Module 2 Flashcards

(189 cards)

1
Q

What is Substance Use Disorder (SUD)?

A

> defined and clinically diagnosed by a number of criteria; once an individual fits 2 criteria they are classified as having a mild SUD

> the more criteria an individual meets, the more severe the SUD

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2
Q

SUD Criteria

A
  • social impairments
    -risky use
    -impaired control
    -withdrawal
    -tolerance
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3
Q

social impairments

A
  • individual fails to fulfill major roles and/or has persistent interpersonal problems
  • Activities/roles reduced
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4
Q

risky use

A

the individual may use the substance in hazardous situations or despite problems caused by use

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5
Q

impaired control

A

the individual may have persistent craving for the substance

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6
Q

withdrawal

A

individual may experience withdrawal syndrome after stopping use

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7
Q

Tolerance

A

the individual may develop a tolerance to the substance

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8
Q

Addiction

A
  • impaired control associated with SUD manifests as emotional and mental preoccupation with the drugs effects with cravings of the drug regardless of the consequences
  • State in which stopping or abruptly reducing dose of a given drug produced non-physical symptoms
  • not only for drugs but stimuli as well (gambling, video games, shopping)
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9
Q

Dopamine

A

—> the predominant hypothesis to explain addiction:

Dopamine Increase

  • commonly misused drug increase dopamine in the reward systems of the brain
  • other neurotransmitter systems are involved in substance misuse, but the increase in dopamine appears to be a key component of the brains reward system
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10
Q

Effect on reward systems

A
  • these dopaminergic systems are also responsible for natural rewards such as food ad sex, as well as for stimulus related rewards such as gambling
  • drugs associated with addiction cause an exaggerated increase in dopamine, altering communication in the brain
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11
Q

Characteristics of Addictive Drugs

A
  1. Increase dopamine
  2. Produce novelty
  3. Reduce anxiety
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12
Q

Types of drugs that Increase Dopamine

A
  • CNS stimulants
  • Alcohol & Cannabis
  • Opioids
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13
Q

CNS Stimulants

A
  • cocaine
  • Amphetamines
  • Nicotine
  • Caffeine
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14
Q

Opioids that increase dopamine

A
  • morphine
  • Heroin
  • Oxycodone
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15
Q

Addictive drugs that produce novelty

A
  • produce a novel feeling in the person
    • Lysergic acid diethylamide (LSD)
    • Ecstasy, aka MDMA
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16
Q

Addictive drugs that reduce anxiety

A
  • reduce anxiety in the person
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17
Q

CNS depressants that reduce anxiety

A
  • Benzodiazepines
  • Barbiturates
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18
Q

Drug Withdrawal

A

an abnormal psychological state produced by repeated administration of a drug that leads to the appearance of withdrawal syndrome when drug administration is discontinues or dose decreased

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19
Q

severity of withdrawal syndrome increases with

A

the speed of drug withdrawal b/c biological processes that have accommodated to the presence of a drug do not have time to reverse themselves

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20
Q

fear of withdrawal

A

a factor that contributes to continued drug-intake

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21
Q

withdrawal symptoms are usually opposite to

A

the effects of the drug

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22
Q

Two common stimulant drugs are cocaine and amphetamines, there withdrawal symptoms include:

A
  • Sleepiness
  • muscle pain
  • anxiety
  • temors
  • low mood
  • suicidal ideations
  • cardiovascular problems
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23
Q

common opioids include heroin, morphine, and prescription pain meds like oxycodone, their withdrawal symptoms include:

A
  • sweating
    • muscle aches
    • agitation
    • diarrhea
    • abdominal cramping
    • vomiting
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24
Q

Drug tolerance

A
  • usually expressed as a shortened duration of action and a decreased magnitude of effect
  • extent and rate of development of tolerance is specific for each drug
  • tolerance does not develop to all drugs not to all aspects of drug action
  • tolerance is reversible upon drug discontinuation
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25
Cross Tolerance
- can occur b/w pharmacologically similar drugs - defined as the resistance or tolerance to one drug because of the resistance or tolerance to a pharmacologically similar drug
26
example of cross tolerance
if a person is tolerant to the CNS depressant alcohol, they will also be tolerant to the CNS depressant benzodiazepines, even if they have never taken it before
27
Factors influencing a SUD
- genetic factors - pre-existing disorders - environmental factors - Developmental factors
28
Genetic factors that influence SUD
- can predispose an individual to an SUD - ex. genetic mutations in the dopaminergic pathways in the brain, which are associated with addiction, confer as increased risk of SUD
29
Pre-existing disorders
individuals with major affective disorder (depression or bipolar), anxiety, or schizophrenia are at a higher risk for SUD than the general population
30
environemtnal factors influencing a SUD
- certain environments can increase the likelihood of drug misuse and SUD - exposure to environments that promote drug use, family dynamics, trauma, and social/work groups have been shown to alter the risk of SUD - even after taking into account genetic factors, those with spouses or siblings with an SUD are at higher risk for developing an SUD
31
Developmental Factors that influence SUD
- individuals are more vulnerable during certain developmental timeframes - adolescence and early adulthood are primarily associated with initiation of SUD
32
Stigma of SUD
- people with SUDs have been stigmatized not only by society in general, but also by medical professionals - stigmatization can lead to isolation and low self esteem - therefore individuals do not receive the medical or social help they need
33
How do we help stigma around SUDs
- help stigma by changing the language you use - instead of abuser, addict, druggie, or junkie USE: - Person with SUD - Instead of abuse USE: - Use/misuse - Instead of Clean USE: - in recovery/not currently using
34
Harm Reduction
- approach that seeks to reduce/prevent the negative consequences of substance use and improve health without judgement, coercion or discrimination and without necessarily requiring the person to stop using the substance
35
Health harm goals
- decrease morbidity - transmission of blood borne diseases, such as HIV?AIDS, hepatitis, infections - decrease mortality - from overdose and secondary to associated morbidity
36
Societal harms goals
decrease lost productivity, apprehension of children, and criminal activity
37
Prescription use vs Misuse of Substances
misuse is defined as using the drug in ways/amounts other than what was prescribed
38
Potential for Misuse of a drug:
- misuse potential refers to the tendency of a drug to be misused - varies from drug to drug and person to person
39
Misuse potential is detemined by 5 factors
- nature of drug -route of administration -amount/frequency of use -availability -inherent harmfulness
40
Misuse potential: Nature of drug
- drugs are natural reinforcers - the pleasurable effects produced by a drug increases the probability the drug will be taken again
41
Misuse potential: route of administration
drugs that can be administered by routes that give rapid absorption, and hence rapid effects, have a greater potential for misuse than drugs which produce the effect more slowly
42
Misuse potential: Amount/frequency of use
the greater the dose and frequency, the greater the potential for development of tolerance, withdrawal and addiction
43
Misuse potential: availability
- the availability of a drug in society is a major factor in determining potential for misuse - the more widespread a drug, the more likely it iwll be misused
44
Misuse potential: Inherent harmfulness
- refers to the potential of a drug to cause harm - if a drug is widely perceived to be serious risk, it will not be used even if available
45
What class of drugs does NOT produce withdrawal symptoms
hallucinogens
46
5 classes of drugs
1. Opioids 2. CNS depressants 3. CNS Stimulants 4. Hallucinogens 5. Cannabis
47
Amphetamines
- controlled substances in Canada ( use is restricted to certain medical conditions like narcolepsy) - drug class includes amphetamine, dextroamphetamine and methamphetamine
48
Amphetamine related compounds include:
- Methylphenidate (Ritalin): used to treat ADHD - MDMA (Ecstasy): derivative of methamphetamine that is often misused
49
MDMA
- fosters the feeling of intimacy and empathy while improving intellectual capabilities - neurotoxic, causing neuronal damage and death - long lasting - permanent
50
Chemistry of amphetamines
- synthetic organic compounds - structurally similar to endogenous neurotransmitters norepinephrine and dopamine - can be synthesized readily, resulting in the illicit manufacturing of these substances, especially meth. - purity of illicit substances is variable, may contain side-products and filling agents
51
Standard overall effect of amphetamines
- increase excitation by increasing dopamine or norepinephrine in the synaptic cleft -amphetamines compete with dopamine for the dopamine transporter
52
amphetamines are substrates for
dopamine transporter - this transporter clears dopamine from the synaptic cleft
53
result of amphetamines compete with dopamine for the dopamine transporter
- amphetamines end up in the presynaptic nerve - then, they block the vesicular monoamine transporter (responsible for bringing dopamine into vesicles to be packaged for release when next nerve impulse arrives)
54
Since dopamine is blocked from vesicles, there is a large increase in concentration of free dopamine in the neuron causing...
- this large [ ] forces dopamine to travel through the dopamine transporter in the reverse direction - Result: increase of dopamine in the synaptic cleft and increase in CNS excitation
55
Four main effects of amphetamines within the CNS:
1. decreased threshold for transmitting sensory input to the cerebral cortex, leading to CNS excitation 2. a feeling of euphoria and reward 3. temperature-regulation and feeding centre modifications leading to appetite suppression 4. an increase in aggressive behaviour and mood swings
56
common amphetamines differ in
magnitude of their CNS effects
57
Increased CNS excitation leads to:
increased alertness, feeling of power, reduced fatigue, increased responsiveness, heart rate and blood pressure
58
Amphetamines: Effects of (non-CNS) short term use:
- chest pain/heart attack - cardiovascular collapse (high doses) - increased respiratory rate - overdose: seizure, high fever or stroke
59
Amphetamines: Effects of (non-CNS) long term use:
- chronic sleeping problems - poor appetite - anxiety, repetitive behaviour, psychoses, aggressive behaviour - elevated BP and abnormal cardiac rhythm
60
Concurrent drug use:
- other drugs may be sought concurrently in an attempt to antagonize toxic effects of amphetamines - ex. someone on amphetamines with sleeping problems may seek a CNS depressant to help them sleep - these ca lead to SUD, misusing and drug-drug interactions
61
Therapeutic use of Amphetamines:
Narcolepsy & ADHD
62
Therapeutic use of Amphetamines: Narcolepsy
chronic sleep disorder
63
Therapeutic use of Amphetamines: ADHD
hyperactivity, impulsivity, and/or difficulty controlling or refocusing attention >drug therapy can calm hyperactivity and improve attention and control
64
Ritalin
(methylphenidate) can be used to treat both of these disorders due to decreased incidence of both cardiovascular and appetite suppressing effects, compared to amphetamine
65
Amphetamines potential for Misuse and SUD:
- because amphetamines produce euphoria and are effective CNS stimulants, they are widely misused - most commonly taken orally, injected or smoked - occasionally sniffed/snorted
66
Amphetamines potential for misuse
- potential is extremely high - water soluble salt forms of the drug allow for large doses that are readily injectable, resulting in a rapid intense response - inherent harmfulness is due to their long term toxicities (cardiovascular effects and drug-induced psychoses) - this does not appear to be a deterrent to misuse
67
Amphetamines potential for Tolerance
- develops euphoria and mood elevating effects, the anorectic (loss of appetite) effects, cardiovascular and respiratory stimulatory effects and lethal effects - tolerance does not develop to therapeutic effects or drug-induced psychosis
68
Amphetamines potential for Withdrawal
cessation of use results in mood depression that may be profound, prolonged sleep, huge appetite, lack of energy and fatigue
69
Amphetamines potential for addiction
- usually self-administered to produce euphoria and abrupt awakening sensation - effects act as rewards and those who take the drug will crave its effects
70
Cocaine
- classified as local anesthetic and CNS stimulant - in terms of law it is classified as a narcotic - one of the most popular recreational drugs - almost indistinguishable from amphetamine in its accute effects and pattern of toxicity
71
which has a shorter duration of action cocaine for amphetamines??
cocaine has shorter duration of action than amphetamine (>1hr for cocaine and up to 12 hrs for amphetamine)
72
cocaine common route of administration
cocaine commonly sniffed/smoked
73
Cocaine mechanism of action
- causes generalized CNS stimulation in a dose-dependent manner - more cocaine = more CNS stimulation -Reuptake inhibition -Postsynaptic neuron activation
74
Reuptake inhibition:
inhibits the active re-uptake of primarily dopamine and serotonin into the presynaptic neuron
75
Postsynaptic neuron activation:
increases concentration of neurotransmitters in the synaptic cleft and in turn, increases the activation of the postsynaptic neurons receptors
76
Therapeutic Use of Cocaine
- only legit use is as a local anesthetic for the mouth and throat - rarely used therapeutically, as better anesthetics have been developed that have similar chemical structures to cocaine but do not have associated potential for misuse and SUD
77
Effects of long term use of Cocaine
- toxic psychosis (paranoia) - hallucinations or sensations of insects crawling under skin - impaired sexual function - permanent brain damage and impairment of neuronal function - high BP and irregular heart rhythm - changes to nasal mucosa, as drug is sniffed
78
alcohol reacts with cocaine to form
an active metabolite: cocaethylene. this temporarily increases euphoria, BP, aggressive and violent thoughts and poor judgement
79
Cocaine: Potential for Misuse and SUD
- widely misused and often concurrent with other types of psychoactive drugs - usually sniffed, smoked but can be injected too
80
Cocaine potential for misuse
- has one of the highest misuse liabilities - due to powerful euphoria, which can be reached rapidly by injecting the drug or smoking the freebase - freebase: purified form of cocaine that has low melting point - the inherent harmfulness involves physical and psychological deficits - these do not deter misuse
81
Cocaine potential for SUD: tolerance
- tolerance develops towards mood-elevating effect of cocaine but not to the drug-induced psychotic effect - tolerance does not develop as readily to the hallucinatory and behavioural effects compared to amphetamines
82
Cocaine potential for SUD: Withdrawal
symptoms similar to those associated with amphetamines
83
Cocaine potential for SUD: addiction
can occur. behavioural effects are usually perceived as pleasurable and rewarding, therefore reinforce repeated use
84
amphetamines: Mechanism of action
- blocks vesicular monoamine transporters -increases dopamine/norepeinephrine at synapse
85
amphetamines: short term effects
-feeling of euphoria and reward, -overstimulation -insomnia -appetite suppression -increased blood pressure and respiration
86
amphetamines: long term effects
chronic sleeping problems, poor appetite, psychoses, elevated blood pressure, complications from IV drug use
87
amphetamines potential for misuse
extremely high
88
amphetamines potential for tolerance
yes, to some effects
89
amphetamines potential for withdrawal
yes
90
amphetamines potential for addiction
yes
91
therapeutic use of amphetamines
narcolepsy & ADHD
92
cocaine mechanism of action
blocks reuptake of dopamine and serotonin, increasing dopamine and serotonin at the synapse
93
short term effects of cocaine
same as amphetmines, but shorter duration of action
94
long term effects of cocaine
same as amphetamines; plus impaired sexual function, potential permanent brain damage, changes to nasal mucosa from sniffing the drug
95
cocaine potential for misuse
extremely high
96
cocaine potential for tolerance
yes to some effects
97
cocaine potneital for withdrawal
yes
98
cocaine potential for addiction
yes
99
therapeutic uses for cocaine
vary rarely used as local anesthetic
100
what is the leading cause of preventable disease death in Canada
tobacco use
101
nicotine
nicotine is a occurring substance found in tobacco, and is responsible for smoking addiction
102
absorption of nicotine
- nicotine exists in cigarette smoke in small particles and when inhaled, these are rapidly absorbed - it is also absorbed from GI tract, oral mucosa, and across the skin - smokers can control dose of nicotine absorbed by the depth of inhalation and frequency of smoking
103
distribution of cocaine
nicotine is distributed throughout the body and rapidly gains access to the brain
104
metabolism of nictone
Nicotine is rapidly metabolized in the liver
105
excretion of nicotine
- metabolites are excreted in the urine - the half life of nicotine in the body is about two hours
106
Mechanism & Action of Nicotine
- nicotine stimulates nicotinic receptors at synapses, simialr to ACh - activation of nicotinic receptors increases psychomotor acitivty, congitive function, attention and memory - in large doses, nicotine can cause agitation, tremors and seizures - effects of the CNS are mediated by nicotinic receptor-mediated release of the CNS neurotransmitters dopamine and serotonin
107
Therapeutic use of nicotine
- only therapeutic use is smoking cessation programs, where nicotine is administered in chewing gum, patches or buccal spray - this attempts to maintain blood nicotine levels and satisfy craving for a cigarette, allowing for tapering of nicotine dose
108
Short term effects of smoking tobacco
- mild euphoria, enhanced arousal, increased ability to concentrate, relaxation - may cause small increase in heart rate and blood pressure, and may suppress appetite
109
Short term effects of smoking tobacco in a non regular smoker
- a few puffs may result in dizziness, headache, nausea, vomiting, and abdominal cramps - smoke may trigger cough or gagging - these symptoms disappear in a chronic smoker
110
Long-term effects of smoking
long term respiratory and carcinogenic effects are related to products of combustion not the nicotine itself - cardiovascular disease -lung disease - cancer
111
Cardiovascular Disease from smoking
- a smoker has higher risk of death due to cardiac causes than a non-smoker - nicotine has been related to cardiovascular disease (aside from the products of combustion) - carbon monoxide reduces the capacity of the RBC to carry oxygen - nicotine and carbon moxoxide increase the incidence of atherosclerosis and formation of thrombi
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atherosclerosis
narrowing and hardening of arteries due to plaque buildup
113
thrombi
blood clots
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Lung Disease from smoking
- the incidence of lung disease is increased by smoking - smokers syndrome: difficulty in breathing, wheezing, chest pain, congested lung and increased lung infections - increased risk of emphysema and other forms of chronic obstructive lung disease
115
cancer from smoking
- 30% of all cancers are estimated to be caused by cigarette smoke - cigarette smoke is known to increase the risk of cancer of the lung, oral cavity, throat, bladder, and uterus
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Other effects of smoking
- exposure to passive smoke (second hand smoke) is associated with increased risk of cardiovascular disease and cancer - in children, passive smoke increases the risk of bronchitis, pneumonia, asthma, and SIDS - During pregnancy, a 2-3 fold increase exists in the incidence of the fetus being small for gestational age or born preterm - this appears to reverse if stop smoking early pregnancy - exposure to passive smoke during pregnancy can increase the risk of low birth weight neonate - due to decreased oxygen delivery to the fetus
117
Nicotine Potential for Misuse and SUD
- high degree of misuse potential - tobacco products meet all the requirements of addictive substances - smoking cessation programs generally include counselling and pharmacological support
118
Nicotine blood levels
-most smokers will smoke to keep nicotine blood levels in a certain range (30-40ng/mL) -the # of cigarettes smoked each day is the number needed to keep nicotine at this level
119
nicotine withdrawal
-withdrawal from smoking involves a # of symptoms such as -irritability -restlessness -anxiety -insomnia -fatigue -inability to concentrate -upon wakening in the morning, a smoker is in a state of nicotine withdrawal
120
nicotine addiction
-does occur as the extreme urge to smoke
121
mechanism of action of nicotine
stimulates nicotinic receptors
122
short term effects of nicotine
mild euphoria, enhanced arousal, increased ability to concentrate, a sense of relaxation
123
long term effects of nicotine
cardiovascular disease, lung disease and cancer due to smoking
124
potential for nicotine misuse
very high
125
potential for nicotine tolerance
no
126
nicotine withdrawal
yes
127
nicotine addiction
highly addictive
128
therapeutic uses of nictoine
smoking cessation
129
lethal dose of caffeine
lethal dose of caffeine is equal to 10g (~50 cups)
130
absorption of caffeine
- taken orally, caffeine is rapidly and completely absorbed - blood levels are significant at 30 minutes and they peak 2 hours after ingestion
131
distribution of caffeine
caffeine distributes to all parts of the body and freely crosses the brain and placenta
132
metabolism of caffeine
- genetics determine the rate we metabolize and excrete caffeine - there are rapid metabolizers and slow metabolizers - explains why coffee at night keeps some awake and some not
133
excretion of caffeine
the half life of caffeine varies, from 2.5 hours to 10 hours
134
Mechanism of action of caffeine
100-250mg of caffeine increases mental performance and motor activity while decreasing drowsiness and fatigue
135
Mechanism of action WITHOUT caffeine
in the brain, activation of receptors termed adenosine receptors stimulates GABAergic neurons that then inhibit dopamine release
136
mechnism of action WITH caffeine
- The actions are exerted by competitively blocking adenosine receptors in the brain. - When caffeine blocks these receptors, the neurons are released from the adenosine inhibition - decreasing GABA activation and thereby increasing dopamine release - overall effect: stimulation of the CNS.
137
Short Term Effects of Caffeine on the CNS
- mild mood elevation and reduced fatigue - small increase in performance - flow of thought may be clearer and more rapid - when taken by abstainers, produces nervousness and can interfere with sleep - high doses will produce irritability, rambling flow of thoughts and speech and psychomotor agitation
138
Short Term Effects of Caffeine on cardiovascular
- constriction of cerebral blood vessels (useful during headache) - increases peripheral blood flow - stimulates cardiac muscle (increases heart rate) - rapid, irregular heart beat with high doses
139
Short Term Effects of Caffeine on respiration
- mild stimulation of respiratory rate and relaxation of bronchial smooth muscle occurs with caffeine - used to stimulate breathing in preterm newborns, as it helps immature brains and lungs remember to breathe
140
Long Term Effects of Caffeine
- restlessness - nervousness - insomnia - increased urinary output - gastric upset - rambling speech and thought
141
effects of Caffeine and smoking
- cigarette smoke increases the metabolism of caffeine - in smokers, the duration of action of caffeine is shortened - when a person quits smoking, the metabolism of caffeine return to normal, thus smoking cessation should prompt decreased caffeine intake
142
effects of caffeine and pregnancy
- Caffeine is NOT teratogenic, in that consumption is not associated with fetal abnormalities - large doses of caffeine during pregnancy increase risk of stillbirth, slightly decreased fetal growth rate and increased chance of miscarriage - modest doses were without any measurable effect on the featus - metabolism of coffee is slower in pregnant people - caffeine remains in the body 2x longer in the 2nd trimester and 3x longer in the third trimester
143
caffeine Potential for Misuse and SUD
potential for misuse and SUD is low
144
caffeine Misuse:
>potential is low >acts as a mild reinforcer, however, the euphoria is mild intensity >inherent harmfulness is very low -low to moderate intake of caffeine does not appear to be associated with adverse effects -larger doses will result in irritability, nervousness, insomnia, and irregular rhythym of the heart
145
caffeine tolerance
Some evidence suggests that tolerance does develop to caffeine
146
caffeine withdrawal
abrupt cessation of caffeine will result in mild withdrawal -headache, fatigue, and drowsiness
147
caffeine addiction
mild can occur
148
caffeine mechanism of action
competitive inhibitor at adenosine receptors, prevents inhibition
149
short term effects of caffeine
increases mental performance and motor activity, decreases drowsiness and fatigue
150
long term effects of caffeine
restlessness, nervousness, insomnia, no definite link to disease states
151
cafeine misuse
low
152
caffeine tolerance
in some individuals
153
caffeine withdrawal
mild
154
caffeine addiction
mild
155
therapeutic use of caffeine
to stimulate breathing in preterm newborns.
156
History of Drugs in Sports : 1950s
- performance enhancing substance use started with amphetamines and anabolic steroids - use increased rapidly until sports regulatory bodies banned these
157
History of Drugs in Sports: 1976
first steroid testing occurred at the Montreal olympics, 11 tested positive
158
History of Drugs in Sports : 1988
Canadian Ben Johnson was tripped of his gold medal after positive steroid test
159
History of Drugs in Sports: 1999
- World Drug Anti-Doping Agency was established - responsible for the anti-doping policies in all sports and countries
160
History of Drugs in Sports: 2007
US athletes Marion Jones admitted to drug use and was sentences to prison for perjury in 2007
161
History of Drugs in Sports: 2012
Lance Armstrong, Tour de France winner, was stripped of his seven titles for having an elaborate doping scheme
162
History of Drugs in Sports : 2016
Numerous Russian athletes vying to compete at the 2016 Rio Olympics were banned from competition due to an elaborate state-run doping scandal leading up to the games
163
History of Drugs in Sports : 2019
- Due to state run doping, the WADA banned russia from all major sporting events, including olympics for 4 yrs - at 2020 tokyo olympics, russian athletes were allowed to compete as neutral athletes if they could prove they had no link to doping scandal - the athletes competed as russian olympic committee
164
what classes of drugs increase endurance and speed
amphetamines; blood doping
165
what classes of drugs increase strength
anabolic steroids
166
what class of drugs reduces body weight
diuretics & amphetamines
167
what classes of drugs reduce anxiety
benzodiazepines
168
why are amphetamines desirable for athletes
- increased alertness, feeling of power, reduced fatigue, increased aggression, and increased responsiveness - increases heart rate and BP - the effects increase endurance and speed - also induce appetite suppression, beneficial for weight loss in sports
169
Amphetamines impact on endurance
- duration was extended by 40%v when 10mg of methamphetamine was administered - as the athletes were nearing exhaustion, the meth allowed them to continue
170
Amphetamines impact on speed
when given meth, 14 of 15 swimmers were faster and 73% improved their times
171
toxicity of amphetamines
- large doses can lead to fatal increases in blood pressure - as the drug wears off, people experience lows or crashes - produce withdrawal symptoms and tolerance develops quickly
172
Anabolic steriods
- use to increase muscle mass and strength - testosterone is an anabolic steroid - typically synthetic steriods are used in sports - these have reduced androgenic effects but maintain the anabolic effects - Androgenic effects: effects on secondary male characteristics - anabolic effects: building of muscle mass
173
anabolic steriods mechanism of actions
1. Anti-catabolic response 2. anabolic response 3. Motivation
174
anabolic steriods Anti-catabolic response:
- athletes can train so hard they use protein from their muscles to fuel their training - this action is blocked by anabolic steroids allowing athletes to maintain muscle mass
175
anabolic steriod anabolic response
- anabolic effects result in protein production - greater effects at high doses - protein supplementation important
176
anabolic steriods motivation
- can produce aggressive behaviour “roid rage” - beneficial for sports
177
effects of anabolic steriods
- greater effects on individuals with lower basal circulating levels of testosterone - effects differ depending on whether low to moderate or large dose is administered
178
low-moderate effects of anabolic steroids
- modest effects ex. effect in inexperienced weightlifters is less than a good exercise program
179
Large effects of anabolic steroids
- yields significant increases in body mass, strength and body weight - at peak training with diet high in protein - aggressive behaviour contributes to performance enhancement effects
180
Side Effects of anabolic steroids
- mood swings - acne (face and body) - cardiovascular disease - bc increased plasma levels of low density lipoproteins (bad cholesterol) and decrease high density lipoproteins (good cholesterol) - altered liver function - hepatitis, liver failure and cancer - reduced testosterone levels - block release of gonadotropin releasing hormone therefore reduction in testosterone levels and sperm production - leads to infertility, reduced libido and impotence
181
in those with low basal testosterone levels (females) synthetic anabolic steroids do still produce
anderogenic effects which increase facial and body hair, lower voice, enlarge clitoris, increase libido and amenorrhea. may or may not be reversible
182
Benzodiazepines
- lorazepam (ativan) or diazepam (valium) are often used to combat insomnia and anxiety in elite athletes ` - reported to help them sleep - good nights rest and recover fast from intense training - also impair psychomotor coordinationand focus at higher doses
183
Blood Doping and Erythropoietin
- used for performance enhancement - both increase RBCs and hematocrit levels
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blood doping
- is an effort to raise RBC by taking blood out, and reintroducing it to get a boost of RBC - these carry higher amount of oxygen to muscle
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EPO
- boosts the bodys natural production of RBC - injection of EPO stimulates bone marrow to make more RBC - inappropriate use r its derivatives can result in thrombotic events (stroke/heart attack)
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detection of blood doping
Blood doping can be detected via measuring the age of RBC
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detection of EPO
EPO can be detected by testing urine for presence of recombinant EPO
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Diuretics
- drugs that enhance the excretion of salt and water through the kidneys - used just before competition to reduce body water and allow athlete to compete in lower weight class - also taken to hasten the excretion of other banned drugs to avoid detection - toxicities are associated with excess electrolyte and water depletion
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Why Ban Performance Enhancing Drugs?
- at least 192 substances are banned 1. Athlete protection 2. Unfair Advantage 1. drugs do not provide a level playing field