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47 Cards in this Set

  • Front
  • Back
Examples of monoamines
Dopamine
Serotonin
Norepinephrine
Epinephrine
Examples of synthetic/nonsynthetic psychomotor stimulants
-Cocaine
---Crack
-Cathinone
---Bupropion
-Amphetamines
---Adderal
-Methamphetamine
-Ephedrine
A prominent psychologist who promoted cocaine as a "cure for many of the ills of mankind"
Freud
Characteristics of ephedrine
In pill form.
Works similar to epinephrine.
Stimulates the sympathetic nervous system to dilate the airways in lungs and help breathing.
Crack vs Cocaine
Crack is cocaine mixed with sodium bicarbonate.
It is more lipid soluble and more easily absorbed by body.
Impurities in cocaine make it cheaper.
Neurophysiological effects of amphetamines
--Amphetamines do not need an action potential because they cause spontaneous leak of neurotransmitters into synaptic cleft, thereby increasing stimulation at post-synaptic receptor.
--When an action potential does arrive, there is an additional increased release of neurotransmitter.
--Amphetamines also block reuptake and the end result is more neurotransmitter in the synapse stimulating and binding to the post-synaptic receptors.
Symptoms of amphetamine-induced monoamine psychosis
Caused by high doses and after repeated use of cocaine, cathinone and amphetamines:

-Auditory and visual hallucinations
-Delusions of persecution, delusions of grandeur
-Hostility and violence triggered by paranoid belief of imminent danger
-Flattened affect
-Depression
-Anxiety
Formication
Cocaine bugs, Crank bugs
--Feeling of bugs crawling around under the skin
Symptoms of stimulant withdrawal
Rebound effect:

-Severe depression
-Suicidal feelings
-Intense cravings
-Fatigue
-Vivid and disturbing dreams
-Sleep disturbances
-Irritability
-Increased appetite
-Physical slowing down
Speed ball
Mix of heroin and cocaine.
Users believe heroin reduces jitteriness of cocaine and cocaine reduces sleepiness of heroin.
Differences between methamphetamine and cocaine
Methamphetamine
-Stimulant
-Manmade
-Smoking produces long lasting high
-Longer half-life
-Increased dopamine release and blocks dopamine reuptake
-Limited medical use

Cocaine
-Stimulant and local anesthetic
-Plant-derived
-Smoking produces brief high
-Short half-life
-Blocks dopamine reuptake
Short-term and long-term effects of methamphetamine use
Short-term effects
-Increased attention, decreased fatigue
-Increased activity and wakefulness
-Decreased appetite
-Euphoria and rush
-Increased respiration
-Rapid/irregular heartbeat
-Hyperthermia

Long-term effects
-Addiction
-Psychosis: paranoia and hallucinations
-Repetitive motor activity
-Changes in brain structure and function
-Memory loss similar to amnesia
-Aggressive or violent behavior
-Mood disturbances from a loss of dopamine and serotonin cells
-Severe dental problems
-Weight loss
Narcotics
Drugs that cause sleepiness
Analgesics
Drugs that produce loss of sensitivity to pain
Examples of synthetic and semisynthetic opioids
Opium
Heroin
Thebaine
---Oxycodone
Demerol
Methadone
Heroin vs Morphine
Morphine
-Strong opiate
-Primarily acts on mu receptors
-Not rapidly absorbed from digestive system
---Significant first-pass metabolism
-Parenteral administration causes very reinforcing, sudden high
-Only small amount crosses blood-brain barrier
---Not much is needed to create effect
-Half-life is 2 hours, most of it is eliminated within 24 hours

Heroin
-Semisynthetic opiate
---Derived from trying to improve morphine
-10x more lipid soluble than morphine, therefore more gets to the brain at higher doses
-10x more potent than morphine
-Half-life is 15-30 minutes
-Effects felt within minutes when injected intravenously; 15-30 minutes when injected intramuscularly
Endorphins
Endogenous substance that exhibits pharmacologic properties of morphine.
-Found in brain areas rich in opiate receptors and stored in synaptic vesicles.
-Neuromodulators that influence presynaptic membranes of nearby synapases and effect release of NE, DA, Ach
Naloxone
Opiate antagonist that blocks the action of opiates. Naloxone is used in overdose subjects.
Naloxone displaces opiates from the mu receptor, and there is no opiate effects on its own.
--Because it displaces opiates from receptor, they cause immediate withdrawal effects.
Types of brain opioid receptors
Mu
-Alleviate wide range of pain
-Found in limbic system, thalamus, LC, VTA, NA
-Agonists: effective against broad range of pain
-Activation of mu receptor causes inhibition of substance p in spinal cord and acts as analgesia

Delta
-Found in limbic system, cortex, hypothalamus, NA, medulla
-Agonist more effective against thermal and mechanical pain

Kappa
-Found in NA, VTA, hypothalamus, thalamus
-Agonist against visceral pain
-Also effective against low-intensity thermal and mechanical pain
Effects of opioid use
-Analgesia
-Euphoria
-Decreased anxiety
-Depressed respiration
-Cough Suppression
-Pupil constriction is indication of overdose
-Suppression of vomiting after first use
---May cause nausea and vomiting on first administration
-Gastrointestinal symptoms
---Causes constipation and interferes with urination
-Sexual dysfunction
---Diminished fertility, irregular ovulation, spontaneous abortion and miscarriage
Effects of opioids on sleep
Causes sedation and drowsiness. Individuals doze but awaken easily

Causes nodding out or dozing off. Prior to nodding out there are increased levels of activity.
Yen sleep
Deep sleep for 8-12 hours caused by heroin withdrawal. It is preceded by chills, and goosebumps.
Maturing out
Many Heroine addicts spontaneously discontinue use after they reach their 30s and 40s or after 5-10 years of use.
Maintenance drugs for heroine addicts
-Naloxone

Methadone
-Full mu agonist
-Extremely long half-life
-Good for maintenance therapy, taken orally
-Prevents withdrawal for 24 hours
-Blocks effects of heroin

Buprenorphine
-Semisynthetic opiate and partial mu agonist
-Produces less euphoria than morphine and heroine
-Less sedation and respiratory depression at prescribed dose
---Risk of overdose
-Longer duration of action than morphine
-More effective orally
-Half-life of 20-73 hours
Psychoactive ingredients in cannabis
Delta-9-tetrahydrocannabinoidol

THC
Hashish vs Hash Oil
Hashish is made from the dried resin from the top of the female plant

Hash oil is hashish boiled in alcohol. It is more potent than hashish.
Effects of cannabis use on neurotransmission
Cannabis modulates GABA and controls the amount of inhibition and the fluidity of neurons.
It also indirectly stimulates the dopamine pathways from the VTA to the NA.
There is an alteration of other neurotransmitters and inhibition of calcium uptake.
Anandamide
an endocannabinoid that is naturally occurring in the body.
Medical uses of marijuana
-Chemotherapy: can reduce nausea and vomiting in cancer patients
-Lowers pressure within the eye for Glaucoma patients
-Reduces muscle spasms in people with nerve problems like MS
-Can relieve some types of pain
-Increases appetite for Wasting syndrome, neuropathic pain and nausea associated with HIV/AIDS
Cannabis withdrawal symptoms
Physiologic
-Nausea
-Tremor
-Perspiration
-Weight loss
-Salivation
-Increased body temperature
-Decreased appetite

Sleep
-Altered sleep/wake cycles
-Insomnia

Behavioral
-Restlessness and agitation
-Irritability
-Depressed mood
-Anxiety
-Thoughts of cannabis and drug craving
A "freak out"
Feelings of an acute psychotic reaction when marijuana is taken in an unusual or stressful circumstance, higher than normal dose or when mixed with other drugs.
Carcinogens in marijuana smoke
Marijuana contains 50-70% more carcinogenic hydrocarbons than tobacco smoke
Effects of cannabis on cognitive functioning and the brain
Cerebellum
--impaired body movement coordination and muscle control
Hippocampus
--impaired learning and memory
Cerebral cortex
--impaired cognitive functions
Basal Ganglia
--rewarding
Hypothalamus
--impaired movement control
Amygdala
--impaired body functions
Spinal Cord
--evokes emotional response, particularly fear and paranoia
Central Gray
-sleepiness, analgesia
Psychedelics
Phantasticant- perceptual distorters
---LSD
Psychedelics- mind manifesters
---Psilocybin
Entactogens- touching within
---DMT
Empathogens- empathy enhancers
---DMT
Psychotomimetrics- mimic psychosis
---Mescaline
Club drugs- hallucinogens and psychedelics used in party situations
---Ketamine
Neurotransmitters associated with hallucinogenic effects
5-HT
NE
Ach
to a lesser extend DA
Half-life of LSD
175 minutes- 300 minutes
Pattern of tolerance and withdrawal with LSD use
Tolerance develops rapidly. If taken repeatedly, tolerance to effects can disappear within 2-3 days. The tolerance dissipates quickly if stopped.

There is no withdrawal because there is no persistent use of the drug
Mescaline vs LSD
Mescaline
-2000x less potent than LSD
Neurophysiology of MDMA
-Binds to 5-HT transporters and prevents reuptake. Increases amount of 5-HT released into synapse.
-Increases stimulation of DA and NE receptors
-Greater serotonin release than methamphetamine and less dopamine release
Subjective and harmful effects of MDMA use
Subjective effects
-wakefulness, endurance, energy, euphoria, sharpened sensory perception, extroversion, connectedness to others

Harmful effects
-Selective serotonin neurotoxin
---Reduction in metabolites of 5-HT even with recreational users
-Causes death: from heart and circulatory problems, liver damage, swelling of brain, overheating, suicide and accident
Subjective effects of salvia
-Intense hallucinations, laughter, loss of motor coordination, perceptional changes, emotional mood swings similar to bipolar characteristics
-Perceptual effects short lived compared to LSD
Examples of dissociative anesthetics
-PCP- phencylidine
-Ketamine
-Dextromethorphan (cough syrup)
Neurophysiology of dissociative anesthetics
-Blocks NDMA receptors and is responsible for dissociative effects
PCP vs LSD
PCP
-Greater addiction potential than LSD
PCP withdrawal symptoms
Vocalizations, grinding teeth, diarrhea, anxiety, confusion, tremors
Neurophysiology of GHB
-Binds to its receptors and in high doses to GABA receptors
-Acts presynaptically and postsynaptically to affect neurotransmission
-May modulate GABA levels and cause surge in DA
Effects of GHB
Behavioral effects
-Alcohol-like intoxication from surge of DA
-Relaxation and euphoria from stimulation of GABA
-Increases sexual pleasure
-Amnesia for events during and after drug use
-Anxiolytic properties to lower anxiety by acting on GABA

Effects on sleep
-Normalizes sleep patterns