One of the commenest psychiatric condition must be studied

1. 1
Substance-related disorders
Desalegn Bekele, MD
Tuesday,03/19/13, 1:30-3:00 P.M

2. Global risk factors
11
1. Underweight
2. Unsafe sex
3. High blood pressure
4. Tobacco consumption
5. Alcohol consumption
6. Unsafe water, sanitation, &
hygiene
7. Iron deficiency
8. Indoor smoke from solid
fuels
9. High cholesterol
10. Obesity
Top 10 risk factors for disease globally

3. In Ethiopia
Substance dependence: 4.0%
Problem drinking: 2.7-3.7%
Khat abuse: 22-64%

4. Substance:
• Refers to a drug of abuse, a medication or a
toxin.

5. What are psychoactive drugs?
…Any chemical substance which, when
taken into the body, alters its function
physically and/or psychologically....”
(World Health Organization, 1989)

6. What are psychoactive drugs?
Psychoactive drugs interact with the central
nervous system (CNS) affecting:
mental processes and behaviour
perceptions of reality
level of alertness, response time, and
perception of the world

7. Classifying psychoactive drugs
Depressants Stimulants Hallucinogens
Alcohol Amphetamines LSD, DMT
Benzodiazepines Methamphetamine Mescaline
Opioids Cocaine PCP
Solvents Nicotine Ketamine
Barbiturates Khat Cannabis (high
doses)
Cannabis (low
doses)
Caffeine Magic mushrooms
MDMA MDMA

8. Substance related disorder
1.Substance use disorders
Substance dependence
Substance abuse
2.Substance induced disorders
Substance intoxication
Substance withdrawal
Substance induced persisting dementia
Substance induced persisting amnesia

9. Substance-Induced Disorders
Psychiatric illnesses that occur following use of
a substance and remit after cessation.

10. Substance-Induced Disorders
1. Substance intoxication delirium
2. Substance withdrawal delirium
3. Substance-Induced Persisting dementia
4. Substance-Induced Persisting amnestic
disorder

11. 5. Substance-Induced Psychotic disorder
6. Substance-Induced Mood disorder
7. Substance-Induced Anxiety disorder
8. Substance-Induced Sexual dysfunction
9. Substance-Induced Sleep disorder
Substance-Induced disorders

12. Substance dependence
A maladaptive pattern of substance use leading to
clinically significant impairment or distress
Manifested by three or more of the following
occurring at any time in 12months:

13. Substance dependence
1)Tolerance:
a. Need for markedly increased amounts of the
substance to achieve intoxication or desired effect
b. Markedly diminished effect with continued use of
the same amount of the substance

14. Substance dependence
2) Withdrawal :
A substance specific syndrome that occurs after
stopping or reducing the amount of the drug or
substance that has been used regularly over a
prolonged period of time
3)Substance is taken in larger amounts or over a
longer period than was intended

15. Substance dependence
4)There is a persistent desire or unsuccessful efforts to
cut down or control substance use
5)A great deal of time is spent in activities necessary to
obtain the substance.
6) Important social ,occupational or recreational
activities are given up or reduced because of
substance use

16. Substance dependence
7)The substance use is continued despite knowledge of
having a persistent or recurrent physical or
psychological problem
 Substance abuse: a maladaptive pattern of
substance use leading to clinically significant
impairment or distress, as manifested by one or more
of the following occurring within a 12 month period

17. Substance abuse
Defn. : a maladaptive pattern of substance use leading
to clinically significant impairment or distress, as
manifested by one or more of the following occurring
within a 12 month period:

18. Substance abuse
1) Recurrent substance use resulting in failure to
fulfill major role obligations
2) recurrent substance use in situations in which
it is physically hazardous
3)recurrent substance related legal problems
4)Continued substance use despite having
persistent or recurrent social or interpersonal
problems

19. Practical Approach
Substance as cause or aggravating factor of
psychosis
Management of alcohol withdrawal
Substance abuse/misuse by health
professionals

20. Practical Approach
Health professionals
Addis Ababa or Regions
General hospitals or Health Centers
Medical, Substance, Psychiatric or Stress

21. Practical Approach
Medical
GMC
Substance
Intoxication, Withdrawal, Substance-Induced
Primary Psychiatric
Stress
Psychosocial, Coping-style, Personality

22. Screening Questions
What are your drinking habits?
Was there ever a time in your life that you
drank too much?
How old were you?
Has anyone in your family said that you drank
too much?
Doctor, friend or anyone else?

23. Screening Questions
CAGE Questionnaire
Ever feel the need to Cut down?
Ever get Annoyed by others?
Ever feel Guilty about your drinking?
Ever have an Eye-opener?
1 or more for F, 2 or more for M

24. Screening Questions
Have you ever used khat? Hashish or
Marijuana? Pethidine or other prescription
pills for pain relief? IV drugs?
How many times?
If < 10 times, abuse or dependence is unlikely
How old?
Family said too much?
Anyone else?

25. Screening Questions
Did you ever get hooked or addicted?
Did you over use more than prescribed?
If YES to any of these questions, assess for
abuse and dependence.

26. Problems related to drug use
Types of problems: Clinical samples
Intox.
Regular Use
Dependence

27. 14
Problems related to substance use (1)
Acute intoxication (immediate effects from use):
 Physical
 Overdose
 Fever, vomiting
 Behavioural
 Accidents and injury
 Aggression and violence
 Unintended sex and unsafe sexual practises
 Reduced work performance

28. 15
Problems related to substance use (2)
Effects of regular use include:
 Specific physical and mental health problems
 Increased risk for infectious diseases
 Psychiatric symptoms
 Sleep problems
 Financial difficulties
 Legal, relationship, or work problems
 Risk of dependence
 Withdrawal symptoms when use is reduced or stopped

29. Types of problems
Intoxication
Accident/injury
Poisoning
Absenteeism
High risk behavior
Regular/excessive use
Health
Finance
Relationship
Child neglect
Dependence
Impaired control
Drug centered behavior
Isolation/social problems
Withdrawal symptomsand
psychiatric problems
Health problems

30. withdrawal
21
Withdrawal
The following symptoms may occur when drug
use is reduced or discontinued:
 Tremors, chills
 Cramps
 Emotional problems
 Cognitive and attention deficits
 Hallucinations
 Convulsions
 Death

31. Alcohol related disorders

32. Ethanol- Basic Facts (1)
Gastrointestinal side effects
Metabolic derangements
Risks of administration/ titration
Hepatic
Hematologic
Neurologic
Nutritional
Recommendation: No. Thanks.
Mayo-Smith, M et al. Pharmacological Management of Alcohol Withdrawal. JAMA. 1997;278:

33. Alcohol related disorders
Alcohol use disorder
Alcohol dependence
Alcohol abuse
Alcohol-induced disorders
Alcohol intoxication
Alcohol withdrawal
Alcohol delirium
Alcohol induced persisting dementia

34. Alcohol induced persisting amnesia
Alcohol induced psychotic disorder
Alcohol induced mood disorder
Alcohol induced anxiety disorder
Alcohol induced sexual dysfunction
Alcohol induced sleep disorder

35. 26
Alcohol: Basic facts (2)
Withdrawal Symptoms:
 Tremors, chills
 Cramps
 Hallucinations
 Convulsions
 Delirium tremens
 Death

36. 27
Long-term effects of alcohol use
 Decrease in blood cells leading to anemia,
slow-healing wounds and other diseases
 Brain damage, loss of memory, blackouts,
poor vision, slurred speech, and decreased
motor control
 Increased risk of high blood pressure,
hardening of arteries, and heart disease
 Liver cirrhosis, jaundice, and diabetes
 Immune system dysfunction
 Stomach ulcers, hemorrhaging, and
gastritis
 Thiamine (and other) deficiencies
 Testicular and ovarian atrophy
 Harm to a fetus during pregnancy

37. Alcohol-related brain injury
 Cognitive impairment may result from
consumption levels of >70 grams per day
 Thiamine deficiency leads to:
 Wernicke’s encephalopathy
 Korsakoff’s psychosis
 Frontal lobe syndrome
 Cerebellar degeneration
 Trauma

38.  Co morbidity:
Other substance related disorder
Antisocial personality disorder
Mood disorders 30-40%
High daily consumption of alcohol and family
history of alcohol abuse.

39.  Anxiety disorder 25-50%
 Use to alleviate anxiety
 Phobias and panic disorder are frequent co morbid
diagnoses in these patients
 Suicide is common 10-15%
MDD, weak psychosocial support ,unemployment,
living alone, serious coexisting medical conditions

40. Sleep effect
Ease of falling asleep
Decrease in rapid eye movement sleep and
deep sleep
Fragmentation of sleep

41. Physiological effect
Liver:
Accumulation of fat and protein
Association between fatty infiltration of the liver and
serious liver damage remains unclear
Associated with alcoholic hepatitis and cirrhosis

42. Gastrointestinal system
Long term heavy drinking is associated with
development of esophagitis,gastritis, achlorhydria,
gastric ulcers and esophageal varices
Pancreatitis, pancreatic insufficiency and pancreatic
cancer

43. Interfere with the normal processes of food digestion
and absorption as a result consumed food is
inadequately digested
Inhibit the intestine’s capacity to absorb various
nutrients such as vitamins and amino acids

44. The poor dietary habits of those with alcohol related
disorders can cause serious vitamin deficiencies,
particularly of the B vitamins.

45. Other bodily systems
Increased blood pressure , dysregulation of
lipoprotein and triglycerides, increased risk of
myocardial infarction.
Increased risk of cancer of the head, neck,
esophagus, stomach , colonic and lung cancer.

46. Hypoglycemia which could be the cause of death in
some persons who are intoxicated.
Increase in estradiol levels in women.

47. Symptoms of Alcohol intoxication
Slurred speech , Incoordination
Unsteady gait ,Nystagmus
Impairment in attention or memory
Stupor or coma

48. Symptoms of alcohol withdrawal
Autonomic hyperactivity
 Increased hand tremor
 Insomnia
Nausea or vomiting

49.  Transient visual,tactile,or auditory hallucinations or
illusions
 Psychomotor agitation
 Anxiety
 Grand mal seizures

50. Alcohol Withdrawal Syndrome
Stage I: Tremulousness
Stage II: Hallucinations
Stage III: Seizures
Stage IV: Delirium tremens
Not necessarily sequential*

51. Aggravating and predisposing factors
malnutrition
depression
fatigue
physical illness

52. Treatment Strategy
Reduce symptoms
Prevent seizures
Prevent delirium tremens
Prevent medical
complications

53. Clinical feature of alcohol withdrawal
Tremulousness 6-8hours
Psychotic and
perceptual disturbance
8-12hours
Seizures 12-24hours
Delirium tremens 72hours

54. Withdrawal seizures
Are stereotyped, generalized , and tonic-clonic in
character.
Patients often have more than one seizure 3-6 hours
after the first seizure.
Status epilepticus is relatively rare and occurs in less
than 3% of patients.

55. Delirium Tremens
Occurs within one week of cessation or reducing
alcohol.
30s-40s after 5-15 years of heavy drinking ,typically
of the binge type.
5% of admitted patients with alcohol-related
disorders develop DT.

56. Mortality rate is 20%
Physical illness e.g. hepatitis or pancreatitis
predispose to the syndrome ; rare in good physical
health.
Death is secondary to intercurrent pneumonia, renal
disease, hepatic insufficiency.

57. Treatment
A high calorie, high carbohydrate diet supplemented
by multivitamins.
Dehydration can be corrected with fluids given by
mouth or iv.
Warm, supportive psychotherapy
Skillful verbal support is imperative for patients are
often bewildered, frightened, and anxious.

58. Prevention is best:
Benzodiazepines :
25-50 mg of chlordiazepoxide q 2-4 hrs until they
seem to be out of danger
DTs : 50- 100mg chlordiazepoxide q 4hrs po or
lorazepam iv 0.1mg/kg at 2mg/min
Vitamins (thiamine 100mg iv/po tid)

59. Alcohol-induced persisting amnestic
disorder
Diagnosis and clinical features
A disturbance in short term memory
The disorder usually occurs in persons who have
been drinking heavily for many years.
The disorder is rare in persons younger than age 35.

60. Wernicke-korsakoff syndrome
Set of acute symptoms
Secondary to thiamine deficiency
Wernicke’s encephalopathy is characterized by ataxia ,
vestibular dysfunction , confusion.

61. Ocular motility abnormalities (horizontal
nystagmus, lateral orbital palsy and gaze palsy)
Wernicke’s encephalopathy is completely reversible
with treatment.

62. Treatment
Respond rapidly to large doses of parenteral thiamine
which is believed to be effective (thiamine in IV bag)
OR
Thiamine 100mg BID or TID p.o 1-2 weeks.

63. Korsakoff’s syndromes
Caused by thiamine deficiency.
Onset is gradual ; is often associated with
Wernicke’s encephalopathy.
Most commonly associated with the poor nutritional
habits of people with chronic alcohol abuse.

64. TREATMENT
Thiamine 100mg 3-4 months.
With treatment, patients may remain amnestic for 3
months and then gradually improve over the
ensuing year.
Administration of thiamine may prevent the
development of additional amnestic symptoms.

65. Approximately one third to one fourth of all patients
recover completely.
Approximately on fourth of all patient have no
improvement of their symptoms.

66. Alcoholic Blackouts
Characteristically, these persons awake in the
morning with a conscious awareness of being unable
to remember a period the night before during which
they were intoxicated.
Can perform complicated tasks and appear normal to
casual observers.

67. Alcohol induced psychotic disorder
Most common auditory hallucination
After the episode, most patients realize the
hallucinatory nature of the symptoms.

68. Treatment and rehabilitation
Three general steps
intervention
 detoxification
 rehabilitation

69. Intervention: The goal is to break through feelings
of denial and help the patient recognize the adverse
consequences likely to occur if the disorder isn't
treated.
Is a process aimed at maximizing the motivation for
treatment and continued abstinence.

70. Motivational interviewing(MI) &
motivational enhancement
therapy(MET)
Precontemplation stage :
does not recognize the need for change or is
not actively considering change
Contemplation :
recognizes problem and is considering
change
Preparation : action has initiated change

71. Maintenance : is adjusting to change and is
practicing new skills and behaviors to sustain
change
Relapse : has begun using drug again.

72. Detoxification
The first step in detoxification is a thorough physical
examination
The second step is to offer rest, adequate nutrition.
And multiple vitamins, especially those containing
thiamine

73. Mild or moderate withdrawal
Treatment is the administration of 25mg of
chlordiazepoxide by mouth three or four times a day
on the first day gradual reduction in dose
With a notation to skip a dose if the patient is asleep
or feeling sleepy

74. Severe withdrawal
First step is to ask why such a severe and relatively
uncommon withdrawal syndrome has occurred
The answer often relates to a severe concomitant
medical problem that needs immediate treatment
Withdrawal symptoms can then be minimized
through the use of either benzodiazepines.

75. Diazepam
Day 1 and 2 10mg tid
Day 3 and 4 10mgbid
Day 5 and6 5mg bid
Day 7 5mg at bed time
Thiamine 50-100mg/day

76. Rehabilitation
Components
Continued efforts to increase and maintain high
levels of motivation for abstinence
Work to help the patient readjust to a lifestyle free of
alcohol
Relapse prevention

77. First identify situations in which the risk for relapse
is high
The counselor must help patient develop modes of
coping to be used when the craving for alcohol
increases
Or when any event or emotional state makes a return
to drinking likely

78. Important aspect of recovery involves helping family
members and close friends understand alcoholism
and realize that rehabilitation lasts for 6-12 or more
months
Follow up
Monitor liver function tests periodically

79. Disulfiram 250mg daily before the patient is
discharged from intensive first phase of outpatient
rehabilitation or from inpatient care
The goal is to place the patient in a condition in which
drinking alcohol precipitates an uncomfortable
physical reaction including nausea vomiting and a
burning sensation

80. Naltrexon
Opioid antagonist decrease the craving for alcohol or
blunt the rewarding effects of drinking
Using of this drug had potentially promising results

81. 29
Tobacco: Basic facts (1)
Description: Tobacco products contain nicotine
plus more than 4,000 chemicals and a dozen
gases (mainly carbon monoxide)
Route of administration: Smoking, chewing
Acute Effects: Pleasure; relaxation; increased
concentration; release of glucose; increased
blood pressure, respiration, and heart rate

82. 30
Tobacco: Basic facts (2)
Withdrawal Symptoms:
 Cognitive / attention deficits
 Sleep disturbance
 Increased appetite
 Hostility
 Irritability
 Low energy
 Headaches

83. 31
Long-term effects of tobacco use
Aneurysm
Cataracts
Cancer (lung and other types)
Chronic bronchitis
Emphysema
Asthma symptoms
Obstructive pulmonary diseases
Heart disease (stroke, heart attack)
Vascular disease
Harm to a fetus during pregnancy,
low weight at birth
Death

84. 33
Cannabis: Basic facts (1)
Description: The active ingredient in cannabis is
delta-9-tetrahydrocannabinol (THC)
 Marijuana: tops and leaves of the plant Cannabis
sativa
 Hashish: more concentrated resinous form of the
plant
Route of administration:
 Smoked as a cigarette or in a pipe
 Oral, brewed as a tea or mixed with food

85. Cannabis: Brain receptors
 Two types of cannabinoid receptors
CB1 & CB2
 CB1 receptors in brain (cortex, hippocampus, basal
ganglia, amygdala) and peripheral tissues (testes,
endothelial cells)
 CB2 receptors associated with the immune system
 Most cannabis effects are via THC acting on CB1
receptors, which facilitate activity in mesolimbic
dopamine neurones

86. 35
Cannabis: Basic facts (2)
Acute Effects:
 Relaxation
 Increased appetite
 Dry mouth
 Altered time sense
 Mood changes
 Bloodshot eyes
 Impaired memory
 Reduced nausea
 Increased blood
pressure
 Reduced cognitive
capacity
 Paranoid ideation

87. 36
Cannabis: Basic facts (3)
Withdrawal Symptoms:
 Insomnia
 Restlessness
 Loss of appetite
 Irritability
 Sweating
 Tremors
 Nausea
 Diarrhea

88. Short term, high-dose effects
Cannabis also affects:
 Short-term memory
 ability to learn and retain new information
 task performance
 balance, stability, mental dexterity
 the cardiovascular and respiratory systems
Short-term, high-dose use may result in:
 synaesthesia
 pseudo- or true hallucinations
 delusions, feelings of depersonalisation
 paranoia, agitation, panicky feelings, “psychosis”

89. 37
Long-term effects of cannabis use
 Increase in activation of stress-
response system
 Amotivational syndrome
 Changes in neurotransmitter levels
 Psychosis in vulnerable individuals
 Increased risk for cancer, especially
lung, head, and neck
 Respiratory illnesses (cough, phlegm)
and lung infections
 Immune system dysfunction
 Harm to a fetus during pregnancy

90. Drugs and Psychosis:
The Cannabis story

91. Dopamine is the
“Wind of Psychotic Fire”
When individuals are acutely psychotic, they show an excessive release
of dopamine1
Dopamine normally mediates the attachment of salience to ideas and
objects2
Heightened DA transmission leads to aberrant assignment of salience to
external and internal stimuli3
Delusions arise from attempts to explain this abnormal salience4
1Laruelle et al 1996; 2Berridge and Robinson 1998; 3Kapur 2003; 4Maher 1983

92. Psychosis

93. Gene-Environment Interaction
Psychosis
COMT
Adolescent
cannabis use

94. Could Susceptibility Be Related
to Genotype?
Cannabis is thought to have its
effects via the dopamine system
COMT encodes a key enzyme
that metabolises dopamine in
the frontal cortex
2 alleles – VAL and MET
Some, but not all, family studies
show the VAL allele confers risk
for schizophrenia
Li T, et al. Psychiatr Genet. 1996;6(3):131-133.
Egan MF, et al. Proc Natl Acad Sci USA. 2001;98(12):6917-6922.
22q
COMT

95. Schizophrenia spectrum disorder:
Cannabis use interacts with genotype
Caspi et al. 2005 (Biol. Psychiatry)
0
5
10
15
Met/Met Val/Met Val/Val
Percent
with
schizophreniform
disorder
at
age
26
Can yes Can no

96. Why should cannabis cause
PSYCHOSIS?

97. Using the dopamine D2/D3 receptor tracer [11C]raclopride and
positron emission tomography in seven healthy subjects, it was
demonstrated that THC inhalation reduces [11C]raclopride
binding in the ventral striatum and the precommissural dorsal
putamen…. This is consistent with an increase in dopamine
levels in these regions.
Bossong et al, 2008
THC Induces Dopamine
Release in the Human Striatum

98. Bad for some … not for others
“Barack Obama on Weed”

99. GENETICS and Psychosis
(GAP ) Study
SLAM: South London and Maudsley
Mental Health NHS Trust
South
London
•517 subjects in their 1st episode of
psychosis (FEP)
Diagnosis defined using the SCAN, (scale
for clinical assessment in neuropsychiatry) CEQ-
GAP modified version 2008 and 10 hours more
assessment …
•306 matched healthy controls
( screened for psychosis)

100. Table 2. Cases
N=159
Controls
N=109
Unadjusted
OR
*Adjusted
OR
Duration of
Cannabis use
0-5 years 65 (40.8%) 68 (62.5%) 1 /
6 years and above 94 (59.2%) 41 (37.5%) 2.4 1.8
Weekly frequency
Only at week-end or ≤
3 days a week
37 (23.1%) 73 (66.7%) 1 /
Everyday 122 (76.9 %) 36 (33.3%) 6.9 6.6
Type of cannabis
used
Resin (Hash)-Imported
Herbal
THC/CBD=1
34 (21.6%) 68 (62.6%) 1 /
Skunk/Sinsemilla
THC 12-18%; CBD=0
125 (78.4%) 41 (37.4%) 8.1 6.1
* age, gender, ethnicity, other stimulants, employment and level of education.

101. In conclusion
Causality Bradford-Hill criteria
1.Strength of association?
2.Consistency of data?
3.Temporal association?
4.Specificity?
5.Dose response?
6.Biological plausibility?
7. Experimental evidence?
Y
Y
Y
?
Y
Y
Y

102. Cannabis: Abuser’s Experience
"When I first started it was just to relax. It reduced the
tension after a days work. We just used to sit around giggling
and playing music and then getting the munchies and eating
our heads off. And next morning I felt fine. No hangover at
all".
"Now I need to smoke it most of the time. At the moment it's
all I really think about. My daily routine is work, think about
a joint, get stoned, sleep, back to work. I can't imagine life
without it. Whilst I'm stoned my memory sometimes goes.
Where did I put the keys? Why did I walk into this room?
What have I got to do? I've reached a point where I was
smoking so much and I couldn't take any more spliff. The
paranoia was too much. Your life tends to float along in a
haze".

103. Stimulants: Basic facts
Description:
Stimulants include: (1) a group of synthetic drugs
(ATS) and (2) plant-derived compounds (cocaine)
that increase alertness and arousal by stimulating
the central nervous system
Route of administration:
Smoked, injected, snorted, or administered by
mouth or rectum

104. Problems of drug use
13
Psycho-stimulant and sexual risk
behaviour
 Psycho-stimulant (cocaine and
methamphetamine.,khat) use is
associated with high risk sexual
behaviour, e.g., unprotected
sex, multiple partners
 Psycho-stimulant users are at
risk for sexually transmitted
diseases (STDs) including HIV
infection

105. Acute effects:
Euphoria, rush, or flash
Wakefulness, insomnia
Increased physical
activity
Decreased appetite
Increased respiration
Hyperthermia
Irritability
Tremors, convulsions
Anxiety
Paranoia
Aggressiveness

106. Long term effects
Strokes, seizures, headaches
Depression, anxiety, irritability, anger
Memory loss, confusion, attention problems
Insomnia, hypersomnia, fatigue
Paranoia, hallucinations, panic reactions
Suicidal ideation
Nosebleeds, chronic runny nose,
hoarseness, sinus infection
Dry mouth, burned lips, worn
teeth
Chest pain, cough, respiratory
failure
Disturbances in heart rhythm
and heart attack
Loss of libido
Weight loss, anorexia,
malnourishment,
Skin problems

107. Cocaine: Abuser’s experience
"It makes you feel great and powerful and all that. The
trouble is it can make you really wired. And it doesn't last
that long so the temptation is to have another go. That's
why it cost me a fortune".
"The first hit is always the best...I've never had anything
like it. With crack once you've got that hit of the day, no
matter how much you take you don't get it back. If the rock
is there, I can't leave it, even though I don't get anything
off it. But you can't just have one (rock) and leave it,
you've got to have more".

108. Stimulant: Abuser’s experience
"It's a wide awake buzz. It intensifies everything.
It makes me feel really confident and energetic.
You don't feel hungry and can skip sleeping. It
makes me talk a lot even though it's probably
bollocks. I used to get a lot of good rushes like
feeling hot and cold, your hairs standing up all
over your body and your head spinning. The
problem now is all the crap. Whizz can be cut with
anything from baking soda to battery acid. I only
buy from people I know and stuff I've used
before"

109. Stimulant: Abuser’s experience
"I've had paranoia experiences. You can get someone walk
past you in the street and you think My God. They just
looked at me. They've got it in for me. They've got my
number'. It can get really scary. I've had bad come downs
on speed. It stops you sleeping and it is literally speedy,
keeping you going all the time. It doesn't inspire me in any
way. It doesn't give you time to stop and think. You're just
moving and doing all the time. Your body tells you to
sleep but your mind's constantly on the go. And then you
come right down and you are low and knackered for ages".

110. Khat

111. Khat

112. Background
Ethiopia is a country of origin of use.
Evergreen shrub, can be grown in droughts.
Most people chew it.
Small number make a drink or more rarely
smoke it.
Khat chewing takes place in social groups.
Men chew more commonly than women.

113. Effects of Khat chewing
Initially atmosphere of cheerfulness and
optimism.
After 2 hours, mounting tension, emotional
irritability and irritability.
Later, feelings of low mood and
sluggishness.

114. Pharmacology
Most effects from cathinone and cathine-
structurally related to amphetamine.
Cathinone 7-10 times more potent than
cathine.
Act on dopamine and noradrenalin pathways.
Effect of cathinone maximal after 15-30
minutes- metabolised rapidly- 2% excreted in
urine.
Cathine –slower onset excreted unchanged in
urine after 24 hours.

115. Addiction, Tolerance and
Withdrawal
Cathinone- dependence producing
constituent.
Possible withdrawal syndrome- lassitude,
lack of energy, nightmares, trembling.

116. Psychological sequelae
Small amounts increased sense of well-
being while chewing.
After chewing- insomnia, numbness, poor
concentration, low mood.

117. Psychiatric consequences
Short-lived schizophreniform psychotic illness-
resolves in 3-11 days
Mania- resolves within hours
Depression
Presentations may be associated with self-harm or
harm to others
Alem and Shibre (1997) described a case where a
patient murdered his wife and daughter.
Alem also described a case of combined homicide
and suicide after chewing large amounts of khat.

118. Physical consequences of Khat
CVS- arrhythmias, tachycardia, palpitations,
infarction
Respiratory- bronchitis, TB, dyspnoea
GI- gastritis, weight loss
Hepatobiliary - cirrhosis
GU-- impotence, urinary retention
Obstetric- still births, impaired lactation
CNS-dizziness, headaches, insomnia, fine
tremor

119. Opioids: Basic facts
Description:
Opium-derived or synthetic compounds that
relieve pain, produce morphine-like
addiction, or relieve symptoms during
withdrawal from morphine addiction.
Route of administration:
Intravenous, smoked, intranasal, oral, and
intrarectal

120.  Cross the blood brain barrier faster and has a more rapid
onset than morphine.
 One effect of all opioids is decreased cerebral blood flow
in selected brain regions in persons with opioids
dependence (PET study)
 Peak of the withdrawal syndrome is during the second or
third day and subsides during the next 7 to 10 days,
but some symptoms may persist for 6 months or long.

121. Opiate related
disorders

122. Opioid dependence: is a cluster of physiological
behavioral and cognitive symptoms which together
indicate repeated and continuing use of opioid drugs
despite significant problems related to such use.

123. Opioid abuse :a pattern of maladaptive use of an
opioid drug leading to clinically significant
impairment or distress and occurring within a 12
month period; but one in which the symptoms have
never met the criteria for opioid dependence.

124. Neuropharmacology
Endorphins are involved in neural transmission and
pain suppression
Opoids also have significant effects on the
dopaminergic and noradrenergic neurotransmitter
system.

125. Addictive rewarding properties of opioids are
mediated through activation of the ventral tegmental
area dopaminergic neurons that project to the
cerebral cortex and the limbic system.

126. Co morbidity
90% of persons with opioid dependence have an
additional psychiatric disorder.
Most common co morbid psychiatric diagnoses are
major depressive disorder, alcohol use disorders,
antisocial personality disorder, and anxiety disorders.

127. Morphine and heroin
Morphine and heroin withdrawal syndrome begins 6
to 8 hours after the last dose.
Usually after a 1to2 week period of continuous use
or after the administration of a narcotic antagonist.
Heroin is the most commonly abused opioid and is
more potent and lipid soluble than morphine.

128. Etiology
Social factors
Children of single or divorced parents
Children from families in which at least one
other member has a substance-related disorder

129. Biological and genetic factors:
Monozygotic twins are more likely than dizygotic
twins to be concordant for opioid dependence .

130. Opioid intoxication
 initial euphoria followed by apathy, dysphoria,
psychomotor agitation/retardation
drowsiness or coma
Slurred speech
Impairment in attention or memory
 Pupillary constriction or dilation.

131. Opioid withdrawal
Dysphoric mood
Nausea or vomiting
Muscle aches
Lacrimation or rhinorrhea
Pupillary dilation,piloerection,sweating
Diarrhea, Fever
Insomnia,Yawning

132. Clinical features
Route of administration
p.o, snorting intranasally and i.v
Adverse effects
The most common and serious are hepatitis and HIV
through the use of contaminated needles by more
than one person.

133. Persons can experience idiosyncratic allergic
reactions to opioids, which result in anaphylactic
shock, pulmonary edema, and death if they do not
receive prompt and adequate treatment.

134. Opioid overdose
Death from an overdose of an opioid is usually
attributable to respiratory arrest from the respiratory
depressant effect of the drug.
Symptoms of overdose
Marked unresponsiveness , coma ,slow respiration,
hypothermia ,hypotension and bradycardia.

135. Suspect opioid overdose when you meet the clinical
triad of coma, pinpoint pupils, and
respiratory depression.
Inspect the patient’s body for needle tracks in the
arms , legs , ankles , groin and even the dorsal vein
of the penis.

136. TREATMENT
Overdose treatment
First task
Ensure adequate airway
Tracheopharangeal secretion should be
aspirated
Airway may be inserted

137. Naloxene i.v slow rate
Signs of improvement:
Increased respiratory rate
Pupillary dilation
Medically supervised withdrawal and
detoxification
Opioid agents for treating opioid withdrawal

138. Education and needle exchange
 Attention to education on transmission of HIV, HBV
& HCV.
 Users of i.v/s.c must be taught available safe sex
practice
 Free needle exchange program where allowed should
be made available to persons with opioid
dependence.

139. Acute effects:
Euphoria
Pain relief
Suppresses cough reflex
Histamine release
Warm flushing of the
skin
Dry mouth
Drowsiness and lethargy
Sense of well-being
Depression of the central
nervous system (mental
functioning clouded)

140. Withdrawal symptoms:
Intensity of withdrawal varies with level and chronicity
of use
Cessation of opioids causes a rebound in functions
depressed by chronic use
First signs occur shortly before next scheduled dose
For short-acting opioids (e.g., heroin), peak of
withdrawal occurs 36 to 72 hours after last dose
Acute symptoms subside over 3 to 7 days
Ongoing symptoms may linger for weeks or months

141. Long-term effects of opioids
Fatal overdose
Collapsed veins
Infectious diseases
Higher risk of
HIV/AIDS and
hepatitis
Infection of the
heart lining and
valves
Pulmonary
complications &
pneumonia
Respiratory problems
Abscesses
Liver disease
Low birth weight and
developmental delay
Spontaneous abortion
Cellulitis

142. Heroin: Abuser’s Experience
"It is probably one of the most pleasurable
experiences I've had. All the pain goes. All the
anger is gone. I was lying on the sofa floating
happily. It makes you feel safe and warm like
being wrapped up in a blanket".
"You can get addicted pretty quickly and start
feeling you have to have it all the time. It's cut
with all sorts of rubbish but you don't really care.
The only goal in life became getting more. It kind
of took all my feelings away".

143. “Benzodiazepines:
the opium of the masses”
(Source: Malcolm Lader, Neuroscience, 1978)
Benzodiazepines

144. General medical / psychiatric indications
for benzodiazepine use
 Anxiolytic – chronic / phobic anxiety & panic
attacks
 Sedative and hypnotic – sleep disturbance &
anaesthesia / premedication
 Anticonvulsant – status epilepticus, myoclonic
& photic epilepsy
 Muscle relaxant – muscle spasm / spasticity
 Alcohol withdrawal

145. BZDs and long-term use
 Long-term use is common and associated with:
 altered use patterns (from nighttime to daytime use)
 excessive sedation
 cognitive impairment
 increased risk of accidents
 adverse sleep effects
 dependence and withdrawal (even at therapeutic
doses)
 BZDs have an additive effect with alcohol / other CNS
depressants, increasing the risk of harm
 BZDs have limited long-term efficacy

146. BZD and illicit drug use
 Illicit BZD use is usually oral, although around 5% are likely to
inject (usually males)
 Often 2nd drug of choice for illicit drug users, as BZDs assist
withdrawal from opioids, stimulants, and alcohol
 Estimated around 70% of people using >50 mg per day are
polydrug users, who tend to:
 be younger
 have higher daily doses and higher lifetime exposure
 use in combination with other CNS depressants to increase
intoxication
 prefer fast-acting BZDs (diazepam, flunitrazepam)
 may convert form to enable injection

147. Effects: High dose
Short term
 Sedation
 Intoxication
 Drowsiness
Other effects
 Paradoxical excitement
 Mood swings
 Hostile and erratic
behaviour
Toxicity
 Performance deficits
 Emotional blunting
 Muscle weakness
 Sensitivity
 Potentiates other drugs
 Euphoria, hypomania

148. Drug + alcohol interactions
 CNS depressants,
e.g., benzodiazepines
 Antipsychotics,
antidepressants
 Opioid analgesics,
antihistamines (some)
 Hypoglycaemics
(chlorpropamide),
metronidazole,
cephalosporins (some)
Confusion, depressed
respiration
Decreased metabolism,
toxicity & CNS depression
CNS depression
Facial flushing, headache

149. 1. Low dose dependence occurs among women and
elderly prescribed low doses over long time periods
(up to 40% experience withdrawal symptoms)
2. High dose dependence occurs among polydrug users
Dependence
Two groups of patients are especially likely to
develop dependence.

150. Withdrawal
 40% of people on long-term therapeutic BZD doses will
experience withdrawal if abruptly ceased
 Symptoms occur within 2 “short-acting” to 7 day “long-acting”
forms
 BZD withdrawal:
 is not life-threatening & usually protracted
 initial symptoms / problems re-emerge on cessation
 issues usually more complicated on cessation
 Seizures uncommon (unless high dose use or abrupt withdrawal,
+ alcohol use)
 Two main groups of users:
 prescribed (older women)
 high level, erratic polydrug use

151. 3 Areas of BZD withdrawal
Anxiety and anxiety-related symptoms
 anxiety, panic attacks, hyperventilation, tremor
 sleep disturbance, muscle spasms, anorexia, weight loss
 visual disturbance, sweating
 dysphoria
Perceptual distortions
 hypersensitivity to stimuli
 abnormal body sensations
 depersonalisation/derealisation
Major events
 seizures (grand mal type)
 precipitation of psychosis

153. Today’s message!
I cannot teach anyone
anything
I can only make them think
Socrates
400 BC
The soul is immortal and
possesses all knowledge