mod 2 - drug misuse & addiction Flashcards
(81 cards)
1
Q
definition of S U D
A
substance use disorder
2
Q
SUD diagnoses criteria (5)
A
- social impairments
- one fails to fulfill major roles (ex. school) - misuse/risky use
- one uses substance in hazardous situations - addiction/impaired control
- persistent craving for the substance - withdrawal
- withdrawal syndrome after stopping use of the substance - tolerance
- develop tolerance
3
Q
addiction
A
state in which stopping or reducing the dose of a given drug produces non-physical symptoms
- can also happen to gambling, shopping, etc…
4
Q
what is the predominant hypothesis in explaining addiction
A
the dopamine hypothesis
5
Q
what does the dopamine hypothesis entail (2)
A
- dopamine increase
- commonly misused drugs increase dopamine in brain’s reward systems - limbic system - effects on rewards system
- dopaminergic systems responsible for natural rewards (ex. food, sex, video games, gambling)
- ex. cocaine causes increase in dopamine, altering brain communication
6
Q
characteristics of addictive drugs
A
- increases dopamine in brain reward systems
- produce novelty (new feelings) in the person taking the drug
- reduce anxiety
7
Q
drugs that increase dopamine
A
CNS stimulants
- cocaine
- amphetamines
- nicotine
- caffeine
opiods
- morphine
-heroine
- oxycodone
other drugs
- alcohol
- cannabis
8
Q
drugs that produce novelty
A
- LSD
- Ecstacy
9
Q
drugs that reduce anxiety
A
- benzodiazepines
- barbiturates
10
Q
drug withdrawal
A
- severity increases with the speed of drug withdrawal
- fear of withdrawal contributes to drug-taking behaviour
11
Q
stimulant drug withdrawal symptoms
A
stimulants: cocain + amphetamines
w/d symptoms:
- sleepiness
- muscle pain
- anxiety
- tremors
- low mood
- suicidal ideals
- cardiovascular problems
12
Q
opiod drug withdrawal symptoms
A
drugs: heroine, morphine, oxycodone, pain meds
drug withdrawal symptoms:
- sweat
- muscle ache
- agitation
- diarrhea
- ab cramps
- vomiting
13
Q
how would a dose-response curve change after drug tolerance is developed
A
shifts to the right (same efficacy, inc in potency)
14
Q
drug tolerance
A
- specific per drug
- reversible upon cessation
15
Q
cross tolerance
A
- occurs b/w pharmacologically similar drugs
- resistance to one drug due to tolerance to a similar-acting drug
16
Q
genetic influence in SUD
A
- make someone more vulnerable to sud
- ex. genetic mutation in dopaminergic pathways
17
Q
pre-existing disorders influence in sud
A
- major affective disorder, anxiety, or schizo are higher risk for sud
18
Q
environmental influence in SUD
A
- exposure to environemnts that promote drug use
- family
- trauma
- etc…
19
Q
developmental influence in SUD
A
- vulnerable at certain time frames of life
- smoking usually begins before 18
- most alcohol sud begin using before 30
- illicit drug use, usually b/w 15-18
20
Q
harm reduction
A
- reduce health and social harms associated with addiction and substance use
- ex. nicotine patch instead of smoking
- ex. wearing a seatbelt while driving
21
Q
health harms
A
- goal: decrease morbidity and mortality
22
Q
societal harms
A
- goal: decrease lost productivty, apprehension of children, criminal activity
23
Q
prescription vs misuse
A
- prescribing drugs will inherently also cause withdrawal – not misuse
- misuse occurs when one meets other criteria for SUD (craving, etc..)
- prescriptions can lead to SUD or while (using it in ways other than what was prescribed or against social norms)
24
Q
assessing the potential for misuse (5)
A
- nature of the drug
- route of administration
- amount/freq of use
- availability
- inherent harmfulness
25
nature of the drug
- drugs usually are natural reinforcers (like food and sex)
- pleasurable effects of the drug increases probability of being taken again
- ex. heroin produce intense pleasure, high intrinsic mis use
26
route of administration
- drugs that can be administered that give rapid absorption (rapid effects) have greater misuse potential
- ex. sniffing, intravenous, inhaling
27
amount/freq of use
- greater dose and freq of use leads to greater potential for tolerance, withdrawal, and addiction --> misuse
- ex. occasional drinking will barely lead to tolerance, withdrawal and addiction
28
drug availability
- more widespread, easier misuse
- ex. alcohol easy
29
inherent harmfulness
- potential of drug to cause harm (is it a serious risk to life)
- ex. methanol is widely available but can cause blindness and death -- not commonly misused
30
drug classes and their abilities to cause tolerance, withdrawal and addiction
| opiods, cns stim/dep, hallucinogens, cannabis
1. opiods: t, w, a
2. cns depressants: t, w, a
3. cns stimulants: t, w, a
4. hallucinogens: t, a (no withdrawal)
5. cannabis: t, w, a
31
misuse vs withdrawal
misuse: using drug in ways or amounts other than prescirbed or against social norms
withdrawal: sumpyoms opposite to primary effect
32
amphetamine related compounds
- methylphenidate (ritalin): treat ADHD
- MDMA (ecstacy): often isused, fosters feelings of intimacy and empathy and improves intellectual capbilities
amphetamines are CNS stimulants
33
chemistry of amphetamines
| which neurotransmitters are they similar to
- synthetic organic
- similar to endogenous neurotransmitters: norepinephrine and dopamine
- side products (unreacted chemicals during manufacturing) can be dangerous -- ex. baking soda
34
process of amphetamines
- they are substrates for the dopamine transporter making them a competitive inhibitor with dopamine (taken from synaptic cleft back to presynaptic nerve)
- results in amphetamines in the presynaptic nerve and blocks the vesicular monoamine transporter (VMAT) (blocking the ability to bring dopamine into vesicles to be released)
- dopamine is blocked from exiting and a large inc of free dopamine happens in the neuron --> forcing dopamine to travel through the dopamine transporter in the reverse direction (back out into the synaptic cleft)
- result: inc of dopamine in synaptic cleft = inc in CNS excitation
35
effects of amphetamines in CNS (4)
1. decreased threshold for transmitting sensory input to the cerebral cortex = CNS excitation
2. feeling of euphoria and reward
3. modification of temperature and feeding leading to smaller appetite
4. inc in aggressive behaviour and mood swings
36
other effects of amphetamines
short term
- chest pain or heart attack
- cardiovascular collapse
- inc respiratory rate
- overdose: seizure, high fever, stroke
long term
- chronic sleeping problems
- poor appetite
- anxiety, repetitive behaviour, aggression
- elevated blood pressure
- abnormal cardiac rhythm
37
amphetamines and other drugs
- using other drugs to suppress amphetamine effects
- ex. using benzos to help combat sleep issues
- ex. someone sleepy may use amphetamines to simulate
38
therapeutic use of amphetamines
1. narcolepsy - chronic sleep disorder
2. ADHD
methylphenidate (ritalin) used to treat these bc have dec incidences of cardiovascular and appetite adverse effects
39
amphetamines potential for misuse
- extremely high
- powerful euphoria
- water soluble = easily injectable
- inherent harm = not high enough to cause deterrents to misuse
40
amphetamines potential for SUD
tolerance: yes to some effects
- develops to euphoria, mood elevating effects, anorectic, resp and cardio stimulating effects, and lethal effects
- does not develop to therapeutic effects or psychosis
withdrawal: yes
- mood depression, prolonged sleep, huge appetite, lack of energy, fatigue
addiction: yes
- self administered to produce euphoria and abrupt awakening = rewards that are craved intensely
41
pharmacology of cocaine compared to amphetamines (duration of action, routes of admin)
duration of action:
- cocaine: shorter (less than an hour)
- amphetamines is up to 12 hrs
routes of administration
- cocaine: sniffed or smoked
- amphetamines: iv
42
mechanism of action of cocaine
- dose dependent cns stimulation
1. reuptake inhibition: inhibits active re-uptake of dopamine and seratoning into presynaptic neuron (like amphetamine)
2. postsynaptic activation: inc conc of dopamine and seratonin in synaptic cleft and inc activation of postsynaptic neuron's receptors
43
therapeutic uses of cocaine
- local anesthetic for mouth and throat
- rarely used
44
long term effects of cocaine
- toxic psychosis, paranoia
- hallucinations or sensations of insects under skin
- impaired sex function
- permanent brain damage
- high bp and irregular hr
- change to nasal mucosa (sniffing)
45
cocaine potential for misuse and SUD
misuse: extremely high
- one of the highest
- powerful euphoria and rapid
- inherent harm does not deter misuse
SUD:
1. tolerance: yes to some effects
- develops to mood elevation effects
- doesn't develop to psychotic effect
- less development to hallucinatory and behavioural effects compared to amphetamines
2. withdrawal: yes
- similar to amphetamines
3. addiction: yes
- cocaine gives pleasure and rewarding feeling
- high addiction
46
what kind of drug is nicotine and caffeiene
CNS stimulant
47
social and economic debt of tobacco
- 48K Canadians die from tobacco use
- costs $16B per year in Canada
48
ADME of nicotine
| *half life?
1. absorption
- nicotine in cigarette smoke in very small particles inhaled
- rapid absorption
- absorbed by GI tract, oral mucosa, across the skin
- dose can be controlled by depth of inhalation
2. distribution
- distributed throughout the body
- rapidly gains access to the brain
3. metabolism
- rapid metabolization in the liver
4. excretion
- metabolites excreted in urine
- half life of nicotine is about 2 hours
49
nicotine mechanism of action
- nicotine stimulates nicotinic receptors at synapses (similar to a-CoA)
- activation inc psychomotor activity, cognitive function, attention and memory
- large doses: agitation, tremors, seizures
- nicotinic receptors mediate release of dopamine and seratonin
50
.therapeutic uses of nicotine
- in smoking cessation programs
- nicotine in the form of gum, transdermal patches, or buccal spray
- maintain blood nicortine levels to satisfy craving without cigarette use
51
short term effects of smoking
short term
- mild euphoria
- arousal
- concentration
- relaxation
- inc in hr and bp
- suppress appetite
52
non regular smoker effects
- dizzines
- nausea
- vomiting
-cramps
53
long term smoker effects
cardio disease:
- CVD
- carbon monoxide reduces RBC ability to carry oxygen
- inc atherosclerosis and formation of thrombi
lung disease:
- smoker's syndrome
- difficulty in breathing, wheezing, chest pain, congested lung, and inc lung infections
- emphysema
cancer
- 30% of all cancers estiamtd to be caused by cigar smoke
- lung, oral cavity, throat, bladder, and uterine cancers
54
passive smoke
- second hand smoke
- fetus from a mother smoking during pregnancy = 2-3X increase in fetus being small for gestational age or bron prematurely, low birth weight
- decreased oxygen delivery to fetus
55
nicotine potential for misuse and SUD
misuse: high
- powerful reinforcer and addictive
- cessation of smoking often fail
- great cravings
SUD
1. tolerance: yes
- keep blood levels at a 30-40ng/ml range
2. withdrawal: yes
- irritability, restlessness, anxiety, insomnia, fatigue, inability to concentrate
3. addiction: yes
56
lethal dose of caffeiene
10g of caffeine for adult
- 50 cups of mediium strength coffee
57
average cup of coffee
200mg caffeine
58
energy drink caffeine
over 300mg
59
ADME of caffeine
| when is peak?*
1. absorption
- rapid and complete
- blood levels significant at 30 min
- peak after 2 hours
2. distribution
- all parts of the body
- crosses into brain and placenta
3. metabolism
- genetic determinator for rate (some people are rapid and some are slow)
4. elimination
- half life is 2.5-10 hours
60
caffeine mechanism of action
100-250mg increase performance and motor activity
without caffeine
- adenosine receptors activate to stimulate GABAergic neurons that inhibit dopamine realease
with caffeine
- caffeine are competitive inhibitors that block adenosine receptors, releasing neurons
- decrease GABA activation and increase dopamine release
- stimulating CNS
61
short term effects of caffeine
CNS
- mood elevation
- reduce fatigue
- increase performance and flow of thought
- interfere with sleep
- high doses cause irritability and tremers
cardiovascular
- constriction of cerebral blood vessels (good for headaches)
- increases peripheral blood flow
- stimulates cardiac muscle -- inc hr
- rapid and irregular heartbeat
respiration
- inc respiration rate
- relax bronchial smooth muscle
62
caffeine in new borns
- stimulate breathing in preterm babies
- helps immature brains and lungs to remember to breathe
63
long term caffeine effects
- restlessness
- nervousness
- insomnia
- increase urinary output
- gastric upset
- rambling speech and thought
64
caffeine and smoking
- cigar smoke inc metabolism of caffeine
- duration of action of caffeine dec
65
caffeine and pregnancy
- not teratogenic (no fetal abnormalities)
- large caffeine risks stillbirth
- decrease fetal growth rate
- inc chance of miscarriage
- metabolism is slowed -- extending duration of actionc
66
caffeine potential for misuse and SUD
misuse: low
- mild reinforcer
- euphoria is mild
inherent harm: very low
SUD
1. tolerance: yes
2. withdrawal: yes
3. addiction: yes, mildly
67
summary of stimulants
amphetamines, cocaine, nicotine, caffeine
68
amphetamines in sports
- inc edurance and speed
- masks pain/fatigue
- reduce body weight
ex: reduces feelings of lactic acid in a 400m race
69
toxicity of amphetamines
- large doses can lead to fatal increases in bp
- when drug wears off someone may experience "crashes"
70
anabolic steroids in sports
- most common
- inc muscle mass and strength
- reduced androgenic effects
- inc anabolic effects
71
anabolic and androgenic effects
anabolic: inc musccle mass
androgenic: effects on secondary male characteristics
72
anabolic steroids mechanism of action
anti-catabolic response (reduces breakdown of proteins and muscle tissue)
- athletes can train and maintain muscle mass instead of using protein as fuel
anabolic
- protein production
motivation
- aggressive behaviour "roid rage"
73
effects of anabolic steroids
| low-meddose, large dose
low-med dose
- modest effects
large dose
- during peak training times for athletes in combination with diet high in protein, will yield sig inc in lean body mass, body weight, and strength
- aggressive behaviour to performance enhancement
74
toxicities of anabolic steroids
- mood swings
- acne
- cardiovascular disease: steroids inc plasma levels of LDL cholesterol and dec HDL cholesterol
- altered liver function: hepatitis, liver failure, liver cancer
- reduces testosterone: block release of gonadotropin leading to dec testosterone and sperm; cause infertility, reduced libido, impotence
---> women: produce androgenic effects like hair, low voice, enlarged clit, inc libido, and amenorrhea (absence of menstration)
75
benzodiazepines in sports
ex. lorazepam and diazepam
- treat insomnia and anxiety
- recover faster from intense training
- high doses impair motor psychomotor function and focus
76
blood doping and erythropoietin in sports
blood doping:
- reinfusion of athlete's own RBC into their circulation
- enhances oxygen carrying capacity
eryhthropoietin:
- hormone that inc RBC amount
- enhance oxygen carrying capacity
77
inappropriate use of erythropoietin or its derivatives can lead to
thrombotic events
78
detection of blood doping and erythropoietin
blood doping:
- measure the age of the RBCs
erythropoietin:
- test urine for erythropoietin recombinant
79
diuretics in sports
enhance excretion of salt and water through kidneys
- reduces body water
- allows athletes to compete at lower weight class
- hasten excretion of other banned drugs in attempt to avoid detection
80
toxicities of diuretics
- excess electrolyte
- water depletion
81
reasons to ban performance-enhancing drugs
1. athlete protection - pressure gets to them
2. unfair advantage
