Substance Use Flashcards
Early Remission vs Sustained Remision
Early: 3-12 months with nothing except cravings
Sustained remission: at leat 12 months without meeting criteria
Alcohol and CDT
CDT is a transferrin. Think of it as a deer with horns. In normal people, the horns have 4-5 branches. In alcoholics, they have 0-2 branches (carbohydrate Deficient transferrin) .
Ethyl Gulcuronide (EtG)
metabolite of ethanol which is formed din the body by glucouronidation usually from drinking. Lets you know if someone drank in the last 5 days. (pilots, etc)
What types of seizures happen in alcohol withdrawal?
Generalized Tonic clonic seizures
Peak incidence of alcohol withdrawal seizures after last drink?
24 hours
Benzos NOT metabolized by the liver?
‘out the liver’ : oxazepam, temazepam, lorazepam.
4 Symptoms of Wernicke’s Encephalopathy
confusion, ataxia, nystagmus, opthalmoplegia (paralysis of eye muscles)
What enzyme is inhibited by disulfiram?
Aldehyde dehydrogenase
Alcohol withdrawal is due to overabundance of what neurotransmitter?
glutamate
How is acamprosate metabolized?
Renally which defers it from naltrexone and disulfiram.
How does acamprosate work?
Leads to less glutamate transmission presynaptically, and also binds to post synaptic glutamate receptors. Helps to reduce hyperglutamatergic state in alcohol withdrawal .gg
When does acamprosate work?
Initiate as soon as possible after alcohol withdrawal when patient achieves abstinence. Maintain treatment if patient relapses. It increases the likelihood of abstinence.
What is the clonidine MOA?
Presynaptic noradrenergic a2 agonist
Methadone MOA
synthetic opioid AGONIST that is very long acting so it prevents the withdrawal sx. Keeps them comfortable and blunts cravings. Used for pregnant women.
Anandamide vs THC
Anandamide is the endogenous cannabinoid. THC has a much stronger and longer effect than anadamide on brain cells. THC interferes with Anandamide’s function of protecting neurons and keeping brain activity in balance.
THC and Hippocampal Neurons
THC suppresses activity of hippocampal neurons below the level needed to trigger memory formation. With chronic thc expsoure, neuron connections involved in memory are gradually lost due to continual suppression.
Marijuana Psychosis Gene
AKT1 gene governs an enzyme that affects Dopamine brain signaling, leading to psychosis (c/c is bad). Another is COMT gene which governs an enzyme that breaks down dopamine (val/val is bad).
Marijuana and collisions
2012 meta analyssis found marijuana use doubled collision risk.
NAC for cannabis use disorder
Modulates glutamate at 1200 mg bid. Side effects are vivid dreams, gi sx. No significant decrease i ncravings for cannabis .
Stimulant withdrawal dreams
unpleasant and vivid.
Cocaine MOA
Causes transient increase in extracellualr dopamine levels in dopaminergic pojections from the VTA area to the nucleus accumbens by binding to the dopamine transporter, thereby inhibiting dopamine reuptake.
Cocaine metabolite
BE (benzoylecgonine) is present in urine for ~48 hourspost use.
Off label disulfiram use in cocaine use disorder
It inhibits dopamin-beta-hydroxylase, plasma esterases, and aldehyde dehydrogenase involved in metabolism of cocaine . It will lead to anxiety, paranoi, and dysphoria after cocaine use which leads to less use overall.
Ketamine and vets
Ketamine used on animals. May have a vet or nurse who can access it.
Dextromethorphan MOA
NMDA receptor antagonist
Adverse events of inhalants
sudden cardiac death or seizures.
Pacifier at a rave party
Person is on MDMA which causes tooth grinding/bruxism.
Most common complication of hydrocarbon use?
Pneumonitis (sniffing paint thinner)
Biggest risk factor for developing cannabis use disorder
Early use of cannabis before 15 yo.