NURS660 Exam 4 Flashcards
What meds do you use for ETOH withdrawal and which one first
Benzos: valium, ativan, librium
Ativan first bc it’s easy on the liver
What are the neurotransmitters for alcohol and what goes on during drinking and withdrawal
GABA: while drinking GABA increases – calm and relax
Glutamate: alcohol leaves and glutamate kicks in
Withdrawal: glutamate causes excitement, restlessness, jittery, hyperactivity, tachy, HTN
MOA for ETOH detox:
mimicking the effects of the substance with benzos
CIWA scores for ETOH
10 or more you start benzo protocol
ETOH use and needed vitamins … what are we trying to prevent?
MV, folic acid, thiamine (B1)
To prevent Warneke encephalopathy
Alcohol use and wellbutrin
Don’t use wellbutrin because it lowers the seizure threshold
Antidote for sudden bizzare behavior, confusion, disorientation with ETOH withdrawal:
IV thiamine 250mg TID x 5 days
When do withdrawal cravings occur
During RESENSITIZATION
S/S of opiate withdrawal
pain, diarrhea, shivering, tachy, dilated pupils, shaking, anger, HTN
Treatment for opiate withdrawal
clonidine and suboxone
What to check while on suboxone
- Prescription monitoring system
- UDS
Non-threatening withdrawal substances
cocaine, meth, THC
Desensitization is the _____ part of substance abuse
tolerance
Acute ETOH r/t CYP
- decreases metabolism - inhibits
- can cause toxicity for other drugs
Chronic ingestion of ETOH r/t CYP
vs prolonged chronic
- Increased liver enzymes - increased metabolism
- Prolonged - dmgs liver and CYP is inhibited vs increased
Which receptor do hallucinogenic drugs work on? And how?
Agonism of 5HT2A
What is the neurotransmitter for cocaine
DA
What loop is associated with ADHD
CSTC loop
PFC r/t ADHD
cognition and attention
Anterior cingulate cortex r/t ADHD
selective attention – details, not listening, careless mistakes
Dorsolateral PFC r/t ADHD
problem solving – sustained attention
Orbital PFC r/t ADHD
impulsive behavior
Dorsal striatum r/t ADHD
compulsive behavior
VTA r/t ADHD
controls reward and impulse
Prefrontal motor cortex r/t ADHD
Hyperactive: fidgeting, leaving seat, running
Orbitofrontal cortex r/t ADHD
Impulsive: excessive talking, blurting, not waiting for turn
Hippocampus r/t Dementia
memory center
Benzos, Meclizine, and Sennakot r/t dementia
Benzos and meclizine can make memory worse
Sennakot can cause aggression
Alzheimer’s s/s
- Gradual
- Marker: beta-amyloid plaques
- Hereditary
Frontotemporal dementia s/s
Aggression
Hypersexual behaviors
Hyperverbal
Nosey
Lasts up to a year - then death
Lewy Body dementia s/s
- Rapid eye movement
- hallucinations
- Usually die within 6 mo
Vascular Dementia s/s
hx of TIA or TBI or CVA
Parkinson’s dementia s/s
can’t dx for a year
shuffling
Huntington’s chorea dementia
- hyperreflexia, chorea
- chorea is marker
Acamprosate (Campral)
- Use
- MOA
Use
- ETOH disorder
MOA
- blocks presynaptic glutamate so if patient drinks they don’t get the euphoria
Amphetamine (Adderall)
- Which pathway
- What causes dependency
- Before starting …
- Mesolimbic pathway to increase DA via DAT
- Dependency caused by competitiveness at the DAT
- UDS
- Drug monitoring system
- Hx of structural cardiac concerns?
Why is ER amphetamine better for addiction?
occupy NET in the PFC slow enough and long enough that they enhance TONIC NE and DA signaling but not quickly or potentently to the point phasic signalling is increased in the NA
Tonic: even tone
Phasic: short bursts
Atomoxetine (Strattera)
- MOA
- CYP
- liver?
- Non stimulant NE reuptake inhibitor
- Increases DA in PFC – not via DAT
- CYP2D6 so inhibitors causes problems
—- Paroxetine, fluoxetine, quinidine, wellbutrin - Rare: liver failure
Clonidine
- Use
- When not to use
detox r/t alpha2 agonism
Don’t use if hypotensive –> use suboxone
Donepezil (aricept)
- what kind of med
- When used
- MOA
- SE
Anticholinesterase
Helps with hippocampus
Improves cognition but doesn’t stop progression
Lots of GI SE: diarrhea/n/v
Disulfram
Aversion therapy for ETOH disorder
– makes violently ill
Blocks enzymes that break down acetaldehyde – leads to accumulation.
SE: throbbing HA, diaphoresis, flushing, stomach upset, n/v
Last drink should be at least 12 hrs
Wait to drink 2 weeks after taking the medication
Galantamine
acetylcholinesterase
Positive allosteric modulation on nicotinic receptor
Alzheimer’s
Lisdexamphetamine
Hair loss over 50mg
Memantine (Namenda)
NMDA receptor antagonist
Methylphenidate (Ritalin)
Similar to cocaine
Blocks DAT/NET – increaesed availability
Can induce psychosis with too much DA
Naloxone (Narcan)
opioid overdose antidote
Naltrexone (Revia)
blocks mu receptor only
for ETOH and Opiate use disorder
reduces excitement (glutamate) and cravings
No desensitization of the GABA – so no cravings
Rivastigmine (exelon)
anticholinesterase
comes in patch due to bad GI problems
– caused by peripheral inhibition of the butyrylcholinesterase and acetylcholinesterase
Viloxazine
Same as Strattera: Non stimulant NE reuptake inhibitor
- Increases DA in PFC – not via DAT
but
also has 5HT2B/C
OK for liver issues
1A2 vs 2D6
What order do we treat different disorders
ETOH/Substance use dependence
Mood disorders
Anxiety
ADHD
Nicotine dependence
Amphetamine based meds
MOA
Amphetamine based meds
Increase DA and NE
Competitively inhibits DAT (gets taken up by DAT)
Packed into vesicles so displaces DA into terminals
Ritalin (methylphenidate)
Blocks DAT and NET
This leads to increased availability in the synaptic cleft
Doesn’t lead to increased release – just more availability by blocking transporters
At mu opioid receptors, naltrexone acts as a/an:
Antagonist
Which of the following interact with the mu opioid receptors as full agonists
Endogenous opioids
Heroin
Rx opioids
Which of the following MATs is effective against fentanyl overdose?
NALOXONE – NOT NALTREXONE
Deep repetitive transcranial magnetic stimulation (drTMS) may be helpful in treating AUD, because it has been shown to
Reduce cravings
Reduce intake of alcohol
Impulsivity associated with ADHD is hypothetically regulated by the
Orbital frontal cortex
Problems with selective attention associated with ADHD are hypothetically regulated by the:
Anterior cingulate cortex
As individuals with ADHD progress into adulthood, they generally experience a decline in:
Impulse and hyperactive symptoms
In individuals with comorbid substance abuse and ADHD, it is generally advisable to address which condition first?
Substance use
Why does atomoxetine lack abuse potential?
It increases dopamine levels in the prefrontal cortex but not in the nucleus accumbens
Rita is a 28-year-old patient with untreated ADHD. You are currently deciding between guanfacine and clonidine as potential treatments for this patient. The selective alpha 2A agonist guanfacine appears to be:
Better tolerated than the alpha 2 agonist clonidine
George is an 81-year-old patient with Alzheimer’s dementia. He is currently taking rivastigmine 4 mg/day but is experiencing treatment-induced nausea and diarrhea. These gastrointestinal side effects may be due to which action of rivastigmine?
Peripheral inhibition of acetylcholinesterase & butyrylcholinesterase
Which of the following dementia treatments has the secondary property of positive allosteric modulation at nicotinic receptors?
Galantamine
Which of the following properties of memantine may be useful in treating Alzheimer’s disease?
NMDA antagonism at the magnesium site
Addiction may be explained by neuroadaptation, such that _____ cortico-subcortical loops supporting impulsive reward seeking give way to _____ cortico-subcortical loops supporting compulsive behaviors.
Ventral, dorsal
The addition of clonidine also functions to reduce the intensity of withdrawal via what action?
Alpha 2A agonism
Alcohol has what effect on GABA and glutamate within the ventral tegmental area?
Increases GABA and decreases glutamate
Guanfacine and food
ABSORPTION OF GUANFACINE IS SIGNIFICANTLY INCREASED WHEN TAKEN WITH A HIGH-FAT MEAL
