Pharmacology Substance Abuse Xi-Xvi

Front 1

What are the theories on the mechanism of alcohol?

Back 1

-Enhancement of GABA mediated inhibition similar to the actions of the benzodiazepines
-Inhibition of Ca2+ entry through voltage gated calcium channels
-Inhibition of glutamate receptor function -especially at the NMDA receptor

Front 2

What is fetal alcohol syndrome?

Back 2

-Increase in stillbirths and spontaneous abortions in women who consume 2-3 drinks/day
-Fetal alcohol syndrome
-The lowest level of daily consuption of alcohol that has found to produce FAS is 2.5oz of pure alcohol or 6.25oz of 80 proof spirits
-FAS characterized by CNS dysfunction, slowed growth, a characteristic facies and other rmalformations

Front 3

What type of seizure is associated with alcohol withdrawal?

Back 3

Grand mal

Front 4

What drug is initially used in treatment of alcohol addiction?

Back 4

Benzodiazepines

Front 5

Describe the use of disulfiram in alcohol addiction treatment

Back 5

-Interferes with ethanol metabolism
-Irreversible inactivates aldehyde dehydrogenase, leading to accumulation (up to 5-10x normal levels) of acetaldehyde metabolite of ethanol.
-Increased acetaldehyde leads to a constellation of other symptoms
-Flushing, pulsating headache, respiratory difficulties, nausea, vomiting, sweating, thirst, chest pain, vertigo, orthostasis, potential death

Front 6

What are the problems with disulfiram in alcohol therapy?

Back 6

-Compliance
-Toxic reactions in individuals who drink

Front 7

Describe the use of Naltrexone in treatment of alcohol addiction

Back 7

-Decreases chance of relapse
-Minimal size effects (nausea, no mood changes)

Front 8

Describe methanol metabolism

Back 8

Metabolized at a much slower rate than ethanol by alcohol dehydrogenase. End product is formaldehyde

Front 9

What are the toxic effects and treatment for methanol poisoning

Back 9

Toxic effects include:
-Severe acidosis, coma, death
-Blindness

Treatment
-Treat acidosis
-Ethanol - to slow metabolism of methanol to formaldehyde by competing for alcohol dehydrogenase
-Dialysis

Front 10

What does alcohol have cross tolerance with?

Back 10

Benzodiazepines
Barbituates

Front 11

Describe barbituate withdrawal

Back 11

Generally more severe (than benzo withdrawal) in terms of autonomic instability, more frequenctly life-threatening, characterized more often by hallucinations and delirium, and may respond much more robustly to treatment with barbiturates with a dramatic resolution of symptoms

Front 12

What are barbituates prescribed less frequently than benzodiazepines?

Back 12

-Lowe therapeuric index
-May have a higher likelihood of producing dependence
-More dangerous withdrawal symptoms

Front 13

What are the treatment of barbituate/benzo withdrawal syndromes?

Back 13

1. Use benzodiazepines for benzodiazepine withdrawal and barbiturates for barbiturate withdrawal
2. Substitution of longer acting agetns
3. Barbiturates may be used to manage benzo withdrawal but benzos are generally ineffective for barbiturate withdrawal

Front 14

Describe the mechanism of action of THC

Back 14

-CB-1 receptors highly localized in cortex, hippocampus, cerebellum of brain
-Physiological function of receptor unknown, but may regulate mood
Increases EC dopamine in nucleus accumbens
-CB-2 receptors generally located peripherally and not in the CNS may be responsible for other cannabinoid effects

Front 15

What is the association of THC and psychiatric disorders?

Back 15

Associated with earlier onset of schizophrenia in vulnerable individuals and concern about possible psychosis in others, especially with early onset of use and continued heavy use

Front 16

What is the mechanism of symptoms in THC withdrawal?

Back 16

Enhanced formation and release of corticotropin releasing factor (CRF)

Front 17

Dronobinol

Back 17

A schedule III oral drug that is THC

Front 18

What are the medical uses of THC

Back 18

-Antiemetic after cancer chemotherapy
-Appetite stimulant
-Muscle relaxant
-Decrase ocular pressure in glaucoma
-Alleviation of neuropathic pain

Front 19

What is the common name of MDMA (methylenedioxymethamphetamine?

Back 19

Ecstasy

Front 20

How do hallucinogens exert thair effects?

Back 20

By binding at the 5HT2A serotonin receptor.

Front 21

Describe tolerance and physical dependence of MDMA.

Back 21

-Tolerance develops rapidly (3-4 days)
-Addiction does not generally occur
-Tolerance disappears quickly (one week)
-Cross tolerance occurs among the different hallucinogens
-Physical dependence is not a problem

Front 22

What does MDMA cause?

Back 22

-Increased awareness of sensory input
-Synesthesia
-Out of body experiences
-Flashbacks, weeks ,months or years after the last use of the drug (can be triggered by other drugs or stress)

Front 23

What are the effects of MDMA?

Back 23

-Combination of mescaline and methamphetamine
-No high like cocaine
-Produces an energized state (sudden rush with increased sensory perception, followed by psychedelic effect, followed by adverse effects)
-Adverse effects
-Decreased appetite and ability to perform mental and physical tasks
-Inability to have sex, depressed mood, prolonged headaches
-Heavy used have loss of serotonin axons that persist for months after last use
-Suppression of thirst
-Long term adverse effects include sleep, mood, and anxiety disturbances, increased impulsiveness, memory and attention problems. Can last for up to 2 years after last use.

Front 24

What are the symptoms of MDMA intoxication?

Back 24

-Illusions
-Intense perceptions
-Rare hallucinations
-Mystical feelings
-Dilated pupils
-Flushing
-Elevated heart rate and BP
-Blurry vision

Front 25

What are the toxic effects of MDMA

Back 25

-Psychosis
-Confusion, anxiety, panic
-Autonomic instability, including fever, shock, convulsions
-Flashbacks
-Spontaneous recurrence while sober of intoxicated experiences
-Persistent and chronic flashbacks suggest a separate psychiatric disorder

Front 26

What drugs are arylcyclohexylamines?

Back 26

Phencyclidine (PCP)
Ketamine

Front 27

Describe the actions of PCP

Back 27

-Non competative antagonism at NMDA receptor complex
-Act by blocking NMDA-associated Ca ion channel
-Bind at PCP binding site where other noncompetitive NMDA antagonists also block this channel

-PCP binds sigma opioid receptor

Front 28

What are the signs of PCP intoxication?

Back 28

Marked variability in responses
-Relaxation, euphoria
-Dysphoria, anxiety, emotional liability, paranoia
-Slowness of time perception
-Feelings of numbness
-Agitation, violence
-Tachycardia, flushing, drooling, miosis
-Dizziness, uncoordination, slurred speech, nystagmus

Front 29

What are the toxic reactions to PCP?

Back 29

-Psychosis
-Muscular rigidity
-Rhabdomyolysis
-Seizures
-Respiratory depression
-Hypotension

Front 30

What is the management of PCP toxicity?

Back 30

-Benzodiazepines for sedation, muscle rigidity
-Treat elevated BP cautiously
-Gastric suction to reduce enterohepatic recirculation
-Acidification of the urine
-Diazepam for convulsions