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Physiological Psychology > Exam 3 Review > Flashcards

Exam 3 Review Flashcards

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1
Q

glucostatic mechanism set point

A

-hypothalamus tells pancreas to secrete insulin or glucagon

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2
Q

glucostatic mechanism detector

A

-ventricle walls in brain

-

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3
Q

glucostatic effector

A
  • pancreas and liver
  • liver takes glucose in response to hormones released by pancreas
  • liver is sugar bank
  • pancreas tells liver what to do
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4
Q

why does insulin release cause dip in blood sugar

A

-sends messages to convert glucose to fat, glycogen, or energy

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5
Q

why don’t brain cells have to rely on insulin

A
  • can’t cross BBB
  • glucose gets in via active transport
  • don’t need insulin
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6
Q

ad agencies and conditioning

A
  • cs: picture of food/logo

- cr: sugar level drop so call company to bring back up

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7
Q

argument that diet drinks make you fat

A
  • encourage one to consume more calories b/c sweet taste leads to sugar drop
  • have to eat more to get back to baseline
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8
Q

ucs diet drinks

A

-insulin release in response to blood sugar rise

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9
Q

cs diet drinks

A

-insulin release in response to sweet taste

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10
Q

ucr diet drinks

A

-insulin release

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11
Q

cr diet drinks

A

-insulin release

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12
Q

why is insulin familiar and not glucagon

A

-famous insulin deficit (diabetes)

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13
Q

causes of diabetes

A
  • type 1: pancreas can’t produce insulin- autoimmune (attack producing cells)
  • type 2: decreased sensitivity to insulin
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14
Q

argument against exercise to lose weight

A

-burn relatively few calories during actual activity

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15
Q

argument for exercise to lose weight

A
  • raises body temp for hours
  • increases muscle tone
  • increases serotonin levels (appetite suppressant)
  • stress hormone release (endorphines and glucagon)
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16
Q

why isn’t CCK on open market

A
  • only works if actually in brain and can’t cross BBB

- brain must release

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17
Q

would CCK work as appetite suppressant

A
  • no b/c can’t cross BBB
  • ingestion: pill broken down
  • even if injected, too big
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18
Q

what happened when circulatory system of obese and slim mouse intermingled

A
  • obese mouse got slim
  • slim mouse stayed slim
  • means that obese mouse lacked leptin prior to intermingling
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19
Q

why incentive to develop taste for spicy food

A

-natural preservative

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20
Q

why is SCN above optic chiasm

A
  • receives input directly from retinal ganglion cells

- resets with exogenous sun cycle

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21
Q

evidence to support repair and restoration explanation of sleep

A
  • babies

- sleep more after activity

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22
Q

what does repair and restoration theory leave unexplained

A
  • why large predators sleep so much and small prey don’t
  • prey are herbivores and move much more, but sleep much less
  • sloths hardly move, but sleep a ton
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23
Q

evidence for evolutionary theory of sleep

A
  • dolphins
  • learned to sleep for the necessary restore and restoration but in a way that is not evolutionarily harmful to them
  • one hemisphere at a time
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24
Q

what is paradoxical about paradoxical sleep

A
  • emergent stage 1
  • EOG energetic
  • EEG indicates light sleep (energetic)
  • EMG indicates deep sleep (low muscle tone)
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25
Q

after initial stage 1 sleep, what are later stage 1s

A

-emergent stage 1

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26
Q

part of brain more active during REM

A
  • pons
  • amygdala
  • parietal/temporal lobes
  • some of frontal lobe
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27
Q

emotional urgency of dreams

A

-amygdala

28
Q

vivid imagery during dreams

A
  • parietal/temporal lobes

- space and faces

29
Q

randomness of dreams

A

-pons

30
Q

lucid dreams

A

-frontal lobe

31
Q

why sleep more easily in cool room

A
  • part of getting to sleep requires lowering body temperature
  • chilling brain slows chemical processes
32
Q

why does anxiety increase incidence of insomnia

A
  • anxiety is opposite of relaxtion

- since sleep is relaxation, insomnia is often caused by anxiety

33
Q

why sleep study for impotence

A
  • to make sure it’s not a physiological problem

- if psychological parasympathetic is active during REM and relaxed state allows for penile erections

34
Q

how is sleep apnea misdiagnosed

A
  • recommended therapy would be

* bad idea b/c

35
Q

features of REM

A
  • light sleep EEG
  • deep sleep EMG
  • paralysis if occurs during wakening
  • high activity of limbic system
  • paralysis leads to cataplexy
36
Q

one therapy for sleep apnea

A
  • CPAP
  • anti-histamines
  • weight loss
37
Q

what if REM occurred during waking

A
  • one would have sleep paralysis where only part of the brain is conscious
  • one would also display cataplexy (strong emotions)
  • many also report being wakened during dreaming
38
Q

what if novice administered same dose as habitual user

A

-novice would easily overdose

39
Q

how does habitual user tolerate what novice can’t

A
  • metabolic tolerance- more NZ
  • cellular tolerance- less receptor sensitivity
  • cross tolerance
  • behavioral tolerance
40
Q

cs with drug but not ucs

A

-desperate need

41
Q

ucs with drug, but not cs

A

-easy overdose

42
Q

why cliche to say I can quit anytime I want

A

-habitual users can quit under social pressures, but addict cannot

43
Q

brain chemistry consequences addiction

A
  • physiological- frontal lobe damage (impulse control loss)

- behavioral- hard time imagining future

44
Q

why unlikely to see GABA antagonist on market

A

-brain would be oblivious to effects of alcohol, but the rest of the body would still suffer the consequences

45
Q

clinical uses for marijuana

A
  • anti-enemic

- cranks up appetite too

46
Q

clinical uses for nicotine

A

-none

47
Q

clinical uses for cocaine

A

-topical analgesic or vasoconstrictor

48
Q

clinical uses for opiates

A
  • analgesics reduce pain
  • reduce brain stem activity- codeine cough suppressant
  • reduces digestive activity -> constipation
49
Q

clinical uses LSD

A

-targets emotional aspect of pain

50
Q

heroin attractive for abuse

A
  • targets nucleus accumbens

- stimulates dopamine release

51
Q

marijuana attractive for abuse

A
  • doesn’t target nucleus accumbens
  • doesn’t stimulate dopamine release
  • not addictive
52
Q

cocaine attractive for abuse

A

-stimulates dopamine release

53
Q

barbiturates attractive for abuse

A
  • eases anxiety

- doesn’t give pleasure

54
Q

alcohol attractive for abuse

A
  • cause pleasure

- stimulates dopamine release

55
Q

drawbacks of R015-4513

A
  • GABA antagonist

- would sober, but could encourage over drinking

56
Q

drawbacks of barbiturates

A

-dangerously low TI (30x effective dose)

57
Q

how does marijuana differ from other drugs of abuse

A
  • marijuana is not addictive

- it targets anadamide receptors, not the nucleus accumbens dopamine receptors

58
Q

final exam

A
  • 50 multiple choice questions
  • 35 questions all lecture from previous exams
  • questions from old exams reworded
  • 15 brand new questions (comprehensive)
  • don’t take final if 90% or above
59
Q

effects of duodenum release of CCK

A
  • close pyloric sphinter- food in stomach, full

- stimulates vagus nerve which leads to CCK release in brain

60
Q

nicotine as agonist

A

-direct of ACh

61
Q

barbiturate as agonist

A

-indirect of GABA (alcohol too)

62
Q

cocaine as agonist

A

-indirect agonist of dopamine

63
Q

marijuana as agonist

A

-direct of anandamide

64
Q

opiates as agonist

A

-direct of endorphins

65
Q

LSD as agonist

A

-direct of serotonin

66
Q

direct agonist

A

-binds to and activates receptive sites

Physiological Psychology (7 decks)

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