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Clinical Neuroscience 2 > Pharm- 18 > Flashcards

Pharm- 18 Flashcards

1
Q

What is substance dependence/addiction?

A

maladaptive use leading to significant impairment or distress
Symptoms: loss of control, salience to the behavioral repertoire, and neuroadaptation
Fundamental element: drug-seeking

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2
Q

What is tolerance?

A

decreased effect of a drug that develops w/ continued use; the dose-response curve shifts to the right as larger doses are needed to produce the same response

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3
Q

What is acquired tolerance?

A

epeated administration of a drug shifts the dose-response curve of the drug to the right, therefore a larger dose of the drug is required to produce the same effect

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4
Q

What is innate tolerance?

A

preexisting interindividual variations in sensitivity to the drug ; exist prior to the first administration of the drug

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5
Q

What pharmacokinetic properties of tolerance result from the increased capacity to metabolize or excrete the drug?

A

Results in a lower concentration of drug at its site of action for any given dose

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6
Q

What are the pharmacodynamic causes of tolerance?

A

caused by neuronal adaptations resulting in reduced response to the same concentration of drug at its site of action in the NS.

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7
Q

What are the short-term exposure dynamics of tolerance?

A

induces neuroadaptive changes in NT release and clearance from the synapse, ↓ in the number of NT receptors, altered conductance of ion channels, or modified signal transduction

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8
Q

What are the long-term exposure dynamics of tolerance?

A

euroadaptive changes in the expression of genes of relevant to the pharmacologic action of the drug

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9
Q

What is dependence?

A

defined only indirectly by: 1) tolerance, 2) emergence of a withdrawal syndrome upon drug discontinuation or administration of a specific antagonist, 3) drug “craving”, 4) drug-seeking behavior manifested as a result of conditioned stimuli after withdrawal has abated

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10
Q

What is physical dependence?

A

initial symptoms experienced after withdrawal; results from the same mechanisms that produce tolerance

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11
Q

What is psychological dependence?

A

resetting of the reward system of the brain as a result of repeated drug use

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12
Q

What is dependence syndrome?

A

need for the drug to be present in the brain to maintain “near-normal” functioning

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13
Q

What happens in acute withdrawl syndrome?

A

occurs when the drug eliminated from the body therefore it no longer occupies its site of action as a result the adaptations that produced dependence are expressed; these symptoms last until the system re-quilibrates to the absence of the drug (days)

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14
Q

What happens in protracted withdrawl syndrome?

A

characterized by a craving for the drug and may emerge and continue for forever; intense preoccupation with obtaining the drug

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15
Q

Medial forebrain bundle and ventral tegmental area (VTA) in the midbrain are the source for what?

A

pleasure/reward centers ;-)

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16
Q

What is the fxn of the nucleus accumbens?

A

crucial for the brain reward pathway
Reinforces motivated behavior and facilitates learning and memory via links to the hippocampus, amygdala, and prefrontal cortex

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17
Q

What is the main NT for the reward pathway of the brain?

A

Dopamine

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18
Q

What class of drug does oxycodone and heroin belong to?

A

opioid

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19
Q

What happens in cross-dependence?

A

multiple inputs into brain reward circuits underline the potential for co-occurrence of addiction to opioids and to other pharmacologically disparate drugs of abuse

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20
Q

Opioids- mech of action

A

Interacts w/ Brain Reward System via μ- opioid receptor: 1) Venral tegmental area- disable GABAergic interneurons; these interneurons naturally inhibit dopaminergic; disinhibit dopaminergic neurons in the VTA 2) Localized in the Nac; inhibit GABAergic neurons that project back tot he VTA (inhibitory feeback loop)

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21
Q

Opioids- Sx

A

Euphoria, followed by sedation, respiratory depression (heroin is hydrophobic –> quickly cross BBB –> quicker high –> more addictive)

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22
Q

Opioids- withdrawl Sx

A

High potential for withdrawal symptoms upon discontinuation of an opioid therfore pt needs to be tapered off

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23
Q

How does buprenorphine Tx opioid detox?

A

partial agonist; binds to and modulates μ-opioid receptor- mediated reward circuits –> diminishes cravings for opioids

24
Q

How does naloxoneTx opioid detox?

A

competitively block binding of opioids to the μ- opioid receptor (Naloxone [opioid overdose; rapid reversal of opioid activity] & Naltrexone [opioid dependence])

25
Q

How does methadone Tx opioid detox?

A

synthetic opioid agonist that binds and activates the μ-opioid receptor; opioid detox and severe pain

26
Q

The drugs triazolam, Phenobarbital, diazepam, clonazepam belong to which class?

A

Benzos/barbs

27
Q

Benzos/barbs- abuse potential

A

All sedative-hypnotics are can cause dependence; however risk of abuse is decreased if they are used cautiously in a time-limited fashion; rarely cause death due to overdose when used alone [combine with EtOH –> death]

28
Q

Benzos/barbs- mech of action

A

Increase efficiency of GABAergic (GABAA receptors) pathways; chronic use lead to down-regulation of these pathways by neuroadaptation –> leaves the brain “uninhibited” –> increasing the possiblity of seizures and derlirium [actions of barbituates are more widespread than those of GABAA- specific benzodiazepines]

29
Q

Benzos/barbs- Sx

A

sedation, respiratory depression, hypnotic; euphoric feelings

30
Q

Benzos/barbs- Withdrawl Sx

A

anxiety, sleep disturbance, dizziness, and emotional concomitants (ex: fear and panic) [barbituate dependence is associated w/ more serious withdrawal symptoms than benzodizipines]

31
Q

What drug is used to manage barb withdrawl?

A

Phenobarbital

32
Q

What drug is the most prevalent drug problem in the US?

A

alcohol

33
Q

Alcohol- mech of action

A

increases GABA mediated Cl conductance and enhances hyperpolarization of neurons. NMDA recepot leads to the development of tolerance and dependence.

34
Q

Alcohol- Sx

A

intoxication, sedation, memory loss, eurphoria

35
Q

Alcohol- withdrawl Sx

A

Emotional volatility, rapid emotional changes, anxiety, fatigue, hand tremors, delirium tremons; can be severe and even life-threatening

36
Q

How does disulfiram treat alcohol withdrawl?

A

inhibits aldehyde drhydrogenase, .’. inhibits the metabolism of acetaldehyde (the produce of EtOH)

37
Q

How does acamprosate treat alcohol withdrawl?

A

stimulates GABAnergic neurotransmission in the brain and antagonizes the affects of glutamate. active at GABA(B) receptors. For ABSTINENCE.

38
Q

Nicotne/ Tobacco- addiction potential

A

high addiction potential due to strong and direct effects on the mesolimbic reward path, inhalation route, and short half-life

39
Q

nicotine- mech of action

A

activates nicotinic acetylcholine receptors that are located centrally, peripherally, and NM junctions. Cholinergic neurons arising from the laterodorsal tegmental area (border of midbrain and pons) activate nicotinic and muscarinic acetycholine receptors on dopaminergic neurons in the ventral tegmental area –> activates dopaminergic brain reward path

40
Q

Nicotine- Sx

A

anxiolytic effects, increased arousal, suppresses appetite, increases bp and stimulates smooth muscle contraction

41
Q

Nicotine- withdrawl Sx

A

strong spontaneous withdrawal syndrome: irritability, anxiety, autonomic arousal, and intense craving and associated drug-seeking behavior

42
Q

How does varencline treat nicotine withdrawl?

A

It’s a partial α4β2 nicotinic receptor agonist that prevents nicotine stimulation of mesolimbic dopamine system.

43
Q

How does buproprion treat nicotine withdrawl?

A

inhibits reuptake of dopamine and NE and aids in qutting smoking

44
Q

Cocaine/Amphetamine- abuse potential

A

substantial abuse liability

45
Q

Cocaine- mechanism

A

Blocks/reverses the direction of neurotransmitter transporters that mediate reuptake of the monoamines (dopamine, NE, and serotonin) into presynaptic terminals thereby aiding in neurotransmission [cocaine blocks Dopamine Transporter (DAT) & and amphetamines reverse the direction of all three monoamine transporters (most effective at NE transporter)]

46
Q

Cocaine- Sx

A

Sense of well-being, energy, and optimism associated, with stimulant intoxication, euphoria, alertness, hypertension, paranoia (these drugs act on the locus ceruleus [maintaing alertness and and responsiveness to unexpected stimuli] & midbrain dopaminergic neurons

47
Q

Cocaine- withdrawl Sx

A

bradycardia, sleepiness, and fatigue, dyphoria, anhedonia (inability to experience pleasure) [symptoms of withdrawal can appear even when the drug levels in the plasma are high; occurs bc of allostatis of the reward path and bc of tachyphylaxis (target tissue becomes less response to constant concentrations of a drug due to depletion of NT)]

48
Q

What do desipramine and fluoextine treat cocaine withdrawls?

A

reduce cocaine craving but do not prevent cocaine use.

49
Q

Cannabinoids- abuse potential

A

slightly addictive

50
Q

Cannacinoids- mech of action

A

Δ9- tetrahydrocannabinol (THC) is a partial agonist for the G protein-coupled type-1 cannabinoid receptor (CB1) which are found in the prefrontal cortex, hippocampusm amygdala, basal anglia, and cerebellum

51
Q

Cannabinoids- Sx

A

euphoria, laughter, giddiness, and depersonalization; after 1-2 hrs, cognitive functions such as memory, rxn time, coordination, and alertness are comprimised, difficulty concentrating; tolerance is due to down regulation of CB1 receptors expression and post-translational modifications FDA approved cannabinoid used for the treatment of chemotherapy related nausea and vomiting and AIDS associated weight loss

52
Q

Cannabinoids- withdrawl Sx

A

generally mild; insomnia, loss of appetite, irritability, and anxiety

53
Q

Phencyclidine (PCP)- mechanism

A

NMDA antagonist

54
Q

PCP- Sx

A

hallucinations and hostile behavior, anesthesia, delirium, intense paranoia, and amnesia

55
Q

MDMA (ecstasy)- mech of action

A

serotonin (mainly affected; causes serotonin release into the extracellular space, inhibition of synthesis, and blocks reuptake [increase conc in extracellular space and depletion]), dopamine, adrenergic (reuptake inhibitors, multiple actions)

56
Q

MDMA- Sx

A

euphoria, alertness, hypertension, and hallucinations; central stimulant effect w/ hallucinations

57
Q

Inhalants- Sx

A

dizziness and intoxication; low doses (mood changes and ataxia) & high doses (dissociative states and hallucinations)

Clinical Neuroscience 2 (16 decks)

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