Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PSY1003 SEMESTER 2 > PSY1003 SEMESTER 2 WEEK 2 > Flashcards

PSY1003 SEMESTER 2 WEEK 2 Flashcards

1
Q

what are acquired brain injury

A

during life. can be traumatic or non traumatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are congential brain injury

A

resulting from genetic factors affecting neurodevelopment pre-birth or birth related trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

outline the different type brain injuries

A

acquired (traumatic (open, closed), non-traumatic) or congenital

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

outline traumatic brain injury

A

sudden such as getting hit over head (intracranial injury). can be specific or widespread, affecting brain tissue directly or indirectly by damaging blood supply (circulatory system)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

give the 2 type of traumatic brain injury

A

open or closed head injuries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

outline closed head injury

A

no penetration of skull, sudden hit causes brain to hit skull wall as not enough cushioning from CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

define contusion

A

closed-head injuries involving damage to cerebral circulatory system, producing internal haemorrhage and result in haematoma (localised collection of clotted blood in organs or tissue)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

define contrecoup injury

A

blow causes the brain to strike inside of skull on other sides of head

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

define concussion

A

disturbance of consciousness following blow to head and no evidence of contusion or other structural damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is dementia puglistica/punch drunk syndrome

A

repeated powerful blows to head. cumulative structural damage can result in dementia like symptoms, increases likelihood of Parkinson’s or Alzheimer’s, occur in boxers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is CTE (chronic traumatic encephalography)?

A

dementia, general intellectual deterioration, cerebral scarring due to repeated concussive, sub-concussive blows

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

define open head injury

A

skull not remaining intact, object penetrates skull and enters brain. bone fragments can damage tissues. damage can be localised but other complications can occur such as bleeding, infection, swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what can swelling from open head injury cause

A

intracranial pressure and can compress brain area controlling breathing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

name 4 type of non-traumatic brain injury

A

stroke, infection, tumour, hypoxia/anoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how common is a stroke

A

4th biggest killer, >400 children have stroke per year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

define infarct

A

area of dead or dying tissue produced by stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

define penumbra

A

tissue surrounding infarct, dysfunctional, may recover or die in ensuing days. primary goal of treatment is to save penumbra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

name 2 main causes of stroke

A

cerebral haemorrhage, cerebral ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what happen in cerebral haemorrhage

A

ruptured cerebral blood vessel, blood leaks into brain and prevent blood going where its needed, so loos of blood supply to brain. intercranial pressure. blood is toxic to neural tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what happen in cerebral ischaemia

A

caused by interruption of blood supply to part of brain due to blockage of blood vessel eg: clot, thrombus, embolism, atheroscleosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what does cerebral haemorrhage often result from

A

aneurysm (pathological balloon like dilation in wall of artery at point where elasticity of artery wall is defective). can be congenital or result of vascular poison/infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what should those at risk of aneurysm do

A

avoid smoking, alcohol and hyppertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what can we do to aid aneurysms if spotted before rupture

A

aneurysm clips, maintain low BP, avoid strenuous activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

define thrombosis

A

plug called thrombus is formed, blocks blood flow at site. composed of blood clot, fat, oil, air bubble, tumour cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

define embolism

A

embolus plug carried by blood from larger vessel to smaller, becomes lodged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

define arteriosclerosis

A

thicken wall of blood vessels, channels narrow due to fat deposit, blocks blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what can thrombosis, embolism, arteriosclerosis lead to

A

prevent O2 and glucose, leading to excitotoxicity- neuronal cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what part of brain is most suceptible to ischemia-induced brain damage

A

hippocampus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

why is glutamate, a excitatory NT, important in a cerebral ischemia

A

after blood vessels blocked, many blood-deprived neurons becomes overactive and release too much glutamate that overactivate glutamate receptors in membranes of postsynaptic neurons. causes lots of Na and Ca enter, trigger release of lots of glutamate from neuron, so spread toxic cascade, trigger sequence of internal reactiosn eventually killing postysnaptic neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what did glutamate lead to the discovery of as a stroke treatments option

A

prevent glutaminergic cascade using NMDA-receptor antagonists administered immediately post-stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is tissue plasminogen activator for strokes

A

drug which breaks down blood clots, administering 3-4 hours post stroke leads to a better chance of recovery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

name the main goal of stroke treatments

A

rescue penumbra by reopening blocked vessel via clot busting drugs that if administered in time can break down clot and prevent stroke damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

which artery tend to be affected by stroke

A

middle cerebral artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is FAST (strokes)

A

Face
Arms
Speech
Time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

name some exogenous neurotoxins

A

mumps, herpies, rabies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

define endogenous neurotoxin

A

produced by body eg: antibodies that can attack components of nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is a neurodegenerative disease?

A

progressive, occur over time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

give 3 neurodegenerative disease

A

Parkinson’s, Alzheimer’s. other dementias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

name some other brain disease (can include neurodegenerative components, but not limited to)

A

ccerebrovascular disease, cancer, epilepsy, infections, other movement disorders, psychaitric disorders

40
Q

what NT is lost in alzheimers

A

acetlycholine

41
Q

what NT is lost in parkinsons

A

dopamine

42
Q

is Alzheimers associated with wiespread or direct neuron loss?

A

diffuse change occuring to brain structures/volume and widespread neuronal loss’

43
Q

is Parkinson’s associated with widespread neuronal loss?

A

mainly attributable to loss of single neurons type, in specific brain region

44
Q

who founded Parkinsons

A

English physician, ‘shaking palsy’

45
Q

how common is Parkinson’s disease

A

0.5% population and 1-2% of elderly population, 2.5x more common in males

46
Q

why is Parkinsons idiopathic

A

each case has own origin, no known general cause. could be stroke, brain infections and neurotoxins, very small % due to genetic mutations, but rest seem to be a spontaneous occurrence

47
Q

give the original Parkinson’s description

A

involuntary tremulous motion, with lessened muscular power, in parts not in action and even when supported, with a propensity to bend the trunk forward, and to pass from walking to a running pace, the senses and intellects being uninjured

48
Q

name some Parkinson’s symptoms

A

-paucity of spontanous movement (insufficiency of movement)
-bradykinesia (very slow movement)
-akinesia (no movement)
-increased muscle tone (rigidity)
-resting tremor (4-5Hz)
-shuffling gait and flexed posture, impaired balance
-mask like expressions

49
Q

what causes rigidity in Parkinson’s

A

both agonist and antagonist muscles are activated at same time

50
Q

explain how a Parkinsons patient could ride bike?

A

difficulty in initiating movement, but once going are okay

51
Q

Parkinson’s- where is the lack of dopamine

A

substantia nigra (midbrain nucleus with neurons projecting via nigrostriatal dopamine pathway to striatum in basal ganglia)
Parkinson’s patients are deficient in striatum

52
Q

how much of brains dopamine is in the basal ganglia

A

80%

53
Q

what has autopsy shown in Parkinson patient

A

clumps of protein (Lewy Bodies) present in surviving dopamine neurons in substantia nigra

54
Q

how much of neuronal mass in substantia nigra is lost before see Parkinson’s symptoms

A

80%

55
Q

outline how drug addiction research gave insight into Parkinson’s

A

1980’s, USA, synthetic heroin users showed Parkinsons symptoms. MPTP unwanted byproduct and becomes converted to highly neurotoxic MPP+. gave big insight as found single drug could recreate symptom
no impact on cats, dog etc but devastating impact on non-human primates

56
Q

Parkinson’s - outline how the lack of dopamine burst in basal ganglia results in symptoms

A

burst of dopamine to basal ganglia allows action in motor system but without dopamine basal ganglia block access meaning inactive motor system. in Parkinsons, basal ganglia in a constant inhibition mode, excessive inhibitory output prevent movement, as cells releasing dopamine in Parkinsons are dying

57
Q

how could lesions work as a Parkinson’s treatment (stop basal ganglia being stuck in inhibition mode)

A

lesion globus pallidus (key part of basal ganglia). reduces symptoms but not a common treatment option

58
Q

briefly state some drugs that could be used to replace dopamine when treating Parkinson’s

A

Levodopa (dopamine precursor)
apomorphine (dopamine agonist)
deprenyl (monoamine and dopamine/serotonin agonist)
cannabis (dopamine agonists, lacking evidential supports)

59
Q

why does LevoDopa not work when treating Parkinson’s

A

a dopamine precursor, but in Parkinsons there is death in dopamine production cells, meaning no dopamine would actually get produced

60
Q

why can we not give Parkinson’s patients just more dopamine

A

it can’t cross BBB

61
Q

outline surgical intervention as Parkinson treatments

A

lesion inhibitory output structure, but only in very severe case

62
Q

explain how deep brain stimulation works to treat Parkinson

A

target same site as lesioning basal ganglia however electrical currents able to be tuned to shut down or inhibit output, reversible, controllable, adjustable

63
Q

name some side effects of deep-brain stimulations

A

cognitive issue, speech impairement and gait problems

64
Q

name a stem cell potential treatment for Parkinson’s development

A

replace lost dopamine cells by using fetal or stem cells transplant

65
Q

define dementia

A

chronic, persistent disorder of mental processes causes by brain disease or injury and marked by memory disorders, personality changes and impaired reasoning

66
Q

how much of dementia does Alzheimer account for?

A

two thirds

67
Q

name some other type of dementia

A
  • vascular dementia
  • dementia with Lewy bodies
  • frontotemporal dementia
  • mild cognitive impairment
  • posterior cortical atrophy
  • primary progressive aphasia
68
Q

how prevalent is Alzheimers in 65+, and 85+

A

10% age 65+
35% age 85+

69
Q

give early stage symptoms of Alzheimers

A

selective decline in memory, attention deficit, personality change

70
Q

give intermediate stage symptoms of Alzheimers

A

confusion, anxiety, irritability, speech deterioration

71
Q

give final stage symptoms of Alzheimers

A

swallowing, bladder control

72
Q

outline assessment of Alzheimer’s

A

MMSE- mini mental state Examination
map score and compare to a standard, potentially measure at different time points

73
Q

what correlation has been found between dementia and other lifestyle characteristics

A

education, cardiovascular health, general physiological health

74
Q

outline the role of amyloid plaque in Alzheimer

A

clumps of scar tissue of degenerating neurons and lumps of amyloid proteins (b-amyloid) interfer with neuronal function

75
Q

what is AmyloidPrecursorProtein (APP) and what goes wrong in Alzheimers

A

APP meant to be broken down, but the way it is broken down when in Alzheimer creates little sticks of b-amyloid that clump to form b-amyloid plaques. function of APP not fully understood yet, but a main focus for research on how it can be interfered with to prevent damaging impacts

76
Q

outline the role of tau in Alzheimers

A

muddles and becomes tangled up with microtubules in cytoplasm (cytoplasm keep cell shape)
microtubules are made from MAPs (microtubule associated proteins) and tau is also a MAP

77
Q

what are neurofibrillary tangles in Alzheimers

A

threadlike protein tangles in neural cytoplasm

78
Q

what are microbleeds in Alzheimers

A

small dot-like lesion, result from microhemorrhage

79
Q

where are microbleeds most prevalent in Alzheimers

A

medial temporal lobe (entorhinal cortex, amygdala, hippocampus)

80
Q

how common is Alzheimers in immediate families

A

x2 as likely if live to old age

81
Q

name what early research into genetics for Alzheimer has found

A

mutations to 3 different genes contribute to early onset, but only 1% later onset

82
Q

what is APP (genetic), founds on chromosomes 21 which links to Alzheimers?

A

also link to down syndrome, develop Alzheimer pathology by 40, 150% of normal APP levels

83
Q

what is apoE in Alzheimers (genetic

A

alpolipoprotein-E = a risk or protective factor, 3 common alleles (E2-good, E3, E4-bad)
involved in transport of cholesterol

84
Q

name animal reserach for Alzheimers

A

genetic modification creating excessive APP, TAU, or copies of genes coding for apoE E4 allele in mice
“double”/”triple” transgenics including genetic encoding for 2 or 3 of these features
able to replicate a key feature of Alzheimer’s so we can study and look at solution

85
Q

name what are current developing treatments for Alzheimers?

A

those focusing for Tau, Amyloid or apoE related features of Alzheimers. immuno and gene therapy approaches

86
Q

what do current Alzheimers treatments target

A

loss of neurons producing Acetylcholine (vital in normal cognitive functions and memory)

87
Q

what does treatments targeting cholinesterase (AchE) do in Alzhimers

A

enzyme that breaks down Ach and prevents Ach continuing to act on neurons. increasing AchE increases effect of Ach on neurons

88
Q

what has staining research evidence found in Alzheimers

A

cholinergic neuron profound loss widespread across cortical regions

89
Q

what is a main drug for Alzheimers

A

cholinesterase inhibitorm

90
Q

name 3 cholinesterase inhibitors (Alzheimers drug)

A

donepezil hydrochloride (Aricept)
rivastigmine (Exelon)
galantamine (Reminyl)

91
Q

what is the current dominant amyloid hypothesis in Alzheimers

A

amyloid plaques are primary symptom of disorder and cause symptom
genetic analysis of families with early onsets found all 3 gene mutations impacts synthesis of b-amyloid

92
Q

what is high-plaque normals in non-dementia individual

A

many people without dementia have significant levels of amyloid plaques - are at risk of cognitive decline

93
Q

outline similarities of down syndrome and Alzheimers pathology

A

at 40 develop numerous amyloid plaques, neurofibrillary tangles
at 60 two-third have dementia
genetic coding of b-amyloid located on chromosome 21

94
Q

what is pathogenic spread hypothesis for Alzheimers

A

many common neurodegenerative diseases result from presence of misfold proteins iniating chain reactions causing other protein to misfold

95
Q

in what ways can brain injury teach us about normal brain functioning

A
  1. study brain localisations
  2. basis of treatments and rehab
  3. allows developmental trajectories and milestones for congenital injuries
  4. neuroremappings in rehab
96
Q

what are limitations of using brain damage findings in clinical practice?

A

correlation not causation
inability to replicate
individual difference
node network involved so not necessarily specific functions

PSY1003 SEMESTER 2 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions