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Pharm final > Drugs of abuse > Flashcards

Drugs of abuse Flashcards

1
Q

Ethanol influences several cellular functions:

A
  • GABAA receptors
  • Kir3/GIRK channels
  • Adenosine reuptake
  • Glycine receptors
  • NMDA receptors
  • 5-HT3 receptors.
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2
Q

Delirium tremens

A

Occurs 48-72 hours post alcohol withdrawal.

Delirium tremens is associated with 5-15% mortality

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3
Q

Three drugs are FDA-approved for treatment of alcoholism:

A
  • Disulfiram: Aldehyde dehydrogenase inhibitor. Used to create aversion to drinking.
  • Naltrexone: Orally available opioid antagonist. Reduces craving for alcohol.
  • Acamprosate: NMDA receptor antagonist. Prevents relapse.
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4
Q

TREATMENT OF ALCOHOL WITHDRAWAL

A
  • Long half-life benzodiazepines are the preferred agents: Diazepam and chlordiazepoxide.
  • Because of their long half-life, withdrawal is smoother, and rebound withdrawal symptoms are less likely to occur.
  • Lorazepam and oxazepam are intermediate-acting drugs.
  • Not as dependent on hepatic metabolism as other benzodiazepines,
  • They may be preferable in the elderly and those with liver failure.
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5
Q

TREATMENT OF ALCOHOL ADDICTION:

Topiramate

A
  • Facilitates GABA function, antagonizes glutamate receptors.
  • May reduce cravings.
  • Not FDA-approved
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6
Q

BENZODIAZEPINES: WITHDRAWAL SYNDROME

A
  • Signs and symptoms include: tremors, anxiety, perceptual disturbances, dysphoria, psychosis, and seizures.
  • The syndrome can be life-threatening.
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7
Q

MANAGEMENT OF BENZODIAZEPINE WITHDRAWAL

A
  • If the patient is on a short-acting drug, they are switched to a long-acting drug.
  • Diazepam is the most used agent.
  • Then the dose is gradually reduced
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8
Q

PSYCHOSTIMULANTS

A

Methylxanthines
- Caffeine, theophylline & theobromine.
Cocaine
Amphetamines

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9
Q

Methylxanthines
- Caffeine, theophylline & theobromine.
MOA

A
  • Methylxanthines block presynaptic adenosine receptors.
  • Activation of adenosine receptors inhibits norepinephrine release.
  • Therefore blockade of adenosine receptors increases norepinephrine release
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10
Q

METHYLXANTHINES: ACTIONS on CNS

A
  • 100–200 mg caffeine (1 - 2 cups of coffee) cause decrease in fatigue and increased mental alertness.
  • 1.5 g caffeine (12 to 15 cups of coffee) produces anxiety and tremors.
  • The spinal cord is stimulated only by very high doses (2–5 g) of caffeine.
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11
Q

COCAINE: MECHANISM OF ACTION

A
  • Cocaine inhibits dopamine, norepinephrine and serotonin reuptake.
  • The prolongation of dopaminergic effects in the brain’s limbic system produces the intense euphoria that cocaine initially causes.
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12
Q

COCAINE: ACTIONS CNS

A

CNS
• Stimulation of cortex and brainstem.
• Increases mental awareness and produces a feeling of well-being and euphoria.
• Paranoia may occur after repeated doses.
• At high doses: tremors and convulsions, followed by respiratory and vasomotor depression.

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13
Q

COCAINE: ACTIONS SNS

A

SYMPATHETIC NERVOUS SYSTEM
• Peripherally, cocaine potentiates the action of norepinephrine resulting in adrenergic stimulation.
• Adrenergic stimulation produces the characteristic physical findings of tachycardia, hypertension, mydriasis, and diaphoresis.

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14
Q

COCAINE: WITHDRAWAL SYNDROME

tx for addiction?

A
  • Dysphoria, depression, sleepiness, fatigue, cocaine craving and bradycardia.
  • Cocaine withdrawal is generally mild.
  • Treatment of withdrawal symptoms is usually not required.
  • No effective tx for cocaine addiction!
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15
Q

AMPHETAMINES: MECHANISM OF ACTION

A
  • Amphetamines increase release of catecholamines.
  • They are also weak inhibitors of MAO.
  • They are also possible direct catecholaminergic agonists in the brain.
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16
Q

AMPHETAMINES: USES

A
  • Attention deficit syndrome: Amphetamine and methylphenidate.
  • Narcolepsy: Amphetamine and methylphenidate
17
Q

NICOTINE: MECHANISM OF ACTION

A
  • Full agonist of the nicotine receptor.
  • The rewarding effect of nicotine requires involvement of the ventral tegmental area , where nicotinic receptors are expressed on dopamine neurons.
  • When nicotine excites these neurons, dopamine is released.
18
Q

NICOTINE: ACTIONS CNS

A
  • Cigarette smoking or administration of low doses of nicotine produces some degree of euphoria and relaxation.
  • Improves attention, learning, problem solving, and reaction time.
  • High doses of nicotine result in central respiratory paralysis and severe hypotension caused by medullary paralysis.
  • Nicotine is an appetite suppressant.
19
Q

TREATMENT FOR NICOTINE ADDICTION

A

NICOTINE REPLACEMENT THERAPY
• Nicotine can be administered by transdermal patch, gum, nasal spray, vapor inhaler or by lozenge for buccal absorption.
SUSTAINED-RELEASE BUPROPION
• Mechanism unclear.
VARENICLINE
• Partial agonist at nicotinic receptors in the CNS.

20
Q

OPIOIDS
most commonly abused?
Among health professionals?

A

The most commonly abused opioids are heroin, morphine, codeine and oxycodone, and –among health professionals- meperidine and fentanyl.

21
Q

OPIOIDS: TOLERANCE, DEPENDENCE & WITHDRAWAL

A
  • All opioids induce strong tolerance and dependence.
  • Addiction to heroin or other short-acting opioids produces behavioural disruptions and usually is incompatible with a productive life.
  • The withdrawal syndrome is unpleasant but not life-threatening.
  • It includes dysphoria, lacrimation, rhinorrhea and yawning.
22
Q

OPIOIDS: TREATMENT OF OPIOID WITHDRAWAL

A

DETOXIFICATION USING OPIOID AGONISTS
• The illicit agent is replace by a long-acting opioid.
• The dose is slowly reduced.
• Drugs used: Methadone or buprenorphine.

23
Q

OPIOIDS: TREATMENT OF OPIOID WITHDRAWAL:

DETOXIFICATION USING ADRENERGIC AGONISTS

A

Drugs used: Clonidine and lofexidine. They are α2 agonists.
• Chronic opioid intake leads to tolerance to the effects of opioids on the ANS, mediated by adrenergic pathways.
• Withdrawal leads to a rebound firing of the neurons.
• A noradrenergic storm results and is responsible for many of the withdrawal symptoms.

  • NALTREXONE for those who choose to remain opioid free
24
Q

MARIJUANA: MECHANISM OF ACTION

A
  • Two cannabinoid receptor subtypes:CB1 & CB2.
  • Both are G protein-linked receptors.
  • Both couple to Gi.
  • CB1 receptors are found primarily in the brain and mediate the psychological effects of THC.
  • CB2 receptors are present mainly on immune cells.
25
Q

MARIJUANA: ACTIONS

A
  • THC can produce euphoria, followed by drowsiness and relaxation.
  • Affects short-term memory and mental activity.
  • Impairs highly skilled motor activity.
  • Other effects: appetite stimulation, xerostomia, visual hallucinations, delusions, enhancement of sensory activity.
  • At high doses: toxic psychosis
26
Q

MARIJUANA: USES

A
  • Therapeutic THC is called dronabinol.
  • Dronabinol is FDA-approved for:
  • Anorexia associated with weight loss in patients with AIDS.
  • Nausea and vomiting associated with cancer chemotherapy (second line).
27
Q

PSYCHEDELIC AGENTS

A 
LSD
MESCALINE
PSILOCIBIN
PHENCICLIDINE
MDMA
28
Q

LSD: MECHANISM OF ACTION

A

The hallucinogenic actions of LSD appear to be mediated by agonist effects at 5-HT2 receptors in the CNS.

29
Q

LSD: CLINICAL PRESENTATION

A

present with a combination of somatic and psychomimetic symptoms.
• Somatic symptoms are usually due to sympathomimetic effects.
• Somatic symptoms include: mydriasis, hypertension, tachycardia, increased body temperature, flushing, sweating, tremors and piloerection.

30
Q

PHENCYCLIDINE (PCP) MOA

A
  • Dissociative anesthetic.
  • Blocks reuptake of norepinephrine and dopamine.
  • Causes cholinergic and anticholinergic effects.
  • Has actions at nicotinic and opioid receptors.

The dissociative properties of PCP are believed to be due to its actions as a non-competitive antagonist at NMDA recept

31
Q

PHENCYCLIDINE: CLINICAL PRESENTATION

A
  • Clinical manifestations include violent or bizarre behavior, psychosis, nystagmus, tachycardia, hypertension, diaphoresis, miosis, anesthesia, and analgesia.
  • An important diagnostic clue is nystagmus.

Pharm final (19 decks)

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