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Year 2 NSB > Cognitive impairment and confused states > Flashcards

Cognitive impairment and confused states Flashcards

1
Q

What is confusion?

A
  • lack of clarity in thinking

- everyday issues can be challenging

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2
Q

What is cognition?

A
  • the mental process involved in making sense of and learning about the world around us
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3
Q

What is crystallised cognitive ability?

A
  • cumulative skills and memories from cognitive processing that occurred in the past
  • tests of general knowledge, vocabulary, reading comprehension, maths, science
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4
Q

What is ‘fluid’ cognitive ability?

A
  • processing of new information to quickly solve problems
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5
Q

In ageing does crystallised and fluid cognitive abilities decline equally?

A
  • no

- fluid has a more dramatic decline

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6
Q

What are some common conditions where a healthy individual may experience cognitive impairment?

A
  • alcohol/drugs
  • acute illness
  • sleep deprivation
  • extreme exercise
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7
Q

What is delirium, often called acute confusional state?

A
  • rapid acute onset
  • causes serious impairments in mental abilities
  • causes confused thinking and reduced awareness of the environment
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8
Q

Are patients who experience delirium all old patients, or what is the other cause?

A
  • can affect anyone
  • usually caused by an acute illness
  • always has a cause
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9
Q

If a patient has delirium, will the impairment in mental thinking and confusion present before the cause or after?

A
  • can be both

- patients may present with delirium and then the infection presents later

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10
Q

What are some of the main presentations of delirium?

A
  • impaired awareness, attention and concentration
  • disorientated
  • memory present, but lack of awareness
  • hallucinations, especially visual
  • delusions
  • mood
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11
Q

Can delirium be treated?

A
  • yes

- treat the underlying cause, like the infection

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12
Q

In patients with delirium, do they always experience a suppression of their normal cognitive state?

A
  • no

- can be hyper, hypo or mixed

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13
Q

Who is most at risk of experiencing delirium?

A
  • older patients and young children
  • patients with hospital stays
  • polypharmacy patients
  • multi-comorbidities
    ALL have increased risks of other disorder or increased infection risk
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14
Q

If delirium and its underlying cause are not treated, will delirium just go away?

A
  • no
  • if left it can become worse
  • increases risk of dementia
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15
Q

What is potentially the most common cause of delirium?

A
  • acute systemic infection

- infection that is in the blood and can spread throughout the body

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16
Q

How can delirium be prevented?

A
  • early diagnosis and treatment of underlying cause
  • maximise healthy sleep patterns
  • prevent dehydration and constipation
  • ensure good nutrition
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17
Q

How can a calm and quiet environment help treat delirium?

A
  • patients have hallucinations and delusions

- so remove any stimulus making these worse

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18
Q

Are medications commonly used to treat delirium?

A
  • avoided at all costs

- generally last option for treatment

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19
Q

What is dementia, which is latin for out of ones mind?

A
  • umbrella term

- group of progressive, neurodegenerative brain disorders

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20
Q

When we talk about dementia, what is one of the key attributes for it to be called dementia, regarding the symptoms?

1 - progressive worsening of symptoms over time
2 - rapid onset of symptoms
3 - rapid onset and then slow progression
4 - slow progression with intermittent rapid deterioration of symptoms

A

1 - progressive worsening of symptoms over time

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21
Q

What are some of the common signs of dementia?

1 - muscle pain, stiffness, impaired memory, thinking and behaviour
2 - impaired memory, thinking and behaviour and altered ADL
3 - insomnia, hyper-mania and and altered ADL
4 - depression, elation and impaired memory and thinking

ADL = activities of daily living

A

2 - impaired memory, thinking and behaviour and altered ADL

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22
Q

Instead of using senile dementia, which is essentially an older patient living with dementia, what should we describe this as?

A
  • late onset dementia

- or just dementia

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23
Q

Instead of using demented, which is essentially someone living with dementia, what should we describe this as?

A
  • living with dementia
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24
Q

Instead of using dementia patient, which is essentially someone living with dementia, what should we describe this as?

A
  • a person living with dementia
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25
Q

Instead of using ‘this person is dementing’, which is essentially someone who may be developing dementia, what should we describe this as?

A
  • person who may be developing dementia
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26
Q

Instead of using ‘presenile dementia’, which is essentially a younger person who may be developing dementia, what should we describe this as?

A
  • young onset of dementia
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27
Q

Instead of using ‘depressive pseudodementia’, which is essentially someone who may be developing dementia associated with depression, what should we describe this as?

A
  • cognitive due to depression
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28
Q

What is the prevalence of dementia in the 65-69 year olds?

1 - 1:10
2 - 1:100
3 - 1:1000
4 - 1:10,000

A

2 - 1 in 100

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29
Q

What is the prevalence of dementia in the 70-79 year olds?

1 - 1:10
2 - 1:25
3 - 1:100
4 - 1:500

A

2 - 1 in 25

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30
Q

What is the prevalence of dementia in the >80 year olds?

1 - 1:6
2 - 1:25
3 - 1:100
4 - 1:500

A

1 - 1 in 6 people

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31
Q

How many people in the Uk are living with dementia, and what is the estimated cost of this per year?

A
  • 850,000 people

- £34.7 billion per year

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32
Q

CVD, cancer and stroke are leading causes of disability in the UK, but what is the main cause of disability in later life in the UK?

A
  • dementia
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33
Q

When we compare dementia and delirium, which has rapid onset and which has a gradual development over time?

A
  • rapid onset = delirium

- gradual decline = dementia

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34
Q

When we compare dementia and delirium, which can cause a change in alertness?

A
  • delirium = alertness can increase or decrease

- dementia = remains normal

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35
Q

When we compare dementia and delirium, which has changes in attention?

A
  • delirium = impaired attention

- dementia = normally preserved

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36
Q

When we compare dementia and delirium, which is more likely to have hallucinations?

A
  • delirium = common

- dementia = rare (except in Dementia with Lewy bodies)

37
Q

When we compare delirium and dementia, which has fluctuations in cognition and awareness?

A
  • delirium = fluctuations during day

- dementia = gradual change over time

38
Q

When we compare delirium and dementia, which has changes in mood?

A
  • delirium = mood often fluctuates

- dementia = mood may be low, doesn’t usually fluctuate

39
Q

Dementia is an umbrella term covering a number of neurodegenerative brain conditions. Which is the most common?

1 - Parkinsons disease
2 - Lewy body dementia
3 - Alzheimers disease
4 - Vascular dementia

A

3 - alzheimers disease

40
Q

Dementia is an umbrella term covering a number of neurodegenerative brain conditions. The most common is Alzheimers, what is the second most common cause?

1 - Parkinsons disease
2 - Lewy body dementia
3 - Frontal-Temporal dementia
4 - Vascular dementia

A

4 - vascular dementia

- dementia caused by cerebrovascular disease

41
Q

What is alpha synuclein?

1 - protein found inside neurons, maintains microtubule structure
2 - protein aggregates that form extracellular plaques in the brain
3 - protein in brain involved in synaptic trafficking and neurotransmitter release
4 - protein found outside neurons, maintains pre-synapse

A

3 - protein in brain involved in synaptic trafficking and neurotransmitter release

42
Q

How can a-synuclein, a normal protein in the brain that is involved in synaptic vesicles trafficking and regulation of neurotransmitter release cause lewy bodies?

1 - clump together forming plaques that build up around synapses causing neuronal cell death
2 - mis-folded form of a-synuclein aggregate around synapse causing neuronal cell death
3 - excessive levels inhibit neurotransmitter release despite action potential
4 - binds to vesicles and inhibits vesicle binding to pre-synapse membrane

A

2 - mis-folded form of a-synuclein aggregate around synapse causing neuronal cell death

  • the aggregates of misfolded protein are called Lewy bodies
  • lewy bodies can cause neurons to die
43
Q

There are 2 types of dementia (that we need to know about) that are associated with lewy bodies (misfolded a-synuclien), what are these?

1 - Parkinsons disease and dementia with lewy bodies
2 - Lewy body dementia and Alzheimers disease
3 - Alzheimers disease and Parkinsons disease
4 - Vascular dementia and Lewy body dementia

A

1 - Parkinsons disease and dementia with lewy bodies

44
Q

Most dementias are causes by a misfolding of different proteins. What are the 3 main proteins we need to be aware of?

1 - Tau protein, a-synuclein, B-Amyloid
2 - SMN-1 protein, a-synuclein, B-Amyloid
3 - Tau protein, a-synuclein, SMN-1 protein
4 - Tau protein, SMN-1 protein, B-Amyloid

A

1 - Tau protein, a-synuclein, B-Amyloid

45
Q

Tau protein is a protein located in the brain. What is one of the key roles of Tau protein?

1 - stabilisation of the internal microtubules
2 - regulation of vesicle trafficking at synapse and neurotransmitter release
3 - regulate neurotransmitter trafficking to and from nucleus
4 - ensure vesicles bind with pre-synaptic membrane

A

1 - stabilisation of the internal microtubules

- important for neurogenesis

46
Q

a-synuclein is a protein located in the brain. What is one of the key roles of a-synuclein?

1 - stabilisation of the internal microtubules
2 - regulation of vesicle trafficking at synapse and neurotransmitter release
3 - regulate neurotransmitter trafficking to and from nucleus
4 - ensure vesicles bind with pre-synaptic membrane

A

2 - regulation of vesicle trafficking at synapse and neurotransmitter release

47
Q

What are amyloids?

A
  • involved in growth and repair following injury
  • BUT can become misfolded and not destroyed by proteases
  • aggregate together and accumulate in tissue
48
Q

Amyloids are proteins which have incorrectly folded and have not been degraded by proteases. How can this lead to dementia?

A
  • collect on outside of neurons and interfere with signalling
  • can also collect in blood vessel walls causing damage
49
Q

Misfolded proteins are common in dementia. Which 2 proteins are commonly reported in Alzheimers disease?

A

1 - B-amyloid (extracellular)

2 - Tau protein (intracellular)

50
Q

B-amyloid (extracellular) and Tau protein (intracellular) can become misfolded, and has been linked with dementia. One of these can build up and cause plaques, and one can causes tangles, which is which?

A
  • B-amyloid = plaques

- Tau protein = tangles

51
Q

Misfolded proteins are common in dementia. Which protein is commonly reported in Parkinsons disease dementia and Lewy bodies dementia?

1 - Tau protein
2 - a-synuclein
3 - B-Amyloid
4 - SMN-1 protein

A

2 - a-synuclein

52
Q

Misfolded proteins are common in dementia. Which protein is commonly reported in frontal-temporal dementia?

1 - Tau protein
2 - a-synuclein
3 - B-Amyloid
4 - SMN-1 protein

A

1 - Tau protein

53
Q

It can be really difficult to diagnose patients with dementia, but what is potentially the most effective method?

A
  • good clinical history
54
Q

It can be really difficult to diagnose patients with dementia, but a good clinical history is really important and potentially the most effective method. What other methods can be useful?

A
  • physical examination
  • blood tests
  • neuroimaging
  • cognitive testing
  • lumbar puncture (mainly in young)
55
Q

It can be really difficult to diagnose patients with dementia, but a good clinical history is really important and potentially the most effective method. Although lumbar puncture is not commonly used, it can be useful in which group of patients?

1 - older patients with late dementia onset
2 - young dementia onset
3 - patients who have had dementia for a long time

A

2 - young dementia onset

56
Q

Alzheimers is the most common dementia. From the time of diagnosis, what is the general survival rate?

1 - 1-4 years
2 - 2-8 years
3 - 4-14 years
4 - 4-20 years

A

4 - 4-20 years

57
Q

In patients with Alzheimers disease, there are 2 pathological mechanisms, one intracellular and one extracellular involving tau protein and amyloid. What is the intracellular pathology?

A
  • Tau protein becomes abnormally phosphorylated
  • forms paired helixes
  • form neurofibrillary tangles causing neuronal cell death
58
Q

In patients with Alzheimers disease, there are 2 pathological mechanisms, one intracellular and one extracellular involving tau protein and amyloid, respectively. What is the extracellular pathology?

A
  • B-amyloid plaques form around neurons and in blood vessels
  • inhibit neuronal function
  • damage blood vessels
59
Q

in patients with Alzheimers disease, there are 2 pathological mechanisms, one intracellular and one extracellular involving tau protein and amyloid. There is also a markedly reduced activity in which receptors in the cerebral cortex?

1 - cholinergic receptors
2 - adrenergic receptors
3 - receptor tyrosine kinase receptors
4 - ligand gates channels

A

1 - cholinergic activity

  • nicotinic and muscarinic receptors
  • BOTH are linked with memory and learning, so if damaged this is affected
60
Q

In Alzheimers, amnesia is commonly reported. Does this affect short and long term memories equally?

A
  • initially short- term memory

- later impairs long-term memory

61
Q

In Alzheimers, amnesia is one of the most dominant clinical feature. What other clinical features do patients present with?

A
  • disorientation
  • loss of motor skills (apraxia)
  • disturbances in recognition of objects and faces (agnosia)
  • disturbances of speech (dysphasia)
  • difficulty in performing complex tasks
  • planning, organization, sequencing, abstraction
  • behavioural and psychological disturbances
62
Q

The genetics that can contribute to Alzheimers disease are complicated, but can be divided into young and late onset. Which 2 genes from the list below are commonly found to be mutated in young onset of dementia?

1 - amyloid precursor protein (APP)
2 - apolipoprotein 4 cholesterol carrier
3 - presenilin 1 and 2 (PSEN-1 and 2) (enzymes involved in amyloid formation)
4 - a synuclein

A

1 - amyloid precursor protein (APP)

3 - presenilin 1 and 2 (PSEN-1 and 2) (enzymes involved in amyloid formation)

63
Q

The genetics that can contribute to Alzheimers disease are complicated, but can be divided into young and late onset. What are the genes that are mutated involved in late onset?

1 - amyloid precursor protein (APP)
2 - apolipoprotein 4 cholesterol carrier
3 - presenilin 1 and 2 (PSEN-1 and 2) (enzymes involved in amyloid formation)
4 - a synuclein

A

2 - apolipoprotein 4 cholesterol carrier

  • supports lipid transport and injury repair in the brain
  • LARGEST KNOWN RISK FACTOR IN LATE ONSET DEMENTIA!!!!!
64
Q

When doing a lumbar puncture, what are we looking for in the amyloid protein?

A
  • ratio between alpha and beta (we want more alpha)
  • GOOD = gamma and alpha
  • BAD = beta and gamma
65
Q

Vascular dementia shares common risk factors with atherosclerosis and thrombosis. What are the most common risk factors for this?

A
  • age
  • vascular risk factors (hypertension, cholesterol)
  • inactivity
66
Q

Which 2 forms of dementia from the image can often co-exist due to the cross over of risk factors?

1 - alzheimers and parkinsons disease
2 - alzheimers and vascular dementia
3 - parkinsons disease and vascular dementia
4 - lewy body dementia and vascular dementia

A

2 - alzheimers and vascular dementia

67
Q

Patients can develop dementia following a common cause of cerebrovascular disease neuropatholgy. What is a cerebrovascular disease neuropatholgy?

A
  • stroke

- 15-30% of patients develop dementia 3 months following stroke

68
Q

The symptoms of vascular dementia are variable due to the range of underlying vascular pathology (stroke). But there is a classical stepwise progression. What does this mean?

1 - slow progression from onset
2 - rapid decline following vascular pathology but then improved symotins
3 - abrupt decline associated with an infarct (small stroke)
4 - slow progression, followed by a rapid decline

A

3 - abrupt decline associated with an infarct (small stroke)

69
Q

The symptoms of vascular dementia are variable due to the range of underlying vascular pathology. Patients are at increased risk of injury due to a slowing of what?

1 - heart rate
2 - working
3 - gait
4 - muscle contraction

A

3 - gait (walking)

- increased risk of falls

70
Q

What are dementia with Lewy bodies and Parkinson’s disease dementia both linked with?

1 - Tau protein
2 - a-synuclein misfolding
3 - B-Amyloid
4 - SMN-1 protein

A

2 - a-synuclein misfolding

- folded proteins aggregate forming Lewy bodies

71
Q

Dementia with Lewy bodies and Parkinson’s disease dementia are both linked with abnormal folding of a-synuclein, which then aggregate and forms Lewy bodies. Where in the brain do these lewy bodies form in dementia with Lewy bodies and Parkinson’s disease dementia?

A
  • dementia with Lewy bodies = cortical = cognitively impaired
  • parkinson’s disease dementia = subcortical = motor function
72
Q

In Dementia with Lewy bodies and Parkinson’s disease dementia the lewy bodies form in the cortical and subcortical structures, respectively. How do we know this is the case in each of these diseases?

A
  • dementia with Lewy bodies = cortical, which is involved with cognitive thought
  • Parkinson’s disease dementia = subcortical, which is involved with movement, memory etc..
73
Q

Patients who have parkinsons who live with the disease for long periods are likely to develop what?

1 - stroke
2 - CVD
3 - dementia
4 - CKD

A

3 - dementia

74
Q

How can we distinguish between dementia with Lewy bodies and Parkinson’s disease dementia?

A
  • dementia with Lewy bodies - begins with cognitive symptoms (cortical)
  • Parkinson’s disease dementia - begin with movement symptoms (subcortical)
75
Q

What clinical features do patients with dementia with Lewy bodies present with?

A
  • motor features of Parkinsons disease
  • visual hallucinations
  • marked fluctuations in cognition and alertness
  • rapid eye movement sleep behaviour disorder
76
Q

Patients with dementia with Lewy bodies are highly sensitive to antipsychotic drugs, what does this mean?

A
  • can have dangerous reactions

- AVOID AT ALL COSTS

77
Q

When we investigate patients with dementia with Lewy bodies, it is very difficult to be able to determine where the build up of lewy bodies (aggregates of a-synuclein misfolded proteins) is in the brain and therefore make a diagnosis until post mortem. What else can be used to help diagnose?

A
  • MRI/CT scans = may show atrophy or be normal
  • Single-photon emission computed tomography may be able to identify where the lewy bodies are or the atrophy of the involved receptors are
78
Q

Single-photon emission computed tomography (SPECT) imaging using a ligand for dopamine transporter proteins can be used to detect atrophy of dopamine receptors. This can help identify if a patients symptoms are due to dementia with lewy bodies (cortical) or parkinsons dementia disease (sub-cortical), due to where is affected in the brain. In the image below, which is Alzheimers?

A
  • 1
  • can see atrophy in hippocampus
  • large dark spaces in cortical area and ventricles
  • uptake of ligand in caudate putamen (involved in motor control, cognition, and emotion)
79
Q

Single-photon emission computed tomography (SPECT) imaging using a ligand for dopamine transporter proteins can be used to detect atrophy of dopamine receptors. This can help identify if a patients symptoms are due to dementia with lewy bodies (cortical) or parkinsons dementia disease (sub-cortical), due to where is affected in the brain. In the image below, which is dementia with Lewy bodies?

A
  • 2
  • some atrophy of cortical area
  • no significant hippocampus atrophy
  • poor uptake by the caudate putamen (motor control, cognition, and emotion)
80
Q

What is frontaltemporal dementia?

A
  • least common dementia
  • group of conditions commonly cause young onset dementia
  • progressive atrophy of frontal and/or temporal lobes
81
Q

Which patients are at risk of frontaltemporal dementia?

1 - 20-30 year olds
2 - 40-60 year olds
3 - adults aged 50-60 years old
4 - adults >75 years old

A

3 - typically people aged 50-60s

- generally genetically causedYEAR

82
Q

In frontaltemporal dementia there are 2 main symptoms that patients present with, what are they?

A
  • behavioural - personality, memory

- language - speech

83
Q

Dementia has multiple brain process involvement that are disrupted. Although cognitive impairment is a central feature behavioural and psychological symptoms of dementia (BPSD) are also very important. What aspects of a patients behavioural and psyche are generally affected?

A
  • perception
  • thought content
  • mood
  • behaviour
84
Q

Cholinesterase inhibitors essentially stop the breakdown of ACh in the synaptic clefts, and therefore maintain higher levels of ACh. This is especially relevant in disorders where there are low levels of ACh. Which form of dementia is this commonly used to treat and does this reveres the disease?

1 - Alzheimers disease
2 - Parkinsons disease
3 - Vascular dementia
4 - Lewy bodies dementia

A

1 - Alzheimers disease

  • mild to moderate onset
  • slows disease, but does not reverse
85
Q

Memantine is a drug that is used to treat mild to moderate Alzheimers disease. What is its mechanism of action?

1 - NMDA antagonist, reducing glutamate binding
2 - NMDA agonist, increasing glutamate binding
3 - inhibitor of cholinesterase and degrades acetylcholinesterase
4 - binds reversibly to acetylcholinesterase

A

1 - NMDA antagonist, reducing glutamate binding

86
Q

Memantine is a drug that is used to treat mild to moderate Alzheimers disease, acting as a NMDA antagonist, reducing glutamate binding. Why is this important in Alzheimers?

A
  • glutamate continues to be released, even in neuronal cell death in Alzheimers
  • excess levels of glutamate results in over-excitation of nerve cells
  • over-excitation leads to excitotoxicity and cell death
87
Q

Donepezil is a core drug that is used to treat Alzheimers only, but not other dementias. What is the mechanism of action of this drug?

1 - increases vesicles containing ACh to be released into pre synaptic cleft
2 - ACh receptor agonist
3 - inhibitor of cholinesterase and degrades acetylcholinesterase
4 - binds reversibly to acetylcholinesterase

A

4 - binds reversibly to acetylcholinesterase

  • inhibits the hydrolysis of ACh
  • increases ACh and cholinergic activity
88
Q

Young onset dementia is defined as those <65 years old. How long does it generally take to diagnose these patients?

A
  • 4.4. years

- very little in specialist services

89
Q

There is evidence that we can actually prevent dementia. Around 30% are described as modifiable risk factors, which are what?

A
  • limited education
  • smoking
  • obesity/diabetes
  • depression
  • inactivity
  • social isolation
  • hearing loss

Year 2 NSB (53 decks)

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