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Psych 660 > NURS660 Exam 4 > Flashcards

NURS660 Exam 4 Flashcards

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1
Q

What meds do you use for ETOH withdrawal and which one first

A

Benzos: valium, ativan, librium

Ativan first bc it’s easy on the liver

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2
Q

What are the neurotransmitters for alcohol and what goes on during drinking and withdrawal

A

GABA: while drinking GABA increases – calm and relax
Glutamate: alcohol leaves and glutamate kicks in

Withdrawal: glutamate causes excitement, restlessness, jittery, hyperactivity, tachy, HTN

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3
Q

MOA for ETOH detox:

A

mimicking the effects of the substance with benzos

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4
Q

CIWA scores for ETOH

A

10 or more you start benzo protocol

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5
Q

ETOH use and needed vitamins … what are we trying to prevent?

A

MV, folic acid, thiamine (B1)
To prevent Warneke encephalopathy

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6
Q

Alcohol use and wellbutrin

A

Don’t use wellbutrin because it lowers the seizure threshold

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7
Q

Antidote for sudden bizzare behavior, confusion, disorientation with ETOH withdrawal:

A

IV thiamine 250mg TID x 5 days

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8
Q

When do withdrawal cravings occur

A

During RESENSITIZATION

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9
Q

S/S of opiate withdrawal

A

pain, diarrhea, shivering, tachy, dilated pupils, shaking, anger, HTN

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10
Q

Treatment for opiate withdrawal

A

clonidine and suboxone

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11
Q

What to check while on suboxone

A
  • Prescription monitoring system
  • UDS
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12
Q

Non-threatening withdrawal substances

A

cocaine, meth, THC

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13
Q

Desensitization is the _____ part of substance abuse

A

tolerance

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14
Q

Acute ETOH r/t CYP

A
  • decreases metabolism - inhibits
  • can cause toxicity for other drugs
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15
Q

Chronic ingestion of ETOH r/t CYP
vs prolonged chronic

A
  • Increased liver enzymes - increased metabolism
  • Prolonged - dmgs liver and CYP is inhibited vs increased
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16
Q

Which receptor do hallucinogenic drugs work on? And how?

A

Agonism of 5HT2A

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17
Q

What is the neurotransmitter for cocaine

A

DA

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18
Q

What loop is associated with ADHD

A

CSTC loop

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19
Q

PFC r/t ADHD

A

cognition and attention

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20
Q

Anterior cingulate cortex r/t ADHD

A

selective attention – details, not listening, careless mistakes

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21
Q

Dorsolateral PFC r/t ADHD

A

problem solving – sustained attention

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22
Q

Orbital PFC r/t ADHD

A

impulsive behavior

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23
Q

Dorsal striatum r/t ADHD

A

compulsive behavior

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24
Q

VTA r/t ADHD

A

controls reward and impulse

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25
Q

Prefrontal motor cortex r/t ADHD

A

Hyperactive: fidgeting, leaving seat, running

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26
Q

Orbitofrontal cortex r/t ADHD

A

Impulsive: excessive talking, blurting, not waiting for turn

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27
Q

Hippocampus r/t Dementia

A

memory center

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28
Q

Benzos, Meclizine, and Sennakot r/t dementia

A

Benzos and meclizine can make memory worse

Sennakot can cause aggression

29
Q

Alzheimer’s s/s

A
  • Gradual
  • Marker: beta-amyloid plaques
  • Hereditary
30
Q

Frontotemporal dementia s/s

A

Aggression
Hypersexual behaviors
Hyperverbal
Nosey
Lasts up to a year - then death

31
Q

Lewy Body dementia s/s

A
  • Rapid eye movement
  • hallucinations
  • Usually die within 6 mo
32
Q

Vascular Dementia s/s

A

hx of TIA or TBI or CVA

33
Q

Parkinson’s dementia s/s

A

can’t dx for a year

shuffling

34
Q

Huntington’s chorea dementia

A
  • hyperreflexia, chorea
  • chorea is marker
35
Q

Acamprosate (Campral)
- Use
- MOA

A

Use
- ETOH disorder

MOA
- blocks presynaptic glutamate so if patient drinks they don’t get the euphoria

36
Q

Amphetamine (Adderall)
- Which pathway
- What causes dependency
- Before starting …

A
  • Mesolimbic pathway to increase DA via DAT
  • Dependency caused by competitiveness at the DAT
  • UDS
  • Drug monitoring system
  • Hx of structural cardiac concerns?
37
Q

Why is ER amphetamine better for addiction?

A

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

38
Q

Atomoxetine (Strattera)
- MOA
- CYP
- liver?

A
  • Non stimulant NE reuptake inhibitor
  • Increases DA in PFC – not via DAT
  • CYP2D6 so inhibitors causes problems
    —- Paroxetine, fluoxetine, quinidine, wellbutrin
  • Rare: liver failure
39
Q

Clonidine
- Use
- When not to use

A

detox r/t alpha2 agonism

Don’t use if hypotensive –> use suboxone

40
Q

Donepezil (aricept)
- what kind of med
- When used
- MOA
- SE

A

Anticholinesterase

Helps with hippocampus

Improves cognition but doesn’t stop progression

Lots of GI SE: diarrhea/n/v

41
Q

Disulfram

A

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

42
Q

Galantamine

A

acetylcholinesterase

Positive allosteric modulation on nicotinic receptor

Alzheimer’s

43
Q

Lisdexamphetamine

A

Hair loss over 50mg

44
Q

Memantine (Namenda)

A

NMDA receptor antagonist

45
Q

Methylphenidate (Ritalin)

A

Similar to cocaine

Blocks DAT/NET – increaesed availability

Can induce psychosis with too much DA

46
Q

Naloxone (Narcan)

A

opioid overdose antidote

47
Q

Naltrexone (Revia)

A

blocks mu receptor only

for ETOH and Opiate use disorder

reduces excitement (glutamate) and cravings

No desensitization of the GABA – so no cravings

48
Q

Rivastigmine (exelon)

A

anticholinesterase

comes in patch due to bad GI problems
– caused by peripheral inhibition of the butyrylcholinesterase and acetylcholinesterase

49
Q

Viloxazine

A

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

50
Q

What order do we treat different disorders

A

ETOH/Substance use dependence
Mood disorders
Anxiety
ADHD
Nicotine dependence

51
Q

Amphetamine based meds
MOA

A

Amphetamine based meds
Increase DA and NE

Competitively inhibits DAT (gets taken up by DAT)

Packed into vesicles so displaces DA into terminals

52
Q

Ritalin (methylphenidate)

A

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

53
Q

At mu opioid receptors, naltrexone acts as a/an:

A

Antagonist

54
Q

Which of the following interact with the mu opioid receptors as full agonists

A

Endogenous opioids
Heroin
Rx opioids

55
Q

Which of the following MATs is effective against fentanyl overdose?

A

NALOXONE – NOT NALTREXONE

56
Q

Deep repetitive transcranial magnetic stimulation (drTMS) may be helpful in treating AUD, because it has been shown to

A

Reduce cravings
Reduce intake of alcohol

57
Q

Impulsivity associated with ADHD is hypothetically regulated by the

A

Orbital frontal cortex

58
Q

Problems with selective attention associated with ADHD are hypothetically regulated by the:

A

Anterior cingulate cortex

58
Q

As individuals with ADHD progress into adulthood, they generally experience a decline in:

A

Impulse and hyperactive symptoms

59
Q

In individuals with comorbid substance abuse and ADHD, it is generally advisable to address which condition first?

A

Substance use

60
Q

Why does atomoxetine lack abuse potential?

A

It increases dopamine levels in the prefrontal cortex but not in the nucleus accumbens

61
Q

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:

A

Better tolerated than the alpha 2 agonist clonidine

62
Q

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?

A

Peripheral inhibition of acetylcholinesterase & butyrylcholinesterase

63
Q

Which of the following dementia treatments has the secondary property of positive allosteric modulation at nicotinic receptors?

A

Galantamine

64
Q

Which of the following properties of memantine may be useful in treating Alzheimer’s disease?

A

NMDA antagonism at the magnesium site

65
Q

Addiction may be explained by neuroadaptation, such that _____ cortico-subcortical loops supporting impulsive reward seeking give way to _____ cortico-subcortical loops supporting compulsive behaviors.

A

Ventral, dorsal

66
Q

The addition of clonidine also functions to reduce the intensity of withdrawal via what action?

A

Alpha 2A agonism

67
Q

Alcohol has what effect on GABA and glutamate within the ventral tegmental area?

A

Increases GABA and decreases glutamate

68
Q

Guanfacine and food

A

ABSORPTION OF GUANFACINE IS SIGNIFICANTLY INCREASED WHEN TAKEN WITH A HIGH-FAT MEAL

Psych 660 (6 decks)

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