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Psychophysiology > Week 4 > Flashcards

Week 4 Flashcards

1
Q

Regions in the brain that are activated by substances

A

Basal Ganglia – motivation, habits, routines
* Repeated Exposure = ↓ sensitvity = Tolerance)

Amygdala - anxiety, irritability, and unease
* Withdrawal feelings = Motivation to seek out drug

PFC - plan, solve problems, make decisions, and exert self-control over impulses
* reduced impulsive control, not done in adolescents so at risk for substances

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2
Q

The structures involved in the reward system

A

Ventral Tegmental Area (VTA)

Nucleus Acumbens

Amygdala

Hippocampus

Prefrontal cortex

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3
Q

Reward system: VTA

A
  • Dopamine-rich nucleus that mediates reward system
  • Located in midbrain, next to the substantia nigra
  • Sends dopamine to the nucleus accumbens, amygdala, hippocampus,and prefrontal cortex. –> START of system
  • ↑ VTA pathways – implicated in OCD
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4
Q

Reward system: Nucelus Acumbens

A

Involved in all motivationally-relevant stimuli –> both rewarding or aversive.

Interface between motivation + action (connection to caudate nucleus)

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5
Q

Reward system: Amygdala

A

Happiness & Enjoyment

Anxiety, irritability, and unease - Withdrawal feelings = Motivation to seek out drug

helps you like soemthing, and not .ike something

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6
Q

Reward system: hippocampus

A
  • Memory and learning
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7
Q

Reward system: Prefrontal cortex

A

Reasoning, problem-solving, impulse control, creativity, perseverance

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8
Q

What are the two dopamine pathways

A

Mesolimbic and mesocortical

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9
Q

Mesolimbic

A

route between VTA, Nucleus accumbens, and
limbic system (hippocampus & amygdala)
* Key Pathway in Pleasure and Reward.
* Substance use

EMOTIONAL aspect of wanting to use a substance again

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10
Q

Mesocortical

A

route between VTA/Nucleus accumbens and
PFC.

BEHAVIORAL aspect of going adn getting drug

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11
Q

What hormone is released in stress and what does it do (substance use)

A

cortcotropin-releasing hormone (CRH) is released
* Strengthens the Amygdala (strengthens emotional response)
* Weakens the hippocampus & prefrontal cortex (hippocampus: don’t want to remember)

You are then at greater risk for substance use:
* Negative emotional state
* Lack of executive control =↑ risk of relapse
* Memory of relief/cravings

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12
Q

Substance use and stress research studies

A
  • 1/3 adol with reported abuse/neglect will develop a SUD before 18.
  • 2-4x of those with PTSD developing chemical dependencies.
  • SGM across lifespan = ↑ risk of TUD and AUD + homelessness = 5x
  • COVID-19 = ↑ 23% increase in AUD
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13
Q

Is stress a universal construct?

A

Yes and no

Asian show more physical symptoms of stress
Americans report emotional feeling of stress

East asiains more stress with relationships
Europeans more stress around indivdiual
stuff

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14
Q

Neural effects of SUD

A

Cocaine, pathological gambling, nicotne = ↓
gray matter in PFC

Leads to hypofrontality: decreased PFC activity
–> see this in Schizophrenia

Schizophrenia:
- high comorbidites with SUD
- 70-90% nicotine dependence
- Smokers with psychiatric conditions = 34% of all
cigarette use
- AUD = 10.1%; Schizophrenia = 9.0%; together = 16%

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15
Q

Chicken or Egg: shchizophrenia and nictoine

A

Does schizophrenia cause nicotine addiction,
or does nicotine addiction cause schizophrenia

See high rates of smoking before onset, also see onset after

Does high rates of smoking before onset cause hypofrontality that we see in schizophrenia? or does hypofrontality seen in schizophrenia cause individuals with schizo. to be more susceptible to drug use

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16
Q

Peptides

A

Peptides are two or more amino acids linked by peptide bonds

Many of these are: Endogenous Opioids Receptors

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17
Q

Endogenous opioid receptors

A

Widely distributed throughout the CNS and PNS – produced by the body itself

Fxns include =
* Modulation of pain response
* Reward and reinforcement
* Inhibits flee response

18
Q

Endogenous peptides vs exogenous peptides and substance use

A

Endogenous peptides mediate the reward and reinforcement properties
* Natural opioid receptors exist in the body
* Your body naturally produces and releases opioids to opioid receptors

Drugs of abuse/Exogenous Peptides = ↑ endorphins and enkephalins –> GIANT DOPAMINE SURGE
- Our brains are like wow that was amazing, lets do that again

19
Q

CDC Guidlines for drinking

A

Moderate drinking not good for you, but can be made better through healthy lifestyle

Moderate drinking guidelines (CDC)
* Females = up to 1 drink per day
* Males = up to 2 drinks per day

Heavy Drinking
* Females = 8 or more per week
* Males = 15 or more per week

Binge Drinking (in 2-3 hours)
* Females = 4 or more
* males = 5 or more

20
Q

Marketing of alcohol towards woman

A

Sugar = ↓ absorption (prolongs effects) –> drunk longer

Carbona􀆟on = ↑ absorption –> drunk faster

Menstruation = ↓ etoh metabolism –> drunk faster

21
Q

SES and alcohol

A
  • Greatest etoh use at ends of SES ranges.
22
Q

Pharmacokinetics of Ethanol

A

Absorption: GI Tract = 20% stomach & 80% small intestine (several variables)

Metabolism: Primarily hepatic (90%) (see next slide for details)

Excretion = Urine
* Diuretic properties –> decreased nutrients & dehydration

Intoxication = consuming etoh faster than liver can break it down

23
Q

Pharmacokinetics of Ethanol: metabolism

A
  • Metabolized by Alcohol Dehydrogenase (ADH) (requires B vitamins) –> Acetaldehyde
  • Acetaldehyde (toxic, carcinogenic, prevents absorption of nutrients) metabolized by aldehyde dehydrogenase (ALDH) –> Acetate

(Approximately 36% of East Asian subjects experience an alcohol induced flush reaction d/t deficient enzyme levels of aldehyde dehydrogenase.

24
Q

Thiamine deficiency

A

80% of ind. With AUD = Thiamine Deficiency D/T ↓ Vitamin
Absorption & ↑ Thiamine use by ADH

Reason one: alcohol dehydrogenase requires B vitamins

Reason two: alcohol impacts your ability to absorb nutrients

25
Q

Neural effects of Alcohol use

A

OVERALL: CNS DEPRESSANT

  • ETOH is an Indirect GABAA Receptors Agonist = has Sedation effect (like benzos)
    –> Impairs memory functioning (hippocampus)

Over inhibition: Receptor Downregulation
- Cerebellum –> loss of coordination & consciousness
* PFC –> decreased inhibition
* Blocks Vasopressin = ↑urination & dehydration

Exception = ETOH = indirect antagonist of GABAA in the
mesolimbic pathway –> so it decreases the amount of GABA in the mesolimbic pathway, which leads to increase of serotonin and dopamine, which is why you get
addicted

Because of receptor downregulation: Withdrawal =↑ seizures
* your body doesn’t want to be in constant state of sedation, so your body has to exciite iteself more. When you take away that sedation (alcohol), you have seizures (too excited)

26
Q

Wernicke-Korsakoff Syndrome

A

From thiamine deficiency
* Thiamine plays roles in brain cell energy production & maintenance and synthesis of myelin

Two conditions:
* Wernicke’s Encephalopathy (WE) – ACUTE phase, WILL DIE = delirium, incoordination, ataxia, decreased consciousness, memory deficits, abnormal gait

Korsakoff Psychosis – can develop after (WE) or without – CHRONIC phase = anterograde > retrograde amnesia & confabulation –> not reversible

27
Q

Alcoholic Neuropathy

A

Nerve Damage

28
Q

Alcoholic Cerebellar Damage

A

Deterioration of cerebellar neurons

Chronic incoordination, slurred speech, jerky movements, tremor, nystagmus

29
Q

Alcoholic Myopathy

A

Progressive muscle damage

Symptoms include muscle atrophy, stiffness, spasms & cramps

30
Q

Fetal alcohol syndrome disorders

A

FASD is an umbrella term for a range of
physical, cognitive, and behavioral disorders
caused by prenatal alcohol exposure

  • 1-5% of 1st grade children has FASD`
31
Q

Stimulant Pharmacokinetics

A

Stimulants impact the brain’s levels of epinephrine/norepinephrine (E/NE), dopamine (DA), and serotonin (5-HT).
* Stimulants impact each to a varying degree (selectivity).
* Cause alertness, attention, energy.

Primary risk factors:
* Reduced seizure threshold (body too excited)
* ↑ BP, HR, HTN = ↑ risk of stroke, MI
* Poor appetite, mood swings, anxiety, insomnia
* Toxic levels = paranoia, psychosis

32
Q

ADHD – improvement in symptoms from medication

A

Fewer excitatory NTs available in their nervous system?

80% improvement in symptoms with medication

33
Q

Nicotine Pharmacokinetics

A

Absorption
* Tobacco smoke – enters blood stream via lungs (inhalation)
* Smokeless tobacco – mucosal membrane of mouth, nose, or skin
* Reaches the brain in 7 seconds
* Mimics Ach = arousal, learning, memory, and emotions

Effects
* Binds to nicotinic receptors –> changes cerebral metabolism
* Stimulates adrenal glands –> increases BP, HR, respiration, alertness + epinephrine

Metabolism & Excretion
* ↑ metabolism in general
* Metabolized by liver, lungs, kidneys
* Excreted via urine

34
Q

Endocannabinoid system

A

The endocannabinoid system comprises a
vast network of chemical signals and cellular
receptors that are densely packed throughout
our brains and bodies. A neuromodulation
system.

CB1 receptor –> THC
* ↑ in brain and lower conc. wide spread
* Mediates most of the psychoactive
effects of cannabinoids.

CB2 receptor –> CBD
* Principally involved in anti-inflammatory
and immunosuppressive actions.

35
Q

Phytocannabinoid

A

biologically active compound found in
cannabis.

36
Q

THC vs HEMP

A

THC Content = <.3% = hemp; >.3% = marijuana

37
Q

Anandamide

A

an endocannabinoid (neuromodulator) found in the
endocannabinoid system.

  • THC mimics anandamide –> effecting the endocannabinoid system.
  • THC much more potent than anandamide
  • Effects energy, mood, appetite, and perception of time.
38
Q

Pharmacokinetics of Cannabis (Cannabinoids)

A

Absorption
* Inhalation – peak plasma conc. 3-10 mins; bioavailability = 10%-35%
* Oral – peak plasma conc. ~ 120 mins, bioavailability = 6%- 20%

Distribution
* Rapidly to well-vascularized organs
* Accumulates in adipose tissue

Metabolism
* Predominantly hepatic
* Able to cross the placenta; released in breast milk
* Excreted through urine, feces, and sweat.

39
Q

THC Neural Effects

A

↓ GABA & ↑ Glutamate = ↑↑ Dopamine (Reward
System)

↑ hunger and thirst (hypothalamus
and thalamus)
↓ coordination, reaction time, and
time perception (Cerebellum)
↓ memory (hippocampus)

Body wants balance –> receptors close –> tolerance

40
Q

Sugar

A

Glucose = primary source of fuel for the brain
* ~20% of glucose-derived energy
* Is necessary - provides precursors for NT synthesis & apoptosis
* Glucose levels correlated with thinking, memory, learning

High sugar diets = ↓ brain-derived neurotrophic factors (BDNF)
* increases risk of neurodegenerative

Should only have: 6-9 tsps

41
Q

Halluciongens

A

2 categories

Classic (e.g., LSD, psilocybin, peyote)
* Impact serotonin

Dissociative (e.g., PCP, ketamine) – contribute to reduced control and disconnection
* Dextromethorphan (cough syrup)
* Interferes with glutamate

42
Q

Technology Addiction/”Internet Gaming Disorder”

A

Teens aged 13-18 spent about 8.4 hours a day on screens

  • “Likes”, “Re-Tweets”, “Novelty” = ↑ Mesolimbic Activation
  • Need to check alerts = Compulsion?
  • ↑ use = ↑ SUD, ADHD, Depression, Anxiety, poor coping
  • Role of COVID-19
  • Triggers = boredom, isolation, low self-esteem

Psychophysiology (13 decks)

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