Physiological Psychology Lecture #6 Flashcards

1
Q

Language

A
  • Larynx changes location 300,000 years ago.
  • More sounds, greater vulnerability to choking.
  • Speech gene evolved by natural selection 100,000 to 200,000 years ago.
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2
Q

When did language emerge?

A

over 100,000+ years ago.

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3
Q

Lateralization Issues

A

Left: language in most person (95%)

Right: narrative speech, map reading, prosody, also language.

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4
Q

Left Handedness

A

10% of the population
- Excel in visual spatial analysis?
- Top 0.1% of SAT 2x as likely to be left-handed.
- Higher level of education.
- Overly represented at the other end of the continuum = criminals
- 2018, more than 2x the risk of developing breast cancer before reaching the menopause than right-handed women.
- Less lateralization than right-handers: 70% (15% R; 15% both).

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5
Q

Future of Language

A

6000 languages exist.
-80% have not been documented
-90% will become extinct in the coming century.
-One language dies every 14 days.

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6
Q

Broca’s Aphasia

A

“Broken, Non-fluent”
- Anterior to motor cortex = impaired speed processing.
- Expressive aphasia.
- Worsens with anxiety or pressure demands.
- Generally aware.

BMF = Broca, motor, frontal lobe

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7
Q

Wernicke’s Aphasia

A

“Fluent”
- Posterior portion of temporal lobe and by the primary auditory cortex = impaired comprehension.
- Receptive aphasia.
- Impaired language comprehension.
- Often unaware.
- Can occur in those who are deaf.

W = wacky, words, or word salad.

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8
Q

Global Aphasia

A

Impairments in both.

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9
Q

Learning

A

Acquisition for new information.

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10
Q

Stages of Learning

A
  1. Sensory Information
  2. Short-Term Memory
  3. Long-Term Memory
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11
Q

Stage 1 of Learning

A

Sensory Information
- Information is first processed through out senses.
- <1 second

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12
Q

Stage 2 of Learning

A

Short-Term Memory
- Meaningful/salient information.
- <1 minute.
- Can support via repetition and chunking (7 +/- 2 Rule)

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13
Q

Stage 3 of Learning

A

Long-Term Memory
- Short term memories are converted into long term memories = consolidation.
- Can be retrieved across a lifetime.
- Increase retrieval (rehearsal = strengthening of memory)
- Involves the hippocampus.

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14
Q

What is the 7 +/- 2 Rule?

A

*Can remember 7 +/- 2 things at a time

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15
Q

What are the types of learning?

A
  1. Stimulus-Response Learning
  2. Motor Learning
  3. Perceptual Learning
  4. Observational Learning
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16
Q

Stimulus Response Learning

A

Perform behavior when stimulus is present.

Classical Conditioning involves the:
- Amygdala
- Hippocampus
- Thalamus

Operant Conditioning involves the:
- Positive and negative reinforcement/punishment.
- Mesolimbic and mesocortical system support learning.
- Basal Ganglia - takes over actions as “over learned motor behaviors.

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17
Q

Motor Learning

A

Learning a skilled task and then practicing with a goal in mind until the skill is executed automatically.
- Moving an action from the conscious to unconscious –> Basal Ganglia.

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18
Q

Perceptual Learning

A

When repeated exposure enhances the ability to discriminate between two (or more) otherwise confusable stimuli.
- Allows us to identify and categorize objects.
- Prior experience influence your perception of stimuli (attribution bias, confirmation bias)

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19
Q

Observational Learning/Social Learning Theory

A

Process of learning by watching behaviors of models.
- Occurs via operant conditions and vicarious conditioning.

More likely to mimic models who:
- Positive perception
- Shared (perceived) traits
- Stand out
- Familiarity
- Self-Efficacy in mimicry

  • Social Media
  • Violence in games and entertainment.
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20
Q

Prosocial Modeling

A

Prompts engagement in helpful and healthy bx.

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21
Q

Antisocial Modeling

A

Prompts other to engage in aggressive/unhealthy bx.

EXAMPLE: Bandura Bo Bo Doll–physical aggression.

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22
Q

Mirror Neurons

A

Type of brain cell that respond equally when we perform an action and when we witness someone else perform the same action.
- Essential Neurons for social interactions.
- Lower number is psychopathy and ASD.
- Brain responds the same way to performing, witnessing, and hearing an action.

Believes to enable:
- Empathy/intention
- Skill building through mimicry
- Vicarious experience

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23
Q

No Evidence for What Learning Types?

A
  • Learning styles exist.
  • “Mozart Effect”
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24
Q

Evidence exists for what kind of learning?

A
  • Interleaving/spacing learning
  • Writing rather than typing
  • Studying in natural light.
  • Power nap (caffeine hack)
  • Context-Dependent Learning
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25
Q

Interleaving

A

Concerns shorter periods of time–altering between topics during on study session.

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26
Q

Spaced Learning

A

Enhances when knowledge is repeated after certain intervals.

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27
Q

Procedural Memory

A

Unconscious recall of how to perform an action or skill. (i.e. how to ride a bike)

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28
Q

Episodic Memories

A

Involve context–must be learned all at once (i.e. where you park your car)

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29
Q

Semantic Memories

A

Involve facts without context.
- Facts for which the context does not matter (i.e. the sun is s star)
- Can be acquired gradually over time.

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30
Q

HM and the Hippocampus

A

Prior to Surgery: suffered from severe, intractable epilepsy. Seemed to have epileptic foci in both medial and temporal lobes.

Bilateral medial temporal lobectomy.
- Included removal of hippocampus and amygdala.

RESULTS:
- Convulsions reduced in severity and frequency.
- IQ increased from 104 to 118
- Remained emotionally stable with generally superior psychological abilities.
- Also produced devastating amnesia.

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31
Q

When does memory peak?

A

Age 8

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32
Q

What strengthens long term memory/storage?

A

Reviewing/rehearing materials.
- Storage is not permanent for a few hour to days.

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33
Q

Anterograde Amnesia

A
  • Failure in explicit memory
  • Declarative
  • Info available to consciousness
  • Capable of perceptual, motor, and SR learning
  • Failure of relational learning
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34
Q

Retrograde Amnesia

A
  • Failure of implicit memory.
  • Non-declarative.
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35
Q

Strokes

A

“Occurs when something blocks blood supply to part of the brain or when a blood vessel in the brain bursts”.

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36
Q

Infarcts

A

Tissue necrosis d/t stroke

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37
Q

Incidence rates of strokes in the U.S.

A

averaages over 750,000 per year

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38
Q

Risk Factors for CVDs

A
  • Hypertension
  • Diabetes
  • Smoking
  • OSA
  • Obesity
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39
Q

Ischemic Strokes

A

Obstruct the flow of blood.
- Thrombus or Embolus

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40
Q

Thrombus

A

Blood clot in the blood vessels

41
Q

Embolus

A

A piece of material that breaks off and is carried through the bloodstream until it reaches an artery too small to pass through.

42
Q

Hemorrhagic Strokes

A

Cause by bleeding in the brain.
88% ischemic; 12% hemorrhagic

43
Q

Transient Ischemic Attack (TIA)

A

Stroke that lasts only a few minutes.
- 1/3 will eventually have a stroke.
- 50% within 1 year.

44
Q

Initial Damage in Ischemic Stroke d/t Glutamate Ecotoxicity

A

Immediate cause of neuron death is the presence of excessive amounts of glutamate.

Decrease O2 leads to neural membranes becoming depolarized which increases glutamate.
- Inflammation attract microglia.
- Microglia attracts WBC that attach to the region which results in CELL DEATH.

45
Q

Stroke Risk Factors

A

Age (non-modifiable)
Race (non-modifiable)
Family history (non-modifiable)

  • High blood cholesterol
  • Smoking
  • Obesity
  • Medications
  • Heart Disease
  • Physical Inactivity
  • Stress
  • Alcohol
  • High BP
  • Diabetes
46
Q

Circle of Willis

A

Where the internal carotid arteries branch into smaller arteries that supply oxygenated blood to over 80% of the cerebrum.

47
Q

Middle Cerebral Artery (MCA) Stroke

A

90% of strokes.
- Largest of the brain arteries.
- Supplies most of the outer surface of the frontal, parietal, temporal lobes and the basal ganglia.
- Includes pre-central (sensory) and post-central (motor) gyrus.

48
Q

MCA Stroke Symptoms

A
  • Contralateral weakness and sensory loss in upper extremities.
  • Homonymous hemianopia (loss of visual field)
49
Q

Left MCA Stroke Results in…

A
  • Speech Deficits
    Broca’s aphasia and wernicke’s aphasia
50
Q

Right MCA Stroke Results in…

A

Neglect and poor motivation.
- Flat prosody.

51
Q

Anterior Cerebral Artery (ACA) Stroke

A

Less Common.
- LACA > RACA
- Feeds deep structures in the brain, frontal, parietal, corpus callosum and bottom of the cerebrum.

52
Q

Symptoms of ACA Stroke

A
  • Contralateral motor and sensory loss in lower extremities.
  • Poor gait and coordination = clumsy
  • Slowed initiation (abulia)
  • Flat affect
  • Urinary incontinence.
53
Q

Posterior Cerebral Artery (PCA) Stroke

A

5-10% of strokes

54
Q

Symptoms of PCA Stroke

A
  • Impaired consciousness.
  • Nausea/Vomiting
  • Ataxia
  • Vision changes
  • Nystagmus
55
Q

Anteriovenous Malformation (AVMs)

A

Tangle of arteries and veins without connecting capillaries. (1-2% of all strokes)
- Acquired through inborn genetic mutation followed by secondary mutation.
- Variable Size

Damage: compression of neighboring structures, stealing of blood flow from surrounding regions.

Presentation: symptoms onset between 10-40. Intracranial hemorrhage most common presentation.

56
Q

Depression and Stroke

A
  • Post stroke depression = 1/3 of survivors.
  • 6x increase risk of depression 2-3 years post stroke.
  • more common in L frontal and basal ganglia strokes.
  • adversely effects functional recovery.
  • increase risk factors = premorbid depression and social isolation post stroke.
57
Q

Anxiety and Stroke

A
  • 1/4 meet GAD criteria post stroke
  • Less common
58
Q

Psychosis and Stroke

A
  • more common in right-temporo-parietal-occipito are lesions, seizures, and subcortical atrophy.
  • pseudobulbar affect = 10-15% post stroke patients.
  • hypmoanic symptoms = 1%
59
Q

BE-FAST

A

Balance
Eyes
Face
Arms
Speech
Time

*Tissue Plasminogen (tPA) can be administered within 4.5 hours.
- Helps to restore blood flow to brain regions affected by a stroke.
- After that time, has hemorrhagic effect.

60
Q

Ingestive Behavior

A

Correlational mechanisms that replenish the body’s depleted stores of water or nutrients.

61
Q

Intracellular Fluid

A

2/3 volume

62
Q

Extracellular fluid

A

1/3 volume

63
Q

What are the 2 types of extracellular fluid?

A

Intravascular = blood plasma
Interstitial = fluid that bathes the cells

64
Q

Tonicity

A

Ability of a surrounding solution to cause a cell to gain or lose water via osmosis.
- Relationship between interstitial and intercellular.
- Solute concentrate determines movement.

65
Q

Isotonic

A

equal concentration on both sides

66
Q

hypertonic

A

more solute
- water moves out of cells

67
Q

hypotonic

A

less solute
- water moves into cells

68
Q

Negative Feedback Loop

A

Essential characterist of all regulatory mechanisms.

69
Q

Satiety Mechanism

A

empty stomach
triggers hunger
eating
trigger satiation

stop behavior in anticipation of replenishment.
- hunger negative feedback loop takes times to reach the brain (20 min delay)

70
Q

2 Types of Thirst

A

Osmometric Thirst
Volumetric Thirst

71
Q

Osmometric Thirst

A

When tonicity of interstitial fluid increases.
- Salty foods.
- Thirst triggered by cell dehydration.

72
Q

Volumetric Thirst

A

When intravascular (blood plasma) volume decreases aka hypovolemia.
- Causes - bleeding, vomiting, diarrhea.
- Leads to: increased BP, inhibition of water and sodium secretion.

73
Q

Osmoreceptors

A

Neuron that detects change in solute concentration of interstitial fluid.
- Located in the Lamina terminalis (anterior walls of the third ventricle)

74
Q

Natural Dying

A

Dehydration of cells in part of body’s natural dying process.

75
Q

IV fluids do not remain in the vascular system instead cause

A
  • Edema
  • Swelling
  • Eventual respiratory distress
76
Q

Reduction in eating = ketosis which results in…

A
  • reduction in appetite and thirst
  • pain relief
  • euphoria
77
Q

Ghrelin

A

Hormone released by the stomach when individuals are fasting, or the digestive system is empty.

Binds to receptors in the hypothalamus.
- Activates orexin producing neurons.
- Stimulates eating behaviors/hunger (i.e. stomach growling)
- Increases before eating; decreases after eating.

78
Q

High Ghrelin

A

Increased cortisol = stress/anxiety

79
Q

Low Ghrelin

A

Decrease in cortisol = reduced stress and anxiety.

80
Q

Prader-Willi Syndrome

A

Genetic multi-system diagnosis.
- Experience hyper-phagia d/t excessive levels of ghrelin. Never feel satiated.

81
Q

Later Hypothalamus and Hunger

A
  • Stop eating and drinking when destroyed.
  • Overeating when activated.
  • Produces orexin-motivation to eat.

Rats will continue to eat as long as LH is stimulated and will eat double their weight when VMH is removed.

82
Q

Ventromedial Hypothalamus and Hunger

A
  • Suppression of eating when activated.
  • Overeating when destroyed.
83
Q

Adjustable Gastric Band

A

Reduced for first 8 months.
- Reduced volume = ghrelin levels drop sooner.

  • At 8 months, 53% higher than pre-surgery.
  • Not seen in gastric bypass.
84
Q

Wegovy (Semaglutide)

A

Augments insulin secretion to inhibit release of glucagon.
- Increased risk of problems with gall bladder, kidney, diabetic retinopathy, depression, suicidal thoughts/behaviors.

85
Q

Obesity

A

Complex, chronic disease which requires medical attention.
- BMI >30 (flawed method).
- Increased 2x in adults and 3x in adolescents since 2000.

86
Q

Pandemic and Obesity Rates

A

Adults increased 3%
5-11 year olds, increased 9%

87
Q

Food Addiction

A

Dopamine level changes resulting in withdrawal symptoms.

Combination of naltrexone (opioid antagonist) and bupropion (dopamine agonist) produce significant weight loss among individuals with obesity.

88
Q

Sensory and Social Factors

A
  • Experience of eating helps us feel satiated.
  • Nutrition value important.
  • Increase age = decrease in taste.
  • More options = increased intake
  • Larger plate size = increased intake
89
Q

Deficiency in Vitamin D

A
  • Nearly 40-50% of men and women in Denver metro area are deficient in vitamin D.
  • More melanin your skin has, the harder it is to synthesize vitamin D
  • Concurrent use with anti-depressant support.
90
Q

Magnesium Deficiency

A
  • w/ stress can increase agitation, anxiety, sleeplessness, headache, and apathy.
  • Can treat restless leg syndrome.
  • Slow response time to reach steady state via oral supplementation (30+ weeks).
91
Q

Omeg-3 Fatty Oils Deficiency

A

Add on treatment for depression (strong evidence)
- For ADHD (some evidence)

92
Q

Anorexia

A

Twin Studies: 58-78% heredity. Risk increases with premature birth or birth trauma.

93
Q

Associations with Anorexia

A
  • Loss of gray and white matter in the brain.
  • Enlarged ventricles and widened sulci (shrinkage of brain tissues)
  • Inhibited emotional facial expression despite reporting similar or more intense emotions.
  • Tissue loss can. be reversed with successful treatment of the eating disorder.
94
Q

Starvation Study (Anorexia)

A
  • 6 months ate at 50% baseline.
  • Loss 25% of body weight.
  • Demonstrated preoccupation w/ food, ritualistic eating, erratic mood, impaired cognition, slowed eating/lingering.

Post Study = complained of fat on their abdomens and legs.

95
Q

Gender Differences in Anorexia

A

Women ate less post-fast than men.

96
Q

TX for Anorexia

A

CBT, increasing eating speed, stimulation of ACC.

97
Q

Bulimia Nervosa Associated with

A
  • Decreased blood flow to the precuneus (self-perception/memory)–food as a means of distraaction.
  • Amygdala activation. Higher activation when eating than control. Stable when eating post-fasting.
  • Feedback loop of DA, 5HTP, and NE
    Anticipation of binge, consumption of junk foods, anticipation of purging, purging, stress.
98
Q

Vomiting and Bulimia

A

Only eliminates approx. 25% of the calories consumed BUT prolonged dehydration and electrolyte depletion = 5x increased risk of heart attack, overall risk of hypovolemic shock, kidney failure, UTI.