AMPHETAMINE USE

MODIFIABLE RISK FACTORS:

Psychological:
 History of psychiatric disorders (such as NON-MODIFIABLE RISK FACTORS:
ADHD, schizophrenia, anxiety, PTSD and Age: (18-44 y/o)
depression)
Enters the presynaptic axon terminal Gender: Male
 Academic stress Race/Ethnicity: Non-hispanic white
 Stressful lifestyle (Diffusion/Uptake)
vc  prior substance abuse
Family History of Psychiatric disorders
(Substance Abuse Disorder, etc)
 Poor coping mechanism
Physical:
 Obesity
Biological:
 Sexual interest Inhibits MAO Stimulates TAAR1
Inhibition of VMAT2 Dysruption of the
 Having homosexual/bisexual lifestyle
Environmental: (Vesicular monoamine electrochemical gradients
 Early exposure to amphetamines transporter 2)
 Easy access to amphetamine
 Unstable home life during childhood
Inhibits metabolism of Induces transporter
 Living/Growing up in a socio-economically
disadvantaged community MAN reversal of DAT
Social:
 Association to Amphetamine abusers
 Deviant peer relationships
 Popularity  Increased stimulation Increased efflux of
 Association with gangs Increase in monoamine with decreased dopamine into the
 Social exclusion and marginalization neurotransmitters lethargy synaptic cleft
Familial:
 Socio-economic status (unemployment,
poverty) Enhancing the release of
Pleasurable effects
 Child maltreatment (neglect, physical, catecholamines
emotional and sexual abuse)  Euphoria Inhibits reuptake of
 Parental or familial substance abuse  Increased alertness certain neurotransmitter
Stimulation of
 Marital status of parents  Wakefulness CNS/PNS Increased neurotransmission of
 Level of parental education (Lack of  Increased
environmental involvement, lack of future locomotor activity DA, 5-HT, histamine and NE
goals)  Loss of appetite Affects peripheral
 Parent-child relationships (poor support receptors
system)
 Child perception that parents approve Activation of sympathetic
substance abuse Anticholinergic activity
 Death of family member against M3 muscarinic nervous system
receptor s/sx:
 Euphoria
drymouth/decreased  Increase in alertness
salivation, tooth damage Fight or flight response  Agitation
 Feelings of well-being
 grandiosity
Stimulation of the mesolimbic  chest pain
Increase in dopamine and Heart attack
dopaminergic system  palpitations
norepinephrine levels Arrhythmias
 Elevated blood pressure
 Tachycardia
 Diarrhea
Enhancing amphetamine-  Dilated pupils (Mydriasis)
rewarding effects  Diaphoresis
 Changes in reward circuit  Taking amphetamine in higher or frequent doses s/sx:
 Unable to control use  Hyperthermia
process
 Spending a lot of time using the drug  Psychosis
 Strong urges to use stimulants
 Euphoria
 Continued used despite having social or relationship
Elevated levels of chemicals problems  Movement disorders
Loss of appetite (dyskinesia, dystonia, tics,
connected with reward & Drug craving  Giving up social, occupational or recreational activities
Weight loss & Muscle  Using substance in situations where it is physically stiffness, tremor, etc.)
feeling good (dopamine)
wasting, malnutrition dangerous to do so (intake of alcohol when under  Tachycardia
influence of amphetamine)  Hypertension
 Continuing to use stimulants even though you have
 Increased respiratory rate
developed a psychological or physical problem that is
Addiction (High  Formication
probably caused by the drug.
dosage/Frequent use)
 Experiencing tolerance (needing more amphetamine to  Increased sex drive
achieve previous effects)  Difficult micturition (urinary
 Withdrawal retention)

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

Hyperthermia
Nausea and vomiting
Generation of free radicals and
Overproduction of toxic nitric oxide (NO)
metabolites metabolites of DA
oxidation, including free radicals
and quinones. Activation of apoptopic
s/sx pathways
 Memory loss
Oxidative stress  Decreased
learning ability Failure of cellular organelles
(mitochondria and endoplasmic
reticulum)
Increase in intracellular DA
levels Impairs memory ability
Breakdown of cytoskeletal
proteins

Destruction of dopaminergic
terminals
DNA damage

Seizure, dizziness Neuronal Cell Death

Excitotoxicity
 AMPHETAMINE TOXICITY

Enhance ROS production

Induce polymerization of
proteins

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

Irreversible damage to the brain

Stroke

Death/Loss of
consciousness