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Psychiatry > pharm of drugs of abuse > Flashcards

pharm of drugs of abuse Flashcards

drugs of abuse

1
Q

Alcohol acts on which receptors

A

GABA-A (agonist) , NMDA/Glutamate (antagonist), opiod (indirect stim of B endorphins), dopamine (indirect)

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2
Q

Does ADH enzyme acitivty increased NADH or NAD+

A

NADH

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3
Q

metabolic effects of alcohol metabolism

A

increaeed production of lactic acid , ketosis, increased triglyceride synthesis, decreased gluconeogenesis= hypoglycemia

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4
Q

2 enzymes involved in alcohol metabolism

A

alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH)

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5
Q

units for BAC

A

mg/dL

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6
Q

thiamine action in body

A

breaks down sugars in the diet and helps correct neuro problems

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7
Q

thiamine is metabolized and eliminated where?

A

liver , renal

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8
Q

Lorazepam short or long duration?

A

short

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9
Q

Oxazepam short or long duration?

A

short

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10
Q

Chlordiazepoxideshort or long duration?

A

long

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11
Q

Diazepam short or long duration?

A

long

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12
Q

when should long acting BZDs not be used

A

elderly or peeps w/ underlying neuro or liver issues

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13
Q

Lorazepam mechanism

A

allosteric modulation of GABA receptors which potentiates GABA activity

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14
Q

how well is lorazepam absorbed?

A

well and rapidly

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15
Q

lorazepam is metabolized wehre and excreted wehre

A

liver, urine

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16
Q

lorazepam peak onset

A

1-2 hours

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17
Q

lorazepam half life

A

10-20 hours

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18
Q

lorazepam routes

A

PO, IM, IV

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19
Q

disadvantage of lorazepam

A

short acting and possible withdrawal seizures

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20
Q

chlordiazepoxide mechanism

A

allosteric modulation of GABA receptors which potentiates GABA activity

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21
Q

chlordiazepoxide bioavailability

A

over 90%

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22
Q

where is chlordiazepoxide metabolized, is the metabolite active? if so what is it called

A

liver
yes

desmethyldiazepam

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23
Q

chlordiazepoxide peak onset

A

1.4-4 hrs

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24
Q

chlordiazepoxide half life

A

5-30 hours, but active metabolites= 36-200 hours

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25
Q

Gabapentin mechanism

A

exact mechanism isn’t known, but interacts w/ voltage gated Ca channels

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26
Q

Gabapentin bioavailability

A

27-60%

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27
Q

Gabapentin peak

A

2 hrs

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28
Q

Disulfiram brand name

A

Antabuse

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29
Q

Disulfiram mechanism

A

irreversible inhibitor of ALDH causes acetaldehyde to accumulate which causes discomfort when drinking alcohol ie hangover: flushing, headache, dizziness, nausea, vomiting, rapid heart rate, hypotension, and mental confusion

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30
Q

what is Disulfiram’s bioavailabilityqualitiatively

A

high

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31
Q

Disulfiram onset

A

5-30 minutes

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32
Q

Disulfiram half life

A

7 hours

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33
Q

Disulfiram duration of effect

A

up to 2 weeks

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34
Q

Disulfiram adverse rxns

A

fulminant hepatitis (use with care in liver disease)
peripheral neuropathy
neuropsych changes
caution over 60, CAD, cerebrovascualr disease

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35
Q

Naltrexone drug class

A

opioid antagonist so decreases rewarding effects of alcohol

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36
Q

Naltrexone side effect

A

nausea, headache, constipation, dizziness, nervousness, insomnia, drowsiness

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37
Q

when does naltrexone have to be used cautiously?

A

liver disease

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38
Q

acamprosate drug class

A

GABA analogue

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39
Q

acamprosate mechanism

A

NMDA antagnoist + GABA A recepcotor activator plus acts on serotonergic noradrenergic and dopaminergic receptors which may lead to restoration of neuronal excitation and inhibition balance

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40
Q

where is acamprosate metabolized/ excreted?

A

it’s not metabolized, excreted in urine

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41
Q

when should acamprosate not be used

A

depressed patients, renal impairment

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42
Q

Topiramate therapeutic class

A

anti-epileptic

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43
Q

Topiramate mechanism

A

blocks voltage gated Na channels
augmentation of GABA at GABA-A receptor
Antagonism at AMPA glutamate receptors

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44
Q

Qualitatively what is Topiramate’s bioavailability

A

high

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45
Q

Topiramate metabolism

A

70% excreted unchanged rest is hydroxylated, hydrolyzed, or undergoes glucuronidation

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46
Q

Topiramate adverse rxns

A

metabolic acidosis, paresthesias, URI , diarrhea, nausea, anorexia, memory/cognitivedistrubance

47
Q

morphine route (3)

A

po, iv im

48
Q

morphine oral bioavailability

A

35-70%

49
Q

morphine half life

A

2-3.5 hours

50
Q

morphine duration

A

4-6 hours

51
Q

morphine metabolism

A

hepatic glucuronidation

52
Q

morphine withdrawal onset, peak, duration

A

8-12 hours after last dose, peaks 48 hours, and lasts 3-5 days

53
Q

codeine route

A

PO only

54
Q

codeine bioavailability

A

~90%

55
Q

codeine half-life

A

2.5-3 hours

56
Q

codeine duration

A

4-6 hours

57
Q

how does heroin have such a rapid effect?

A

lipid soluble, rapid penetration of BBB

58
Q

relative potency b/w morphine and heroin

A

heroin is 2x more potent

59
Q

heroin withdrawal onset, peak, and duration

A

8-12 hours after last dose, peaks 48 hours, and lasts 3-5 days

60
Q

oxycodone is what schedule of drug

A

2

61
Q

oxycodone onset PO

A

1 hr

62
Q

oxycodone half life

A

3-4 hours

63
Q

oxycodone duration

A

6-8 hours

64
Q

oxycontin duration

A

12 hrs

65
Q

oxycodon bioavailability

A

60-87%

66
Q

does oxycodon have active metabolites? If so what is it called

A

yes, oxymorphone

67
Q

Oxycodon metabolized by which enzymes

A

3A4 and 2D6

68
Q

Hydrocodone onset

A

30 min

69
Q

hydrocodone peak

A

1 hr

70
Q

hydrocodone half-life

A

2-3 hours

71
Q

hydrocodone duration

A

3-4 hours

72
Q

hydrocodone pain relief relative to oxycodone

A

thought to be about 50% of oxycodone

73
Q

hydrocodone is which drug schedule

A

II

74
Q

methadone mechanism

A

full mu agonists

75
Q

methadone bioavailability

A

> 90%

76
Q

methadone half life

A

24 hrs

77
Q

methadone onset

A

6-8 hours

78
Q

methadone withdrawal onset, peak, and withdrawal

A

36-48 hrs after last dose, peak at 3-4 days, lasts up to 3 weeks

79
Q

buprenorphine classified as what

A

opiate

80
Q

buprenorphine mechanism

A

partial opioid agonist with very high affinity so it kicks full agonist out

81
Q

what are implications of buprenorphine’s ceiling effect (4)

A

low abuse potential
lower level of physical dependence ie less withdrawal
less opioid effect than methadone
safety in overdose quantities

82
Q

route in which buprenorphine should be taken

A

sublingual

83
Q

Buprenorphine withdrawal onset, peak, duration

A

36-72 hours after last dose, peak 3-4 days= softer landing

84
Q

Suboxone is combination of what

A

buprenorphine and naloxone

85
Q

why is naloxone added to suboxone

A

leads to withdrawal if taken IV and it blunts high

86
Q

cocaine IV/ smoked , euphoria lasts how long

A

4-7 minutes; effect diminished by half 17-30 minutes

87
Q

cocaine snorted, peaks when

A

30 min

88
Q

cocaine is metabolized to what and excreted how

A

benzoylecgonine excreted in urine

89
Q

cocaine mechanism

A

blocks dopaimine reuptake transported in presynaptic membrane

90
Q

Cocaine desired effects

A

alertness, well-being, euphoria, energy and motor activity, self confidence, increased sexuality, maybe increased athletic performance, minor withdrawal

91
Q

Cocaine toxic effects

A

CNS Stimulation
anxiety, restlessness
paranoia / delusions
hallucinations, seizures
hyperpyrexia (increased temp)
Adrenergic Effects
tachyarrythmias
increased BP
tremor
Vasoconstrictive
heart attack
stroke

92
Q

cocaine long term consequences

A

neuroadaptation
decreased dopamine transporters
decreased dopamine receptors

93
Q

Amphetamine mechanism

A

enter dopamine neurons via reuptake transporters and interact intracellularly to release dopamine in presynaptic terminal. Dopamine= reverse transported out of neuron …damages vesicles which leads to release

94
Q

methamphatmine is which schedule drug? and approved for what

A

II approved for ADHD ad obesity

95
Q

crystal meth route

A

oral, IN, IV, smoked

96
Q

crystal meth effects

A

euphoria, well being, confidence, sexual enhancement, alertness, hyperactivity, increased energy, increased HR, BP, temperature, tremors, and RR

97
Q

psych effects of crystal meth

A

hypomania, insomnia, irritability, appetite suppression, weight loss, 10% frank psychosis

98
Q

meth neurotransmitter toxicity

A

chronic use leads to reduction in dopamine transporter levels which leads to depletion of dopamine in presynaptic terminal which leads to impaired motor and verbal fxn and eventually long term cognitive defects

99
Q

meth withdrawal signs and consequences

A

terrible Tuesday: depression, irritability, suicidal ideation, carbohydrate craving. Long term use can lead to chronic depression. 62% remain depressed 2-5 years after abstinence

100
Q

short term Medical complications of meth and what are they caused by

A

mediated by release of DA and NE ( tachy, HTN, tachypnea, hyperthermia, CNS, excitation)
Rhabdomyolysis and CV events
vasoconstriction, vasculitis, focal myocyte necrosis
CV events associated w/ long term use include MI and stroke
bruxism and periodontal disease ie meth mouth

101
Q

marijuana is metabolized by which enzyme and eliminated where

A

CYP 2C9 and elimianted in feces and urine

102
Q

desired effects of marijuana

A

sense of well being, relaxation, euphoria
modified level of consciousness
altered perception, time sense
intensified sensory experiences
sexual disinhibition

103
Q

marijuana withdrawal

A

irritability
decreased appetite
anxiety
physical discomfort
low mood
increased aggression/anger
insomnia
restlessness

104
Q

ecstasy (MDMA) mechanism

A

blocks serotonin reuptake acutely and decreases serotonin chronically by depleting stores and synthesis

105
Q

Serotonin Syndrome

A

hyperthermia, dehydration
kidney failure (rhabdomyolysis)
elevated BP and hR
nausea, vomiting, diarrhea, sweating
hallucinations, hypomania, seizures
muscle cramps and bruxism

106
Q

GHB prescribed as

A

Xyrem for narcolepsy and cataplexy

107
Q

what effect does GHB have on body ie sedative or stimulant

A

CNS depressant, sedative-hypnotic

108
Q

pharmacodynaically GHB affects/ is related to which NT

A

precursor and catabolite of GABA

109
Q

GHB is what schedule drug

A

I unless Xyrem which is III

110
Q

ketamine prescribed as

A

anesthetic

111
Q

ketamine has what affect as or on NTs

A

antagonist of glutamate NMDA receptors

112
Q

Ketamine effects

A

analgesic, dissociative, neuroprotective effects in brain trauma

113
Q

rohypnol prescibed use

A

muscle relaxant

Psychiatry (4 decks)

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