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BSP Exam I > Dementia Pharm, Sedative Hypnotics, Alcohol, Drugs of Abuse > Flashcards

Dementia Pharm, Sedative Hypnotics, Alcohol, Drugs of Abuse Flashcards

1
Q

Central AChE inhibitor originally approved for dementia, but newer agents are now preferred due to high incidence of hepatotoxicity

A

Tacrine

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2
Q

Noncompetitive, reversible, centrally-acting AChE inhibitor approved for mild, moderate, or severe dementia of the Alzheimer type

A

Donepezil

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3
Q

3 AChE inhibitors approved for use in pts with dementia

A

Donepezil
Galantamine
Rivastigmine

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4
Q

Reversible AChE inhibitor utilized in mild, moderate, and severe dementia of Alzheimer type as well as mild to moderate dementia associated with Parkinson disease

A

Rivastigmine

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5
Q

Competitive, reversible centrally-acting AChE inhibitor that also modulates nAChR to increase from surviving presynaptic nerve terminals and may increase glutamate and serotonin levels; utilized in mild-to-moderate Alzheimers

A

Galantamine

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6
Q

Pts with Alzheimer type progressive dementia have a deficiency of intact _____ neurons, which explains the utility of AChE inhibitors in the treatment of these pts. Pts with dementia associated with _____ disease also benefit

A

Cholinergic; Parkinson

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7
Q

Signs of acute intoxication with AChE inhibitors like donepezil, rivastigmine, and galantamine

A

Signs of mAChR stimulation = miosis, salivation, sweating, bronchoconstriction, vomiting, diarrhea

With poisoning from lipid-soluble agents, CNS involvement follows rapidly — confusion, ataxia, generalized convulsions, coma, respiratory paralysis

Time of death after a single acute exposure may range 5 minutes to 24 hours and is caused primarily by respiratory failure

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8
Q

Treatment for acute AChE intoxication

A

Atropine, pralidoxime, and a benzodiazepine are typically combined

[atropine acts at mAChRs, pralidoxime reactivates AChE by removing phosphorus group from active site, Benzodiazepine acts as an anticonvulsant]

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9
Q

________, the primary excitatory amino acid in the CNS, may contribute to the pathogenesis of Alzheimer’s disease by overstimulating various receptors leading to excitotoxicity and neuronal cell death

A

Glutamate

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10
Q

Antagonist of the NMDA type of glutamate receptor by binding to the intra-pore magnesium site with longer dwell-time, thus functioning as a receptor blocker only under conditions of excessive stimulation (does not affect normal neurotransmission)

A

Memantine

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11
Q

Benzodiazepine with the fastest rate of onset after oral administration

A

Diazepam

[followed by alprazolam, flurazepam, chlorazepate > chlordiazepoxide, lorazepam, triazolam, clonazepam > oxazepam]

Slowest is oxazepam!

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12
Q

3 intermediate-to-long acting benzodiazepines

A

Diazepam

Lorazepam

Clonazepam

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13
Q

5 short-to-intermediate acting benzodiazepines

A 
Alprazolam
Oxazepam
Temazepam
Midazolam
Triazolam
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14
Q

4 benzodiazepines with significant active metabolites

A

Chlordiazepoxide
Diazepam
Flurazepam
Chlorazepate

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15
Q

Newer sedative-hypnotic utilized for sleep maintenance

A

Zolpidem

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16
Q

Newer sedative-hypnotic good for pts who awaken early in sleep cycle

A

Zaleplon

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17
Q

______ and _____ are newer sedative-hypnotics that cause less amnesia and day-after somnolence than zolpidem or benzodiazepines

A

Eszopiclone; zaleplon

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18
Q

Newer sedative-hypnotic good for sleep-onset and maintenance; most common adverse effect is next-day somnolence

A

Suvorexant

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19
Q

Symptoms of benzodiazepine overdose are that of CNS depression — including disorientation, drowsiness, ataxia, slow slurred speech, etc. what agent is utilized to reverse benzodiazepine-induced sedation?

A

Flumazenil

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20
Q

MOA of flumazenil

A

Competitive antagonist at GABA-A receptor (same binding site as benzodiazepine)

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21
Q

MOA of benzodiazepines

A

Binds GABA-A receptor and enhances GABA’s effects

Increases Cl- influx, increased hyperpolarization, decreased number of APs (CNS depression)

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22
Q

MOA of barbiturates

A

Binds the GABA-A receptor; increases the duration of GABA-gated channel openings

Increases Cl- influx, increased hyperpolarization, decreased number of APs (CNS depression)

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23
Q

The MOA of ______ is unknown but it has a high affinity for 5-HT1A and 5-HT2 receptors and moderate affinity for D2 receptors, without affecting benzodiazepine GABA receptors

A

Buspirone

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24
Q

________ is a highly effective, rapid onset sedative hypnotic with minimal hangover effects and a longer half life than zolpidem and zaleplon; may interact with GABA receptor complexes at binding domains located close to or allosterically coupled to benzodiazepine receptors

A

Eszopiclone

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25
Q

Potent selective agonist of melatonin receptors MT1 and MT2 (with little affinity for M3) within suprachiasmatic nucleus of the hypothalamus, an area responsible for determination of circadian rhythms and synchronization of the sleep-wake cycle

A

Ramelteon

[MT1 agonism —> sleepiness; MT2 agonism —> regulation of circadian rhythms]

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26
Q

_______ is a newer sedative-hypnotic that interacts with the benzodiazepine GABA receptor complex; possibly at omega-1 recepto on alpha subunit of GABA-A receptor

A

Zaleplon

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27
Q

Imidazopyridine hypnotic that enhances activity of GABA via selective agonism at benzodiazepine-1 receptor —> increased Cl conductance, neuronal hyperpolarization, inhibition of action potential, decrease in neuronal excitability

A

Zolpidem

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28
Q

Sedative-hypnotic that affects the thalamus and limbic system; also appears to inhibit multineuronal spinal reflexes

A

Meprobamate

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29
Q

CNS depressant due to active metaboite trichloroethanol

A

Chloral hydrate

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30
Q

_____ competes with histamine for H1 receptor sites on effector cells in GI tract, blood vessels, and respiratory tract; has skeletal muscle relaxing, bronchodilator, antihistamine, antiemetic, and analgesic properties

A

Hydroxyzine

31
Q

Describe the relationships between dose of benzodiazepines and barbiturates and their CNS effects

A

Most sedative-hypnotics exhibit graded dose-dependent depression of CNS function

Older sedative-hypnotics like barbiturates and alcohols: increase in dose higher than that needed for hypnosis may lead to state of general anesthesia —> higher doses lead to respiratory and vasomotor center depression in medulla leading to coma and death

Benzodiazepines and newer sedative-hypnotics: require proportionately greater dosage increments to achieve CNS depression more profound than hypnosis

32
Q

Describe biotransformation pathway for benzodiazepines

A

Hepatic metabolism; mostly via phase I reactions via CYP450 enzymes (esp CYP3A4), then phase II reactions to form glucuronides that are excreted in urine

Many phase I metabolites of benzodiazepines are pharmacologically active — those metabolites with long half lives are more likely to cause cumulative effects with multiple doses

33
Q

4 drugs utilized in the treatment of acute alcohol withdrawal syndrome

A

Diazepam
Lorazepam
Oxazepam
Thiamine (B1)

34
Q

3 drugs used for the prevention of alcohol abuse

A

Acamprosate
Disulfuram
Naltrexone

35
Q

2 drugs utilized in the treatment of acute methanol or ethylene glycol poisoning

A

Ethanol

Fomepizol

36
Q

What receptors are affected during acute ethanol exposure?

A

Acute ethanol exposure enhances the action of GABA and GABA-A receptors

Ethanol also inhibits the ability of glutamate to open NMDA-subtype of glutamate receptors [the NMDA receptor is implicated in aspects of cognitive function including learning/memory]

37
Q

The overall metabolism of ethanol involves extensive first pass metabolism by gastric and liver enzyme __________________, followed by ________________.

Metabolism follows ____-order kinetics in that the rate of biotransformation is independent of time and concentration of ethanol; enzymes are almost immediately saturated

A

Alcohol dehydrogenase (ADH); aldehyde dehydrogenase

Zero

38
Q

Drug used in the setting of alcohol cravings that acts as a mu-opioid receptor antagonist (long-acting), and reduces craving for alcohol and rate of relapse to either drinking or alcohol dependence in the short-term

A

Naltrexone

39
Q

T/F: individuals physically dependent on alcohol and opioids should not stop their opioid use prior to initiating therapy with naltrexone in order to avoid an acute withdrawal syndrome

A

False!

Individuals physically dependent on alcohol and opioids must be OPIOID-FREE before initiating naltrexone therapy, because naltrexone precipitates an acute withdrawal syndrome

40
Q

Drug used in the setting of alcohol cravings that acts as a weak NMDA receptor antagonist and GABA-A receptor agonist (also affects serotonergic, noradrenergic, and dopaminergic systems)

Reduces short-term and long-term relapse rates (more than 6 mos)

A

Acamprosate

41
Q

Drug used in the setting of alcohol cravings that irreversibly inhibits aldehyde dehydrogenase —> accumulation of aldehyde; causes extreme discomfort in pts who drink alcohol — flushing, headache, N/V, sweating

A

Disulfiram

42
Q

T/F: When combined, alcohol, benzodiazepines, barbiturates, and sleep aids have additive effects on CNS depression

A

True

43
Q

When consumed, methanol is converted by alcohol dehydrogenase and aldehyde dehydrogenase into toxic metabolites _________ and _______

When consumed, ethylene glycol is converted into toxic ______ and _______

A

Formaldehyde; formate

Aldehydes; oxalate

44
Q

How is methanol toxicity treated?

A

Fomepizole

Ethanol

45
Q

MOA of fomepizole in tx of methanol or ethylene glycol poisoning

A

Inhibits alcohol dehydrogenase —> reduction of toxic metabolite formation

46
Q

Wernicke’s encephalopathy vs. Korsakoff’s psychosis (clinical features)

A

Wernicke’s encephalopathy — paralysis of the external eye muscles, ataxia, and confusion; can progress to coma and death

Korsakoff’s psychosis — chronic disabling memory disorder following Wernicke’s encephalopathy

47
Q

Appropriate drug therapy for Wernicke’s encaphalopathy

A

Benzodiazepines

Thiamine

48
Q

As a general rule, all addictive drugs activate the ______ dopamine system. Dopamine within this system codes for the difference between expected and actual reward, thus constituting a strong learning signal. This system continuously scans for reward, increasing its activity when reward is larger than expected, and shutting down when reward does not occur.

By directly increasing ________, addictive drugs generate a strong but inappropriate learning signal, thus hijacking the reward system and leading to pathologic reinforcement.

What hypothesis does this describe?

A

Mesolimbic

Dopamine

The dopamine hypothesis of addiction

49
Q

Drugs of abuse can be placed into 3 categories: Drugs that activate GPCRs, Drugs that bind ionotropic receptors and ion channels, and Drugs that bind to transporters of biogenic amines.

What are 4 drugs of abuse that activate GPCRs?

A

Opioids

Cannabinoids

y-Hydroxybutyric acid (GHB)

LSD

50
Q

Drugs of abuse can be placed into 3 categories: Drugs that activate GPCRs, Drugs that bind ionotropic receptors and ion channels, and Drugs that bind to transporters of biogenic amines.

What are 5 drugs of abuse that bind ionotropic receptors and ion channels?

A

Nicotine

Alcohol

Benzodiazepines

Phencyclidine

Ketamine

51
Q

Drugs of abuse can be placed into 3 categories: Drugs that activate GPCRs, Drugs that bind ionotropic receptors and ion channels, and Drugs that bind to transporters of biogenic amines.

What are 3 drugs of abuse that bind transporters of biogenic amines?

A

Cocaine
Amphetamine
Ecstasy

52
Q

General MOA of opioids as drugs of abuse

A

Agonists at mu-opioid receptor (Gi) —> disinhibition on dopamine neurons

53
Q

Signs and symptoms of opioid intoxication

A

Pupil constriction

Decreased body temp

Decreased HR and BP

Sleepiness, droopy eyelids, soft low voice, euphoria

54
Q

Signs/symptoms of opioid withdrawal

A 
Dysphoria
N/V/D
Myalgias
Lacrimation
Rhinorrhea
Mydriasis
Piloerection
Sweating
Yawning
Fever
55
Q

Treatment options for opioid withdrawal

A

Naloxone — reverses effects of morphine or heroin in minutes; provokes an acute withdrawal syndrome in a dependent pt who has recently taken an opioid

Methadone, buprenorphine, morphine sulfate — longer acting opioids that act as substitution therapy

56
Q

MOA of cannabinoids as drugs of abuse

A

Agonist at cannabinoid-1 (Gi) receptor —> disinhibition on dopamine neurons

57
Q

Signs and symptoms of cannabinoid intoxication

A

Euphoria and relaxation, feelings of well-being, grandiosity, and altered perception of time passage, increased appetite

58
Q

Signs/symptoms of cannabinoid withdrawal

A

Restlessness, irritability, mild agitation, insomnia, nausea, cramping

[mild and short-lived]

59
Q

MOA of y-hydroxybutyric acid (GHB)

A

Weak agonist at GABA-B (Gi) receptors —> disinhibition on dopamine neurons

60
Q

Signs and symptoms of intoxication with GHB

A

Before causing sedation and coma, causes euphoria, enhanced sensory perceptions, feeling of social closeness, and amnesia

61
Q

MOA of LSD

A

Ergot alkaloid; partial agonist at 5-HT2A (Gq) receptor

62
Q

Signs/symptoms of LSD intoxication

A

Induction of perceptual symptoms including shape and color distortion

Can induce abortion via stimulation of uterine contractions

63
Q

MOA of nicotine as a drug of abuse

A

Agonist at nAChR —> excitation of dopamine neurons (direct stimulation)

64
Q

Signs and symptoms of nicotine intoxication —> increased pulses and BP, odor on breath, stained fingers or teeth. Signs/symptoms of withdrawal may include irritability and sleep problems.

How is nicotine withdrawal treated?

A

Nicotine given in slowly absorbing forms — gum, inhaled, transdermal

Varenicline, plant-extract cytisine — occupy nAChRs on dopamine neurons of VTA, preventing nicotine from exerting its action

Buproprion — weak inhibitor of neuronal uptake of NE and DA

65
Q

MOA of alcohol has a drug of abuse

A

Acts at GABA-A, 5-HT3, nAChR, NMDA, and Kir3 channels —> excitation, disinhibition on DA neurons

66
Q

Signs and symptoms of alcohol withdrawal at 6-12 hours, 12-24 hours, 24-48 hours, and 48-72 hours after cessation

A

6-12 hrs — tremor, N/V, excess sweating, agitation, anxiety

12-24 hrs — visual, tactile, auditory hallucinations

24-48 hrs — generalized seizures

48-72 hrs — alcohol withdrawal delirium (delirium tremens): hallucinations, disorientation, autonomic instability; 5-15% mortality

67
Q

Treatment for alcohol withdrawal includes benzodiazepines that rely less on oxidative hepatic metabolism, such as ____ and _____

A

Oxazepam; lorazepam

68
Q

Signs/symptoms of benzodiazepine withdrawal

A

Irritability, insomnia, phonophobia, photophobia, depression, muscle cramps, seizures

69
Q

MOA of phencyclidine and ketamine as drugs of abubse

A

Antagonists at NMDA receptors

70
Q

Signs/symptoms of intoxication with phencyclidine or ketamine

A

Unpleasant vivid dreams, hallucinations, psychedelic effects, increased BP, impaired memory function, visual alterations, out-of-body experiences

71
Q

MOA of cocaine

A

Inhibitor at dopamine transporter (DAT), SERT, and NET —> blocks dopamine uptake

72
Q

MOA of amphetamine

A

Reverses transport at DAT, NET, SERT, and vesicular monoamine transporter (VMAT) —> blocks DA uptake, synaptic depletion

73
Q

MOA of ecstasy

A

Reverses transport at SERT > DAT, NET —> blocks DA uptake, synaptic depletion

74
Q

______ is a BZD effective for status epilepticus and muscle spasticity. _________ is another BZD that is effective for status epilepticus

A

Diazepam; lorazepam

BSP Exam I (9 decks)

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