Transcript 12-SUBSTANCE - RELATED disorder2.ppt

Fahad Alosaimi MBBS, SSC-Psych
Psychosomatic medicine Consultant
Assistant professor
King Saud University
‫ارتفاع نسبة االدمان في شرق السعودية ‪ %300‬خالل عامي ‪2006-2005‬‬
‫‪CNN‬‬
‫وقال ماثيو نايس‪ ،‬خبير مكافحة المخدرات‬
‫في المكتب‪ ،‬إن الكميات األكبر من‬
‫األمفيتامين يجري مصادرتها في‬
‫المملكة العربية السعودية‪ ،‬وأضاف‪ ،‬في‬
‫حديث لـ‬
‫‪CNN‬‬
‫أن الرياض صادرت خالل ‪ 2008‬أكثر‬
‫من ‪ 12.8‬طن متري من األمفيتامين من‬
‫أصل ‪ 15.3‬مليون طن على مستوى المنطقة‬
‫ككل‬
‫أما علي الحقوي‪ ،‬الطبيب في مستشفي الملك‬
‫سعود بن عبدالعزيز‪ ،‬فقال‬
‫إن المرضى لديه يقولون بأن االتجاه‬
‫األكبر لإلدمان هو على الكحول‪ ،‬ومن ثم‬
‫األمفيتامين‪.‬‬
What is addiction?
 In Aug 2011, The American Society of Addiction
Medicine (ASAM) has officially recognized Addiction
as mostly:
a) a social problem
Addiction is not a choice, but
b) a moral problem
choice still plays an important
c) a criminal problem
role in getting help.
d) a primary chronic brain problem
e) a behavioral disorder occur as the result of other
causes such as emotional or psychiatric problems.
Terminology
 Abuse: Self-administration of any substance in a
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culturally disapproved manner that causes adverse
consequences.
Dependence: The physiological state of neuroadaptation
produced by repeated administration of a drug,
necessitating continued administration to prevent the
appearance of the withdrawal state.
Addiction: A nonscientific term that implies dependence.
Intoxication:
Withdrawal:
Tolerance:
Substance Use Disorders
(DSM IV-TR)
 Substance Abuse:
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Repetitive problems in  1 major life areas
 Substance Dependence (3 criteria):
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Tolerance
Withdrawal
Amount /  time
Urges, failure to cut down
Excessive time obtaining, using & recovering
Activities given up
Use despite problems
Common Routes of Substance
Abuse
Route
substances
Oral
alcohol
hypnotics - sedatives
stimulants
 hallucinogens
Injections
Opioids
 stimulants
Smoking
cannabis
 PCP
Sniffing
cocaine
 volatile substances
Photo courtesy of the NIDA Web site. From
A Slide Teaching Packet: The Brain and the
Actions of Cocaine, Opiates, and Marijuana.
Case of Mr.A
 26 year old male.
 He came to ER with a runny nose, stomach cramps,
dilated pupils, muscle spasms, chills despite the warm
weather, elevated heart rate and blood pressure, and is
running a slight temperature.
 He has no other adverse medical problem and no
psychological problems.
 At first he is polite and even charming to you and the
staff. He’s hoping you can just give him some “meds” to
tide him over until he can see his regular doctor.
 However, he becomes angry and threatening to you and
the staff when you tell him you may not be able to comply
with his wishes.
Case of Mr.B
 He is an older man in his late sixties and was a bit disheveled in
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appearance.
He came to ER accompanied by his neighbour.
The neighbour tells you that he found him earlier this evening trying to
enter his apartment door.
He was sweaty, his eyes where dilated, and his hands were trembling so
badly that he could not get the key in the door.
He kept calling his neighbour by another name and saying he was
trying to get into his office to do some work though he retired years
ago.
He can correctly identify himself but, also appears confused & unable
to tell you the month or season.
His demeanor is polite and apologetic to you and the staff.
He tells you he has never had a problem with ???? but scored high on
the ???? assessment test. He then admits to an occasional ???? every
now and then.
Questions
 What preliminary Axis I diagnosis would give each of
your patients and why?
 What, if any, medical danger(s), do you see or should
you consider for either patient? Why?
 Management?
Assessement
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Collateral history.
Urine screening tests.
blood screening tests (alcohol, barbiturates).
Pattern of Abuse:
 What? (type, dose, route, effect: nature and duration).
 How? (frequency, duration, how long, source, and
situation)
 Why? (? psychosocial problems).
 Dependence?
 Complications :
Psychosocial…..
Physical…..
Classes of Substances
CNS
depressants
CNS
stimulants
• Alcohol
• Sedatives, hypnotics or anxiolytics
• Inhalants (Volatile Solvents)
•
•
•
•
•
•
Amphetamines, Cocaine
Khat (Qat)
Caffeine, Nicotine (Tobacco)
Cannabis
Opioids
Hallucinogens, Phencycldine
‫‪Alcohol‬‬
‫أم الخبائث‬
Alcohol Kills More Than AIDS, TB or
Violence-WHO report (Feb 2011)
 Alcohol causes nearly 4% of deaths worldwide,
more than AIDS, tuberculosis or violence.
 Alcohol is the world's leading risk factor for death
among males aged 15-59,"
 Alcohol is a causal factor in 60 types of diseases
and injuries.
 Now we have strong evidence of a causal
relationship between drinking and breast cancer.
Epidemiology
 dependence is most common in
those aged 40 – 55 years.
• In USA :
• 13 % men and 4 % women
age 18
 20-40% hospital admissions
 Alcoholics who continue drinking have a
shortened life-span of 15 years why?
20
Assessment
Risk factors of Alcohol abuse
 Vulnerable personality: impulsive, gregarious, less
conforming, isolated or avoidant persons.
 Vulnerable occupation: senior businessmen,
journalists, doctors.
 Psychosocial stresses: social isolation, financial,
occupational or academic difficulties, and marital
conflicts.
 Emotional problems: anxiety, chronic insomnia
depression.
Is your patient ETOH dependent?
CAGE questionnaire
 C = Have you ever felt you must Cut down your
drinking?
 A = Have people Annoyed you by criticizing your
drinking?
 G = Have you ever felt Guilty about your drinking?
 E = Have you ever had a drink first thing in the
morning as an “Eye opener”?
Laboratory Tests
 Identify acute and/or heavy drinking (> 5 drinks/day):
 Blood Alcohol Levels (BAL).

Gamma-glutamyltransferase (GGTP > 35 IU/L)

Carbohydrate Deficient Transferrin (CDT > 20 IU/L)

Erythrocyte mean corpuscular volume (MCV >91.5 3)
 High
AST/ALT
*** CDT + GGTP best diagnostic combination.
Alcohol intoxication
Ethanol plasma concentrations Vs. CNS effects
Ethanol plasma concentration
(per mill)
Effect
0.2
Feeling of relaxation
0.3
Slight euphoria
0.5
Slight motor incoordination
1
ataxia
3
stupor
>4
Coma, death due to the
respiratory failure
Alcohol withdrawal
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70 % of AD patients & Rate in the elderly.
No gender/ethnic differences
85% mild-to-moderate
15% severe and complicated:
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Seizures
Delirium Tremens
 Features :
 Tremulousness (hands, legs and trunk).
 Nausea, retching and vomiting.
 Sweating, tachycardia and fever.
 Anxiety, insomnia and irritability.
 Cognitive dysfunctions.
 Thinking and perceptual disturbances.
Course of AW
Stages
Symptoms
 I (24 – 48 hours):
 Peak severity at 36 hours
90% of AW seizures
Most cases self-limited
 II (48 – 72 hours):
  Stage I symptoms
 III (72 – 105 hours):
 “Delirium Tremens”
 IV (> 7 days):
 Protracted withdrawal
Delirium Tremens
Features:
 delirium.
 gross tremor .
 autonomic disturbances .
 dehydration and elecrolyte disturbances..
 marked insomnia.
Course :
 peaks on third or fourth day, lasts for 3 – 5 days, worsens at night, and
followed by a period of prolonged deep sleep,
Complications :
 seizures.
 chest infection, aspiration.
 violent behaviour.
 coma.
 death; mortality rate: 5-15%. Why ?
Complications of chronic ETOH abuse
Medical
Neurological
Cerebellar
degeneration
Seizures
Periphral neuropathy
Optic nerve atrophy
head trauma
Alimentary
Tumours (oesophagus,
liver..)
gastritis, peptic ulcer
Pancreatitis
hepatitis, cirrhosis
Others:
cardiomyopathy
anaemia
obesity
impotence
gynaecomastia
psychiatric
amnesic disorder
delirium
dementia
psychosis
depression
reduced sexual
desire
insomnia
personality
deterioration
suicide
morbid jealousy
Social
social isolation
job loss
marital conflicts
family problems
legal troubles
social stigma
others
Treatment
 Treating Alcohol Intoxicated Patient:
Conscious : supportive, antipsychotic if agitated. Unconscious: ABC
 Treating Alcohol Withdrawal:
Supportive, thiamine & long acting BDZ (Why?) ± anticonvulsants for
seizure.
 Maintaining Abstinence:
 Medciations:
 Disulfiram – blockade of aldehydedehydrogenase  cummulation of
acetaldehyde - nausea, flushing, tachycardia, hyperventilation, panic…
 Naloxone – reduces alcohol-induced reward.
 Acamprosate – anti-craving effects .
 Psychological: group Tx, AA, relapse prevention.
Sedatives, Hypnotics, and
Anxiolytics
 Similar clinical manifestations to alcohol.
 withdrawal from short-acting substancet (e.g. triazolam)
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can begin within 4 - 6 hours .
Alcohol and all drugs of this class are brain depressants
any risk? , are cross-tolerant and cross-dependant.
withdrawal can be accomplished safely using diazepam,
phenobarbital, and pentobarbital, dose reduced in steps
(about 1/4 - 1/10 of daily benzodiazepine dose, every two
weeks).
BDZ have a large margin of safety & less addiction
potentials.
Flumazenil is a BDZ receptor antagonists used in BDZ
overdose.
Inhalants (Volatile Solvents )
 Examples : Lighter fluids,Spray paints,Cleaning
fluids,Glues,Typewriter correction fluids,Fingernail
polish removers.
 The active compounds : acetone, benzene or
toluene.
 brain depressants, effects appear within 5 – 10
minutes and may last for several hours.
 Common among adolescents in lower
socioeconomic groups, usually as occasional
experimentation.
 features of recent abuse : unusual breath or odour,
rashes around the nose and the mouth or the
residue on the face, hands or clothing.
Inhalants
Acute effects
Euphoria
excitement disinhibition
**High dose:
disturbed conciousness
perceptual disturbances
Impulsiveness
Assultiveness
impaired judgement
Sedation
slurred speech
nystagmus,
ataxia,
 incoordiantion
nausea, vomiting.
*Course of abuse: short
Long term effects
Irreversible multi-organ damages
(brain, lungs, liver, kidneys, muscles,
peripheral nerves and bone marrow).
Psychological dependence.
Death because of:
respiratory depression
asphyxiation
aspiration of vomitus
cardiac arrhythmia
 serious injury
* Treatment : supportive.
STIMULANTS
 Enhance DA & NE, sympathomimitics peripherally.
 amphetamine , Khat (Qat), caffeine, cocaine &
nicotine (tobacco).
 Therapeutic uses : ADHD, narcolepsy,depression &
obesity.
 Abused by students, long distance drivers..etc.
 Crack ( smoked, cocaine ) is highly addictive
why?
 Mild w/drawal Sx : low mood and dec. energy.
* In severe cases : depression, anxiety,
lethargy, headache , sleep disturbances &
craving .
STIMULANTS (Clinical effects)
Psychological
Physical
Enhanced cognitive functions
Elevated mood
Hyperactivity
Over-talkativeness
Increased confidence, self-esteem
 Insomnia.
Reduced sense of fatigue
Reduced appetite (anorexia)
Dilated pupils
Tremor
In high doses / prolonged use:
Nausea, vomiting, cardiac
arrhythmia. hypertension, CVA,
seizures, dizziness, hyperthermia,
respiratory distress, cyanosis.
 rebound rhinitis, nose bleeds &
perforated nasal septum(cocaine
snorting)
Restlessness, irritability
Paranoid psychosis
Aggressiveness, hostility
In high doses / prolonged use:
Treatment
* Intoxication: supportive ( sedation, antiarrhythmic drugs, Antipsychotics &
urine acidification why?
* Planed Withdrawal : counseling ,sedatives & Antidepressants if needed..
Other stimulants
 Khat:
* The fresh leaves are chewed for their stimulant
effect( Cathinone ) .
* Chronic use : infection & loss of appetite.
 Caffeine
* Intoxication >250 mg. :
 restlessness
*
excitement
*
 insomnia
*
diuresis
 tachycardia
*
muscle twitching
agitation
* GI upset
*
flushed face
* Withdrawal (after prolonged use and abrupt cessation)
 headache
 dysphoria
* nausea
* fatigue
*
*
vomiting *
drowsiness
anxiety
Nicotine
 CNS stimulants ,agonist at the nicotinic subtype of Ach
receptors and activating DA and NE. & a skeletal muscle
relaxant.
 Why people like smoking? improved attention, learning,
reaction time, and problem - solving ability.
 Withdrawal features ( peak in 1-2 days, few weeks):
 irritability
 insomnia
* frustration
* poor concentration
* dysphoric mood * increase appetite.
 Smoking causes cancer of the lung, upper respiratory
tract, bladder, pancreas, oesophagus and probably
kidney and stomach.
 Cigarette smoking can induce liver microsomal enzymes
and reduce plasma concentrations of antipsychotic
agents.
OPIOIDS
 This group include: heroin • morphine • codeine •
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
pethidine • methadone .
The medical use of opioids ( e.g. pethidine) is mainly for
analgesia .
They are abused for their powerful euphoriant effects .
Tolerance develops rapidly & diminishes rapidly which is
serious why?
Opioid Withdrawal: flulike Sx , craving.. They are very
distressful but not serious medically. including:
 lacrimation
 muscle and joint pain
 cold and hot flushes
 nausea, vomiting and diarrhoea
 piloerection
Opioids ( clinical effects)
Psychological
euphoria
relaxation
hyperactivity
drowsiness
analgesia
reduced sexual desire
Physical
small pupil
bradycardia
reduced appetite
constipation
respiratory depression
I.V use:
*AIDS
* hepatitis
* endocarditis * septicemia
* Acute local infections
Treatment:
*Opioid overdose : supportive +naloxone
*Opioid Withdrawal: symptomatic treatment, Counseling,
individual or group therapy
* Harm reduction strategies: methadone,buprenophine
CANNABIS(clinical effects)
Psychological
sense of well being
euphoria
relaxation
enhancement of aesthetic
experiences through
hightened perceptual
awareness
 impaired memory
impaired psychomotor
performance.
dysphoria, depression
anxiety, panic attacks
amotivation syndrome ?
(chronic use)
psychosis (risk factor for
SCZ)
Physical
tachycardia
reddening of the conjunctiva
dry mouth
respiratory tract irritation
increased appetite
CANNABIS
 The active ingredient “9-tetrahydrocannibinol” (THC).
 With high dose & prolong abuse, tolerance
psychological dependence may occur.
 Withdrawal from high doses gives rise to a
syndrome of nausea, anorexia, irritability and
insomnia.
 Chronic use of cannabis can lead to a state of
apathy and amotivation (amotivation syndrome)
but this may be more a reflection of patient’s
personality structure than an effect of cannabis.
 Treatment : Symptomatic , support & counseling.
HALLUCINOGENS (clinical effects)
Psychological
Physical
marked perceptual distortion
( changing shapes, colours…)
hallucinations ( visual, tactile… )
false sense of achievement an
strength
depersonalization, derealization
euphoria, anxiety, panic
paranoid ideation
homicide and suicide tendencies
flashbacks after abstinence
Delirium
tachycardia
hypertension
 cerebellar signs
wide pupils
hyperemic conjuncitva
 blurred vision
hyperthermia
Piloerection
PCP
euphoria and peaceful
floating sensations.
delirium
agitation and aggressive
behaviour.
PCP
hypertensive crisis
status epilepticus
malignant hyperthermia
HALLUCINOGENS
 Hallucinogenes can be natural, e.g. Psilocybin
(magic mushroom) or synthetic , e.g. Lysergic acid
diethylamide (LSD).
 Phencyclidine(PCP) is a dissociative anaesthetic
with hallucinogenic effects (a separate category in
DSM IV).
 Tolerance develops rapidly& reverses quickly in
few days.
 Abuser can develop a psychological
dependence.
 Treatment: Supportive & symptomatic.
Questions
 What preliminary Axis I diagnosis would give each of
your patients and why?
 What, if any, medical danger(s), do you see or should
you consider for either patient? Why?
 Management?