Performance enhancing drugs Flashcards

1
Q

6 categories of PEDs

A

stimulants
pain killers
blood doping
B agonists
B blockers
AAS and hormones

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2
Q

AAS

A

anabolic/androgenic steroids
based off testosterone steroid nucleus
altered to enhance muscle building

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3
Q

type 1 AAS

A

esters
prolonged half-lives
hydrolyzed to testosterone
aromatized to estrogens by aromatase

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4
Q

type 2 AAS

A

19-nor-testosterone (nandrolone) derivatives
prolonged half-lives
reduced androgenic effects
80% less aromatization compared to type 1

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5
Q

type 3 AAS

A

17a-alkyl derivatives
greatly reduced liver metabolism
not converted to estrogen
increased anabolic effects

best for building muscles

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6
Q

administration

A

pyramiding
stacking
cycling

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7
Q

pyramiding

A

increasing dose followed by decreasing dose

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8
Q

stacking

A

using multiple steroids

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9
Q

cycling

A

alternating periods of use
co-ordinated with training or testing schedules

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10
Q

absorption

A

injection IM
ingestion
topical

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11
Q

distribution

A

lipophilic
rapid
muscle
widespread

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12
Q

metabolism

A

liver
first-pass metabolism
low bioavailability

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13
Q

excretion

A

kidney = 90%
other 10% in GI tract

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14
Q

physiology

A

sex steroids determine male and female differences
production in reproductive tissues stimulated by FSH/LH from anterior pituitary

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15
Q

5a-reductase

A

converts testosterone to DHT

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16
Q

aromatase

A

converts testosterone to estrogen
rate-limiting step for estrogen production

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17
Q

negative feedback

A

controls levels → cyclical

18
Q

mechanism of action

A

anabolic steroids bind androgen receptor
drug-receptor complexes translocate to nucleus → bind specific DNA sequences
activates gene transcription mRNA production → make new protein

19
Q

stem cell differentiation

A

steroids shift stem cells away from adipose and towards muscle cell differentiation

20
Q

mechanism of reinforcement

A

euphoria
from increased beta-endorphin levels → decrease GABA release onto VTA DA-ergic neurons

steroids modulate GABAA receptors → DA-ergic mesolimbic neurons increase firing rate

21
Q

animal models

A

with AAS
showed increased number of myonuclei; increased muscle fiber cross-sectional area

22
Q

cellular memory

A

allows rapid muscle building after period of inactivity
more pronounced cross sectional analysis after 11 week break in steroid treated animals

23
Q

trenbolone

A

19-nor derivative of testosterone
higher affinity for androgen receptors
not a substrate for 5a-reductase, or aromatase
induces myotrophic effects without unwanted effects

24
Q

MuRF1

A

atrophic gene
expression reduced by trenbolone

25
Q

IGF-1

A

anabolic gene
expression increased by trenbolone

26
Q

tolerance

A

develops after single dose
presence of steroids inhibits their own production (neg feedback)

27
Q

withdrawal

A

depression + mood swings
fatigue, headache
insomnia, lack of energy
no appetite
body dissatisfaction

28
Q

dependence

A

30% of users
more likely at higher doses
psychological - cycle length

29
Q

long term health risks

A

steroid receptors are present in multiple tissues → activation of other genes leads to unwanted, dangerous side effects

hypogonadism
masculinization
gynecomastia

30
Q

heart risk

A

increased blood pressure
cholesterol
heart abnormalities

31
Q

roid rage

A

increased aggression, anger, rage
psychosis and depression
GABAa, NMDA, and 5HT receptors can bind endogenous neurosteroids

32
Q

anterior hypothalamus

A

aggression centre
activation of D2 in AH → aggression + violence
moderate doses in adolescence increases D2 expression

33
Q

arginine vasopressin

A

excitatory
potentiates aggression

enhanced by steroid exposure

34
Q

5HT

A

inhibitory
decreases aggression

reduced by steroid exposure

35
Q

chronic nandrolone

A

increases aggression in mice
reduces 5HT receptor mRNA in PFC, hypothalamus, hippocampus, and amygdala

36
Q

BDNF

A

brain-derived neurotrophic factor levels
stimulates neuronal growth in hippocampus

reduction due to abuse → correlates with depressed behaviours

37
Q

CHLO treatment

A

chlorimipraminie
antidepressant
reverses BDNF reduction

38
Q

testing

A

urine - test for known metabolites
HPLC, ELISA, GC-MS

39
Q

assays

A

chemical and immunoassays

40
Q

chemical haptenation

A

small molecule that binds a macromolecule to produce an immune reaction