Designer Drugs, Hallucinogens, & Cannanbinoids Flashcards
Ecstasy: Give Chemical name (old fashioned)
THANK YOU Petros Levounis, MD
Chemical name; Methylene-dioxy-meth-amphetamine
Ecstasy: EFFECTS:
1) Partly a _______ & partly a _________
An attenuated form of ______________ &
an attenuated form of ______________
2) Emotion that it evokes: ____________
3) It yields ___________ feelings or _________ to the rest of the ____________
Used for psychotherapy in the 1970s
Ecstasy: EFFECTS:
1) Partly a STIMULANT & partly a HALLUCINOGEN
An attenuated form of COCAINE &
an attenuated form of LSD
2) Emotion that it evokes: EMPATHY
3) It yields PROFOUND feelings or RELATEDNESS to the rest of the WORLD
Ecstasy: NEUROBIOLOGY
1) Acutely ___________ ________________ levels by
a) _________ reuptake
b) directly __________ 5-HT
2) Chronically, Ecstasy _____________ 5- HT levels by
a) _____________ 5-HT stores
b) _____________ synthesis of new 5-HT stores
3) Neuro___________ It kills axons that do not regenerate properly- they don’t make the old connections - instead they form a sort of dendritic arborization.
Ecstasy: NEUROBIOLOGY
1) Acutely INCREASES 5-HT levels by
a) BLOCKING reuptake
b) directly RELEASING 5-HT
2) Chronically, Ecstasy DECREASES 5- HT levels by
a) DEPLETING 5-HT stores
b) INHIBITING synthesis of new 5-HT stores
3) NeuroTOXICITY It kills axons that do not regenerate properly- they don’t make the old connections - instead they form a sort of dendritic arborization.
Ecstasy: INTOXICATION
1) “Disco Dump” & B_____M
2) Stimulant effects
a) Wakefulness, endurance & energy
b) Tris____s, A______a, D_____sis & H__ F______S
3) S_______N Syndrome
a) Treat with hydration, cooling & sedation
b) Do NOT treat with beta blockers - which may cause vasospasm and worsen HTN
Ecstasy: INTOXICATION
1) “Disco Dump” & BRUXISM
2) Stimulant effects
a) Wakefulness, endurance & energy
b) TRISMUS, ANOREXIA, DIAPHORESIS & HOT FLASHES
3) SEROTONIN Syndrome
a) Treat with hydration, cooling & sedation
b) Do NOT treat with beta blockers - which may cause vasospasm and worsen HTN
Ecstasy: WITHDRAWAL
1) A______A & D______D MOOD
2) L______Y & F______E for several days
3) True SI is RARE/COMMON in the absence of a co-existing depression
4) Treatment is/is not indicated
Ecstasy: WITHDRAWAL
1) ANHEDONIA & DEPRESSED MOOD
2) LETHARGY & FATIGUE for several days
3) True SI is RARE in the absence of a co-existing depression
4) Treatment IS NOT indicated
Ecstasy: LONG TERM EFFECTS Associated with (but no hard evidence of causality) * D *A *P Disorder *Increased/Decreased Impulsivity *S D *C Dysfunction NO FDA approved medications Generic psychosocial treatments (MET, CBT) - NO EVIDENCE
Ecstasy: LONG TERM EFFECTS Associated with (but no hard evidence of causality) * Depression *Anxiety *Panic Disorder *Increased Impulsivity *Sleep Disorder *Cognitive Dysfunction NO FDA approved medications Generic psychosocial treatments (MET, CBT) - NO EVIDENCE
Ketamine: Effects
can induce a “K-XXXX”
*Similar to XXX, but YYYY potent & ZZZZZZ duration
*Distorted perception of
** the BXXX
** the EXXXXXXXXT
** TXXE
*Lack of responsive awareness to
**PXXN
**the GENERAL EXXXXXXXXXT
*DISCONNECTION
*Used to achieve “higher/lower” forms of consciousness
*Heightened capacity to discern CxxxxL CxxxxxxxxS in all things
Ketamine: Effects
can induce a “K-HOLE”
*Similar to PCP, but LESS potent & SHORTER duration
*Distorted perception of
** the BODY
** the ENVIRONMENT
** TIME
*Lack of responsive awareness to
**PAIN
**the GENERAL ENVIRONMENT
*DISCONNECTION
*Used to achieve “HIGHER” forms of consciousness
*Heightened capacity to discern CAUSAL CONNECTIONS in all things
Ketamine: Neurobiology
- It is a
* *NON-ANXXXXXC DXXXXXXXXXE anesthetic
* *NON-CXXXXXXXE NDMA AXXXXXXXXT - NDMA inhibition is related to:
* *SXXXXXXXXXXL symptoms
* *DXXXXXXXXXE symptoms
Ketamine: Neurobiology
- It is a
* *NON-ANALGESIC DISSOCIATIVE anesthetic
* *NON-COMPETITIVE NDMA ANTAGONIST - NDMA inhibition is related to:
* *SCHIZOTYPAL symptoms
* *DISSOCIATIVE symptoms
Ketamine: INTOXICATION
- Mild Doses
* * AXXXXXC state (“sightless stare”)
* * PXXXXXY of thinking - Higher Doses
* * K-XXXE (Zombie-like state), ACCIDENTS
* *Overdose is very RARE/COMMON (LD 50 is apx 3/60 TXXXS the RXXXXXXXXXXL DOSE - Treat with DIRECT CONFRONTATION/CALM REASSURANCE & HIGH/LOW-stimulation environment
- UTILIZE/AVOID antipsychotics
Ketamine: INTOXICATION
- Mild Doses
* * AUTISTIC state (“sightless stare”)
* * PAUCITY of thinking - Higher Doses
* * K-HOLE (Zombie-like state), ACCIDENTS
* *Overdose is very RARE (LD 50 is apx 60 TIMES the RECREATIONAL DOSE - TREAT with CALM REASSURANCE & LOW-stimulation environment
- AVOID antipsychotics
Ketamine: WITHDRAWAL
- Both the anesthetic and behavioral effects REMAIN FOR A LONG PERIOD/REMIT QUICKLY
- Treatment IS/IS NOT indicated
Ketamine: WITHDRAWAL
- Both the anesthetic and behavioral effects REMIT QUICKLY
- Treatment IS NOT indicated
Ketamine: Long Term Features
*TOLERANCE
*SHORT TERM/LONG-LASTING memory impairments among frequent users (Case reports only)
Flashbacks HAVE/HAVE NOT been reported
NO FDA approved medications
TX: MET & CBT
Ketamine: Long Term Features
*TOLERANCE
*LONG-Lasting memory impairments among frequent users
Flashbacks HAVE been reported
NO FDA approved medications
TX: MET & CBT
GHB: Effects
It is really “CLEAN/DIRTY.”
It is a SENSUAL Drug, LIKE/UNLIKE MDMA, resulting in the BEST/WORST sex ever.
It evokes feelings of:
*RELAXATION, TRANQUILITY, PLACIDITY, MILD EUPHORIA, DISINHIBITION”
“ANXIETY, IRRITABILITY, RAGING EUPHORIA, INHIBITION
MEMORY IS
* GREAT
*IMPAIRED (TEMPORARY AMNESIA)
*BLACKOUTS- A DATE RAPE DRUG
GHB: Effects
It is really "CLEAN."
It is a SENSUAL Drug, LIKE MDMA, resulting in the BEST sex ever.
It evokes feelings of:
*RELAXATION, TRANQUILITY, PLACIDITY, MILD EUPHORIA, DISINHIBITION"
MEMORY IS
*IMPAIRED (TEMPORARY AMNESIA)
*BLACKOUTS- A DATE RAPE DRUGGHB: NEUROBIOLOGY
It IS/IS NOT a neurotransmitter
It is BOTH/NOT precursor & a metabolite of GABA
Activity on both GABA & the GHB binding sites results in:
*Temporary suppression of DA
*Subsequent marked release of DA &
*Increased release of endogenous opioids
It is Schedule III - used for narcolepsy
GHB: NEUROBIOLOGY
It IS a neurotransmitter
It is BOTH a precursor & a metabolite of GABA
Activity on both GABA & the GHB binding sites results in:
*Temporary suppression of DA
*Subsequent marked release of DA &
*Increased release of endogenous opioids
It is Schedule III - used for narcolepsy
GHB: INTOXICATION
STEEP/SHALLOW dose-response curve - RESEMBLES/DOES NOT RESEMBLE EtOH
*DOES/DOES NOT CAUSE:
**Ataxia, loss of coordination
**Respiratory Depression, Bradycardia
**Coma, persistent vegetative states, death
**Overdose IS/IS NOT a real danger (LD50 is 5 times/ 50 times the recreational dose
**IS/IS NOT SYNERGISTIC with EtOH & other sedatives
GHB: INTOXICATION
STEEP/SHALLOW dose-response curve - RESEMBLES/DOES NOT RESEMBLE EtOH
*DOES/DOES NOT CAUSE:
**Ataxia, loss of coordination
**Respiratory Depression, Bradycardia
**Coma, persistent vegetative states, death
**Overdose IS/IS NOT a real danger (LD50 is 5 times/ 50 times the recreational dose
**IS/IS NOT SYNERGISTIC with EtOH & other sedatives
GHB: INTOXICATION
*TREAT as a medical emergency
ABC —> ICU
Atropine for bradycardia
GHB: INTOXICATION
*TREAT as a medical emergency
ABC —> ICU
Atropine for bradycardia
