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Biological Psychology > Bio Psych Exam 4 > Flashcards

Bio Psych Exam 4 Flashcards

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1
Q

How do arteries and veins differ?

A
  • arteries carry oxygenated blood and glucose from the heart to the brain
  • veins carry deoxygenated blood, lactic acid etc. from the brain to the heart
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2
Q

What is the Circle of Willis, and why is it important?

A

if one part of the brain fails and is not getting blood supply we have backups to a point

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3
Q

What is a watershed region?

A

some brain regions are on the edge of the territory served by a cerebral artery
- these are called watershed regions
- they are the most susceptible to injury after stroke

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4
Q

What is a stroke?

A

a vascular (blood vessel-related) event that happens in the brain, causing neurological (brain-related) dysfunction
- blood vessels supply oxygenated blood to the brain
- the brain needs a constant supply of blood in order to function
- stroke happens when a blood vessel in the brain gets blocked or bursts
- as blood flow reduces, brain tissue quickly begins to die

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5
Q

What is the difference between an ischemic stroke and hemorrhagic stroke?

A
  • in an ischemic stroke, artery supplying the brain gets occluded (blocked)
  • in a hemorrhagic stoke, artery supply the brain ruptures (bursts)
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6
Q

What is the ischemic cascade?

A

a series of events that happens in brain tissues/cells in response to low blood flow
- lack of oxygen –> glutamate buildup –> excitotoxicity –> generation of harmful chemicals, breakdown of cell membranes/organelles and necrosis (cell death)

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7
Q

What is meant by “Time is Brain”?

A

strokes should be immediately recognized and treated, because neurons die rapidly without blood flow
- the excitotoxic damage happens in seconds to minutes

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8
Q

What is meant by FAST?

A

a mnemonic for typical stroke symptoms to determine if someone is having a stroke
- face droops
- arm weakness
- speech difficulty
- time is critical

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9
Q

What are some of the major risk factors for stroke?

A
  • vascular conditions (i.e., hypertension (high blood pressure), high cholesterol levels in blood)
  • heart conditions (i.e., atrial fibrillation)
  • other medical conditions (i.e., diabetes, family history of stroke)
  • demographic factors (i.e., old age, women at higher risk because they live longer)
  • lifestyle habits (i.e., smoking, eating unhealthy foods, lack of exercise)
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10
Q

How do we treat strokes within the first 24 hours?

A
  • thrombolysis (breaking up the clot using medications) –> intravenous injection of IV-tPA that gives a large increase in chance of excellent recovery when administered within 3 hours of stroke onset
  • thrombectomy (removing the clot using surgery) –> insertion of a stent retriever to snake up into the brain and mechanically pull out the clot; only a second-line treatment after IV-tPA (or if IV-tPA is not possible)
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11
Q

How do we treat strokes after the first 24 hours?

A

chronic stroke management is mostly focused on three aspects: preventing future strokes; recovering lost functions through rehabilitation; providing social, physical, emotional, and mental support

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12
Q

At what point does functional recovery seem to stop?

A

after the first 3 months

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13
Q

What is a TBI?

A

a form of acquired brain injury that occurs when a sudden trauma causes damage to the brain
- can result when the head suddenly and violently hits an object, or when an object pierces the skull and enters brain tissue

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14
Q

How does a TBI differ from other injuries to the brain, like stroke?

A

caused by an external force that damages the brain, whereas other injuries are caused by non-traumatic (internal) factors

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15
Q

How do we diagnose and classify TBIs?

A

classified by mild TBI (concussion), moderate TBI, and severe TBI
- loss of consciousness/mental state and post traumatic amnesia guide diagnoses

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16
Q

What are the symptoms of a TBI?

A
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17
Q

What is the Glasgow Coma Score?

A

a method used to diagnose mild, moderate, and severe TBIs
- uses eye opening response, verbal response, and motor response associated with a point scale

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18
Q

Which is a better score to get on the Glasgow Coma Score, high or low?

A

high

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19
Q

What are the 3 categories of Glasgow Coma Score?

A
  • eye opening response
  • verbal response
  • motor response
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20
Q

Why do we use CT scans for TBI?

A
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21
Q

What is the difference between penetrating and blunt force injuries?

A
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22
Q

What is a coup-contrecoup injury?

A

an initial impact from outside force causes the brain to impact front of the skull –> rebound of the head causes brain to impact opposite side of skull

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23
Q

What are the primary vs. secondary disease mechanisms?

A

primary disease mechanism
- white matter damage
- bleeding (contusions, hemorrhages, hematomas)
secondary disease mechanism
- seizures
- cerebral edema (brain swelling)
- increased intracranial pressure
- ischemia (inadequate blood supply)
- contusions can grow into larger lesions
- breakdown of blood-brain-barrier
- all of these secondary disease mechanisms cause neuronal, axial, and glial injury/death

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24
Q

How do we treat TBI in the short term?

A

surgical intervention or medical management

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25
Q

How do we treat TBI in the long term?

A
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26
Q

What happens if you have a secondary TBI?

A

secondary injuries are exponentially worse (but time helps)

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27
Q

What is CTE?

A

a neurodegenerative disorder caused by multiple concussions or subconcussyve impacts to the brain, especially earlier in life

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28
Q

What do we know about CTE?

A
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29
Q

What is the endocrine system?

A

glands that secrete chemicals into the bloodstream and help control bodily function
- controls the body functions indirectly
- controls the body slowly via hormones
- hormones are chemicals released by the endocrine glands (“the neurotransmitters of the body”)

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30
Q

“Who” is in charge of the endocrine system?

A

mainly controlled by the central nervous system through the hypothalamus
- the pituitary gland releases a wide variety of hormones that spread throughout the body, stimulating actions in the other endocrine glands
- pituitary is the “master” gland, although the hypothalamus is the real power behind the throne; they work together to regulate the body

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31
Q

What is the HPA axis?

A

the hypothalamic-pituitary-adrenal axis; one of the primary stress response systems

32
Q

Where is the HPA axis?

A

hypothalamus –> pituitary gland –> adrenal cortex

33
Q

How does the HPA axis work?

A
34
Q

What is the output that we care about in the HPA axis?

A

cortisol: the most important glucocorticoid
- initially, cortisol prepares individual for fight-or-flight response when exposed to cues indicating potential threat
- then it dampens the stress-induced response so we can shut it down

35
Q

Can you walk through the cascade in the HPA axis?

A
  • too much cortisol is released
  • the sensitivity of the system to that feedback loop decreases
  • cortisol can’t do as good of a job telling the system to shut down once the stressor has passed
  • but more cortisol was released to begin with, so the system is already amped up
  • system continues to act as though the threat of stress is still present, even if there’s not actually a threat (overactive)
  • HPA and stress can directly be related to psychopathology (depression)
36
Q

What is the CAR?

A

cortisol awakening response
- diurnal variation
- CAR variation might be a risk factor of psychopathology

37
Q

What are the effects of cortisol on the HPA axis?

A
  • in a healthy person, cortisol is time-limited
  • it binds to glucocorticoid receptors in pituitary and hypothalamus, which reduces the hormone necessary for creating cortisol
38
Q

What are the effects of cortisol on the immune system?

A
39
Q

What happens specifically to the HPA axis in depression?

A
  • too much cortisol is released
  • the sensitivity of the system to that feedback loop decreases
  • cortisol can’t do as good of a job telling the system to shut down once the stressor has passed
  • but more cortisol was released to begin with, so the system is already amped up
  • system continues to act as though the threat of stress is still present, even if there’s not actually a threat (overactive)
  • HPA and stress can directly be related to psychopathology (depression)
40
Q

What is the immune system?

A
  • set of cells, molecules, and various mechanisms responsible for protecting the organism against foreign substances
  • coordinated response of cells and molecules to foreign agents (immune response)
  • keep the body biologically healthy, especially in times of physical injury, wounds, infections
41
Q

What is a pro-inflammatory cytokine?

A
42
Q

What is an anti-inflammatory cytokine?

A
43
Q

What is inflammation vs. neuroinflammation?

A
44
Q

How does the immune system play a role in Alzheimer’s disease?

A
45
Q

Alzheimer’s was used as a case study to illustrate that…..

A
46
Q

How do the CNS, endocrine systems, and immune systems talk to each other?

A

via 3 systems
- immunotransmitters = functional equivalent of neurotransmitters
- pituitary hormones = those things that trigger cortisol
- neuropeptides = facilitate communication between CNS and immune system (mediator)

47
Q

In a healthy person, how does cortisol affect the immune system?

A
48
Q

In someone with depression, how does cortisol affect the immune system?

A
  • more cortisol is released and negative feedback becomes less sensitive
  • glucocorticoid resistance
49
Q

How do ACEs fit into our discussion about hormones and immunology?

A

early life stress makes things even worse
- childhood maltreatment predicts higher inflammation levels more than 20 years later

50
Q

What is generally going on in the gut-brain axis?

A
51
Q

What is glutamate and how is it implicated in epilepsy?

A
  • primarily excitatory neurotransmitter –> stimulates other neurons to fire action potentials but in excess can lead to excitotoxicity
52
Q

What is GABA and how is it implicated in epilepsy?

A
  • primarily inhibitory neurotransmitter –> inhibits other neurons from firing action potentials
53
Q

Why is the video of Mitch McConnell likely not a stroke?

A
54
Q

What is the cascading effect we know of in regard to epilepsy?

A
  • the neurons in some area(s) of the brain all start to generate action potentials at the same time
  • the synchronous electrical activity involves mass waves of neuronal depolarization
  • as neurons continue firing in a cyclical fashion, normal brain activity cannot be established
  • this abnormal and excessive brain activity causes a variety of physical symptoms, which are collectively called “epileptic seizures”
55
Q

What is meant by “synchronous brain activity”?

A

neurons in area(s) of the brain start to generate action potentials at the same time which is abnormal
- this disrupts the balance of excitation and inhibition
- floods the brain with glutamate –> excitotoxicity –> possible brain damage

56
Q

What is the difference between focal onset vs. generalized onset?

A
  • focal onset seizures occur when synchronous neuronal activity begins in one area of the brain and one hemisphere –> may spread to other parts of the brain and/or to both hemispheres in which case it would become generalized
  • generalized onset seizures occurs when synchronous neuronal activity begins in both hemispheres of the brain at the same time (and this means multiple brain areas must be affected)
57
Q

What is the difference between motor and non-motor symptoms?

A
  • motor symptoms primarily affect the muscles of the body
  • non-motor symptoms primarily affect other systems of the body
58
Q

What are some of the risk factors for epilepsy?

A
59
Q

How do the risk factors for epilepsy fit into other topics we have discussed this unit?

A
60
Q

How do we treat epilepsy?

A

the three main goals of epilepsy treatment are: to become seizure-free; to have minimal side effects (ideally none) from treatment; to have everyday function that the person considers to be normal
- medication
- electric stimulation of the nervous system to control seizures (ex: deep brain stimulation)
- surgery (ex: only for focal onset epilepsy MRI-guided laser that burns off the specific brain area that is causing seizures)

61
Q

What is ASD?

A

a neurodevelopmental disorder

62
Q

What are the symptoms of ASD?

A
  • social communication deficits (socioemotional reciprocity, nonverbal communication, developing and maintaining relationships)
  • restricted interest and repetitive behaviors (repetitive mannerisms, insistence on sameness, circumscribed interests, sensory hypo/hypersensitivity)
63
Q

What kind of disorder is ASD?

A

a neurodevelopmental disorder

64
Q

What is meant by the “spectrum”?

A

there are three functional levels
- Level 1: requiring support; full sentences but stigmatized; rigid, inflexible; difficulty initiating social interactions; organization and planning problems can hamper independence
- Level 2: requiring substantial support; social interactions limited to narrow special interests; frequent restricted/repetitive behaviors; simple sentences; substantial difficulty coping with change
- Level 3: requiring very substantial support; severe deficits in verbal and nonverbal social communication skills; great distress/difficulty changing actions or focus; minimal response to social overture; persistent gross interference with functioning

65
Q

What is a mand?

A

a request for something wanted or needed, or a request to end something undesirable
- one of the first forms of communication naturally acquired

66
Q

What is “stimming”?

A

also known as self-stimulatory behavior; repetitive or unusual movement/noise; helps manage emotions in people with ASD

67
Q

What is the rough prevalence of ASD?

A
  • 4:1 male to female
  • prevalence of 1 in 36 in boys
  • lower SES linked to under-diagnosis
68
Q

What are some risks that have evidence supporting them?

A
  • valproate use during pregnancy
  • older sibling having ASD
69
Q

What are some “risks” with no support?

A

vaccination

70
Q

Why do we care about genetics in ASD?

A
  • highly heritable
  • 60-90% of variance in ASD
  • MZ concordance about 90%
71
Q

In terms of brain structure, what is larger in children with ASD compared to typical children?

A
  • grey matter: general and regional brain enlargement, especially in frontal and temporal in young children
  • white matter: increased white matter volume/integrity in young children, but this reverses
  • increased extra-axial CSF
  • there is hyper connectivity in young children, but as they get older, we see hypo connectivity
72
Q

Where do ASD children tend to focus their gaze? Why might this matter?

A
  • tend to focus their gaze at the mouth
  • helps with communication and avoids emotional connections
73
Q

What is Theory of Mind? How might this play a role in understanding ASD?

A
  • difficulties attributing mental states of others and the self, and understanding that others have mental states that differ from their own
  • most ASD children fail tasks that try to tap into this
  • not related to just general mental slowing, as we see kids with Down syndrome perform normally on these tasks
  • also not related to only language delays: ASD children perform worse on these tasks even when paired with individuals with the same language abilities
74
Q

What are the broad goals of treatment for ASD?

A
  • medical management (psychotropic medications)
  • social and communication based therapies (relationship development intervention, social skills therapy)
  • educational programming (speech, language, occupational therapies)
75
Q

What are the 2 brain mechanisms that we understand for ASD?

A
  • excitation/inhibition imbalance
  • change in the functional interactions of large-scale brain networks
76
Q

What is an unexpected area of the brain that new research is focusing on for ASD?

A

the cerebellum
- cerebellar abnormalities in ASD are present in early life and exist into adulthood
- cerebellum talks to the cortex in stereotyped manners
- connectivity between parts of the cerebellum and parts of the cortex

Biological Psychology (5 decks)

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