| What is Cannabis? | Marijuana, Hash...
Prepared from dried flowering tops and leaves of plants, consists of dried cannabis resin, may be light brown to almost black |
| What is composition of Cannabis? | . |
| How is THC variations in Hash? | Great variation in concentration, Hash Oil very high THC concentration.
Balance between of THC and CBD in street cannabis appears to have changed over the last decade |
| How is method of use of Hash? | Smoked (joints), Water-pipe (bong), Oral (cooked), no injection (THC does not dissolve in water) |
| How is pharmaceutical use of Hash? | Two human cannabinoid receptors (CB), THC and metabolites are highly fat soluble, slow rate of clearance.
May be detected in blood for several days and traces may persist for several weeks.
THC may be stored in body fat for more than 28 days |
| What are clinical effects of Hash? | Lower Doses (relaxation, euphoria, altered time and sensory perception, increased apetite)
Higher Doses (hypervigilance, paranoia, anxiety or panic, derealization or depersonalization, hallucinations)
Increased HR by 20-50% up to 3 hours, BP increased while person is sitting and decreases on standing.
Healthy young users CV effects rarely significant, risk to pt with heart disease.
Driving performance impairment, no fatal poioning in human medical lit. |
| How is cannabis withdrawal? | Cessation of use after heavy and prolonged usage.
3 or more of following 1 week prior cessation
irritable, nervousness/anxiety, sleep difficulty, decreased appetite/weight loss, restlessness, depressed mood, one of physical symptoms causing discomfort [abdo pain, shakiness, sweating, fever, chills, headache]. |
| What are effects of long-term cannabis use? | Medical, Gateway effects
Neurotoxic effects (deficits in cognitive function memory and attention, education and occupational.
Mechanism: THC induce cell death, decreased cerebral blood flow)
Mental health (gateway drug, amotivational syndrome, psychosis/schizophrenia [psychosis among vulnerable, exacerbates symptoms and prolongs illness, helps self medicate psychiatric symptoms or medication side effects]
Depression and anxiety increases + suicide attempts) |
| What is synthetic cannabinoids? | AKA spice/K2, Pot pourri herbal addictives with synthetic cannabinoid chemical compounds, less common may be sold as resin/powder, oils, e-liquid, card, vape...
Smoked by cannabis pipe.
Incentive (cannot be detected w/std urine drug test, affordable, promises a high stronger than cannabis. |
| Compare SC vs THC? | SC have four times more affinity for the CB1 receptor and ten times more affinity for the CB2 receptor
SC are a full agonist In contrast to THC which is a CB1 partial agonist
SC may exert activity on other receptor families as well, like NMDA and 5-HT2A
Spice do not include cannabidiol
SC are 2 to 100 times more potent than THC |
| What are acute/subacute effects of Cannabis? | Agitation, auditory/visual hallucinations, anxiety, intense feelings of paranoia, mood swings, suicidal ideation, suicide attempts….
Seizures, vomiting, hypertension, hypokalemia, respiratory depression…
Both supraventricular and ventricular arrhythmias |
| What is Spiceophrenia? | Higher risk than cannabis:
- no CBD
- full agonist
- dose variation
Longer-lasting induced effects (many weeks)
Psychotic relapse after smoking SC for a day |
| What are opiates? | Opium derivatives: Heroin, Morphine, Codeine
Synthetic opioids: Fentanyl
Opioid receptors: mu, kappa, delta
Opioid drugs: µ agonists
Heroin (diacetylmorphine):
- more potent and more lipid soluble than morphine
- crossing the blood–brain barrier more rapidly
- more rapid onset of subjective effects |
| How are methods of use of opiates? | . |
| What are clinical effects of opiates? | Changes in mood (euphoria in some persons)
Indifference to anticipated distress
Reduced anxiety
Increased self-esteem
Better ability to cope with everyday problems
Decreased sense of boredom.
Physical effects: analgesia, respiratory depression |
| How is opioid intoxication? | A. Recent use of an opioid.
B. Pupillary constriction (or pupillary dilation due to anoxia from severe overdose) and one (or more) of the following signs, developing during, or shortly after, opioid use:
(1) Drowsiness or coma
(2) Slurred speech
(3) Impairment in attention or memory |
| How is opioid toxicity? | Associated with route of admin (HIV/hep/infection/PE)
Opioid injections (sclerosed veins and puncture marks, severe sclerosis causes peripheral edema and individuals switch to injecting in veins, legs, neck, groin then start injecting subcutaneous tissue [skin popping], resulting in cellulitis, abscesses and circular appearing scars)
Life expectancy (infections, overdoses, suicides [3 times higher]) |
| What are signs of opioid overdose? | Slow and shallow breathing
Very sleepy and unable to talk
Unconscious
Blue lips or fingertips
Snoring or gurgling sounds |
| What is overdose? | Overdose is a condition that usually occurs over 1-3 hours
May be caused by:
Excess intake of opioids
Combination of opioid and a depressant
Opioid use in someone with a medical condition |
| What are differences in signs btw overdose and very high opioid use? | . |
| What are do's and dont's when responding to opioid overdose? | Do's (attend persons ABCs admin oxygen chest compression... administer naloxone 1 or 2 doses, put pt in recovery position, stay with person and keep him warm)
Dont's (slap/forcefully stimulate person may be unconscious, put in cold bath due to risk of falling and shock, inject with substance only use naloxone, make him vomit he will choke and lead to lung injury) |
| How is opioid withdrawal? | A. Either of the following:
(1) Cessation of (or reduction in) opioid use that has been heavy and prolonged (several weeks or longer)
(2) Administration of an opioid antagonist after a period of opioid use.
B. Three (or more) of the following, developing within minutes to several days after Criterion A:
(1) Dysphoric mood
(2) Nausea or vomiting
(3) Muscle aches
(4) Lacrimation or rhinorrhea
(5) Pupillary dilation, piloerection, or sweating
(6) Diarrhea
(7) Yawning
(8) Fever
(9) Insomnia |
| What are stimulants (cocaine and amphetamine)? | Increase monoamines:
- dopamine (D1 and D2): reinforcing effects
- norepinephrine: toxic effects
- serotonin: modulates reward potency, behavioral manifestations, cocaine-seeking behavior
Cocaine: Inhibits the normal reuptake of monoamines from the synaptic cleft
Amphetamines: release of monoamines from storage sites in axon terminals. |
| What are effects of stimulants? | Generally enjoyable effects with great increase in self-image. A rapid onset of high with the following components:
- Euphoria, seldom dysphoria
- Increased sense of energy
- Enhanced mental acuity
- Increased sensory awareness (sexual, auditory, tactile, visual)
- Decreased appetite (anorexia)
- Decreased need of sleep
- Postponement of fatigue
- Increased anxiety and suspiciousness
- Increased self-confidence, egocentricity
- Delusions |
| What are signs of stimulant intoxication? | Recent use
Two (or more) of the following, developing during, or shortly after, cocaine use:
- tachycardia or bradycardia
- pupillary dilation
- elevated or lowered blood pressure
- perspiration or chills
- nausea or vomiting
- evidence of weight loss
- psychomotor agitation or retardation
- muscular weakness, respiratory depression, chest pain, cardiac arrhythmias
- confusion, seizures, dyskinesias, dystonias, or coma |
| How is stimulant withdrawal? | Cessation of (or reduction in) use that has been heavy and prolonged.
Dysphoric mood and two (or more) of the following physiological changes, developing within a few hours to several days after:
- fatigue
- unpleasant dreams
- insomnia or hypersomnia
- increased appetite
- psychomotor retardation or agitation |
| What are combinations used with stimulants? | Stimulants used with opioid (in same syringe, better quality than stimulant alone, IV use + Heroin is called speed balling)
Amphetamine and opioid oral also is common, CNS depressants (alcohol/benzodiazepines/opioids/marijuana are used after cocaine use to temper unpleasant effects of cocaine intoxicity (anxiety/paranoia/restlessness) and relieve withdrawal symptoms. |
| How do stimulants induce psychiatric disorders? | Paranoia worsens during binge and appears earlier, psychotic symptoms common w/cocaine and meth, paranoia worries police, drug dealers, others will attack him.
Cocaine-induced psychosis differs from schizo in having less thought disorder and bizzare delusions and fewer negative symptoms (alogia/inattention)
Stimulant-induced hallucinations may be auditory/visual/somatosensory [crawling under skin]
Mood disorders (depressive and manic episodes intoxication) panic disorder exacerbated w/palpitations and hyperventilations. |
| How is cocaine preparation? | Different forms:
- Cocaine hydrochloride “coke”
- Freebase, Crack
Routes of administration:
- Snorting: coke
- Inhaling: freebase, crack
- Injecting: coke |
| How is cocaine pattern of use? | Episodic or daily (or almost daily) use
Cocaine use separated by 2 or more days of nonuse is episodic
Binges: use that typically involve continuous high-dose use over a period of hours or days
All groups, all demographic groups, all levels of society.
Very high psychological dependence |
| What are medical complications of cocaine intoxication and abuse? | Cardiovascular
Central nervous system
Cerebrovascular
Respiratory
Metabolic
Reproductive
Fetal
Neonatal
Infectious |
| What are amphetamines? | Speed, Ice, Crystal Meth, …
Oral, Snorting, Inhalation, Injection
At the present time, amphetamines are used legitimately almost exclusively for the treatment of narcolepsy and attention-deficit/hyperactivity disorder (ADHD)
Crystal meth, powdered crystal meth, meth pills. |
| What are types and names of amphetamines? | Street names: Crystal Meth, Tina, Christine, Ice, Glass, Chabu, etc.
Methamphetamine v/s Amphetamine:
- more potent
- crosses the blood-brain barrier more easily
- more pronounced longer lasting stimulant effects
Methamphetamine v/s Cocaine: short- and long-term effects are similar but:
- last longer
- can be more severe. |
| What are methods of use of amphetamines? | Smoked
Snorted
Injected intravenously (‘’slamming’’)
Anally
Smoking and injecting: more harmful consequences |
| What are harms due to acute use of amphetamines? | Physical:
- Cardiovascular and respiratory: irregular or fast heart rate (common), chest pain, palpitations, hypo or hypertension, respiratory difficulties
- Gastrointestinal: abdominal pain, vomiting
- Neurological: tremor, sweating, confusion, seizures
Psychological: acute psychosis (hallucination, delusions), panic attacks
Death: highest risk of illegal drug- related deaths after opioid drugs. Direct toxic effects:
- strokes, brain hemorrhage, heart attack or failure, high fever, renal failure
- murder, suicide, road traffic accidents |
| What are harms due to chronic use of amphetamines? | CV (angina, irregular heartbeat, strokes, hemorrhage, heart attacks)
Neuro (headaches, tremors, parkinson's involuntary movements)
Pulmonary (bronchitis, pulmonary edema, HTA, cough blood)
Hemato, GI and uro
Oral (meth mouth tooth decay, teeth loss, fractures)
Skin (scratching bacterial infections) blood bourne infections.
Psychological (mental health problems exacerbated, paranoia, delusions, auditory, visual, tactile hallucinations, mood disturbances
Some develope psychosis weeks or months after quitting. |
| How is dependence and withdrawal of amphetamines? | Dependence and withdrawal: The risk of methamphetamine dependence with regular use is high. Dependence results in deficits in memory and decision-making and verbal reasoning, which can continue months after abstinence.
Acute withdrawal (7-10 days): typically begin and peak shortly after someone’s last use (which means within 24 hours after their last use): Features:
- severe, profound unhappiness which can lead to suicidal thoughts
- irritability; anxiety
- extreme sleepiness and fatigue
- intense cravings
- paranoia
Longer term withdrawal (up to months): inability to feel pleasure; profound unhappiness; impaired social functioning; intense craving; anxiety; mood swings; irritability; and disrupted sleep patterns |
| What is captagon? | Large prevalence in Middle East
According to UNODC, the three countries reporting the highest captagon seizures are Saudi Arabia, Jordan and Syria
Fenethylline (Amphetamine and Theophylline)
Fenethylline was first synthesized in 1961 and used in Europe as an alternative to amphetamines
Currently: composition variable (amphetamine-like)
Stimulant-like effects
Less adverse effects and lower abuse potential than amphetamines
Mixed frequently with other substances |
| What are psychodelics? | Hallucinogens
Dissociatives |
| What are molecules of hallucinogens? | A hallucinogenic drug primarily alters perception, cognition, and mood with relatively minimal effects on memory and orientation at usually taken doses.
Molecules:
- LSD
- Psilocybin ( mushrooms)
- Mescaline
Others:
- Ayahuasca
- Salvia |
| What are characterstics of hallucinogens? | Differences:
- potency
- mechanism of action
Oral route most common
Concerts, movies, dances, outdoor activities, mystical experiences
Effect:
- illusions, sometimes hallucinations
- mood and perceptual changes
- somatic symptoms
- sensory symptoms
Duration of effects: a few hours |
| How is hallucinogens intoxications? | Perceptual changes occurring in a state of full wakefulness and alertness (e.g., subjective intensification of perceptions, depersonalization, derealization, illusions, hallucinations, synesthesias)
Two (or more) of the following signs:
- (1) Pupillary dilation
- (2) Tachycardia
- (3) Sweating
- (4) Palpitations
- (5) Blurring of vision
- (6) Tremors
- (7) Incoordination
Self limited, resolves usually within 6 to 12 hours |
| What is bad trip in hallucinogens? | A “bad trip” usually takes the form of an anxiety attack or panic reaction, with the person feeling out of control.
An experience of depersonalization may precipitate the fear of losing one’s mind permanently
Hallucinogen ingestion may result in an acute toxic delirium that is characterized by delusions, hallucinations, agitation, confusion, paranoia, and inadvertent suicide attempts (eg, attempts to fly or perform other impossible activities |
| What are characteristics of dissociatives? | Ketamine, PCP, Dextromethorphan (DXM), and the gaseous anesthetic, nitrous oxide (inhalant ?)
Distinguished pharmacologically and clinically from true hallucinogens:
- hallucinogens affect primarily 5HT2A receptors instead of NMDA receptors
- hallucinogens are associated with a different 5HT2A- associated clinical syndrome of intoxication: dissociation or impaired reality testing is less typically involved and visual hallucinations are more commonly involved |
| What are hypo and hyperglutamatergic actions of dissociatives? | Ketamine, PCP, and related dissociatives may actually increase glutamate in certain brain areas and thereby produce some of the drugs’ behavioral effects
PCP and ketamine: NMDA receptor blockade / increase glutamatergic neurotransmission at AMPA receptors |
| How is ketamine use? | Medical use:
- general anesthesia in both animals and humans
- more often in children, who appear less susceptible than adults to emergent delirium
Recreational use: liquid, powder: snorted, smoked, oral, intramuscular, intravenous |
| What are ketamine effects? | Low dose: euphoria, sensory distortions, lucid intoxication, and heightened feelings of empathy: “K-land”
High dose: hallucinatory state referred to as a “K-hole” : intense dissociative experience that includes visions and distortion of time, sense, and identity, and sometimes out-of- body, near death, or rebirth experiences. Users often report the K-hole as a frightening or aversive experience
Ability to produce both negative and positive symptoms of schizophrenia (related theory that glutamatergic dysfunction is involved in schizophrenia ) |
| What are medical side-effects of ketamine use? | Ketamine stimulates the cardiovascular system, due to decreased catecholamine reuptake. These changes lead to increased heart rate and blood pressure
Patients with a history of chronic ketamine use commonly reported abdominal pain and urinary tract symptoms. A number of cases reports suggest that ketamine abuse can cause suprapubic pain, dysuria and hematuria
Liver damage: caused by chronic use of ketamine: bile duct dilatation, microscopic bile duct injury, and even significant liver fibrosis |
| What is ecstasy (MDMA)? | Mood-improving, stimulant, and hallucinogenic subjective effects: combination of amphetamine and lysergic acid diethylamide (LSD)
Ecstasy is presented for use as tablets-pills, capsules or powder (crystal).
It is usually taken orally, but some user snorted the contents.
The MDMA content of pills or tablets varies widely between regions and different brands of pills and fluctuates. Pills may contain other active substances meant to stimulate in a way similar to MDMA, such as amphetamine, mephedrone, methamphetamine, ephedrine or caffeine. In some cases, tablets sold as ecstasy do not even contain any MDMA
Nonlinear pharmacokinetics: small increases in the dose of MDMA ingested induce disproportionate increases in plasma concentrations of MDMA |
| What are clinical effects of ecstasy? | Use:
- most often recreational (raves, concerts…)
- daily users (psychiatric comorbidity, poly users…)
Subjective Effects: last 4 to 8 hours
- elevated mood
- increased self-confidence
- sensory sensitivity
- peaceful feelings coupled with insight, empathy, and closeness to people
- decreased appetite
Some of the effects differential from those elicited by classical amphetamines (e.g. feeling close to others, increased empathy, increased sociability) are collectively termed as empathetic or entactogenic, and MDMA is considered the prototypical drug producing such effects |
| What are adverse effects of ecstasy? | The acute physical effects of MDMA at low to moderate doses resemble those of a stimulant: increased muscle tension, jaw clenching, tooth grinding (bruxism), restlessness, insomnia, ataxia, headache, nausea, decreased appetite, dry mouth, dilated pupils, and increased heart rate and blood pressure
Cardiac arrhythmias
Severe cerebrovascular accidents
Hepatotoxicity
The most dangerous is hyperthermia, which results from a combination of direct thermogenic effects of the drug (probably via adrenergic mechanisms), increased physical activity (as through vigorous dancing), warm environment (as in a crowded, poorly ventilated dance club), and disruption of thermoregulation by the drug, often exacerbated by dehydration
Severe and potentially fatal hyponatremia induced by (SIADH)
Panic attacks, paranoid psychosis, depression |
| What is GHB? | GHB is classified as a central nervous system depressant
Mechanism of action: binding to GABA, in particular the GABA-B complex
Use of GHB and its precursors, (GBL) and (1,4-BD) have a dose-dependent effect on glutamate and dopamine release. At low dose, stimulation of GHB receptors increases dopamine release resulting in stimulant-like effects, whilst at higher doses, binding to GABA-B receptors results in hypnotic effects and eventually coma
Method of use: orally as a liquid or in a powder mixed into drinks.
Effects begin within 15 minutes of ingestion and last 2-4 hours: patients with GUD typically consume GHB every 2–3 h to prevent withdrawal symptoms |
| How is GHB intoxication? | . |
| How is GHB withdrawal? | . |
| What is GHB rape drug? | Liquid: tasteless, odorless, colorless
Added to a woman's alcoholic beverage to reduce her judgment, inhibition, and physical ability to resist sexual activity
Amnestic properties + memory for the event may also be impaired by the combination of alcohol and GHB
Short interval of detection: Detection: 5h in blood, less than 12 hours in urine |
| What are inhalant products? | Four commercial classes:
- (1) solvents: glues, adhesives, nail polish remover…
- (2) propellants: aerosol paint sprays, hair sprays, shaving cream…
- (3) thinners: paint products, typing correction fluids…
- (4) fuels
Methods of use:
- sniffing vapor through the nose
- huffing (taking deep breaths) through the mouth
- bagging
Transpulmonary absorption with very rapid drug access to the brain |
| What populations use inhalants? | Onset and higher prevalence in adolescents
Low socio-economic background, poor functioning
Frequency of conduct disorder or adult antisocial personality disorder |
| What are sedatives and anxiolytics? | Benzodiazepines
Barbiturates
Hypnotic drugs
Anticholinergics |
| What are properties of anxiolytics? | Therapeutic use of BZD
Different contexts:
- long-term prescription of benzodiazepines at therapeutic doses
- patients escalating their dose of benzodiazepines beyond that prescribed by their physicians
- use of a benzodiazepine by heroin or cocaine addicts to self-medicate symptoms of heroin withdrawal or cocaine toxicity
- intentional benzodiazepine overdose in a suicide or suicide attempt |
| How is anxiolytics intoxications? | A. Recent use of a sedative, hypnotic, or anxiolytic.
C. One (or more) of the following signs, developing during, or shortly after, sedative, hypnotic, or anxiolytic use:
(1) Slurred speech
(2) Incoordination
(3) Unsteady gait
(4) Nystagmus
(5) Impairment in attention or memory
(6) Stupor or coma |
| How is anxiolytics withdrawal? | A. Cessation of (or reduction in) sedative, hypnotic, or anxiolytic use that has been heavy and prolonged.
B. Two (or more) of the following, developing within several hours to a few days after Criterion A:
(1) Autonomic hyperactivity (e.g., sweating or a pulse rate greater than 100 beats per minute)
(2) Increased hand tremor
(3) Insomnia
(4) Nausea or vomiting
(5) Transient visual, tactile, or auditory hallucinations or illusions
(6) Psychomotor agitation
(7) Anxiety
(8) Grand mal seizures |
| How are hypnotics (Zolpidem)? | Chemically unrelated to the benzodiazepines
Pharmacologic profile similar to a benzodiazepine
Tolerance, dependence and withdrawal present |
| What are cholinergics anxiolytics? | Trihexyphenidyl (Artane, Benzhexol)
Studies of abuse since about 30 years ago
Substance of abuse in many Arabic countries (Saudi arabia, Jordan, Lebanon…)
Abusers:
- young, unemployed
- low socio-economic background
- polydrug users
- antisocial personality
Effects: stimulant or euphoric effects, reversible cognitive impairment
Withdrawal symptoms: anxiety, delirium, various physical complaints, orthostatic hypotension, tachycardia |
| What is gambling disorder? | Persistent and recurrent problematic gambling behavior leading to clinically significant impairment or distress, as indicated by the individual exhibiting four (or more) of the following in a 12-month period:
- Needs to gamble with increasing amounts of money in order to achieve the desired excitement.
- Is restless or irritable when attempting to cut down or stop gambling.
- Has made repeated unsuccessful efforts to control, cut back, or stop gambling.
Is often preoccupied with gambling
Often gambles when feeling distressed (e.g., helpless, guilty, anxious, depressed).
- After losing money gambling, often returns another day to get even (“chasing” one’s losses).
- Lies to conceal the extent of involvement with gambling.
- Has jeopardized or lost a significant relationship, job, or educational or career opportunity because of gambling.
- Relies on others to provide money to relieve desperate financial situations caused by gambling |
| What is basis for effective treatment of SUD? | Recovery is a long-term process and frequently requires multiple episodes of treatment.
No single treatment is appropriate for all individuals.
Effective treatment attends to multiple needs of the individual, not just his or her drug addiction (medical, social, psychological, legal…).
An individual’s treatment plan must be assessed often and modified to meet the person’s changing needs.
Multiple responses with different intensity that goes from prevention to more complex treatment. |
| What are essentials in SUD tx? | Retention for an adequate period of time is critical.
Counseling and therapy are essential.
Medications are an important element of treatment, especially when combined with counseling and other therapies.
Coexisting mental disorders should be treated in an integrated way.
Medical management of withdrawal syndrome is only the first stage of addiction treatment.
Therapeutic alliance with drug user is essential. |
| How is detox of SUD? | At hospital or at home
Necessity and intensity depends on the substance
Duration: 1 to 2 weeks |
| What are tx modalities of SUD? | Individual psychotherapy
Psychodynamic
Cognitive behavioral therapies
Relapse prevention
Motivational enhancement
Counseling
Group therapy
12 steps (Alcoholic or Narcotic Anonymous…)
Psychodynamic model
Educational and CBT groups
Family therapy
Alternative treatments: faith based approaches, acupuncture… |
| What are tx settings of SUD? | Inpatient :
Long term residential : ex: Therapeutic communities: longer stay (up to 2 years)
Short residential care (between 4 and 6 weeks) followed by outpatient after
Outpatient facilities :
Low intensity
Intensive day program
Prison based programs |
