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Flashcards in Drugs of Abuse Deck (40)
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1
Q

3.3 Types of Tolerance

A

Innate
Acquired - Pharmokinetic/dynamic, learned
Cross

2
Q

Rimonabant

A

Cannabinoid R inverse agonist, potential cessation aid for a lot of substances

3
Q

Key Addiction Pathway

A

DA neurons from VTA go to inhibit GABA nuclei in NAc, leading to reward in ventral pallidum. Also GABA in VTA that inhibit DA. Opioid in each inhibit GABA as well. Glutamate from cortex excites GABA

4
Q

Opiates Effect

A

Act to inhibit both GABA in VTA (releases DA inhibition) and NAc

5
Q

Opioid Danger

A

Tolerance to desirable effects develops quickly, so users quickly require desirable effects and withdrawal avoidance, increasing risk of overdose (usually respiratory depression)

6
Q

Salvia

A

Activates Kappa-opioid agonist

7
Q

3 Kinds of Effects from Smoking and What They’re From

A

CV: Primarily nicotine
Carcinogenic: Probably tar then enhanced by nicotine
Respiratory: Tar

8
Q

Titration

A

Smokers will alter their behavior to get the exact conc of nicotine they like

9
Q

Nicotine Effect

A

Acts on DA cell bodies and presynaptic terminals both to depol them and make APs more likely

10
Q

Cocaine CV Effects

A

Bradycardia from vagal stimlation, then tachycardia at higher doses. Tolerance develops to CNS effect but not these, where danger lies

11
Q

Cocaine Treatment (3)

A

Alpha/beta adrenergic blockers - labetolol
Calcium channel block
Diezepam for calming

12
Q

2 Most Common Cocaine Administrations

A

Cocaine hydrochloride and cocaine free base (crack)

13
Q

Cocaine Mechs

A

Blocks NE, DA, and 5HT (higher dose) transporters. Peripheral effects due to block of sympathetic neurons

14
Q

Cocaine Elimination

A

Primarily by plasma esterases, not much excreted in urine

15
Q

Amphetamine Treatment

A

Alpha1 blocker - prazosin

16
Q

Amphetamine Tolerance

A

Develops to CNS effects, so move up to huge amounts until reach psychotoxic effects and become so out of it/schizo that they can’t administer anymore

17
Q

Amphetamine Mech

A

Taken up by NET/DAT/SERT, blocks VMAT which reloads vesicles, so MA builds up at nerve terminal and effluxes. Also inhibits MAO which breaks down toxic DA buildup products

18
Q

Ecstasy Mech

A

Acute release of 5HT/action on 5HT transporter

19
Q

Phenethylamine and Tryptamine

A

Scaffolds for DA/NE and 5HT, respectively. Psychadelics

20
Q

Most Potent Cannabinoids

A

Delta9-THC and 11-hydroxy-Delta9-THC (metabolite) - any further metabolism inactivates

21
Q

2/3 Clinical Uses for Cannabinoids

A

Anti-emetic/appetite stimulant for chemotherapy - Marinol and nabilone
Glaucoma - reduces intraocular pressure

22
Q

Notable Feature About LSD

A

Exceptionally potent

23
Q

Notable Aspect of Psychadelic Tolerance

A

Can develop after a few daily doses, but returns after a few drug free days. Maybe due to downreg. Also cross tolerance b/w LSD, mescaline, and psilocin

24
Q

Psychadelic Mech

A

Act on 5HT GPCRs, especially partial agonism at 5HT2, probably responsible for hallucinations

25
Q

PCP Mech

A

Channel blocker of NMDA glutamate Rs. These have learning/memory effects (also this might be responsible for dependence)

26
Q

Standard Dose of Ethanol

A

0.5 oz = 14g

27
Q

EtOH Distribution

A

Everywhere, but very water soluble so really where there’s water. Easily crosses BBB

28
Q

EtOH Elimination via Lungs

A

1st order, so proportional to BAC in exhalation

29
Q

Saturation Kinetics of EtOH Metabolism

A

Saturated, so 0 order. Can metabolize 2/3 standard drink/hr

30
Q

EtOH Metabolism

A

ADH converts to acetaldehyde, ALDH converts to acetate. Each step produces NADH, so produces a lot of reducing capacity that can damage cells

31
Q

2 EtOH Metabolism Polymorphisms

A

ADH: Slow EtOH metabolism, so it lasts longer and increased risk for alcoholism
ALDH - Asian flush, can’t drink

32
Q

Alcohol Mechanisms

A

Not quite sure, just kinda generalized effects like GA but with very low affinity. GABAa Rs seem to be a target

33
Q

2 Alcohol Dependence Treatment Drugs

A

Acamprosate - GABAa activator

Disulfiram - ALDH inhibitor, can’t tolerate EtOH

34
Q

Delirium Tremens

A

Severe alcohol withdrawal w/ hallucinations and delirium and shit

35
Q

Treatment for Alcohol Withdrawal Syndrome

A

Benzodiazepines

36
Q

3 Liver Issues w/ Alcohol

A

Excess reducing capacity
Acute Drug Metabolism: decreased bc enzymes being used/decreased blood flow
Chronic: faster for some drugs bc enzyme induction

37
Q

Methanol

A

Converted to formaldehyde, then formate which is especially dangerous. Can cause retinal damage/blindness, among other things

38
Q

Best Treatment of Methanol and Ethylene Glycol Poisoning

A

Ethanol - ADH has higher affinity for it

39
Q

GHB

A

Looks like GABA, addictive as GABAb agonist (inhibits GABA neurons inhibiting DA ones in VTA)

40
Q

Thujone

A

GABAa R modulator thought to be special factor in Absinthe, turns out not there.