Better cards Flashcards

1
Q

Caffeine base

A

purinergic

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2
Q

adenosine A1

A

normally inhibitory, stops adenylyl cyclase. Found in reward and hippocampus

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3
Q

adenosine A2

A

normally excitatory, starts adenylyl cyclase, found in DA rich regions on GABA neurons

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4
Q

caffeine reward

A

adenosine A1 receptor on DA neuron’s disinhibiting them

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5
Q

Paraxanthine

A

Caffeine metabolite, increases blood glycerol and fatty acids via lipolysis

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6
Q

Theobromine

A

Caffeine metabolite, dilates vessels (periphery) and increases urine

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7
Q

theophylline

A

caffeine metabolite, inhibits PDE increasing cAMP is the increased breathing mechanism

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8
Q

Nootropics

A

cognitive enhancers (BDNF linked to LTP in hippocampus)
-caffeine
-taurine
-nicotine
-ritalin
-afinil family
-l-theane
- ginko and ginseng
-amphetamines

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9
Q

Nicotine base

A

Alkaloid, want it in free base form so burn it

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10
Q

Diacetyl

A

butter flavour destories lungs

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11
Q

vit E acetate

A

in vapes causes allergic reactions

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12
Q

nicotine metabolism

A

CYP2A6, CYP2B6, monooxygenases

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13
Q

Nicotine binding sites

A

An acetylcholine receptor agonist, binds tightly. notably to alpha 4 beta 2 which is located on GABA interneurons which is quickly desensitized disinhibiting dopamine release. alpha 7 controls Glu release

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14
Q

Nicotine tolerance

A

vomiting and dizziness go away quick but no tolerance to heart or vessel effects. Sensitization due to higher expression on alpha 4 beta 2 (most in PFC)

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15
Q

Bupropion

A

nAChR antagonist as a Treatment for nicotine withdrawal has higher affinity. also inhibits NAT and NET to act as antidepressant

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16
Q

Varenicline

A

partial nAChR agonist to reduce craving

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17
Q

Hypnotics

A

cause sleep and drowsiness (Zopiclone, Zolpidem)

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18
Q

Z-Drugs

A

orexin antagonists, melatonin agonists, anti histamines

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19
Q

Sedatives

A

anxiolytic, sedation, anesthesia, anti convulsant

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20
Q

Sedative charaterization

A

based on duration of length. short is used for preanesthetic or insomnia. long acting for anticonvulsants, muscle relaxants and anxiolytics

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21
Q

Sedative metabolism

A

CYP450 creates active metabolites
-chordiazepoxide, diazepam, midazolam

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21
Q

Benzodiazepines

A

sedative, Binds GABA between alpha and gamma to increase frequency of opening when GABA is present. Rapid tolerance

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22
Q

Barbiturates

A

sedative, bind GABA between alpha and beta to increase duration of opening (can activate when GABA not present)

23
Q

Gamma-hydroxybutyric acid

A

precurose of Glu, gly and GABA. at low doses only binds Glu receptors and acts as stimulant
at high dose binds GABA for sedative like effect (alcohol)

24
Q

Flumazenil

A

Overdose treatment for sedatives/ GABA antagonist

25
Q

Sedative reward

A

From disinhibition of GABA interneurons on DA terminals

26
Q

CB1 expression

A

basically everywhere but mainly in CNS

27
Q

CB2 expression

A

on immune cells, spleen and tonsils

28
Q

Cannabis effects

A

-pleasure
-analgesia from CB1 activation
-heart rate increase
-increased energy metabolism and appetite/thirst via CB1
-decreasing sex drive and hormones

29
Q

Cannabis 5HT effect

A

anti-emetic effect from inhibition of 5HT release in medulla all around. But THC and CBD also bind and inhibit 5HT3 directly.

30
Q

cannabis binding targets

A

CB1 and 2 but also TRPV1 and 2 (Na/Ca) channels and 5HT2

31
Q

cannabis reward

A

from presynaptic (on axon) activation of CB1 on GABA interneurons

32
Q

Cannabis acute adverse effect

A

high THC in hippocampus can reduce memory and learning
-blood shot eyes from CB1 activation and dilation of vessels in the eyes

33
Q

The munchies

A

From presynaptic inhibition of Glu neuron’s projecting to nasal GABA interneurons that inhibit nasal mitral cells. The disinhibition sensitizes the mitral cells to smells increasing food drive and pleasure from eating.

34
Q

Cannabis long term effects

A

miscarriage rates go up
lung damage (smoke)
low sex hormones otherwise effecting fertility (male and female)

35
Q

Bath salts structure

A

highly changing but bases around the cathinone nucleus (phenethylamine with a ketone) and then some stuff added to it.
-a pyrolodine ring can increase potency (more lipophilic)
-long chains increase potency

36
Q

Bath salts effects

A

stimulants
-some of the serotonin effects increase heat leading to hyperthermia and maybe rhabdomyolysis and kidney failure
-euphoria
-locomotor activity from increased DA in striatum

37
Q

Bath salts reward/ mechanism

A

two types
-without pyridine ring acts like amphetamine
entering the terminal via SERT and displacing DA and NE while reversing DAT via TAAR
- with pyridine ring is too big so acts like cocaine and blocks DAT

38
Q

DAT/SERT ratio

A

the higher this ratio the more it favours DA and it is more addictive. based on IC50 (concentration to prevent 50% of reuptake) so the higher the concentration the less favoured that receptor is.

39
Q

Bathsalts adverse effects

A

cause violence and homicidal behaviour, self mutilation and excited delirium syndrome
death from surge of NE, DA and 5HT
-hyper thermal and serotonin syndrome leading to water intoxication

40
Q

MDPV

A

bathsalt with very very high abuse potential

41
Q

Type 1 anabolic steroids

A

have esters to be hydrolyzed into testosterone
-but also into estrogen my aromatase

42
Q

Type 2 anabolic steroids

A

19-Nor-testosterone. These have less androgenic effects (secondary sex characteristics) and 80% less aromatization to estrogen

43
Q

Type 3 anabolic steroids

A

extra ring of the A ring
- long lasting and not turned into estrogen and has increased anabolic effects

44
Q

anabolic steroid admin

A

different dose schedules
-pyramiding (up and down)
-Stacking (many types at once)
-cycling (to stay around testing)

45
Q

anabolic steroid action

A

Binds to andro receptor and forms a complex which acts as a transcription factor increasing stem cell development to muscle

46
Q

anabolic steroid metabolism

A

5 alpha reductase converts testosterone to DHT. the introduction of more steroids stops their natural production as it is a negative feedback loop.

47
Q

steroid reward

A

Can come from natural endorphins inhibiting GABA in VTA. also some direct steroid modulation of GABA to increase DA neuron firing

48
Q

anabolic steroid effects

A

the TF produces more anabolic genes (IGF-1) and decreases atrophic genes (MuRF1). this increases myonuclei and muscle fibre size.

49
Q

steroid withdrawal

A

depression, mood swings, fatigue, body dissatisfaction

50
Q

steroid dependance

A

mostly psychological from wanting to avoid negative effects so 30% become dependant

51
Q

steroid long term risks

A

Many other genes activated for a pleiotropic effect
-increased BP, cholesterol and heart defects
-reduced 5HTR expression in PFC, hypo and hippocampus

52
Q

Steroid rage

A

anterior hypothalamus is aggression centre and D2 activation there leads to aggression. steroid dose can increase D2 expression there.
steroids also enhance arginine vasopressin (which increases aggression) and decreases 5HT which calms

53
Q

arginine vasopressin

A

a molecule that increases aggression. activated and increased by sterioids leading to rage

54
Q

Steroid abuse

A

from the DA release but also from BDNF in hippocampus being prevented from stimulating growth leading to depressed behaviours

55
Q

Chemical heptenation

A

a small molecule that binds to macromolecule like protein to produce an immune effects (used in lateral flow assays.