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Addiction Flashcards

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1
Q

What pathway acts on pleasure/ motivation?

A

Mesolimbic pathway mediated by release of dopamine

Ventral tegmental area > Nucleus accumbens

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2
Q

what pathway acts on goal setting/ descicion making?

A

Prefrontal cortex

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3
Q

True/ False Prefrontal cortex can override the mesolimbic pathway

A

True- prefrontal cortex can override the mesolimbic pathway

-drugs can disrupt the frontal cortex

mesolimbic pathway- motivation and pleasure using dopamine
prefrontal cotex- descicion making and goal setting

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4
Q

what part of the brain is the creator of motivation to act?

A

orbitofrontal cortex

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5
Q

what part of the brain is overactive in cravings/ addicts?

A

Orbitofrontal fortex is overactive in cravings/ addicts

-it is the creator of motivation to act

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6
Q

role of hippocampus in addiction?

A

stores memory of pleasure and learned drug associations

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7
Q

what dopamine pathway do addictive drugs act on?

A

Addictive drugs act on the mesolimbic pathway
(pathway that controls pleasure/motivation)

VTA >NA (mediated by dopamine)

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8
Q

what can chronic drug use and overstimulation of the mesolimbic pathway lead to?

A

-reduces dopamine receptor expression and results in tolerance
-the body eventually depends on drug dopamine stimulation to feel normal (negative reinforcement)

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9
Q

recommended units a week- alcohol?

A

14 units/ week

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10
Q

what is classed a hazardous drinking?

A

> 14 units/ week

-increases risk of harm

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11
Q

what harm can hazardous drinking (>14 units a week) cause?

A

Cancer- breast, GI (oesophagus, bowel, oral), liver

Wernicke’s encephalopathy

Korsakoff syndrome

Cardiovascular problems

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12
Q

what cancer can hazardous drinking (>14 units a week) cause?

A

Breast, GI (oesophagus, bowel, oral) and liver

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13
Q

what is Wernickes encephalopathy

A

Acute thiamine (aka B1) deficiency caused by hazardous drinking (usually >14 units/week)

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14
Q

Alcoholic develops ataxia, nystagmus and confusion
-what?

A

Acute thiamine (B1) deficiency
-Wernicke’s encephalopathy

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15
Q

what is Korsakoffs syndrome?

A

Chronic thiamine (B1) deficiency caused by alcohol use

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16
Q

Alcoholic presents with dementia and confabulation (false lies/ think they are telling the truth)
-what is this

A

Korsakoff syndrome

17
Q

what CV SE are there to hazardous drinking (>14 units a week)?

A

Dilated cardiomyopathy
-stroke, hypertension

18
Q

what is considered harmful drinking?

A

> 35 units/ week (women)
50 units/week (men)

19
Q

what medication can be given for alcohol detoxification?

A

benzodiazepine (gradually withdraw) + vitamin supplementation (to prevent thiamine deficiency)

20
Q

MofA benzodiazepines?

A

increase the affects of GABA (so more inhibation/ drowsiness)

inhibits glutamate (excitatory)

21
Q

what can be done as relapse prevention in alcoholics?

A

should not use benzodiazepines beyond detoxification period

1st line= Naltrexone
-Disulfram
-Acamprosate

22
Q

MofA Nalrexone?

A

(used 1st line in relapse prevention of alcoholics)

Opiod anatagonist and reduces rewards from alcohol

23
Q

MofA- dilsulfram?

A

-acetaldehyde dehydrogenase inhibitor

(acetaldehyde build up with alcohol ingestion causing alcohol intolerace)

24
Q

MofA Acromprosate?

A

Acts centrally (GABA/glutamate)

-reduces cravings
-good to use alongside psychotherapy

25
Q

when is peak incidence of delirium tremens?

A

symptoms start 6-12 hours (tremor, sweating, tahcycardia, anxious)

seizures 36 hours

Peak incidence of delirium tremens 48-72 hours (coarse tremor, confusion, delusions, auditory and visual hallucinations, fever, tachycardia)

26
Q

peak incidence of seizures?- delirium tremens

A

36 hours after last drink

27
Q

when do delirium tremens symptoms start?

A

6-12 hours after last drink
-tremor
-sweating
-tachycardia
-anxiety

28
Q

treatment of delirium tremens?

A

long acting benzodiazepine:
-diazepam
OR
-chlordiazepoxide

29
Q

MofA- delirium tremens?

A

-Chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors

-Alcohol withdrawal is thought to be lead to the opposite (decreased inhibitory GABA and increased NMDA glutamate transmission)

30
Q

what is treatment of opiod dependance?

A

Opioid replacement therapy:
-Methadone (solution)
-Buprenorphine (oral tablet)

31
Q

Patient has pinpoint pupils, respiratory depression or is unconscious. Have a history of opioid use

-how will you manage them?

A

Drug reversal= IV naloxone

Symptoms of drug toxicity= unconsciouss, respiratory depression, pin point pupils

psych (18 decks)

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