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Pharm III > Exam 1, Drugs of Abuse > Flashcards

Exam 1, Drugs of Abuse Flashcards

1
Q

physiological vs psychological dependence

A

Physio dependence: Neuroadaptations - abnormal behavior and physical sx (withdrawal) occur if drug is withdrawn

Psych dependence:
dysphoria and intense craving following withdrawal of drug. Occurs with or without physical dependence

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2
Q

What is the basis of withdrawal

A

adverse rxns caused by dc of drug; based on neuroadaptations of brain –> release dynorphine and GABA in nucleus accumbens (reward pathway)

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3
Q

What is tolerance and what forms of tolerance are there?

A

Tolerance = more drug needed to produce effect; dose/ response curve shifted RIGHT

Innate (genetic lack of sensitivty)
PK: increased metab
PD: receptor downregulation
Learned: adapted to degree of intoxication
Conditioned: familiar settings diminish effects, novel enhance
Acute: repeated use over short period of time
Cross: one drug produces tolerance to another

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4
Q

What is sensitization

A

increased responsiveness after repeated use

Dose/response curve shifts LEFT

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5
Q

define addiction related to drugs, contrasted with recreational use

A

compulsive, relapsing drug use in spite of adverse consequences
*recreational use: drug use to achieve pleasurable expericne

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6
Q

How does addiction affect the body

A

neural plasticity alters brain function

  • typically psychological in nature
  • physio dependence usually present (but this dose no mean addiction)
  • abuse is generally a factor, drug is causing harm
  • dev depends on individual, drug, and environment
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7
Q

What are some non drug related addictions that cause the same brain stimulation/pathways affected as drugs

A

Gambling and

Oniomania (addiction to shopping)

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8
Q

What are general properties of abused drugs

A
  • cause euphoria
  • easy to use
  • potency & purity (need effect with small dose)
  • rapid onset/short action (shroter DOA, more often need to reinforce effect, more freq use of drug, greater addiction potential)
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9
Q

Outline the reward pathway in the brain

A

aka Mesolimbic DA pathway
*VTA –> NAc (nucleus accumbens) –> prefrontal cortex

  • reinforcement/reward, motivation, reinforcing effects of drugs (such as opiates)
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10
Q

what various drugs cause addiction by affecting DA release, specifically increasing DA levels

A

Amphetamine, Cocaine, Nicotine, Morphine

*all increase release of DA in nucleus accumbens

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11
Q

How do Addicting drugs like cocaine also have an effect on memory?

A

drug abuse and environmental cues activate cortical regions in brain (ie watching a cocaine video increases amygdala activity - responsible for memory)

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12
Q

Sites of action:

What drugs are considered Class I and where do they act

A

Class I: opioids, THC, GHB,

act on GPCRs in VTA

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13
Q

Sites of action:

What drugs are considered Class II and how/where do they act?

A

Class II: BZ, nicotine, EtOH

act on ion channels in VTA

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14
Q

Sites of action:

what drugs are considered Class III and where do they act?

A

Class III: cocaine, amphetamine, exstasy (MDMA)

act on monoamine transporters (ie MDMA acts on serotonin transporter, cocaine and amphetamine on dopamine) in both VTA and NAc

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15
Q

all addictive drugs…

A

increased DA in NAc

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16
Q

What types of drugs are considered CNS depressants? how do they work?

A

Alcohol: commonly abused, severe withdrawal

Sedative Hypnotics:
Barbiturate - no longer common
BZ - combined with other drugs

Work at GABAa receptor (increase GABAa receptor activity = increased CNS depression)

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17
Q

how do you treat alcohol abuse (a CNS depressant drug of abuse)

A

Naltrexone (opioid antagonist)
Disulfiram (neg SE)
Acamprosate (GABA analogue)

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18
Q

What drugs are considered opioids

A

Heroin
Morphine
Codeine
Oxycodone

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19
Q

How/why are opioids typically used?

A

Recreational use: produce sense of euphoria, reduces anxiety

*tolerance builds quickly, become physically dependent, severe withdrawal

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20
Q

How do you treat opioid (heroin, oxycodone, codeine, morphine) abuse?

A

Naltrexone (opioid antagonist)

Methadone (keeps levels constant)

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21
Q

What drugs of abuse are considered CNS stimulants

A

Amphetamines (ex Ritalin, Adderall, or Meth/ICE)

  • increases release of DA, reverses DA transport through DAT (DA not able to be taken up at postsynaptic receptor)
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22
Q

What are therapeutic uses of CNS stimulants

A

Narcolepsy, ADHD (Ritalin, Adderall)

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23
Q

what CNS effects and peripheral effects due CNS stimulants (ampethamines, ritalin, adderall) have?

A

CNS:

  • alertness, euphoria, excitement
  • appetite suppression
  • aggression, paranoia, delusions

Peripheral: increase BP, cardiac stimulation (may cause HF)

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24
Q

What withdrawal sx present when CNS stimulants (amphetamines) are dc

A

increased appetite, fatigue

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25
Q

Methamphetamine aka ICE, crystal meth… MOA, effect?

A

Increases release of DA and NE in basal ganglia

  • more CNS effects that amphetamine (alert, euphorai, excitement, appetite suppression, aggression, delusions)
  • may produce amphetamine psychosis
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26
Q

What long term/chronic effects does Meth have that are related to its addictiveness?

A

Chronic use may cause permanent neurotoxic damage to Noradrenergic and serotonergic neurons

  • long term personality changes common
  • rapid physical and psych dep
  • craving in abstinence intense
  • withdrawal may be severe and long lasting
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27
Q

What dangerous SE besides the addictive properties, does Meth have

A

Cardiac toxicity - Pulmonary edema and HF

seizures, organ damage, stroke, heart attack

28
Q

DA transporter related SE of Meth include

A

meth induced loss of DA transporters (down reg DA transporters due to continuous stimulation) –> deficiency in both motor and memory

29
Q

other SE of meth include

A

wt loss, whiter skin, odor (hyperthermia), dilated pupils, dental problems “meth mouth”, formication “meth bugs”,

30
Q

What is cocaine and it’s MOA

A

alkaloid found in leaves of erythroxylon coca; ingredient of coca-cola until 1903

MOA: inhibits DA reuptake (blocks DAT, increases DA in cleft)–> physical and psych dependence

31
Q

what effects does cocaine have? CNS, peripheral, Medical

think stimulant, SNS!

A

CNS stimulation: alertness, euphoria, anxiety, hyperactivity

Peripheral effects: cardiac
- tachy, vasoconstriciton, HTN, bronchodilation, hyperprexia, dilated pupils (all SNS)

Medical:
local anestheic, vascoconstrictor

32
Q

Chronic cocaine use can result in

A

reduction in overall brain activity

  • anxiety, insomnia, paranoia, hallucinations, repetitive behaviors, “cocaine bugs” (Formication)
  • nasal congestion and perforated nasal septum
  • intense psychological dependence (dysphoria, craving when levels drop)
  • withdrawal can be severe
33
Q

Describe cocaine potential OD/toxicity effects?

A

ventricular tachycardia and fibrillation, stroke, cerebral hemorrhage, seizures

34
Q

which is worse: cocaine or meth withdrawal

A

meth

35
Q

What is recommended tx/recovery process

A

detox and withdrawal
abstinence
long term support, 12 step, avoid environmental cues
Pharm: Bromocriptine to decrease cocaine craving

36
Q

What drug helps with cocaine recovery

A

bromocription (activates DA receptors to prevent craving)

37
Q

How is cocaine normally taken

A

intranasally (immediate onset of action)
“freebase” (can be inahled) -even faster onset
“crack lung”
“crack babies”

smoking & IV fastest

38
Q

What is Nicotine MOA

A

activates nicotinic receptors in CNS and periphery
*increases 5-HT and DA release
CNS effects

39
Q

What effects does Nicotine have on the body

A

CNS stimulant = mild euphoria, increased arousal, appetite suppression

  • intense psych and physical dependence
  • difficult withdrawal can last mths
40
Q

PK of nicotine?

A

rapid absorption, half life 30 min, CYP450 metab, induces CYP450

41
Q

how do you treat nicotine withdrawal

A

Bupropion

*treats craving, DA reuptake inhibitor

42
Q

how does smoking effect nicotinic receptors

A

smokers have excess nicotinic receptors during first month of abstinence

43
Q

What is MDMA and it’s MOA

A

3.4 Methylenedioxymethamphetamine
aka “ecstasy”
increases 5-HT activity by blocking reuptake and stimulating 5-HT receptors

*increases serotonin activity

44
Q

How does MDMA affect the body

A

produces feelings of peacefulness, empathy, closeness and trust followed by confusion, depression, anxiety and paranoia
*increased BP and HR

45
Q

SE of MDMA?

A

increased BP and HR, Hyperthermia, dehydration, kidney failure can lead to fatalities
Persistent memory loss may occur

46
Q

outline the short term effects of MDMA

A

1) during excstasy, elevated mood due to increased 5-HT (blocked SERT, more serotonin in synapse)
2) After ecstasy: depression like feeling and irritability due to decreased 5-HT (down reg of serotnin receptors)
- decreased cerebral blood flow

47
Q

what are long term effects of MDMA

A

significant decreases of serotonin present in cerebral cortex neurons (even 7 yr post ecstasy)

48
Q

What is marijuana, how is it taken? pk?

A

delta–tetrahydrocannabinol (THC)

  • smoked or eaten;
  • quick absorption,
  • very lipophilic, long half life
49
Q

What are the effects of THC/marijuana?

A

Produces state of mild euphoria, well-being, altered sense of time, difficulty concentrating, introspection, tranquility

*no physical dependence; psych dependence possible

50
Q

what is a unique aspect about THC?

A

no physical dependence or neuro adaptations

51
Q

what is THC/cannabinoids MOA?

A
  1. Targets presynaptic cannabinoid (CB1) receptors
  2. Inhibits NT release (glutamate and ACh)
    * bind CB1, and inhibits glutamate and ACh
52
Q

What are adverse effects of MDMA?

A
  • anxiety, decreased memory, impaired cognitive functioning
  • amotivational “lazy” syndrome
  • bronchial irritation, ^CA risk
  • dec ovulation and test/sperm
  • LBW, fetal malformations
53
Q

What are bath salts? frequency of use?

A

synthetic “cannabinoid” AGONISTS
1/9 HS seniors
- psychoACTIVE effects

54
Q

what effect do bath salts (CB agonists) have?

A

psychoactive:
paranoia, hallucinations, mood swings, aggression, outbursts

  • elevated BP, HR
  • not tested for human effects, high rate ER visits
55
Q

what are some medical uses of marijuana

A
  • decreased IOP (tx glaucoma) not proven to be effective
  • decreased spasticity/ataxia, muscle weakness (tx MS, cerebral palsy, spinal cord injuries
  • analgesic (cancer pain, post op pain, phantom limb)
  • appetite stim
  • antiemetic
  • bronchodilation (asthma)
56
Q

what are LSD, mescaline, & psilocybin?, MOA? effect?

A

Lysergic acid diethylamide (LSD)

  • acts on 5-HT receptors in brain (not addicting, don’t stim DA pathway)
  • euphoria, visual hallucinations, altered sense of time and reality, bad trips/flashbacks
  • Synesthesia: one sensory modality assumes characteristics of another (colors hear or sounds seen)
57
Q

what are SE of LSD

A

may increase BP, HR
flushing, dilated pupils
“bad trips”; flashbacks
altered sense of time, reality, synesthesia, euphoria, visual hallucinations

58
Q

What are PCP, Ketamine, GHB? MOA?

A

Developed as general dissociate anesthetics (ketamine used as horse tranquilizer)

PCP (angel dust) and ketamine are NMDA receptor antagonists (glutamate hypothesis)

GHB is a GABA receptor weak agonist

59
Q

what effects do PCP, Ketamine, and GHB have on the body?

A
  • dissociative anesthetics, sensation of dissociation or “floating”
  • PCP and ketamine may cause analgesia and aggression
  • may produce amnesia and personality changes
  • PCP often produces psychosis, (treat with haloperidol in ER)
  • ketamine, GHB “date rape”
  • increase BP, may cause coma with non reactive pupils
60
Q

what are the date rape drugs

A

ketamine and GHB

61
Q

what does PCP often cause, and how do you treat it?

A

PCP –> psychosis

treat with haloperidol in ER

62
Q

increased BP, coma and non reactive pupils… cause?

A

PCP, Ketamine, GHB

63
Q

what are inhalants and what effect do they have? MOA?

A

chem vapors (huffing)

  • household cleaners, solvents, nitrates, ketones, hydrocarbons
  • produce sense of euphoria
  • mech unknown
  • toxicity in many organs; lesions in brain’s white matter
64
Q

What is nitrous oxide and how is it used

A

inhalant with rapid, short acting pleasurable effects

  • causes peripheral neuropathy with chronic use
  • OD can be fatal
  • overused by dentists
65
Q

what are amyl and butyl nitrite? effect?

A

“poppers” or “snappers”
SM relaxants
euphoria, light headedness, blurred vision, HA, nausea, hypoTN, tachycardia

Pharm III (9 decks)

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