Objectives

ILLICIT DRUGS

Review the history of common illicit drugs

Explain the effects of illicit drugs such as:

HNB3205 Nursing Specific Populations

Monika Taylor

Heroin History

Opioids
Psychostimulants
CNS Depressants
Cannabis

Outline the principles of nursing management

Briefly discuss harm minimization strategies

Opioids

1853 First synthesized from

morphine at St Marys Hospital
London
1898 Bayer exports heroin to
23 countries
It was noticed that people were
consuming large amounts via
cough medicines
1911 Heroin identified as
addictive
1913 Bayer ceases production
1924 USA bans production

Heroin is a semisynthetic drug

derived from the opium poppy
papever somniferum
Natural products morphine &
codeine
Morphine converted to heroin
~20 opioid substances including
endogenous endorphins peptides
Major effects of opioids on CNS &
neural plexuses of GIT

Opioids

Heroin 10 x more potent than morphine due to high lipid

solubility
In brain heroin rapidly converted to 6-mono-acetylmorphine which binds as an agonist to receptors
Morphine (IV) half life is 2.5-3 hours
Methadone (oral) has slow & erratic absorption, peaking
several hours later
Morphine metabolized in liver, small amount of heroin is
excreted in urine unchanged

Effects of Opioids

Analgesia
Drowsiness, mood changes
Respiratory & cough suppression
Pupillary constriction
Slow & slurred speech
Constipation, decreased GIT motility
Peripheral arterial & venous dilation
Stimulates histamine release itchy nose, skin & eyes

Opioids

Routes

IV, oral, IM, SC & intranasal

Oral route not popular as need large doses and no
rush

Long term IV use causes sclerosed vessels,

infections & cellulitis

Effects of Opioids

Soon after injection

Kick or turning in stomach

Heaviness in extremities
Tingling & warmth
Sense of sublime contentment, tranquility & freedom
from worry & anxiety
Mental function is clouded
High doses, people nod off for short periods of time
Can have nausea & vomiting

Effects of Opioids

Most opioids are depressants thus with high

doses suppress respiratory centers in brain stem
Tolerance is rapidly obtained
Deaths usually result when opioids are combined
with other drugs or uncut heroin is used

Complications

Withdrawal

Within a few hours, peak between 24-48 hours and last 1

week
Some may have withdrawal for several months
S & S none are life threatening

Restlessness, muscle & bone pain

Insomnia
Abdominal cramps, vomiting, diarrhoea
Lacrimation, sweating
Anxiety

Scarred, sclerosed & collapsed veins

Bacterial infections
Blood born diseases hepatitis, HIV
Endocarditis, Valvular disease
Soft tissue abscesses
Airway obstruction, aspiration pneumonia
Compartment syndrome or rhabdomyolysis

Management of OD

ABCDE
Naloxone short-acting opioid antagonist
No evidence that naloxone alone reduces mortality
Route IN, IV, IM, SC or ET
Isolated cases of respiratory arrest post administration in
deeply comatosed patients
Dose 0.4 2.0 mg IN, IV or IM in adults
0.01 mg/kg in neonates or child
Can try small incremental doses of 0.1 mg to prevent
abrupt emergence
Half life of narcan ~ 1 hour

Management of OD

Should be observed in ED for ~ 6 hours although

no consensus on minimum time
Opportunity for preventative interventions

Mortality ~ 20% in addicts

No specific antidotes
Treatment is largely symptomatic
Treat and support body systems

ABCDE
Oxygenation and ventilation
Cooling for malignant hyperthermia
Sedation for hyperactivity
Benzodiazepines first line therapy in mild cases of serotonin
syndrome
Fluid resuscitation
Correction of electrolytes and acid base disturbance
Surgery for haemorrhage

Amphetamine types natural or synthetic

Harm prevention strategies

Assistance with withdrawal
Psychological counseling
Social services

Treatment for
Psychostimulants

Psychostimulants

Amphetamine
Dexamphetamine or speed, crystal meth or ice
Methylenedioxy-methamphetamine (MDMA) or
ecstasy
Paramethoxyamphetamine (PMA)
Methylenedioxy-amphetamine (MDA)

Cocaine

Methamphetamine

Amphetamine
derivative
Also known as

Speed
Meth
Crystal
Crank
Tina
Ice (4-methyl-aminorex)

Key points

The use in Australia is increasing.

Ambulance responses and transfer to emergency
departments following overdose is increasing.
Psychostimulant toxicity has been recognized among
both nave and regular users and represents a
medical emergency when severe.
Medical management of some common medical
conditions often differs in the presence of
psychostimulants.

Methamphetamine

Can be taken orally, snorted, smoked or injected

Onset immediate with IV, 30-40 oral
Duration ~4-8 hrs, Half life 4-6 hrs
Drug testing

Urine up to 1-3 days

Blood up to 1-3 days
Hair up to 90 days

Dose

Depends on frequency of use and tolerance.

In pure form ~50 milligrams can be fatal for a non-user

Effects

Similar to cocaine
Euphoria
Hyperexcitability, Extreme nervousness
Tachycardia, Vasoconstriction
Sweating, dizziness
Restlessness, insomnia
Tooth grinding, incessant talking
Bronchodilation
Pupil dilation
Some evidence can improve mental capacity

Serotonin Syndrome

Cognitive effects: headache, agitation, hypomania,

mental confusion, hallucinations, coma
Autonomic effects: shivering, sweating,
hyperthermia, vasoconstriction, tachycardia, nausea,
diarrhoea.
Somatic effects: myoclonus (muscle twitching),
hyperreflexia (manifested by clonus), tremor.
Vigorous dancing at high temperatures can lead to
muscle breakdown - rhabdomyolysis

Hyperthermia

Serotonin Syndrome
Management

Temp >39.5OC

Rapid external cooling, paralysis, intubation and

deep intravenous sedation
Monitor temperature closely
Assess for rhabdomyolysis and electrolyte
problems, hydrate adequately.

Airway management, adequate oxygen, IV fluids, control

seizures initially with benzodiazepines,
Avoid aspirin if cerebral haemorrhage is suspected,
Head CT early and attention to general supportive care,
corticosteroids may be harmful.

Hyponatraemia

Control muscle rigidity & agitation & seizures

Benzodiazepine first line therapy
Cerebrovascular Management

Increased serum osmolality causes antidiuretic hormone

(ADH) release. ADH secretion fails to turn off
Resulting in Syndrome of inappropriate ADH release
(SIADH)

Leads to impaired water excretion water intoxication

Hyponatraemia is a result of excess water rather than low
sodium

However, some may have blunted thirst sensation

Can lead to seizure and death
Assess total body water, fluid restrict if mild. Hypertonic
saline if severe.
Check blood sugar and potassium. Supportive care.

Cardiovascular Management

ECG, electrolytes, glucose, renal function,

creatinine, avoid beta-blockers,
sublingual nitroglycerine for chest pain in
combination with benzodiazepines.
Avoid aspirin if uncontrolled hypertension.

Ecstasy
Chemical name

3,4 methylenedioxymethamphetamine (MDMA)

Related to amphetamines
Combines effects of speed and acid

Other names

E, XTC, Eccy

Adam, Eve, love drug, party drug

Ecstasy

Ecstasy

History

Availability

1914: synthesized, patented as an appetite

suppressant
1950s: experimental military brainwashing drug
1970s: psychotherapy drug, used to heighten
introspection
1980s: growing house party and underground club
subculture

Tablets are most common and contain 50-100mg

of MDMA at $20-50
Can be injected, inhaled or taken rectally
Often engraved with a dove, elephant, bugs
bunny, Ferrari or E, XTC, E, X
Produced in illicit and often clandestine
laboratories with poor quality control

Pharmacokinetics
Oral intake

Initial effects usually 20-40 minutes

Initial rush is followed by plateau phase with
peak effects at 90 minutes and may persist for 48 hours
May take multiple doses stacking
Action duration 8-24 hours with a half life of 1234 hours
Metabolised by liver with renal excretion

Pathophysiology
Similar effects to methamphetamine

Hyperthermia
CVS disturbances

Hypertension surges, Tachycardia, Arrhythmias

Hyperactivity
Neurological effects dilated pupils, IC bleeding
Bruxism (teeth grinding) & trismus (jaw
grinding/clenching) is common

Pathophysiology

Common effects

empathy, euphoria
lack of inhibition, increased sensuality, erectional
dysfunction
deep insight, panic attacks

Rare effects: auditory & visual hallucinations

As the high wanes feelings of depression, fatigue
& irritability known as Tuesday Blues

Emergency Management

Supportive management as no specific antidote

Urine drug screens positive only with very large
doses
No specific serum test exists however drug wipe
has been developed for testing sweat

Emergency Management
Acute panic

reassuring environment
oral benzodiazepine

Severe agitation

History

Aggressive cooling for malignant hyperthermia

Sedation for hyperactivity
Chlorpromazine to block serotonin syndrome
Avoid beta blockers with tachycardia as potential
for unopposed alpha effects
Dantrolene for hyperthermia

DRABCD
IV diazepam or clonazepam

Cocaine

electrolyte management

Seizure

Emergency Management

Personal use dates back as far as 3000 BC

Peruvian Indians known to chew the coco leaves as it reduces
fatigue, increases stamina and reduces hunger
1500s Europe
1850 coca tinctures used in throat surgery
1863 coca extract in Bordeaux wine called Vin Mariani
1884 Fraud recommends use of cocaine for a variety of
conditions including morphine addiction
1886 Coca-Cola contained cocaine laced syrup & caffeine
1901 Cocaine removed from Coca-Cola
1970 Control Substance Act schedule II drug

Cocaine
History

Sigmund Freud was frequent user

William Halsted (1884) who first documented
cocaines local analgesic properties also became
temporarily addicted to it
1880s Coca Cola also had enough cocaine in it to
provide a noticeable euphoria

Cocaine

Is an alkaloid extracted from the erythroxylon

(coco) plant that grows in South America
Cocaine hydrochloride is made from dissolving
cocaine alkaloid in hydrochloric acid to produce a
water-soluble salt that can be dissolved in water
& injected, inhaled or snorted through the nasal
mucosa

Cocaine: Crack

Crack cocaine is made

from dissolving
cocaine hydrochloride
in water, mixing with
baking it

The base precipitates

into a soft mass that
hardens then cools and
makes a cracking
sound when smoked
Results in 6-8 second of
euphoria followed by an
intense craving for more
cocaine
www.crackaddiction.org/Crack_Cocaine_Paraphernalia.htm

Cocaine

Nasal inhalation euphoric effects can last up to 6 hours

Plasma half life of cocaine is 30-120 mins
80% is metabolized into 2 metabolites which have life
4-7 hours
These substances can be detected in the urine for up to
6-14 days
Often taken with alcohol to lengthen effect as liver
converts cocaine into cocaethylene which has similar
effects

Physiological effects

Stimulant with complex actions on the peripheral

nervous system, nerve conduction and CNS resulting
in accumulation of catecholamines increasing cell
receptor stimulation

Sustained stimulation of dopamine receptors causing

intense euphoria
Heightened energy levels, increased self-confidence,
enhanced alertness
Suppression of fear and panic

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Physiological Effects

Repeated use, dopamine stores become depleted

causing extreme exhaustion and need for sleep
Chronic users develop tolerance to the drug requiring
larger doses to achieve the same effects
Acts as local anaesthetic by competitively blocking fast
sodium channels and impeding nerve impulses
In high concentrations acts as an anticholinergic excess
secretion of gastric hydrochloric acid thus ulcers &
perforation

Physiological effects
CNS

Physiological Effects

Gastric

Constricts mesenteric
vessels causing
oedema, ulceration,
perforation, ischaemia
and necrosis
High doses acts as
anticholinergic causing
excessive hydrochloric
acid production

Renal

Acute rhabdomyolysis
renal failure
Renal infarction
Glomerulosclerosis

Cardiovascular

Cerebral ischaemia or
hemorrhagic stroke
Cerebral vasculitis, &
movement disorder
Cerebral emboli originating
from heart during cocaine
induced AMI
Disruption of cerebral
autoregulation cerebral
dilation & increased blood flow
vascular rupture
Seizures (10%) usually within
90 minutes of use

VF
Dramatic increase in BP, heart
rate
Peripheral vasoconstriction
Impairs cardiac electrical
activity arrthymias
Cardiac ischaemia, AMI
Cardiomyopathy
Myocarditis, endocarditis
Aortic rupture & cardiac
standstill

Physiological Effects

Psychological

Chronic use can produce variable effects

Anxiety, depression, panic attacks

Paranoia, feelings of hopelessness
Suicidal ideation, suicide attempts - some are successful
Psychological effects can persist even after stopped using

One theory is that some cocaine users have underlying

psychological problems such as PD, bipolar disorders
or schizophrenia

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GHB

Is a CNS depressant
Chemical name

Gamma-hydroxybutic
acid (GHB)
Neurotransmitter

Other names

gamma G
scoop, grievous bodily
harm
liquid E, liquid X, G, F
fantasy

GHB
History

1960: synthesized as an anaesthetic with capacity to

rapidly induce deep coma
1980: used as a fat burner and growth hormone
promoted by dieters and body builders
Also used as hallucinogenic, euphoric and sleep aid

GHB

Pharmacokinetics

Availability

Oral intake

Powder or liquid form

Small plastic bottle with 10 hits $20-100
Prevalent at rave and dance parties
Mixed with rohypnol as date rape drug
Still used as anaesthetic and addiction therapy
drug in Europe

Rapidly absorbed
Maximal plasma concentration in 20-30 minutes,
dose dependent
Clinical effects evident in 5-15 minutes
Half-life = 30 minutes, dose dependent
Eliminated via expired CO2

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GHB

Naturally found in the CNS

Toxicity hallmark is CNS depression

short term amnesia and hypotonia

respiratory depression and agitation
drowsiness and sleep
profound hypnosis and coma

Pathophysiology
Neurologic effects

Emergency Management
Severe agitation

reassuring environment
electrolytes

Coma

airway protection
O2 therapy and ventilatory support
IV therapy

inhibits noradrenaline
release
low doses inhibit
dopamine release
high doses mediate
dopamine release
produces increase in
growth hormone
mediates release of
endorphins

Cardiovascular

Bradycardia, decreased
SVR and hypotension
Studies have shown
tissue protective effects
from reducing oxygen
requirements and
unknown mechanisms

Marijuana (Cannabis)

Used for thousands of years 4000BC

Produced from hemp plant
Marijuana dried from leaves, flowers, stems & seeds
Hashish more concentrated form concentrated
extract, oils 5 x more potent
Estimated that 200-300 million people use marijuana in
some form
Evidence of increasing use at a younger age
Cigarette smokers are twice as likely to use marijuana

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Pharmacokinetics

Main substance is Delta 9 terahydrocannabinol (THC)

THC binds to protein receptors in certain nerve cells
leading to a series of cellular reactions
Alters the sensory information processed by the
hippocampus part of the brains limbic system that is
crucial for memory, emotions and motivations
High lipid solubility thus readily binds to surfactant lining
of lungs
Oral ingestion results in variable absorption rates but
effects last longer

Behavioral Effects
Within a few minutes of inhalation

Behavioral Effects

Some may feel

Anger, depression, anxiety or a sense of great

personal misfortune
Paranoia & panic reactions may occur with large doses
Evidence to suggest how you react is hereditary

Feel relaxed & tranquil

Increased awareness of surroundings
Perception of increased auditory and visual acuity
Time is distorted
Insight into life & life issues seem enhanced
Things seem funny, laughter comes easily
Alters learned behaviors problems with memory &
learning
Loss of coordination

Physiological Effects

Increased heart rate

Increased peripheral blood flow
Bronchodilation
Reddened conjunctiva
May have muscle weakness, tremors,
unsteadiness
Chronic users develop similar respiratory
ailments as tobacco smokers

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Therapeutic Uses

Lowers intra-ocular pressures glaucoma

Effective anti-emetic properties cancer
chemotherapy
Analgesic properties muscle spasm
Appetite stimulant - anorexics

Long Term Use

Impaired cognitive skills remain with heavy use after 3 days

(or 4 weeks in some studies) of stopping
Increased risk of AIDS mortality in males
No evidence as yet that this impairment is permanent
Some well documented cases of pneumomediastinum due to
valsalva maneuvers (expiration through resistance)
Social and economic consequences of long term heavy users

Harm Minimisation

Principles

Reducing the risk of an individual engaging in

substance misuse

Reducing supply
Reducing demand

Reducing the harm associated with substance abuse

Lower education
Less income
More unemployment
Increased incidence of accidents

Bibliography
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Crespigny, C., & Farquhar, S. (2007), Alcohol and other drug use,
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Kelly, L. Murray, A. Brown & J. Heyworth (eds.), Textbook of
adult emergency medicine (2nd Ed.), Churchill Livingstone,
Sydney.
Hahn, IH. (2015). MDMA toxicity.
http://emedicine.medscape.com/article/821572-overview.
Hansen, K. & Prybys, K. (2004), Hallucinogens. In J. Tintinalli, G.
Kelen & S. Stapczynski (eds.), Emergency medicine. A
comprehensive study guide, pp.1079-1084. McGraw-Hill, New
York

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Jenner, L., Spain, D., Whyte, I., Baker, a., Carr, V.J., Crilly, J.
(2006). Management of patients with psychostimulant
toxicity: Guidelines for Emergency Departments.
Canberra: Australian Government Department of
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Stone, T. & Taylor, A. (2011), Nursing care of clients with
problems of substance abuse, In Le Mone et al,
Medical-surgical nursing: critical thinking in client care,
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