Brainscape's Knowledge GenomeTM

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


See full index

Med 4 > CNS Week 4 Dementia > Flashcards

CNS Week 4 Dementia Flashcards

1
Q

Demographic of the population most likely to get dementia

A

66% are women (could be due to age being a risk factor and women living longer)
1/3 people over 65 will get dementia

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

Signs and symptoms of dementia that you should look out for

A
  • struggling to remember recent events but easily recalling things from the past
  • finding it hard to follow conversations or TV programmes
  • forgetting names of friends or objects
  • repeating yourself or losing the thread of what you are saying
  • issues with thinking and reasoning
  • feeling anxious, depressed or angry about forgetfulness
  • confused even in familar environment
  • decline in ability to talk, read or write
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Psychological disturbances in dementia

A

Delusions and hallucinations

Anxiety and depression

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

Behavioural disturbances in dementia

A

Apathy, aggression, purposeful walking (walking but forgetting where theyre going)
Abnormal vocalisation

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

Biological distubrances in dementia

A

Sleep and appetite

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

What factors does the clinical dementia rating take into account

A 
Memory 
Orientation 
Judgement and problem 
Community affairs 
Home and hobbies 
Personal care
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is a dementia friendly community

A

A place where people with dementia are understood respected and supported
Uses measures eg sign posts on the floor rather than walls as PwD tend to look down when they walk

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

Process of a dementia diagnosis being made

A

Visit to GP: signs / symptoms are noticed by PwD or informant- a feeling that something isnt quite right
Screening tests eg MMSE

Referral to MAS: diagnostic assessments undertaken eg neuropsychological testing, CT head scan, blood testing for biomarkers

Diagnosis disclosed at MAS: the healthcare professional at the MAS will disclose a diagnosis after discussion with the PwD and their supporters

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

Why are scans and biomarkers less helpful in diagnosing old people with dementia

A

Because a mixed pathology is very common

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

How do south asian families view dementia

A

Tend to seek help later as they may prefer to manage symptoms within the family
Older people are shown respect in south asian cultures by no longer being asked to do household chores so impairments can go unnoticed

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

How do sub-saharan african cultures view dementia

A

May perceive dementia as witchcraft or possession and can turn to alternative care such as herbs, prayers or traditional healers

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

Define dementia

A

An umbrella term that describes a collection of symptoms that are caused by disorders affecting the brain. It is not one specific disease
Affects thinking, behaviour and the ability to perform everyday tasks and brain function is affected enough to interfere with the persons normal social or working life

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

What is alzheimers disease

A

The most common type of dementia
Accounting for approximately 40-70% of all dementias
Caused by build up of protein in the brain (amyloid beta and tau)

Insidious onset and gradual progression
Slightly more predictable than other dementias

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

What is vascular dementia

A

The second most common type of dementia
Accounting for approximately 15-25% of all dementias
Caused by interrupted blood flow to the brain which causes cells to die

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

What is lewy body dementia

A

Accounts for approximately 2-20% of all dementias

Deposits of protein called lewy bodies that interrupt the chemical transmission of impulses

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

Symptoms of lewy body dementia

A

Problems with attention and alterness that can fluctuate throughout the day, memory, visual hallucinations which may be distressing, delusions such as thinking there are strangers in the house or that family members have been replaced by imposters, movement problems such as shuffling when walking and balacne problems

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

What are some other types of dementia

A

Demenita associated with parkinsons disease and huntingtons disease
Head trauma
Human immunodeficiency virus
Alcohol related dementia
Crutzfedlt jakob disease
Corticobasal degeneration and progressive supranuclear palsy

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

Link between neuropathology and presentation in alzheimers disease

A

Cell death and difficulties in cells communicating with each other begins in the hippocampus (memory)

Degeneration spreads to areas concerned with language so we start to have problems comprehending and forming speech

Then to the fronal lobes - problems with decison making and planning actions

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

What reduces the risk of developing alzheimers disease

A

Activities than strengthen our neural connections or create extra connections eg white collar jobs, edication, stimulating activities such as reading, museums, sport and sudoku

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

What

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

Symptoms of vascular dementia

A

Problems with thinking speed, concentration and communication, anxiety and depression, memory problems and confusion

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

Treatment of vascular dementia

A

No way of reversing the damage so treatment is about secondary prevention
Use drugs that act on the cardiovascular system eg blood pressure / statins

Lifestyle changes- people with dementia might need extra support to make these changes

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

What is levodopa

A

A drug often given to people with parkinsons disease to help with movement - increases the amount of dopamine precursor available

Sometimes given to people with dementia lewy bodies but is less effective for them

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

What is frontotemporal dementia

A 
Affecting less than 5% of all people with dementia and generally with a younger onset (55) 
Affects frontal (executive function and damage here can lead to a loss of inhibitions, difficulty expressing sympathy or empathy, loss of interest and motivation, difficulties in planning and temporal lobes (language, communication so damage here can lead to difficulties with speech, understanding sentences and finding the right words
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is mild cognitive impairment

A

A concept developed to describe the transitional phase between normal and pathological ageing

Criteria include objective impairment in memory or other cognitive domain, intact general cognitve functioning, intact activies of daily living, absence of dementia, presence of subjective memory complaints

People with MCI are at increased risk of progression to dementia compared to people without cognitve impairment

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

Link of social networks and risk of dementia

A

People with cognitive impairment have less rich social networks than those without

Having weaker social networks is associated with a higher likelihood of having anxiety and depression

Both relatives and friends are important

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

Describe the 3 componenets of reality orientation

A

24 hour - staff present information related to orientation every time they interact with people and give a commentary on what is happening

Small groups of 5 or 6 and 2 staff
Sessions begin with an introduction and a discussion of current information and orientation and then activities to enhance social interaction and learning

Attitude therapy - staff tailor their attitudes towards patients / residents personalities
This can vary from friendliness through no demand and matter of fact to kind firmness

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

What is reminisence therapy

A

Using memory triggers to provide a tangible focus for reminisence

Maintaining the persons identity and assisting in social interaction through sharing memories and experiences

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

What is cognitive stimulation therapy

A

1) experimental learning using all 5 senses to promote cognitive stimulation and memory processes
2) focused psychological interventions relevant to the difficulties of everyday living
3) acknowledgement of the emotional lives and enhancement of the cognitive skills of people with dementia
4) implicit learning rather than explicit ‘teaching’. Extensive rehearsal and consolidation of essential information about themselves and their world
5) the reciprocal, psychological processes in which people with dementia and those who care for them learn more about each others capabilites and vulnerabilities

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

Benefits of cognitive stimulation therapy for PwD

A

Opportunities to engage in pleasurable and mentally stimulating activities

Improved cognition

Improved communication

Maintenance of daily skills

The supportive environment and opportunities for social interaction help to boost confidence

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

Benefits of cognitive stimulation therapy for carers

A

A break whilst the PwD is attending the group

Carer delivered iCST helped carers and PwD to become closer

Strengthen the care giving relationship

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

Define learning

A

The process by which we acquire new information about the world

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

Define memory

A

The product of learning - the persistence of learning in the brain in a manner that enables us to call it up later

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

What are the general stages of memory

A

Encoding: the processing of information ready for storage

Storage: the maintenance of a permanent record, trace or ‘engram’ representing the encoded information

Retrieval: the ‘bringing to mind’ of a stored representation of information, an event or actions

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

What is sensory memory

A

Duration of milliseconds- seconds

Echoic and iconic sensory traces

Larger capacity than STM - icon thought to contain about 12 items but they fade too fast for verbal report

Echoic trace thought to last 10 seconds

Items shift from sensory to STM through attention

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

What is short term memory

A

Duration of seconds
Capacity of 7 +/-2 items (miller
Chunking information creates larger items

Items can be maintained in STM by active rehearsal; if rehearsal is blocked, items decay over time

Items shifted from STM to LTM via rehearsal

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

What is LTM

A

Unlimited capacity store

Duration measured in hours - years

Information can be lost from LTM through interference of new malterial on old

Items can enter LTM only via STM according to the modal model

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

What is working memory

A

The collection of strucures and processes used for temporarily storing and manipulating information eg digit span and digit span backwards

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

What is amnesia

A

A condition characterised by deficits in the recall and recognition of facts and events experienced

STM abilities and intelligence often remain relatively unimpaired

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the 2 types of amnesia

A

Retrograde amnesia: before the onset of brain damage

Anterograde amnesia: after the onset of brain damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the causes of amnesia

A

Organic: the result of damage to the brain through trauma, disease, or drugs

Functional: the resuly of psychological factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is episodic memory

A

Length of storage: minutes to years

Explicit declarative awareness eg remembering a short story, what you had for dinner last night, your birthday

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is semantic memory

A

Length of storage of memory: minutes to years
Explicit declarative awareness eg knowing the PMs during WWII, the colour of an elephant, how a fork is different to a comb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is procedural memory

A

Length of storage of memory: mins to years
Explicit or implicit, declarative or nondeclarative awareness eg driving a car, lerning the sequence of numbers on a mobile without trying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is working memory

A

Length of storage of memory: seconds to minutes

Explicit, declarative awareness
Eg phonologic: keeping a phone number in your head, mentally following a route in your mind

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Neuropathology of AD

A 
Amyloid plaques 
Neurofibrillary tangles 
B-amyloid pathology and tauopathy 
Synaptic dysfunction and neuronal loss 
Reactive gliosis and microgliosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Histopathology of AD

A

Neuritic plaques: extracellular B-amyloid depositions and dystrophic neurites, activated microglia

Neurofibrillary tangles: intracellular acetylated paired helical filaments of hyperphosphorylated tau

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is dementia with lewy bodies

A

Clinically similar to AD
May not have parkinsons
Varying degrees of B amyloid plaques
Neocortical neurofibrillary tangles are less frequent in DLB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the difference between lewy body dementia and dementia with lewy bodies

A

Lewy body dementia includes PD

Whereas dementia with lewy bodies doenst

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are the subtypes of dementia with lewy bodies

A

Brainstem predominant DLB

Limbic DLB

Neocortical or diffuse DLB

Cerebral DLB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Explain how symptoms can vary in frontotemporal dementia

A

If the frontal lobe is more affected then behaviour is affected first
If the temporal lobe is more affected then language is affected first

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Structural neuroimaging techniques for dementia

A

Computed tomography

Magnetic resonance imaging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Functional neuroimaging techniques for dementia

A 
Functional MRI 
Magnetic resonance spectroscopy 
SPECT (if this is positive most likely DLB) 
Positive emission tomography 
Diffusion tensor imaging
54
Q

Different types of B amyloid peptides

A

AB1-40 and AB1-42

AB1-42 aggregates faster, seeds plaques and more neurotoxic
Most familial AD mutatiosn increase the levels of AB1-42

55
Q

Describe the amyloid cascade hypothesis

A

Reduced breakdown clearance, mutations and risk factors all increase B amyloid.
Cuases more plaques, tangles and neurotransmitter changes

Plaques and tangles lead to neuronal loss which increases neurotransmitter changes and has a 2 way relationship with synapse loss

56
Q

What does Tau protein do

A

It is stable and binds to elements in the neuronal membrane

They are abundant in the CNS neurons and have roles in maintaining stability of microtubules in axons

57
Q

What is tauopathy

A

Phosphorylation negatively regulates binding of tau to microtubules
Highly phosphorylated during development and in AD

Insoluble ubiquitinated phosphorylated Tau form filamentous inclusions in neuronal cell bodies, processes and glia

58
Q

Conditions associated with tauopathies

A 
AD 
Pick’s disease 
Frontotemporal dementia with parkinsonism linked to chromosome 17 
Progressive supranuclear palsy 
Corticobasal degeneration 
Postencephalitic parkinsonism 
Niemann pick’s disease
59
Q

Describe synucelinopathy

A

Aggregation of a-synuclein is the key inital step in the formation of lewy bodies

Neurotoxic a-synuclein oligomers

Extracellular a-synuclein oligomers can transmit lewy pathology

60
Q

Neurobiology of DLB

A 
B-glucocerebrosidase 1 deficiency 
Microglial dysfunction 
Mitochondrial dysfunction 
Autophagy lysosome pathway impairment 
Ubiquitin protease system impairment 
Oxidative stress
61
Q

Indicative biomarkers of DLB

A

Reduced dopamine transporter uptake in basal ganglia demonstrated by SPECT or PET scan

Low uptake in 123iodine- MIBG myocardial scintigraphy

Polysomnographic confirmation of REM sleep wihtout atonia

62
Q

Supportive biomarkers of DLB

A

Relative preservation of medial temporal lobe structures

Generalised low uptake on SPECT / PET with reduced occipital activity +/- the cingulate island sign on FDG-PET imaging

Prominent posterior slow wave activity on EEG with periodic fluctuations in the pre-alpha / theta range

63
Q

Role of DNA methylation in epigenetics

A

The methyl group (an epigenetic factor found in some dietary sources) can tage DNA and activate or repress genes and change the histone structure which alters the availability of genes in the DNA to be activated

64
Q

What is causing population ageing

A

Decreasing fertility and increasing life expectancy

65
Q

Implications of population ageing

A

Healthcare utilisation, shrinking workforce, older retirement age, pensions, public finances

66
Q

Define dementia

A

An acquired, persistnet impairment of mental abilities often accompanied by changes in personality and behaviour (aggression, wandering)

Impaired daily living, occupational functioning and social interaction

Caused by disease or head trauma and often associated with increasing age (exc downs syndrome, and early onset dementia)

67
Q

What is mild cognitve impairment

A

A pre clincial stage of dementia

Not 100% cognitive functioning

68
Q

Pathological casues of dementia

A

AD

Vascular

Frontal temoral

Lewy body

69
Q

Breakdown of the cost of dementia in the UK

A

Costs over £26bn
£12bn for cancer, £8bn for coronary heart disease and £5bn for stroke

Cost is actually higher as PwD are usually cared for by unpaired carers eg family members

70
Q

Protective factors of dementia

A 
Educational attainment 
Social engagement 
Mental stimulation 
Physical activity 
Diet (eg fish intake)
71
Q

Risk factors for dementia at different points throughout life

A

Birth: ApoE E4 allele
Early life: less education
Midlife: hearing loss, hypertension, obesity
Late life: smoking, depression, physical inactivity, social isolation, diabetes

72
Q

Drug treatment for dementia

A

Approval for a limited number of drugs
Cholinesterase inhibitors (galantamine, rivastigmine, donepezil)
Memantine (N-methyl D aspartate antagonist; glutamate)

Only approved for mild - moderate cases
Dont work in everyone
Side effects: gastrointestinal, insomnia, nausea, vomiting

73
Q

Non pharmacological interventions for dementia

A

Physical activity, caloric restriction, cognitive training/therapies eg cognitve stimulation therapy and vitamin supplementation

74
Q

Benefits of an ageing population

A

Reflectes success in medicine and technology (childhood disease) as well as advancement in social and environmental conditions

Resource for families and communities in the form of knowledge

75
Q

Challenges of an ageing population

A

Strain pension and social security systems (many LIC where people dont have access to pensions)

Increase demand for acute and primary health care

Require a larger and better trained health workforce

Increase the need for long term care

76
Q

What is the individual impact of dementia

A

Years lived with disability not mortality
Impact on quality of life (cognitive and functional disability)

Contributes much more than other chronic illness to disability, need for care, carer strain, financial strain

77
Q

How can the behaviour of the EO muscles be used to examine the cranial nerves that innervate them

A

CNII, CNIII, CNIV and CNVI usually tested together
Test includes:
Range and accuracy of eye motion (tracking an object)

Pupillary light reflex (shining light into one pupil should
cause both to dilate)

Ptosis (drooping eyelid)

78
Q

What are cranial nerve palsies

A

Affect CN III, CN IV and CN VI often found by opticians and referred to opthalmology

Often found with strabismus (squint) and diplopia (double vision)

79
Q

Common causes of cranial nerve palsy

A

Trauma
Neoplasm / tumour
Something vascualr eg diabetes and hypertension

80
Q

Things to consider in treatment of cranial nerve palsy

A

Affected nerve (cranial nerve examination)
Direction of diplopia (horizontal, vertical, oblique)
Age of onset

81
Q

Role of fixational eye movements in pathology

A

Certain visual disorders influence unconscious eye movement behaviour

Eg they are exaggerated by a factor of 4 in macular disease

82
Q

What are the smallest eye movements

A

Tremors

83
Q

Difference in clincal manifestation of DLB and AD

A

AD is mainly about progressive memory or other non-amnestic symptoms

DLB typically has fluctuating cognition, recurrent visual hallucinations, REM sleep behaviour disorder, plus symptoms of parkinsonism

84
Q

What brain structures are implicated in AD

A

Begins in the hippocampus and medial temporal lobe spreading upwards and outwards to affect other cortical regions
As a result memory is usually affected also language and later other areas such as visuospatial skills
Executive problems quite common due to frontal lobe involvement

85
Q

what neuropathological findings are seen in alzheimers disease at post mortem stage

A

Typically cerebral atrophy, especially medial temporal lobe structures but also often inferior temporal and frontal areas
Consequent ventricular enlargement
Microscopically neurofibrillay tangles of hyperphosphorylated tau protein and beta amyloid plaques

86
Q

Describe the genetic component to alzheimers

A

1) single genes with autosomal dominant inheritance that causes AD eg presenilin mutations
2) ApoE e4 is a gene conferring increased risk of AD or at least of developing AD at an earlier age

87
Q

What are the tests done to determine dementia

A

Clinical assessment - history, collateral history, mental state examination, cognitive testing
Blood tests
Neuroimaging

88
Q

How does dementia look on an MRI

A

Ventricles may be enlarged - depends on the degree of cerebral atrophy which can be variable

89
Q

Whay is montreal cognitive assessment (MOCA) and what does it entail

A

A short neuropsychological scheldule designed as an alternative to the MMSE aimed especially at early dementia / MCI
Tests: orientation, attention, naming, language, memory, delayed recall, abstraction and visuospatial / executive

90
Q

What are normal MOCA and ACE-III scores for a person without dementia

A

MoCA= 26/30 and above; ACE-III various figures quoted between 82-88/100
Higher cutoff has greater sensitivity but lower specificity

91
Q

Differentials for an older patient presenting with memory loss

A 
Dementia 
MCI 
Depression 
Alcohol misuse 
Medication with anticholinergic side effects 
Delirium
92
Q

How is alzheimers dementia different to another type of dementia

A

Progressive memory impairment over a period of time plus a lack of symptoms to suggest another cause eg DLB or depression suggests AD

93
Q

Action of donepezil and how it helps in the management of dementia

A

Acetylcholinesterase inhibitor
Inhibits breakdwon of ACh at synapses thus increasing availability of ACh to muscarininc and nicotinic receptors
ACh is important in memory function however action of AChEIs seems to be as much on alertness as upon improving memory

94
Q

How do urine infections cause delirium

A

Pathophysiology isnt completely understood
Various hypotheses:
- changes in neurotransmitters, altered neuroinflammatory processes and oxidative stress

95
Q

What causes death in dementia

A

In severe dementia people become physically frail and immobile and their swallowing reflex may be impaired
Vulnerable to conditions that affect frail, immobile people
Often eventually die of pneumonia

96
Q

Define quality of life

A

The level of satisfaction and comfort that a perosn enjots

Life gains its quality from the ability and capacuty of the individual to satisfy his or her needs

97
Q

What is response shift

A

The potential of a subjects views, values or expectations changing over the course of a study, thereby adding another factor of change on the end results

98
Q

What is SIDECAR

A

The scale measuring the impact of dementia on carers

99
Q

Describe end of life care in dementia

A

No proven effective interventions on QoL in advanced dementia
Several interventions effective in diminishing mediatiors of QoL ie challening behaviour, mood, sleeping disorders, including pain treatment

100
Q

What symptoms do people with end of life dementia experience

A 
Confusion 
Pain 
Low mood 
Constipation 
Loss of appetite

(Similar to cancer but people with dementia experience them for much longer

101
Q

Barriers to pain recognition in dementia

A

Person with dementia may not be able to remember the pain they experienced earlier
The person with dementia may not be able to verbally communicate what they are feeling
May not be able to identify where their pain is located
Belief that behaviours resulting from the pain are symptoms of the dementia

102
Q

How to assess pain in dementia

A

Asking the patient directly is best

Poor STM: people may not remember their pain

Speech problems- may have difficulty describing their pain

May no longer understand the concept of ‘pain’

May lose abstract concepts of severity

May need to use alternative expressions eg ‘sore’

Ask relatives for any individual pain indicators

Review health records

103
Q

Barriers to good palliative care in dementia

A

Lack of care continuity across the whole trajectory of dementia

Continuity in a palliative care approach in dementia is often not acheived well in the UK largely because of the commissioning divide across health and social care

104
Q

What is the role of the obicularis oculi

A

Has 2 parts (palpebral) and (orbital)

P- involved in blinking
O- needed if you are scrunching the eye shut

Goes to just below the cheek bone

105
Q

What is the role of the levator palpebrae superioris

A

Used for opening the eye

106
Q

What are the origins and insertions of the recti muscles (EO)

A

Recti superior originate in a common tendinous ring

Insert into the sclera

107
Q

Role of the optic nerve

A

Takes information away from the back of the eye

Is cranial nerve 2

108
Q

Origin and insertion of the oblique muscles (EO)

A

Superior oblique originates in sphenoid bone
Inferior oblique originates in maxilla

They both hook through the trochlear and back on self and insert into the sclera

109
Q

What are saccades

A

Intentional eye movements that are fast and omnidirectional

110
Q

What are FEMs

A 
Fixational eye movements 
(The eyes are never stationary) 
3 types: 
- microsaccades 
- drifts 
- tremors
111
Q

Describe the roles of the different types of fixational eye movements

A

Drifts: move the image across the retina
Microsaccafes: snap it back to the centre
Adaptation: causes the image to fade over time

112
Q

Describe testing of cranial nerves 2,3,4,6

A

Range and accuracy of eye motion eg tracking an object

Pupillary light reflex (shining light into one pupil, should cause both to dilate)

Ptosis (drooping eyelid)

113
Q

What cranial nerves do cranial nerve palsies affect and what are the causes

A

CN III, IV and VI

Causes: trauma, neoplasm / tumour, vascular eg diabetes, hypertension

114
Q

What are opsins

A 
Photosensitive proteins (rhodopsin / conopsin) 
Contain vitamin A
115
Q

What is the function of photoreceptors

A

Dark: Na + channel open, Na+ / K+ ATP-ase pump active, cell at baseline depolarised (-40mV)

Light: Na+ channel closed, positive ions build up in the synpase, cell hyperpolarised (more -ve), glutamate prevented from release to bipolar cells

116
Q

Role of choroid layer

A

Absorbs light

117
Q

Role of rods

A 
120 million per eye 
In the periphery 
Monochrome colours 
Low resolution 
Many : 1 with ganglion cells
118
Q

Role of cones

A 
6 million per eye 
In the fovea 
Detect colour 
High resolution 
1:1 with ganglion cells
119
Q

Describe cataracts

A

Increased opacity / cloudiness of the lens (sometimes cornea)

Most common cause of low vision registration worldwide

Key factors:

  • gradual onset
  • can be 1 or both eyes
  • manifests as gradual degradation of acuity, diplopia, reduced sensitivity to colour
  • simple surgical treatment
120
Q

Risk factors for cataracts

A 
Age 
Trauma 
Radiation 
Smoking 
Genetics
121
Q

Describe glaucoma

A

Increased intra-ocular pressure (IOP)

  • fluids in the eye maintain structure - typically 10mmHg
  • if the outflow is blocked, pressure can build (above 21 mmHg is considered high)
  • constricts the optic nerve and artery
  • results in loss of peripheral visual field
122
Q

Describe macular degeneration

A

Dry, age related

  • if the eye stops clearing debris properly, drusen can build up
  • this can block or damage photoreceptors, particularly in the fovea (macula)
  • loss of centra visual field
123
Q

Describe the key factors of a detached retina

A

The detached retina has been pulled away from the choroid layer

  • often connected to trauma (particularly in myopic patients)
  • sudden appearance of ‘floaters’- dark spots that float in the field of vision
  • sudden short flashes of light in one eye
124
Q

Describe colour vision deficiency (colour blindness)

A

Typically genetic but can develop due to other eye diseases

Red-green is most common

XX chromosomes: 0.5% chance due to the gene being carried on the X chromosome
XY: there is an 8% chance that you are coloour blind

125
Q

What is giant cell / temporal arteritis

A

Inflammation of some very important arteries

May affect blood supply to the optic nerve, causing arteritic anterior ischemic optic neuropathy

  • reduced visual acuity
  • diplopia
  • acute loss of vision
126
Q

What happens at the optic chiasm

A

Projections from the contralateral hemifield switch sides at the optic chiasm

127
Q

Role of the optic tract

A

Projects to the LGN in the thalamus and some projections to the hypothalamus

128
Q

What do lesions in the optic nerve lead to

A

Monocular blindness

129
Q

What do lesions in the optic chiasm lead to

A

Temporal hemianopia

130
Q

What do lesions in the optic tract lead to

A

Left or right hemianopia

131
Q

What do lesions in the optic radiations pathways lead to

A

Upper or lower hemianopia

Upper VF defects sometimes caused by temporal lesions

132
Q

What is the 2 stream model in the visual cortex

A

Post V1, information is transmitted via 2 pathways
Dorsal stream: the ‘where’ or ‘how’ pathway
Associated with motion, location, saccadic control

Ventral stream: the ‘what’ pathway
Associated with object recognition and memory

Med 4 (12 decks)

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