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Biological Psychology > Bio Psych Exam 4 > Flashcards

Bio Psych Exam 4 Flashcards

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
How do we treat TBI in the long term?
26
What happens if you have a secondary TBI?
secondary injuries are exponentially worse (but time helps)
27
What is CTE?
a neurodegenerative disorder caused by multiple concussions or subconcussyve impacts to the brain, especially earlier in life
28
What do we know about CTE?
29
What is the endocrine system?
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")
30
"Who" is in charge of the endocrine system?
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
31
What is the HPA axis?
the hypothalamic-pituitary-adrenal axis; one of the primary stress response systems
32
Where is the HPA axis?
hypothalamus --> pituitary gland --> adrenal cortex
33
How does the HPA axis work?
34
What is the output that we care about in the HPA axis?
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
Can you walk through the cascade in the HPA axis?
- 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
What is the CAR?
cortisol awakening response - diurnal variation - CAR variation might be a risk factor of psychopathology
37
What are the effects of cortisol on the HPA axis?
- 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
What are the effects of cortisol on the immune system?
39
What happens specifically to the HPA axis in depression?
- 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
What is the immune system?
- 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
What is a pro-inflammatory cytokine?
42
What is an anti-inflammatory cytokine?
43
What is inflammation vs. neuroinflammation?
44
How does the immune system play a role in Alzheimer's disease?
45
Alzheimer's was used as a case study to illustrate that.....
46
How do the CNS, endocrine systems, and immune systems talk to each other?
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
In a healthy person, how does cortisol affect the immune system?
48
In someone with depression, how does cortisol affect the immune system?
- more cortisol is released and negative feedback becomes less sensitive - glucocorticoid resistance
49
How do ACEs fit into our discussion about hormones and immunology?
early life stress makes things even worse - childhood maltreatment predicts higher inflammation levels more than 20 years later
50
What is generally going on in the gut-brain axis?
51
What is glutamate and how is it implicated in epilepsy?
- primarily excitatory neurotransmitter --> stimulates other neurons to fire action potentials but in excess can lead to excitotoxicity
52
What is GABA and how is it implicated in epilepsy?
- primarily inhibitory neurotransmitter --> inhibits other neurons from firing action potentials
53
Why is the video of Mitch McConnell likely not a stroke?
54
What is the cascading effect we know of in regard to epilepsy?
- 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
What is meant by "synchronous brain activity"?
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
What is the difference between focal onset vs. generalized onset?
- 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
What is the difference between motor and non-motor symptoms?
- motor symptoms primarily affect the muscles of the body - non-motor symptoms primarily affect other systems of the body
58
What are some of the risk factors for epilepsy?
59
How do the risk factors for epilepsy fit into other topics we have discussed this unit?
60
How do we treat epilepsy?
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
What is ASD?
a neurodevelopmental disorder
62
What are the symptoms of ASD?
- 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
What kind of disorder is ASD?
a neurodevelopmental disorder
64
What is meant by the "spectrum"?
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
What is a mand?
a request for something wanted or needed, or a request to end something undesirable - one of the first forms of communication naturally acquired
66
What is "stimming"?
also known as self-stimulatory behavior; repetitive or unusual movement/noise; helps manage emotions in people with ASD
67
What is the rough prevalence of ASD?
- 4:1 male to female - prevalence of 1 in 36 in boys - lower SES linked to under-diagnosis
68
What are some risks that have evidence supporting them?
- valproate use during pregnancy - older sibling having ASD
69
What are some "risks" with no support?
vaccination
70
Why do we care about genetics in ASD?
- highly heritable - 60-90% of variance in ASD - MZ concordance about 90%
71
In terms of brain structure, what is larger in children with ASD compared to typical children?
- 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
Where do ASD children tend to focus their gaze? Why might this matter?
- tend to focus their gaze at the mouth - helps with communication and avoids emotional connections
73
What is Theory of Mind? How might this play a role in understanding ASD?
- 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
What are the broad goals of treatment for ASD?
- medical management (psychotropic medications) - social and communication based therapies (relationship development intervention, social skills therapy) - educational programming (speech, language, occupational therapies)
75
What are the 2 brain mechanisms that we understand for ASD?
- excitation/inhibition imbalance - change in the functional interactions of large-scale brain networks
76
What is an unexpected area of the brain that new research is focusing on for ASD?
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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