Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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
define embolism
embolus plug carried by blood from larger vessel to smaller, becomes lodged
26
define arteriosclerosis
thicken wall of blood vessels, channels narrow due to fat deposit, blocks blood vessels
27
what can thrombosis, embolism, arteriosclerosis lead to
prevent O2 and glucose, leading to excitotoxicity- neuronal cell death
28
what part of brain is most suceptible to ischemia-induced brain damage
hippocampus
29
why is glutamate, a excitatory NT, important in a cerebral ischemia
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
30
what did glutamate lead to the discovery of as a stroke treatments option
prevent glutaminergic cascade using NMDA-receptor antagonists administered immediately post-stroke
31
what is tissue plasminogen activator for strokes
drug which breaks down blood clots, administering 3-4 hours post stroke leads to a better chance of recovery
32
name the main goal of stroke treatments
rescue penumbra by reopening blocked vessel via clot busting drugs that if administered in time can break down clot and prevent stroke damage
33
which artery tend to be affected by stroke
middle cerebral artery
34
what is FAST (strokes)
Face Arms Speech Time
35
name some exogenous neurotoxins
mumps, herpies, rabies
36
define endogenous neurotoxin
produced by body eg: antibodies that can attack components of nervous system
37
what is a neurodegenerative disease?
progressive, occur over time
38
give 3 neurodegenerative disease
Parkinson's, Alzheimer's. other dementias
39
name some other brain disease (can include neurodegenerative components, but not limited to)
ccerebrovascular disease, cancer, epilepsy, infections, other movement disorders, psychaitric disorders
40
what NT is lost in alzheimers
acetlycholine
41
what NT is lost in parkinsons
dopamine
42
is Alzheimers associated with wiespread or direct neuron loss?
diffuse change occuring to brain structures/volume and widespread neuronal loss'
43
is Parkinson's associated with widespread neuronal loss?
mainly attributable to loss of single neurons type, in specific brain region
44
who founded Parkinsons
English physician, 'shaking palsy'
45
how common is Parkinson's disease
0.5% population and 1-2% of elderly population, 2.5x more common in males
46
why is Parkinsons idiopathic
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
give the original Parkinson's description
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
name some Parkinson's symptoms
-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
what causes rigidity in Parkinson's
both agonist and antagonist muscles are activated at same time
50
explain how a Parkinsons patient could ride bike?
difficulty in initiating movement, but once going are okay
51
Parkinson's- where is the lack of dopamine
substantia nigra (midbrain nucleus with neurons projecting via nigrostriatal dopamine pathway to striatum in basal ganglia) Parkinson's patients are deficient in striatum
52
how much of brains dopamine is in the basal ganglia
80%
53
what has autopsy shown in Parkinson patient
clumps of protein (Lewy Bodies) present in surviving dopamine neurons in substantia nigra
54
how much of neuronal mass in substantia nigra is lost before see Parkinson's symptoms
80%
55
outline how drug addiction research gave insight into Parkinson's
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
Parkinson's - outline how the lack of dopamine burst in basal ganglia results in symptoms
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
how could lesions work as a Parkinson's treatment (stop basal ganglia being stuck in inhibition mode)
lesion globus pallidus (key part of basal ganglia). reduces symptoms but not a common treatment option
58
briefly state some drugs that could be used to replace dopamine when treating Parkinson's
Levodopa (dopamine precursor) apomorphine (dopamine agonist) deprenyl (monoamine and dopamine/serotonin agonist) cannabis (dopamine agonists, lacking evidential supports)
59
why does LevoDopa not work when treating Parkinson's
a dopamine precursor, but in Parkinsons there is death in dopamine production cells, meaning no dopamine would actually get produced
60
why can we not give Parkinson's patients just more dopamine
it can't cross BBB
61
outline surgical intervention as Parkinson treatments
lesion inhibitory output structure, but only in very severe case
62
explain how deep brain stimulation works to treat Parkinson
target same site as lesioning basal ganglia however electrical currents able to be tuned to shut down or inhibit output, reversible, controllable, adjustable
63
name some side effects of deep-brain stimulations
cognitive issue, speech impairement and gait problems
64
name a stem cell potential treatment for Parkinson's development
replace lost dopamine cells by using fetal or stem cells transplant
65
define dementia
chronic, persistent disorder of mental processes causes by brain disease or injury and marked by memory disorders, personality changes and impaired reasoning
66
how much of dementia does Alzheimer account for?
two thirds
67
name some other type of dementia
- vascular dementia - dementia with Lewy bodies - frontotemporal dementia - mild cognitive impairment - posterior cortical atrophy - primary progressive aphasia
68
how prevalent is Alzheimers in 65+, and 85+
10% age 65+ 35% age 85+
69
give early stage symptoms of Alzheimers
selective decline in memory, attention deficit, personality change
70
give intermediate stage symptoms of Alzheimers
confusion, anxiety, irritability, speech deterioration
71
give final stage symptoms of Alzheimers
swallowing, bladder control
72
outline assessment of Alzheimer's
MMSE- mini mental state Examination map score and compare to a standard, potentially measure at different time points
73
what correlation has been found between dementia and other lifestyle characteristics
education, cardiovascular health, general physiological health
74
outline the role of amyloid plaque in Alzheimer
clumps of scar tissue of degenerating neurons and lumps of amyloid proteins (b-amyloid) interfer with neuronal function
75
what is AmyloidPrecursorProtein (APP) and what goes wrong in Alzheimers
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
outline the role of tau in Alzheimers
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
what are neurofibrillary tangles in Alzheimers
threadlike protein tangles in neural cytoplasm
78
what are microbleeds in Alzheimers
small dot-like lesion, result from microhemorrhage
79
where are microbleeds most prevalent in Alzheimers
medial temporal lobe (entorhinal cortex, amygdala, hippocampus)
80
how common is Alzheimers in immediate families
x2 as likely if live to old age
81
name what early research into genetics for Alzheimer has found
mutations to 3 different genes contribute to early onset, but only 1% later onset
82
what is APP (genetic), founds on chromosomes 21 which links to Alzheimers?
also link to down syndrome, develop Alzheimer pathology by 40, 150% of normal APP levels
83
what is apoE in Alzheimers (genetic
alpolipoprotein-E = a risk or protective factor, 3 common alleles (E2-good, E3, E4-bad) involved in transport of cholesterol
84
name animal reserach for Alzheimers
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
name what are current developing treatments for Alzheimers?
those focusing for Tau, Amyloid or apoE related features of Alzheimers. immuno and gene therapy approaches
86
what do current Alzheimers treatments target
loss of neurons producing Acetylcholine (vital in normal cognitive functions and memory)
87
what does treatments targeting cholinesterase (AchE) do in Alzhimers
enzyme that breaks down Ach and prevents Ach continuing to act on neurons. increasing AchE increases effect of Ach on neurons
88
what has staining research evidence found in Alzheimers
cholinergic neuron profound loss widespread across cortical regions
89
what is a main drug for Alzheimers
cholinesterase inhibitorm
90
name 3 cholinesterase inhibitors (Alzheimers drug)
donepezil hydrochloride (Aricept) rivastigmine (Exelon) galantamine (Reminyl)
91
what is the current dominant amyloid hypothesis in Alzheimers
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
what is high-plaque normals in non-dementia individual
many people without dementia have significant levels of amyloid plaques - are at risk of cognitive decline
93
outline similarities of down syndrome and Alzheimers pathology
at 40 develop numerous amyloid plaques, neurofibrillary tangles at 60 two-third have dementia genetic coding of b-amyloid located on chromosome 21
94
what is pathogenic spread hypothesis for Alzheimers
many common neurodegenerative diseases result from presence of misfold proteins iniating chain reactions causing other protein to misfold
95
in what ways can brain injury teach us about normal brain functioning
1. study brain localisations 2. basis of treatments and rehab 3. allows developmental trajectories and milestones for congenital injuries 4. neuroremappings in rehab
96
what are limitations of using brain damage findings in clinical practice?
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.
© 2025 Bold Learning Solutions. Terms and Conditions