Class 5 Flashcards

1
Q

Why Do People Abuse Drugs?

A

Drugs of Abuse Engage Motivation and Pleasure Pathways of the Brain.
Stress Reduction
To Feel Good To have novel: feelings, sensations, experiences AND to share them.
To Feel Better To lessen: anxiety, worries, fears, depression, hopelessness.

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2
Q

Natural rewards ??? DA levels but drugs

A

elevate, are mon effective

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3
Q

What is Addiction?

A

Addiction is A Brain Disease
Characterized by:
Compulsive behavior or craving
Continued abuse of drugs despite negative consequences
Persistent changes in the brains structure and function

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4
Q

True or false, addiction can change biology

A

true

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5
Q

Biologic changes following addiction

A

Decreased Brain Metabolism
Decreased DA transporters
Induced suppression of brain activity (ROH, cocaine)
– changes in neurotransmitter levels
– decreased dopamine D2 receptors
– low activity in the orbitofrontal cortex (OFC) and the
anterior cingulate gyrus (CG)
– inhibition of the frontal cortex – effects on memory,
decision making, inhibitory control, poor judgement,
planning and behavioural control

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6
Q

Hallmark of addiction

A

loss of control of the use of substance
compulsive use or craving
continued use despite consequences

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7
Q

Misuse

A

Use of medication other than as directed, whether
wilful or not.
Similar to abuse but usually applies to drugs prescribed by physicians that are then used improperly.

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8
Q

Abuse

A

Maladaptive pattern of substance use leading to
clinical impairment or distress.
Use of medication for non medical purposes.
Use of any drug, usually by self administration, in a
manner that deviates from approved social or medical
patterns.

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9
Q

Withdrawal

A

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. This syndrome is characterized
by physiological signs and symptoms in addition to
psychological changes such as disturbances in
thinking, feeling, and behaviour.

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10
Q

Intoxication

A

A reversible syndrome caused by a specific
substance that affects one or more of the following
mental functions.

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11
Q

DSM 5 Definitions

Substance use disorder

A

A maladaptive pattern of substance use leading to clinically significant impairment or distress as manifested by 2 or more of the following (11 symptoms) occurring
within a 12 month period:

  1. Recurrent substance use resulting in a failure to fulfill major role obligations at work, school, or home.
  2. Recurrent substance use in situations in which it is physically hazardous.
  3. Continued substance use despite having persistent and recurrent social or interpersonal problems caused or
    exacerbated by the effects of the substance.
  4. Tolerance: Need increased amounts to achieve intoxication. Diminished effect with continued use
  5. Withdrawal
  6. Substance is often taken in larger amounts or over a longer period than was intended
  7. Persistent desire or unsuccessful efforts to cut down or control substance use
  8. A great deal of time is spent in activities necessary to obtain the substance, use the substance, or recover from its effects.
  9. Important social, occupational, or recreational activities are given up or reduced because of substance use.
  10. The substance use is continued despite knowledge of having persistent or recurrent physical or physiological problem that is likely to have been caused or exacerbated by the substance.
  11. Craving or a strong desire to use a specific substance.
Severity:
Depends on the number of symptoms
Mild: 2 3
Moderate: 4 5
Severe: 6 or more

Specifiers:
In early remission: no criteria for more than 3 months
but less than 12
In sustained remission: no criteria for more than 12
months
In a controlled environment

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12
Q

10 Classes of Substances

A
Alcohol
Caffeine
Cannabis
Hallucinogens: PCP, others
Inhalants
Opioids
Sedatives, hypnotics, and anxiolytics
Stimulants
Tobacco
Other
(Gambling)
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13
Q

Etiology

A
Bio:
Genetics
Neurotransmitters
Signaling pathways
Psycho:
Psychodynamic
Learning and conditioning: the addiction cycle
Social
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14
Q

Major neurotransmitter systems:

A

Dopamine: activates the reward system/triggers
GABA: indirect activation of reward system
Glutamate: reinforcement, relapse, and drug seeking

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15
Q

Brain reward circuitry

A
Nucleus accumbens
Locus ceruleus
Prefrontal cortex
Amygdala
Hippocampus
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16
Q

Drugs of abuse ????

natural neurotransmitters in the brain

A

resemble/activate or disrupt

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17
Q

Dopamine Pathways Functions

A
  • attention, arousal
  • reward (motivation)
  • motor function
  • decision making
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18
Q

Serotonin Pathways Functions

A
  • mood
  • memory processing
  • sleep
  • cognition
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19
Q

Psycho : Addiction cycle

A

emotional pain = craving for relief = preoccupation with substance/ behaviour = substance use/ compulsive behaviour = short term pain relief = negative consequences resulting from behaviour = depression, guilt, shame =more pain

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20
Q

Social : Addiction

A
Family
Peers
Societal
Cultural
Life events
Stress
Isolation
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21
Q

Predisposing Factors

A

Biological factors: Genetic, 10% addicts have genetic predisposition. Familial

Psychosocial:
Being a male
Peer pressure
Religion
Home conditions
Stability of parents’ marriage
Cultural practices
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22
Q

Precipitating factors

A

Exposure to drink or drugs for social and other

reasons

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23
Q

Perpetuating factors

A

Persistent exposure
Lack of treatment
Lack of social support

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24
Q

Protective Factors

A
female gender
assertiveness
high commitment to school
high educational aspirations
close affective relationships
absence of parental problems
high religiosity
close supportive relationships with
positive influencing peers
high self esteem
self efficiency
creativity
good temperament
high sociability
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25
Q

Indirect stimulation of pleasure pathways: decrease background

A

PCP, ketamin

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26
Q

Indirect stimulation of pleasure pathways: increase signal intensity

A

psychadelics

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27
Q

direct interaction with pleasure pathways: primary DA effect

A

stimulants

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28
Q

direct interaction with pleasure pathways: primary endorphin effect

A

opioids

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29
Q

direct interaction with pleasure pathways: DA + GABA + endorphins

A

sedative hypnotics

ROH

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30
Q

only ??? in 10 person with addiction receives treatment

A

1

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31
Q

Psychosocial therapies

A
Motivational
Cognitive behavioral
Community reinforcement
Contingency management
Behavioral couples family
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32
Q
NIDA: Selected Principles of
Effective Treatment (EBPs)
A
  1. Addiction is a complex but treatable disease that affects brain function and behavior.
  2. No single treatment is appropriate for everyone.
  3. Treatment needs to be readily available.
  4. Effective treatment attends to multiple needs of the individual, not just his or her drug abuse.
  5. Counselling individual and/or group and other behavioural therapies are the most commonly used forms of drug abuse treatment.
  6. Many drug addicted individuals also have other mental disorders.
  7. Medically assisted detoxification is only the first stage of addiction treatment and by itself does little to change long term drug abuse.
  8. Treatment does not need to be voluntary to be effective.
  9. Treatment programs should assess patients for the presence of HIV/ AIDS, hepatitis B and C, tuberculosis, and other infectious diseases as well as provide targeted risk reduction counseling to help patients modify or change behaviors that place them at risk of contracting or spreading infectious diseases.
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33
Q

Scientifically Based Approaches

to Addiction Treatment

A
Cognitive behavioral interventions
Community reinforcement
Motivational enhancement therapy
12 step facilitation
Contingency management
Pharmacological therapies
Relapse Prevention
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34
Q

True or false: Relapse Rates Are Similar to

Other Chronic Diseases

A

True

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35
Q

Management: screening

A
Clinical assessment: Don t forget, patients usually under report their use or sometimes downright lie about their use
CAGE
Screening questionnaires:
DAST
AUDIT
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36
Q

CAGE

A

Have you ever felt you should c ut down on your drinking?
Have people a nnoyed you by criticising your drinking?
Have you ever felt bad or g uilty about your drinking?
Have you ever had a drink first thing in the morning to steady your nerves or get
rid of a hangover ( e ye opener)?

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37
Q

Stages of transtheoretical model of changes:

A
Precomtemplation
Contemplation
Decision
Action
Maintenance
Relapse
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38
Q

Precomtemplation

A

Not a problem

Intervention: raise doubt

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39
Q

Contemplation

A

a problem that maybe needs to change

Intervention: strengthen the will to change

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40
Q

Decision

A

something that needs to change

Intervention: create an action plan

41
Q

Action stage

A

something that is changing via abstinence

Intervention: maintain steps in the action plan

42
Q

Maintenance stage

A

no longer a problem because action is reinforced by the maintenance of a certain way of life
Intervention: avert relapse

43
Q

Canadian standard drink sizes

A

13.6 grams of alcohol
12 ounces of beer = 341 mls = 1 bottle (5%)
5 ounces of wine = 150 mls (12%)
1.5 ounces of hard liquor = 45 mls (40%)

44
Q

ROH Screening options:

Single item screener

A

How many times in the last year have you had (men = 5 or more) (women = 4 or more) drinks in one occasion?”
More than once is positive screen 82% sensitive, 79% specific for unhealthy drinking (at risk and AUDs)

45
Q

Alcohol related disorders

A
Alcohol use disorder
Alcohol intoxication
Alcohol withdrawal
Delirium
Alcohol induced persisting amnestic disorder
46
Q

Short term ROH

A

Short term: Intoxication, injury, violence,
accidents, spousal abuse, suicide, alcohol toxicity
(overdose), death

47
Q

Intoxication ROH

A
Problematic behaviour and psychological changes
Slurred speech
Incoordination
Unsteady gait
Nystagmus
Impaired attention or memory
Stupor or coma
48
Q

Educ alcohol recommendations:

A

2 drinks per day max 10 per week for women
3 drinks per day max 15 per week for men
3 drinks max per day on special occasions for women
4 drinks max per day on special occasions for men
At least one day per week where no alcohol is
consumed

49
Q

Canadian Epidemiology

Alcohol use disorder:

A

2.6%
3.8% for men
1.3 for women
Province with most use: Quebec (82%)

50
Q

Long term: ROH

A

Alcohol dependence, increased risk of several types
of cancer (e.g., cancers of the mouth, throat, liver,
breast, and digestive track), diabetes, cirrhosis,
pancreatitis, low birth weight, fetal alcohol spectrum
disorder (FASD).

51
Q

Alcohol withdrawal

A

GABA down, Glutamate up

  1. Sweating and increased pulse
  2. Increased tremor
  3. Insomnia
  4. Nausea and vomitting
  5. Hallucinations
  6. Agitation
  7. Tonic clonic seizures
52
Q

Minor withdrawal ROH

A

autonomic symptoms

53
Q

Major withdrawal ROH

A

autonomic symptoms+ hallucinations, seizures

54
Q

4 stages of ROH withdrawal

A
  1. autonomic symptoms: tremors 6-8h
  2. Hallu: 10-30h
  3. Neuronal excitation: seizures 6-48h
  4. DT: 2-5 days
55
Q

Treatment: Alcohol withdrawal

A

CIWA (rating scale)
Mild to moderate: no need for pharmacotherapy
Moderate to severe:
Thiamine to prevent encephalopathy
Benzodiazepine to reduce withdrawal severity
Monitoring vital parameters , with a special reference to
blood electrolytes and fluid balance (Na, K, Mg, glucose) glucose),
ECG
Benzodiazepines (diazepam [5 20 mg p.o. every 4 6
hour, starting dose of 10 30 mg i.v. if needed],
chlordiazepoxide) avoid in intoxication and long term
use, risk of respiratory depression and sedation ;
oxazepam or lorazepam if significant hepatic impairment
Thiamine for prevention of Wernicke Korsakoff syndrome
Beta blockers (e.g. propranolol or atenolol for autonomic
hyperactivity)
Valproate or carbamazepine if seizures are present
Haloperidol for hallucinations, delusions, and violence
in delirium [5 10 mg p.o. or i.m.], together with
benzodiazepines (risk of seizures and extrapyramidal
side effects)

56
Q

Wernicke encephalopathy

A

Acute and reversible
Due to lack of thiamine
Confusion, ophthalmoplegia and ataxia

57
Q

Korsakoff s syndrome

A

Chronic (20% recover completely)

Amnesia, confabulation, apathy, and anosognosia

58
Q

Treatment of alcohol use disorder 1st line

A

Naltrexone: Blockage of mu opioid receptor, blocks the reinforcing effect of alcohol: don’t get the buzz + less craving
Acomprosate: GABA agonist and glutamate antagonist really metabolized TID s/e: crazy diarrhea

59
Q

Treatment of alcohol use disorder 2nd line

A

Disulfuram: can’t take anything with alcohol, even hand santizier
Topiramate
Gabapentin
Baclofen

60
Q

Low risk drinking guidelines

A

Women: 10 drinks a week, with no more than 2 drinks a day most days, up to 3 for special occasions
Men: 15 drinks a week, with no more than 3 drinks a day
most days, up to 4 for special occasions

Elderly American guideline (no Canadian guideline)
Men no more than one per day
Women less than one per day on average

61
Q

Cannabis related disorders

A

Cannabis use disorder
Cannabis intoxication
Cannabis withdrawal

62
Q

Cannabis related disorders

epidemiology

A
12 month prevalence
3.4% among 12 17 year olds
1.5% in adults
More males than females
Rates decrease with age
Cannabis is the most widely used illicit drug in Canada
63
Q

SYNTHETIC CANNABINOIDS

A

Pharmacological research tools to study endocannabinoid system
Synthetic cannabinoids sprayed on herbal plants
No cannabidiol
Super agonist at CB 1 receptor
Can cause acute renal failure, hypertension,
myocardial infarction, seizures, psychosis, death
Not detected in standard urine drug screens

64
Q

CANNABIS EFFECTS

A

Cannabis produces euphoria and relaxation, changes in
perception, time distortion, and deficits in attention span.
It also negatively impacts the ability to divide attention and results in deficits in memory, body tremors, and impaired motor functioning.
Cannabis also impairs coordination and balance.
Other physical effects of recent cannabis use include increased heart rate and appetite, decreased blood pressure, dilated pupils, red eyes, dry mouth and throat, and bronchodilation (expansion of breathing passages).

65
Q

Cannabis intoxication

A

30 min. for peak effect
Lasts 2 4 hours
Motor and cognitive effects can last 6 12 hours

66
Q

Effects of Cannabis oral

A

onset: 30 min
duration: up to 8h
subjective effects: greater bad effects
abstinence effects: less subjective abstinence effects
45% increase in appetite

67
Q

Effects of Cannabis smoking

A

onset: sec
duration: 1-2h
subjective effects: greater effects on high and mellow
abstinence effects: greater effects on irritable and miserable
45% increase in appetite

68
Q

Cannabis intoxication

A
Recent use
Behavioural or psychological changes
Two or more of the following:
Conjunctival injection
Increased appetite
Dry mouth
Tachycardia
69
Q

Cannabis use disorder

Long term effects:

A

Chronic cannabis use is associated with deficits in memory, attention, psychomotor speed and executive functioning, particularly among those who started using cannabis during early adolescence.
Chronic use of this drug can also increase the risk of psychosis, depression and anxiety, breathing problems and respiratory conditions, and possibly lung cancer.
Use of cannabis during pregnancy particularly heavy use
can affect children s cognitive functioning, behaviour, future substance use behaviour and mental health.
Decreases testosterone levels in men

70
Q

Cannabis withdrawal

A
Cessation after heavy and prolonged use
Three or more of the following which develop within a week:
Irritability, anxiety, aggression
Nervousness or anxiety
Sleep difficulty
Decreased appetite or weight loss
Restlessness
Depressed mood
Abdominal pain, shakiness/tremors, sweating, fever,
chills, or headache
71
Q

Treatment of cannabis use disorder

A
No effective pharmacological treatment
––? Gabapentin
Non pharmacological treatment options:
CBT
Motivational interviewing
Voucher based incentives
Peer support groups
Family therapy
72
Q

Opioid related disorders

A

Opioid use disorder
Opioid intoxication
Opioid withdrawal

73
Q

Opioid def

A

Definition: Natural and man made chemicals that act at opioid receptors to produce morphine like effects

74
Q

Opioid types

A

Natural: codeine, morphine
Semi synthetic: diacetylmorphine (heroin), hydromorphone, oxycodone, buprenorphine
Synthetic: fentanyl, methadone, meperidine
Endogenous: Endorphins

75
Q

opioid prevalence

A

0.5 3% of Canadians are currently using opioids

76
Q

Opioid intoxication

A
Problematic behaviour or psychological changes
Pupillary constriction
Drowsiness and coma
Slurred speech
Impaired orientation and memory
77
Q

Opioid use disorder

Long term effects

A

Opioids can reduce pain and improve function.
Opioids can also produce a feeling of well being or euphoria high ””).
At sufficiently high doses, opioids cause drowsiness, coma, and death.
Other physical effects are constricted pupils, a slight decrease in respiratory rate, nausea, vomiting, constipation, loss of appetite, and sweating.
Narcotic bowel syndrome: increased abdominal pain with
increasing doses of opioids.
Opioids can also cause increased risk of sleep apnea, mood changes, decreased sex hormone levels resulting in decreased interest in sex and menstrual irregularities, physical dependence, and addiction.
Regular use of large quantities of opioids during pregnancy increases the risk of premature delivery and withdrawal in the infant.
In those people who crush and inject oral opioids, certain filler chemicals in the pills can permanently damage veins and organs.
Sharing needles or injecting with previously used needles greatly increases the risk of getting certain infections (e.g., HIV, hepatitis C).

78
Q

Symptoms of opioid withdrawal

A
Dysphoria
N o/Vo
Muscle aches
Lacrimation/rhinorrhea
Pupillary dilation, pilo erection or sweating
Diarrhea
Yawning
Fever
Insomnia
79
Q

Treatment opioids

A

Pharmacological treatments
Methadone (agonist)
Buprenorphine (agonist)
Naltrexone (antagonist)

Non pharmacological treatments
Individual or group counselling
Peer support groups
Abstinence based treatments

80
Q

Stimulant related disorders

A

Stimulant use disorder
Stimulant intoxication
Stimulant withdrawal

81
Q

COMMON

STIMULANTS

A
Cocaine
Crack cocaine
Methamphetamines
Amphetamines
MDMA (Ecstasy)
Prescription stimulants
Methylphenidate
Dextroamphetamine
Modafinil
Caffeine
Ephedrine
Cathinone ( Khat)
82
Q

Prevalence of Stimulant Use

A

Canadian cocaine use ~1.5 % (past year use

Canadian Drug Summary 2017

83
Q

Mechanism of Action

Cocaine

A
blocks catecholamine ( dopamine ,
adrenaline, noradrenaline) reuptake
84
Q

Mechanism of Action Methamphetamines

A

blocks dopamine reuptake AND promotes direct dopamine release

85
Q

Mechanism of Action MDMA

A

increases serotonin by blocking reuptake and directly releasing

86
Q

Effects of stimulant use

Short term:

A

Cocaine use can cause increased energy and
alertness, euphoria, increased body
temperature, increased heart rate and blood
pressure, agitation, paranoia, suppressed
appetite, muscle spasticity, stroke, fainting,
and overdose.

87
Q

Cocaine An overdose

A

can involve a seizure, heart failure, and respiratory suppression.

88
Q

Effects of Stimulant Use

Long term:

A

Longer term effects of cocaine use are sleep
disturbance, weight loss, tolerance, depression,
cardio vascular problems, nasal damage (through
snorting), throat and bronchial damage (through crack
smoking), headaches, hallucinations, seizure,
attention and memory disruption, and low birth weight
of children born to mothers who use cocaine during
pregnancy

89
Q

Treatment stimulants

A
Non pharmacological treatment:
Contingency management: voucher based
Psychotherapies:
CBT
Motivational interviewing
Pharmacological treatment:
None proven effective
90
Q

Sedative –,hypnotic –, or anxiolytic related disorders

A

Sedative –, hypnotic –, or anxiolytic use disorder
Sedative –, hypnotic –, or anxiolytic intoxication
Sedative –, hypnotic –, or anxiolytic withdrawal

91
Q

Types of Sedative –, hypnotic –, or anxiolytics

A

Benzos, barbiturates, non benzo sleep rx

92
Q

Benzodiazepines (BZD):

mechanism of action

A
Enhance GABA activity
GABA is the major inhibitory neurotransmitter of the
CNS, it decreases neuronal excitation
GABA A : depressant effect
Benzodiazepine ( Bz ) receptors
Bz 1 : Sleep inducing effect
Site of action of zolpidem
Bz 2 and Bz 3 : antiseizure , antianxiety and muscle
relaxation effects
93
Q

Sedatives and Tranquilizers use disorder prevalence

A

Prevalence:
12 17 year olds: 0.3%
18+: 0.2%

94
Q

Effects of Sedative and Tranquilizer Use

Short term:

A

These medications increase the activity of the neurotransmitter gamma aminobutyric acid (GABA), which causes a decrease in brain activity.
Low to moderate doses of sedatives and tranquilizers can relieve mild to moderate anxiety and have a calming and relaxing effect.
Higher doses of these medications can relieve insomnia and severe states of emotional distress, and result in drowsiness and impaired coordination.
Other short term effects of sedatives and tranquilizers include dilated pupils, slurred speech, irregular breathing, decreased heart rate and blood pressure, loss of inhibition, and impaired judgment, learning, and memory.
These medications can also cause side effects such as confusion, disorientation, amnesia, depression and dizziness.

95
Q

Effects of Sedative and Tranquilizer Use Long term

A

term: The long term effects of sedatives and
tranquilizers can include chronic fatigue, vision
problems, mood swings, aggressive behaviour,
slowed reflexes, breathing problems, death due to
respiratory depression, liver damage, sleep
problems, and sexual dysfunction.
These drugs also have the potential for addiction
and this risk is amplified when they are misused.

96
Q

Benzodiazepine withdrawal

A
Symptoms are likely to include
Headaches and anxiety 
Insomnia 
Tremors 
Fatigue 
Perceptual changes
Tinnitus
Sweating
Decrease concentration
Abrupt abstinence after higher doses could cause
delirium and seizures
Irritability
97
Q

Benzodiazepine withdrawal SIGNS / COMPLICATIONS

A
Autonomic hyperactivity
(diaphoresis, tremor, tachycardia, HTN)
Hyperreflexia,
Mydriasis
Seizures, Arrythmias
Psychosis, Delirium
Suicidal Ideation
98
Q

Sedative and Tranquilizer Treatment

A

Pharmacological management
Medication tapering
Switching to long acting benzodiazepine

Non Pharmacological management
Peer support
Individual or group psychotherapy
CBT
Motivational interviewing
99
Q

???? withdrawal are potentially deadly.

A

Alcohol and benzodiazepine