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Neurologic & Psych > EXAM 3 Drugs of abuse Dr. Pond > Flashcards

EXAM 3 Drugs of abuse Dr. Pond Flashcards

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1
Q

What are the two forms of Dependence?

A

Physical dependence = dependence (withdrawal when stopping the drug)

Psychological dependence = addiction (compulsive, relapsing drug despite negative consequences, cravings

all addictive drugs produce a strong feeling of euphoria and reward

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2
Q

What are the forms of Tolerance?

A

reduced effect of drug over time

Pharmacokinetic tolerance: the drug is cleared faster

Pharmacodynamic tolerance: the body adapts to the drug (number of receptors is downregulated or less sensitive)

-sometimes both forms are seen

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3
Q

What do all addictive drugs have in common?

A

a strong feeling of euphoria and reward

activation of the dopamine-reward pathway in some way

-> Mesolimbic pathway

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4
Q

What is the Mesolimbic pathway

A

VTA (brainstem) -> Nucleus accumbens (limbic area)
other factors that activate this pathway: food, water, sex (surviving)

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5
Q

Which substances have the highest risk for addiction?

A

RR = 5
-Cocaine
-Amphetamine

RR = 4
-Nicotine
-Opioids

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6
Q

What are the enzymes involved in alcohol metabolism?

A

Alcohol dehydrogenase (ADH)
Ethanol -> Acetaldehyde

Aldehyde dehydrogenase (ALD)
Acetaldehyde -> Acetate

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7
Q

What kinetics does alcohol metabolism follow?

A

Zero-order kinetics

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8
Q

To which receptors does alcohol bind in the CNS?

A

-NMDA receptor - suppressing its activation
-GABA (A) activation (GABA(A) is inhibitory)

in total inhibitory

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9
Q

Other short-term effects of alcohol

A

-Vasodilator - severe overdose -> hypothermia
-Diuresis: inhibits antidiuretic hormone (ADH)

-sour stomach: stimulates gastric acid secretion
-decreased sexual function
-inhibits REM: although it causes sedation, it disrupts normal sleep pattern

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10
Q

Acute Tolerance of alcohol

A

reduced sensitivity of GABA(A) receptors
-> the first glass of wine has a greater effect than the last one

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11
Q

Chronic tolerance of alcohol

A

-metabolic tolerance: induction of microsomal enzymes (MEOS) -> second way to metabolize Ethanol to Acetaldehyde

-pharmacodynamic tolerance:
decreased sensitivity of GABA(A) receptors
downregulation of GABA(A) receptors in some parts of the brain

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12
Q

How does alcohol affect other drugs?

A

-additive or synergistic with other CNS depressants

-activation of MEOS -> build of toxic metabolites -> depletion of glutathione in liver cells -> acetaminophen toxicity

-increased risk of gastric bleeding when taking NSAIDs or aspirin

-cross-tolerance with other CNS depressants (fe benzos since the GABA(A) receptors become less sensitive)

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13
Q

What are the early withdrawal symptoms?

A

Rum fits
-nausea
-anxiety
-shakes
-sweating, cramps
-nightmares, hallucination
-tonic-clonic seizure (can be life-threatening)

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14
Q

What are the late withdrawal symptoms?

A

Delirium tremens
-confusion, disorientation
-agitation
-sweating
-hyperthermia
-cardiac collapse

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15
Q

What is the treatment for alcohol withdrawal?

A

Sedative hypnotics are common
-> usually benzos like diazepam -> then gradually taper off

-the goal is to prevent seizures

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16
Q

What are the long-term toxicities of alcohol?

A

-liver toxicity
-CNS dysfunction
-liver cirrhosis
-cardiomyopathy
-gastritis
-pancreatitis
-cancer risks

women at higher risk for HTN and the other toxicities

acute toxicities: nausea, vomiting, memory loss, passing out

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17
Q

What are the long-term effects on CNS function?

A

-increases ventricular size, decreases in
grey matter (brain scan)
-> cognitive impairment, memory loss,
anxiety, depression

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18
Q

What is the Wernicke-Korsakoff syndrome?

A

-paralysis of the eye muscle, ataxia, learning and memory deficit-> can progress to coma and death

-> lack of vitamin B1 (thiamine), malnutrition bc they get their calories from alcohol
-> loss of neurons in parts of basal forebrain

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19
Q

Which drug is used for alcoholism?

A

Naltrexone (mu antagonist)

-reduces short-term cravings for alcohol

ADE: GI (N/V, diarrhea), dizziness, headache

20
Q

Why do we use opioid antagonists in alcoholism?

A

alcohol increases the release of endorphins -> which bind mu-opioid receptors on GABA neurons

so the release of GABA is blocked
GABA would have blocked the dopamine release in the reward pathway (nucleus accumbens)

so now we have more dopamine release due to endorphins blocking the GABA neuron -> we need to block the opioid in order to have more GABA

the opioid contributes to the feeling of euphoria -> that’s why we use naltrexone in alcoholism

21
Q

What are the risks associated with Naltrexone?

A

risks: hepatotoxicity, withdrawal in opioid-dependent patients

22
Q

Which drug is used for alcoholism treatment and is mimicking the effects of alcohol?

A

Acamprosate
-> reduces short and long-term relapses

alcohol is a GABA(A) agonist and NMDA antagonist
Acamprosate is a
-weak NMDA-receptor antagonist
-GABA (A) agonist

poorly absorbed and renally eliminated

ADE: GI, insomnia, itching, anxiety, depression

23
Q

Which drug is used for alcoholism and facilitates the side effects of alcohol?

A

Disulfiram (Antabuse)
-inhibits Aldehyde dehydrogenase (ALD)
-> accumulation of acetaldehyde (1st metabolite of ethanol) -> produces N/V, palpitation, blurred vision, flushing, dyspnea (SOB)

risks:
-hepatoxicity
-several DDI

24
Q

Which drugs for alcoholism are hepatoxic?

A

Naltrexone
Disulfiram

25
Q

How does Xylazine express its analgesic effect?

A

alpha-2 agonist on presynaptic neurons (autoreceptors in NE release) -> closes voltage-gated Ca2+ channels -> INHIBITORY

-often used with fentanyl to prolong the euphoria -> risk for respiratory depression

-ADE: drowsiness, amnesia, slow breathing and heart rate

Antidote: Tolazoline (alpha-2 antagonist)

26
Q

What are the two pharmacologically active compounds in Kratom

A

7-α-hydroxymitragynine and mitragynine

MOA not understood
-has opioid and stimulant properties

27
Q

What is the main active ingredient in Cannabis?

A

Δ9-Tetrahydrocannabinol (THC)

the main psychoactive Cannabinoid

28
Q

How does THC work?

A

Synthesized in response to Ca2+ -> they move retrogradely to the presynaptic neuron and bind to CB1 receptors -> blocking the release of NT

same effect with body-made Endocannabinoids:
-> anandamide and 2-arachidonylglycerol

they may act on Glutamatergic neurons or GABA neurons (so different effects seen)

29
Q

Which neurons does THC bind to?

A

partial agonist of CB1 on GABA neurons

-these GABA neurons would inhibit DA neurons in the VTA

-> THC blocks GABA and thereby the inhibition of DA -> more DA effect (disinhibition of DA neuron)
-> Opioids do the same

30
Q

MOA of Cannabidiol (CBD)

A

the drug itself is not psychoactive

it blocks FAAH enzyme

-it prevents the degradation of Endocannabinoids and it increases the amount of Endocannabinoids (anandamide)

31
Q

Other effects of THC

A

-Respiratory (irratation, infection)
-Cardiovascular (increase in HR, MI risk)
-IQ reduction in heavy users as teens (secondary effect since they are not so much engaged in learning events)

-short-term antidepressive effects but long-term contributes to depression, anxiety

-some addiction risk bc it works on the DA reward pathway

32
Q

How is Δ8-THC different from delta 9?

A

change in location of the double-bond

it is psychoactive and not regulated right now
(delta 9 is psychoactive too)

33
Q

What are the targets of Gamma-Hydroxybutyric Acid (GHB)?

A

-high-affinity on protein of unknown function (GHB receptor)

-low-affinity binding site on GABA(B) receptor (weak agonist) -> main target (studies have shown that blocking GABA (B) you will block most effects of the drug

34
Q

What are the effects of GHB?

A

Euphoria, enhanced sensory perception, feeling of social closeness, and amnesia (synergistic with alcohol)

-rapidly absorbed, short half-life (30 min, hard to detect)

-Liquid ecstasy, rape drug

35
Q

To which neurons does GHB bind?

A

GABA(B) receptors are present on GABA neurons which would inhibit DA neurons (like opioids and THC) and on DA neurons

-it prefers to bind to the GABA(B) receptors on the GABA neuron at lower doses-> Disinhibition of the DA neurons

-at high doses it will also hit GHB receptors on DA neurons -> agonist -> IPSP -> decrease in firing -> less DA effect

36
Q

Which receptors are targeted by LSD, Mescaline, and Psilocybin?

A

their structure resembles Serotonin

-they target 5-HT(2A) receptors (agonist/(partial agonist)
-G-protein coupled
-closing K+ channels -> ESPS

37
Q

What are the effects of LSD, Mescaline, and Psilocybin?

A

Hallucination
-Synesthesia (experiencing one than one sense?)
-awareness of sensory input, feeling of clarity
-spectator ego
-autonomic activation, increase in HR and BP
-GI distress with the natural products

38
Q

Which receptor is targeted by Ketamine and PCP?

A

NMDA (antagonist)

-PCP is more potent than Ketamine
-dissociative drug, ego perspective
-similar effects with high doses of Dextromethorphan (DXM)

39
Q

What are the effects of Ketamine and PCP?

A

autonomic: increase in BP and HR, hyperthermia, impaired memory function

effects can be unpredictable
-excitement, agitation
-hallucinations, euphoria, dysphoria

PCP is addictive
-> DA and NE release

40
Q

Which receptor does Salvia bind to?

A

Kappa receptor (like opioids)
-> Kappa receptor causes dysphoria, but it is still used because it also causes psychotomimesis (hallucinations)

41
Q

Which receptors does Nicotine bind to?

A

agonists of Nicotinic ACh receptors (ionotropic, Na+/K channels -> Na+ comes in -> EPSP)

they hit NiACh receptors on DA neurons in the mesolimbic pathway (VTA to nucleus accumbens)

42
Q

Which drugs to treat nicotine addiction?

A

-Nicotine substitution (Nicorette, Nicoderm)
Spray, chewed, inhaled

-Bupropion (Zyban)

-Varenicline (Chantix)

43
Q

Which receptors are targeted by Bupropion?

A

-inhibits NE and DA uptake (weak)
since nicotine activates DA neurons and stopping smoking causes DA withdrawal -> blocking DA reuptake makes more DA available to reduce withdrawal

-nicotine receptor antagonist
smoking when on Bupropion will prevent that high sensation, bc it prevents nicotine from binding and the DA release

44
Q

BBW of Bupropion

A

suicidal ideation particularly in children and adolescents

ADE: aggravation of psychosis (drugs that increase DA have this effect), dizziness, tremor, insomnia,
some sympathomimetic: dry mouth, constipation, increased HR and BP -> since it increases NE

45
Q

Which receptors are targeted by Varenicline?

A

partial agonist of α4β2 nicotinic acetylcholine receptor (major receptor in the VTA)

-partial agonist in the presence of the (stronger) agonist, in this case, nicotine will reduce the effect of nicotine

(in the presence of no other agonist (nicotine) the partial agonist will give a reduced effect of dopamine)

-insomnia, sleep disturbance (dreams), nausea, constipation, flatulence

46
Q

Which chemicals are contained in inhalants?

A

nitrates, ketones, aliphatic and aromatic hydrocarbons

-inhalants produce a rapid high (like alcohol intoxication)

Neurologic & Psych (37 decks)

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