MODIFIABLE RISK FACTORS:

NON-MODIFIABLE RISK FACTORS:

Psychological: Age: (18-44 y/o)
00  History of psychiatric disorders (such as AMPHETAMINE USE Gender: Male
ADHD, schizophrenia, anxiety, PTSD and Race/Ethnicity: Non-hispanic white
depression) Family History of Psychiatric disorders (Substance
 Academic stress Abuse Disorder, etc)
 Stressful lifestyle
 prior substance abuse to other drugs
 Poor coping mechanism
Physical:
Enters the presynaptic axon terminal
 Obesity (Diffusion/Uptake)
Biological:
 Sexual interest
 Having homosexual/bisexual lifestyle
Environmental:
 Early exposure to amphetamines
 Easy access to amphetamine
 Unstable home life during childhood Inhibition of VMAT2 Dysruption of the Inhibits MAO Stimulates TAAR1
 Living/Growing up in a socio-economically (Vesicular monoamine electrochemical gradients
disadvantaged community transporter 2)
Social:
 Association to Amphetamine abusers
 Deviant peer relationships Inhibits metabolism Induces transporter
 Popularity
of MAN reversal of DAT
 Association with gangs
 Social exclusion and marginalization
Familial:
 Socio-economic status (unemployment, Increased efflux of
poverty) dopamine into the
 Child maltreatment (neglect, physical, Increase in monoamine  Increased stimulation synaptic cleft
emotional and sexual abuse) neurotransmitters with decreased
 Parental or familial substance abuse lethargy

 Marital status of parents

 Level of parental education (Lack of Inhibits reuptake of
environmental involvement, lack of future Enhancing the release of certain
goals)
catecholamines neurotransmitter
 Parent-child relationships (poor support
system)
 Child perception that parents approve
substance abuse
 Death of family member Release of Increased
Stimulation
of CNS glutamate neurotransmission

Pleasurable effects
Affects peripheral
receptors
 Euphoria
 Increased alertness Increased in DA Increased in 5- Increased in NE
 Wakefulness level HT level level
 Increased
locomotor activity Anticholinergic activity
 Loss of appetite against M3 muscarinic
receptor Induces positive Activation of
mood
sympathetic
Decreased salivation nervous system

Violence and
aggression

Dry mouth
 s/sx:
 Euphoria
 Increase in alertness
 Agitation
Fight or flight response
 Feelings of well-being
 grandiosity
Stimulation of the mesolimbic
 chest pain
dopaminergic system  palpitations
 Elevated blood pressure
 Tachycardia
Enhancing amphetamine-  Diarrhea
rewarding effects  Dilated pupils (Mydriasis)
 Diaphoresis

 Taking amphetamine in higher or frequent doses

Changes in reward circuit  Unable to control use
 Spending a lot of time using the drug
process  Strong urges to use stimulants
s/sx:
 Continued used despite having social or relationship
problems
 Hyperthermia
 Giving up social, occupational or recreational activities  Psychosis (Belligirent and
Drug craving  Using substance in situations where it is physically aggressive)
dangerous to do so (intake of alcohol when under  Euphoria
influence of amphetamine)  Movement disorders
 Continuing to use stimulants even though you have
(dyskinesia, dystonia, tics,
developed a psychological or physical problem that is
Frequent use of stiffness, tremor, etc.)
probably caused by the drug.
amphetamine  Experiencing tolerance (needing more amphetamine to  Tachycardia
achieve previous effects)  Hypertension
 Withdrawal  Increased respiratory rate
 Formication
 Increased sex drive
Addiction
 Difficult micturition (urinary
retention)
 Agitation

Decrease levels of antioxidants Serotonin terminal Excessive GLU release Depletion of DA Increase DA
in DAergic and/or 5-HTergic depletion in the striatum levels
terminals
Increase in cellular calcium Increases the
s/sx:
increase serotonin levels release of
Disruption of vesicular proton level  Anxiety and depression
acetylcholine
gradient and vesicular  Increased concentration
monoamine transporter
Activation of a variety of
function
calcium-dependent enzymes
Overproduction of
serotonin level

Overproduction of toxic Generation of free radicals and

metabolites metabolites of DA nitric oxide (NO)
oxidation, including free radicals Affects
and quinones. hypothalamus
Activation of apoptopic
pathways

Hyperthermia
Nausea and vomiting
 s/sx
 Memory loss
Oxidative stress Failure of cellular organelles
 Decreased
(mitochondria and endoplasmic
learning ability
reticulum)
Increase in intracellular DA
levels
Impairs memory ability
Breakdown of cytoskeletal
proteins

Destruction of dopaminergic
terminals
DNA damage

Seizure, dizziness Neuronal cell death

AMPHETAMINE INTOXICATION

Enhance ROS production

Induce polymerization of LEGEND:

proteins

Disease processs
Migration of
Regular
inflammatory cells Disruption of BBB barrier
infections Symptoms
(monocytes)

Symptoms present in the client

Irreversible damage to the brain
Stroke

Death/Loss of
consciousness