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Physiological Psychology > Physio Quiz 2 > Flashcards

Physio Quiz 2 Flashcards

1
Q

Lateralization Issues

A
  • Left: Language in most persons (95%)
  • Right: Narrative speech, map-reading, prosody, ALSO language
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2
Q

Left Handedness

A
  • 10% of population
  • Excel in visual spatial analysis
  • higher levels of education
  • overly represented in criminals
  • Less lateralization than right handers
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3
Q

Future of Language

A
  • 6000 languages exist (80% not documented, 90% doomed to extinction in the coming century)
  • one language dies every 14 days
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4
Q

Broca’s Aphasia

A
  • Anterior to motor cortex = impaired speech production
  • expressive aphasia
  • worsens with anxiety or pressure demands
  • generally aware
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5
Q

Wernicke’s Aphasia

A
  • Posterior portion of temporal lobe and by the primary auditory cortex = impaired comprehension
  • Receptive aphasia
  • Impaired language comprehension
  • Often unaware
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6
Q

Learning

A
  • Acquisition of new information
  • Refers to the process by which experiences change our nervous system and our behavior
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7
Q

Learning Stage 1: Sensory Information

A
  • Information is first processed through our senses e.g., echoic memory
  • < 1 second
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8
Q

Learning Stage 2: Short-term Memory

A
  • Meaningful/salient information
  • < 1 minute
  • Can support via repetition or chunking (7+/- 2 Rule)
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9
Q

Learning Stage 3: Long term Memory

A
  • Short term memories are converted into long term memories = CONSOLIDATION i.e., made solid
  • Can be retrieved across a lifetime
  • Increased retrieval i.e., rehearsal = strengthening of memory
  • Involves the hippocampus
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10
Q

Types of Learning

A
  • Stimulus-Response Learning
  • Motor Learning
  • Perceptual Learning
  • Observational Learning
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11
Q

Stimulus-Response Learning

A
  • Perform behavior when stimulus is present
  • Classical conditioning
  • Involves the amygdala, hippocampus, and thalamus
  • Operant conditioning
  • Involves the positive/negative reinforcement/punishment
  • Mesolimbic and mesocortical system support learning
  • Basal ganglia = takes over actions as “over learned motor behaviors”
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12
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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13
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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14
Q

Observation Learning

A
  • Social Learning Theory
  • Process of learning by watching the behaviors of models
  • occurs via operant and vicarious conditioning
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15
Q

Prosocial Modeling

A
  • Prompts engagement in helpful and healthy behavior
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16
Q

Antisocial Modeling

A
  • Prompt others to engage in aggressive/unhealthy behaviors
  • Bandura BoBo Doll - physical aggression
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17
Q

Likely Models to Mimic

A
  • Positive perception (liked, high status)
  • Shared (perceived) traits
  • Stand out
  • Familiarity
  • Self-efficacy in mimicry
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18
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
  • Brain responds the same way to performing, witnessing, and hearing an action
    believed to enable: empathy/intention, skill building through mimicry, vicarious experience
  • Essential brain cells for social interactions
  • Lower numbers in psychopathy and ASD
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19
Q

Learning: Things with no evidence

A
  • Learning styles exist
  • Mozart Effect
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20
Q

Learning: Things with Evidence

A
  • Interleaving/spaced learning
  • Writing rather than typing
  • studying in natural light
  • power nap (caffeine hack)
  • context-dependent learning
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21
Q

Procedural Memory

A
  • Unconscious recall of how to perform an action or skill
  • e.g., remembering to ride a bike
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22
Q

Episodic Memories

A
  • Involve context
  • Must be learned all at once
  • e.g., where you parked your car
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23
Q

Semantic Memories

A
  • Involve facts without context
  • Facts for which the context does not matter
  • e.g., the sun is a star
  • Can be acquired gradually over time
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24
Q

HM Prior to surgery

A
  • Suffered from severe. intractable epilepsy
  • Seemed to have epileptic foci in both medial temporal lobes
  • Bilateral medial temporal lobectomy prescribed for HM (included removal of hippocampus an amygdala)
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25
Q

HM Successful Aspects of Surgery

A
  • Convulsion reduced in severity and frequency
  • IQ increased from 104 to 118
  • Remained emotionally stable with generally superior psychological abilities
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26
Q

HM Surgery Negative Aspects

A
  • Surgery produced devastating amnesia
  • Repeatedly wrote “Today I woke for the first time”
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27
Q

Hippocampal Volume Loss and Mental Health

A
  • Seen in Alzheimer’s Dementia, Depression, Childhood stress, ETOH, PTSD, and Bipolar Disorder
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28
Q

Long Term Memory/Storage

A
  • Memory peaks at age 8
  • Reviewing/rehearsing materials
  • Storage is not permanent for a few hours to days
  • Once established it is mostly permanent (memories change every time you recall)
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29
Q

Anterograde Amnesia

A
  • Failure in EXPLICIT memory (Declarative, Info available to consciousness)
  • Capable of perceptual, motor, and Stimulus-Response learning
  • Failure of relational learning
  • Loss of ability to learn new information/form new memories
  • You cannot retain new information/facts i.e., explicit memories
  • You can repeat a task until that task becomes a procedural memory (habit) for you
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30
Q

Retrograde Amnesia

A
  • Failure in IMPLICIT memory (non-declarative)
  • Loss of memory for events that occurred before a specific injury/time
  • In extreme cases, you cannot recall prior procedural tasks you used to complete i.e., implicit memories such as how to send an email
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31
Q

Stroke

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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32
Q

Infarcts

A
  • Tissue necrosis due to stroke
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33
Q

CVA

A
  • Cardiovascular Accident
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34
Q

Risk Factors of CVDs

A
  • Hypertension
  • Diabetes
  • Dyslipidemia
  • Smoking
  • Obstructive Sleep Apnea (OSA)
  • Obesity
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35
Q

Risk Factor for CVD: Hypertension

A
  • 77% of individuals first strokes have BPs higher than 140/90
  • 50% have history of hypertension
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36
Q

Risk Factor for CVD: Diabetes

A
  • 3x increased risk of ischemic strokes
  • heightened risk in African Americans <55 and whites <65
  • Hyperglycemia at stroke onset = higher brain damage
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37
Q

Risk Factor for CVD: Smoking

A
  • Higher heart rate and blood pressure and lower arterial distensibility
  • Secondhand smoke equal risk
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38
Q

Risk Factor for CVD: Obstructive Sleep Apea

A
  • Prevalence in stroke patients >60%
  • Independently higher risk 4x
  • Linked to other risk factors
  • CPAP and BiPAP reduce risk
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39
Q

Risk Factor for CVD: Obesity

A
  • Abdominal obesity > total body obesity
  • Linked to multiple other risk factors
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40
Q

Types of Strokes (3)

A
  • Ischemic Strokes
  • Hemorrhagic Strokes
  • Transient Ischemic Attack (TIA)
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41
Q

Ischemic Strokes

A
  • Obstruct the flow of blood
  • 88% of strokes
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42
Q

Thrombus

A
  • A blood clot in blood vessels
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43
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
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44
Q

Hemorrhagic Strokes

A
  • Caused by bleeding in the brain
  • 12% of strokes
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45
Q

Transient Ischemic Attack (TIA)

A
  • a stroke that lasts only a few minutes
  • 1/3 will eventually have a stroke
  • 50% within a year
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46
Q

Initial Damage in Ischemic Stroke due to Glutamate Ecotoxicity

A
  • Immediate cause of neuron death is the presence of excessive amounts of glutamate
  • Decreased O2 leads = neural membranes become depolarized = more glutamate
  • NMDA receptors become over-stimulated
  • Inflammation attacks microglia
  • Microglia attracts WBC that attach to the region
  • Cell death
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47
Q

Circle of Willis

A
  • Where the internal carotid arteries branch into smaller arteries that supply oxygenated blood to over 80% of the cerebrum
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48
Q

Middle Cerebral Artery (MCA) Strokes

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 (including pre-central gyrus (Sensory) and post-central (motor) gyrus)
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49
Q

Middle Cerebral Artery (MCA) Stroke Symptoms

A
  • Contralateral weakness and sensory loss in upper extremities
  • Homonymous Hemianopia (loss of visual field)
  • Left MCA stroke = speech deficits (Broca’s Aphasia and Wernicke’s Aphasia)
  • Right MCA stroke = neglect and poor motivation (flat prosody)
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50
Q

Anterior Cerebral Artery (ACA) Stroke

A
  • less common (L ACA> R ACA)
  • feeds deep structures in the brain. frontal, parietal, corpus callosum and bottom of the cerebrum
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51
Q

Anterior Cerebral Artery (ACA) Stroke Symptoms

A
  • Contralateral motor and sensory loss in lower extremities- Poor gait and coordination = clumsy
  • Slowed inhibition (abulia)
  • flat affect
52
Q

Posterior Cerebral Artery PCA Stroke and Symptoms

A
  • 5-10% of strokes
    Symptoms:
  • Impaired consciousness
  • Nausea/vomiting
  • Ataxia
  • Vision changes
  • Nystagmus
53
Q

Arteriovenous Malformations (AVMs)

A
  • Tangle of arteries and veins without connecting capillaries
  • Acquired through inborn genetic mutation followed by secondary mutation (1-2% of all strokes)
  • Variable size (2mm to several cm)
54
Q

Arteriovenous Malformations (AVMs) Damage

A
  • Compression of neighboring structures
  • “Stealing” of blood flow from surrounding regions
55
Q

Arteriovenous Malformations (AVMs) Presentation

A
  • Symptom onset between ages 10-40
  • Intracranial Hemorrhage most common presentation
56
Q

Stroke and Depression

A
  • Post stroke depression = 1/3 of survivors
  • 6x higher risk of depression 2-3 years post stroke
  • more common in L frontal and basal ganglia strokes
  • Adversely effects functional recovery
  • Higher risk factors = premorbid depression and social isolation post stroke
  • EARLY PSYCHOPHARMACOLOGIC TREATMENT IS KEY
57
Q

Stroke and Anxiety

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

Stroke and Psychosis

A
  • More common in right-temporo-parietal-occipto area lesions, seizures, and subcortical atrophy
  • Pseudobulbar Affect = 10-15% post stroke patients
  • Hypomanic symptoms = 1%
59
Q

BE FAST

A

B: Balance (Does the person have a loss of balance?)
E: Eyes (Has the person lost vision in one or both eyes?)
F: Face (Does the person’s face look uneven?)
A: Arms (Can the person raise both arms for 10 seconds?)
S: Speech (Is the person’s speech slurred?)
T: Time (Time is brain, call 911 if you suspect a stroke)

60
Q

Tissue Plasminogen (tPA)

A
  • Can be administered within 4.5 hours
  • Helps to restore blood flow to brain regions affected by a stroke, thereby limiting the risk of damage and functional impairment
  • After that time, has hemorrhagic effect
61
Q

Ingestive Behavior

A
  • Correctional mechanisms that replenish the body’s depleted stores of water or nutrients
62
Q

Intracellular Fluid

A
  • 2/3 volume
63
Q

Extracellular Fluid

A
  • 1/3 volume
  • 2 types: intravascular (blood plasma), interstitial (fluid that bathes the cell)
  • Tiny bit of CSF
64
Q

Tonicity

A
  • The ability of a surrounding solution to cause a cell to gain or lose water via osmosis
  • Relationship between interstitial and intracellular
  • Solute concentration determines movements
65
Q

Isotonic

A
  • Equal concentration on both sides (no movement)
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 Loops

A
  • Essential characteristic of all regulatory mechanisms
69
Q

Satiety Mechanisms

A
  • Empty stomach –> triggers hunger –> eating –> triggers satiation (the opposite response)
  • Stop behavior in anticipation of replenishment
  • Hunger negative feedback loops take time to reach the brain
  • 20-minute delay
70
Q

Osmometric Thirst

A
  • Occurs when the fluid content INSIDE (aka intracellular fluid) the cell decreases - usually because not enough water has been consumed to compensate for food intake i.e., salty food
  • As a result, water is drawn from the OUTSIDE surrounding fluid (aka extracellular fluid) into the cell
  • water moves from extracellular to intracellular
  • Thirst triggered by cell dehydration
71
Q

Volumetric Thirst

A
  • Occurs when the blood volume drops due to a loss of extracellular fluid (the outside surrounding fluid)
  • As a result, water is drawn from inside the cell to the outside
  • Can be caused by sweating, vomiting, diarrhea, and blood loss
  • Hypovolemia
72
Q

Osmoreceptors

A
  • A neuron that detects changes in solute concentration of interstitial fluid
  • Located in the Lamina Terminalis (anterior wall of the third ventricle)
73
Q

Anterior Cingulate Cortex (ACC)

A
  • Activated by thirst
  • ACC responsible for emotional expression, attention allocation, and mood regulation
  • May underlie the affective motivation of drinking behavior demanded by thirst
74
Q

Natural Dying

A
  • Dehydration of cells is part of body’s natural dying process
  • IV fluids do not remain in the vascular system instead cause: edema, swelling, eventual respiratory distress
  • Reduction in eating = ketosis which results in: reduction in appetite and thirst, pain relief, euphoria
75
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
  • Increases BEFORE eating; decreases AFTER eating
76
Q

LOW Ghrelin

A
  • Higher cortisol
  • Stress and anxiety
77
Q

HIGH Ghrelin

A
  • Lower cortisol
  • Reduced stress and anxiety
78
Q

Prader-Willi Syndrome

A
  • Genetic multi-system d.o.
  • Experience hyper-phagia due to excessive levels of ghrelin - never feel satiated
79
Q

Lateral Hypothalamus

A
  • Stop eating and drinking when destroyed
  • Overeating when activated
  • Produces Orexin - motivation to eat
80
Q

Ventromedial Hypothalamus

A
  • Suppression of eating when activated
  • Overeating when destroyed
81
Q

Weight Loss

A
  • Reduced for first 8 months of adjustable gastric band - reduced volume = ghrelin levels drop sooner (at 8 months, 53% higher than pre-surgery; not seen in gastric bypass)
  • Wegovy (semaglutide)
82
Q

Wegovy (Semaglutide)

A
  • Newly FDA approved 2021
  • Augments insulin secretion to inhibit release of glucagon
  • Increased risk of problems with gall bladder, kidney, diabetic retinopathy, depression, suicidal thoughts/behaviors
83
Q

Obesity

A
  • AMA = BMA >30 (flawed method)
  • 2x in adults; 3x in adolescents
  • prevalence went up during pandemic: adults 3% in adults, 9% 5-11 y/o
84
Q

Obesity: Sensory and Social Factors

A
  • Eating high-fat soup > direct tube feed to stomach
  • Nutrition value important
  • Higher age = Less taste
  • More options - increased intake
  • Larger plate size = increased intake
  • “Pepsi Paradox”
85
Q

Deficiency of Vitamin D

A
  • Depression/negative emotions
  • Nearly 40-50% of men and women in the Denver metro area are deficient in vitamin D
  • The more melanin you skin has, the harder it is to synthesize vitamin D
  • Concurrent use with anti-depressants supportive
86
Q

Magnesium Deficiency

A
  • With stress, can increase agitation, anxiety, sleeplessness, headaches, and apathy
  • Can treat restless leg syndrome
  • Slow response time to reach steady state via oral supplementation (30+ weeks)
87
Q

Omega-3 Fatty Oils

A
  • Add on treatment for depression (strong evidence)
  • For ADHD (some evidence)
88
Q

Anorexia: Twin Studies

A
  • 58-76% heredity
  • Risk increases with premature birth or birth trauma
89
Q

Anorexia: Associations

A
  • Loss of gray and white matter in the brain
  • Enlarged ventricles and widened sulci (shrinkage of brain tissue)
  • Inhibited emotional facial expression despite reporting similar or more intense emotions
  • Tissue loss can be reversed with successful treatment of the eating disorder
90
Q

Anorexia: Starvation Study

A
  • 6 months ate at 50% of baseline
  • Loss of 25% body weight
  • Demonstrated preoccupation with food, ritualistic eating, erratic mood, impaired cognition, slowed eating/lingering
  • Post-study = complained of fat on their abdomen and legs
91
Q

Anorexia: Gender Differences

A
  • Women ate less post-fast than men
92
Q

Anorexia: Treatment

A
  • CBT
  • Increasing eating speed
  • Stimulation of ACC
93
Q

Bulimia Nervosa: Associations

A
  • Less blood flow to the Precuneus (self-perception and memory)
94
Q

Bulimia Nervosa: Amygdala Activation

A
  • Higher activation when eating than control
  • Stable when eating post-fasting
95
Q

Bulimia Nervosa: Feedback Loop of DA, 5HTP, and NE

A
  • Anticipation of binge
  • Consumption of junk foods
  • Anticipation of purging
  • Purging - especially vomiting
  • Stress = binge-purge cycle = receptor down regulation and repeat
96
Q

Bulimia Nervosa: Vomiting

A
  • Only eliminates approximately 25% of the calories consumed
  • Prolonged dehydration and electrolyte depletion = 5x higher risk of heart attack, overall risk of hypovolemic shock, kidney failure, and UTI
97
Q

Microbes (7)

A
  • Bacteria
  • Archaea
  • Fungi (mycobiome)
  • Protists
  • Viruses (virome)
  • Phages
  • Microscopic animals
98
Q

Subarachnoid Hemorrhage

A
  • Sudden onset of a severe headache +/- nausea/vomiting
  • Seizure (>25% of patients)
  • Ophthalmologic signs: retinal hemorrhage, papilledema
  • Meningeal signs seen in over 75% of SAH
  • Neck stiffness, low back pain, bilateral leg pain
  • May take several hours to develop
  • Loss of consciousness
99
Q

Subarachnoid Hemorrhage: Loss of Consciousness

A
  • Transient intracranial circulatory arrest
  • the ‘percussive’ blood pressure impact of the hemorrhage increase ICP (intracranial pressure) and therefore reduces CPP (cerebral perfusion pressure)
100
Q

Hunt and Hess Scale

A
  • Grade I: Asymptomatic or mild headache
  • Grade II: Moderate to severe Headache, or occulomotor palsy
  • Grade III: Confused, drowsy, or mild focal signs
  • Grade IV: Stupor (Localizes pain)
  • Grade V: Coma (posturing or no motor response to pain)
101
Q

MCA Syndrome

A
  • Contralateral weakness (face = trunk = arm = leg)
  • Contralateral cortical sensory loss
  • Homonymous hemianopsia or quadrantanopsia
  • Gaze preference
  • Dysphagia
102
Q

MCA Syndrome: Non-Dominant

A
  • Contralateral neglect and anosagnosia
  • Visuospatial distortions
  • Aprosody
  • Apraxias
103
Q

MCA Syndrome: Dominant

A
  • Global aphasia
  • Apraxia
104
Q

Hemiplegia

A
  • Paralysis affecting one side of the body
105
Q

Hemiparesis

A
  • Implies a lesser degree of weakness than hemiplegia
106
Q

Neglect

A
  • Failure to attend to, respond to, and/or report stimulation that is introduced contralateral to the lesion
  • Persistent neglect is a negative functional outcome predictor
107
Q

Apraxia

A
  • Loss of ability to execute skilled or learned movement patterns on command
108
Q

Ideomotor Apraxia

A
  • Plan for the movement is intact, but the execution fails
  • Dominant pre-motor area and dominant inferior parietal region implicated in contralateral ideomotor apraxia
  • Bilateral apraxia may occur with unilateral lesions of the dominant supplementary motor cortex
109
Q

ACA Syndrome: Unilateral

A
  • Leg > arm motor loss (up to 90% of patients)
  • Leg > face = arm cortical sensory loss
  • Frontal release signs/inhibition of reflexes
110
Q

Agnosia

A
  • Acquired inability to associate a perceived unimodal stimulus (i.e., visual, auditory, tactile) with meaning
  • Disorder of recognition (not naming)
111
Q

Anosagnosia

A
  • denial of deficit
112
Q

Prosopagnosia

A
  • Impaired ability to recognize faces
113
Q

Aphasia

A
  • Impairment of Language
  • Associated with damage to the language dominant hemisphere
  • Nearly always involves damage to the left fronto- temporal and/or temporo- parietal regions
114
Q

Intraparenchymal Hemorrhage

A
  • Alteration in level of consciousness (~50%)
  • Nausea and vomiting (40-50%)
  • Headache (~40%)
  • Seizures (6-7%)
115
Q

Traumatic Brain Injury (TBI)

A
  • Occurs when a sudden, external, physical assault damages the brain
116
Q

Closed Brain Injury

A
  • Non penetrating injury to the brain with no break in the skull
117
Q

Penetrating Brain Injury

A
  • Penetrating or open head injuries where there is a break in the skull
118
Q

Diffuse Axonal Injury (DAI)

A
  • The tearing of the brain’s long connecting nerve fibers (axons) that happens when the brain is injured as it shifts and rotates inside the bony skull
  • Damage to white matter
  • Changes are microscopic
  • Can lead to disorders of consciousness
  • Difficult to see on CT Scan or MRI
  • Can occur without other visible damage
119
Q

Chronic Traumatic Encephalopathy (CTE)

A
  • Produces neurodegeneration due to repeated head trauma
  • Prevalence in athletes who participate in contact sports and experience frequent and repeated head trauma
  • Seen as: abnormal tau protein accumulation, reduced brain volume, ventricular enlargement
  • Mood and cognitive impairment can appear years after the injury occurred
120
Q

Glasgow Coma Scale Limitations

A
  • Substance use
  • Administered drugs
  • Intubation
  • Injury to eye
  • Hemiplegia
  • Language
121
Q

Post-Traumatic Amnesia

A
  • State of confusion and disorientation that occurs immediately after TBI, is part of the healing process
  • do NOT ask them to recall the injury (they cannot do this)
  • Brain is unable to form continuous day to day memories
  • Memory is the slowest part of the conscious mind to recover
122
Q

Dose-Response Relationship

A
  • Cognitive changes after mild TBI resolve within weeks to about 3 months at most spontaneously without treatment while changes tend to persist greater than or equal to 2 years following moderate to severe TBI
123
Q

Non-Injury Risk Factors that can Influence TBI Outcomes

A
  • Pre-injury psychiatric status and conduct issues/incarceration
  • age at injury
  • Level of education
  • Stable employment 6 months pre-injury
  • Marital status
  • Other non-neurological injuries sustained
124
Q

TBI: Motor Sensory Impairments

A
  • Paralysis
  • Poor coordination
  • Changes in sensation (visual, hearing, touch, taste, smell)
  • Bowel and bladder control
125
Q

TBI: Communication Impairments

A
  • Dysarthria (motor speech d/o)
  • Social communication
126
Q

TBI: Cognitive Impairments

A
  • Slowed processing speeds = most common impairment
  • Memory
  • Executive functions (need external structures)
127
Q

TBI: Psychosocial Impairments

A
  • Reduced initiation/motivation
  • Control challenges
  • Emotional control
  • Self-centeredness

Physiological Psychology (4 decks)

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