increase duration of Cl channel opening
-> epilepsy, anesthesia effects
intoxication with sedative-hypnotics (benzos and barbiturates) can result in these sx
drowsiness, confusion, impaired judgement
nystagmus, slurred speech, incoordination, ataxia
mood lability
hypotension, RESPIRATORY DEPRESSION
coma, death
confused, wobbly, low vitals
what can exacerbate sedative-hypnotics?
when EtOH or opioids are used in conjunction, as these can result in synergistic effects on the symptoms
treatment for barbiturate OD
NaHCO3 - alkalinizes urine to promote renal excretion
treatment for benzodiazepine OD
precautionary warnings associated with this treatment
flumazenil - short acting BDZ antagonist; can precipitate seizures when treating OD
what is so concerning about sedative-hypnotics withdrawal?
tonic clonic seizures may result; life threatening (in general, withdrawal from sedating drugs is life-threatening due to compensatory hyperactivity, while withdrawal from stimulants is not)
treatment for sedative-hypnotics OD/withdrawal in general?
Benzodiazepine TAPER +/- carbamazepine/valproic acid taper for seizure prophylaxis
common opioid in cough syrup?
dextromethorphan
opioid MoA
stimulates opiate receptors (µ, k, ∂) -> analgesia, sedation, dependence
effects on dopaminergic system -> addiction, reward
serotonin syndrome can result if these recreational drugs are combined with antidepressants
amphetamines
opioids
amphetamines + SSRI
opioids + meperidine OR MAOi
opioid intoxication sx
N, V drowsiness, sedation decreased pain perception decreased GI motility -> constpation pupil constriction seizures respiratory depression -> coma, death
treatment in opioid OD
1) naloxone or naltrexone (opioid antagonist) - can precipitate severe withdrawal
2) clonidine - treatment of moderate withdrawal sx
3) NSAIDs - muscle pain/cramps
4) diclyclomine - abdominal cramps
opioid withdrawal sx
lacrimation, rhinorrhea, sweating dilated pupils yawning piloerection (goosebumps) altered vitals: fever, HTN, tachycardia N, V, abd cramps arthralgia, myalgia cravings
treatment in opioid dependence 3
methadone
buprenorphine
naltrexone
methadone MoA
ADR
long-acting opioid-R agonist
ADR: QT prolongation
best for opioid-dependent pregnant women
buprenorphine MoA
ADR
partial opioid-R agonist
present in SUBOXONE (buprenorphine + naloxone)
what is naloxone? where can it be found? what is the purpose of adding this to buprenorphine?
competitive µ receptor antagonist – rapidly blocks the effects of other opioids (heroin, cocaine) and produces rapid onset of withdrawal symptoms
Naloxone is not active when taken PO, so withdrawal symptoms occur only if injected (lower abuse potential)!
found in suboxone (buprenorphine + naloxone)
how can you quickly tell if someone has opioid overdose?
give IV naloxone - rapid recovery of consciousness is consistent with opioid OD
T/F hallucinogens (LSD) do not cause physical dependence or withdrawal
TRUE
sx of hallucinogens (LSD) intoxication
perceptual changes (illusions, hallucinations, distorted body image, synesthesia) dilated pupils palpitations, tachycardia HTN hyperthermia tremors incoordination
sx of hallucinogens (LSD) withdrawal
flashbacks later in life
sx of marijuana intoxication
*euphoria* conjunctival injection dry mouth, increased appetite mild tachycardia, anxiety perceptual disturbances impaired motor coordination
sx of marijuana withdrawal
irritability, anxiety insomnia, restlessness strange dreams depression HA, sweating N, cravings decreased appetite
caffeine MoA
adenosine antagonist, which results in increased cAMP + stimulant effect via dopaminergic system
3 Rx that is used for treatment of nicotine dependence
1) varenicline (chantix)
2) bupropion (zyban)
3) nicotine replacement therapy (transdermal patch, gum)
varenicline (chantix) - MoA and clinical use
partial agonist of nAChR (nicotinic cholinergic receptor) -> prevents withdrawal sx
bupropion (zyban) - MoA and clinical use
antidepressant
partial agonist at nAChR + inhibitor of Dopamine uptake -> reduces withdrawal sx
