Gerries Flashcards

1
Q

what are the pharmacological managements available for Alzheimers?

A

> the three acetylcholinesterase inhibitors (donepezil, galantamine and rivastigmine) as options for managing mild to moderate Alzheimer’s disease

> memantine (an NMDA receptor antagonist) is in simple terms the ‘second-line’ treatment for Alzheimer’s, NICE recommend it is used in the following situation reserved for patients with
moderate Alzheimer’s who are intolerant of, or have a contraindication to, acetylcholinesterase inhibitors
as an add-on drug to acetylcholinesterase inhibitors for patients with moderate or severe Alzheimer’s
monotherapy in severe Alzheimer’s

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2
Q

When is donepezil contraindicated? and what are the adverse effects?

A

Donepezil
is relatively contraindicated in patients with bradycardia
adverse effects include insomnia

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3
Q

Which kind of medication are associated with increased mortality in dementia patients?

A

antipsychotics

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4
Q

how to distinguish between delirium and dementia?

A

Factors favouring delirium over dementia
acute onset
impairment of consciousness
fluctuation of symptoms: worse at night, periods of normality
abnormal perception (e.g. illusions and hallucinations)
agitation, fear
delusions

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5
Q

what are risk factors for pressure ulcers?

A

malnourishment
incontinence: urinary and faecal
lack of mobility
pain (leads to a reduction in mobility)

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6
Q

what scoring system is used for pressure ulcers?

A

Waterlow score

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7
Q

what investigation is recommended for dementia?

A

Structural imaging in the form of CT or MRI head is recommended in the investigation of dementia, both to exclude reversible causes of cognitive decline (i.e. subdural haemorrhage) and assist with subtype diagnosis. MRI features suggestive of a diagnosis of Alzheimer’s disease, for example, include mesial temporal lobe atrophy and temporoparietal cortical atrophy.

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8
Q

What medications can exacerbate parkinsonian symptoms in Lewy body dementia?

A

neuroleptic drugs like haloperidol

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9
Q

what kind of dementia is most associated with hallucinations?

A

Lewy body dementia

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10
Q

what are the features of Lewy body dementia?

A

progressive cognitive impairment
typically occurs before parkinsonism, but usually both features occur within a year of each other. This is in contrast to Parkinson’s disease, where the motor symptoms typically present at least one year before cognitive symptoms
cognition may be fluctuating, in contrast to other forms of dementia
in contrast to Alzheimer’s, early impairments in attention and executive function rather than just memory loss

parkinsonism

visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)

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11
Q

how is Lewy body dementia diagnosed?

A

usually clinical
single-photon emission computed tomography (SPECT) is increasingly used. It is currently commercially known as a DaTscan. Dopaminergic iodine-123-radiolabelled 2-carbomethoxy-3-(4-iodophenyl)-N-(3-fluoropropyl) nortropane (123-I FP-CIT) is used as the radioisotope. The sensitivity of SPECT in diagnosing Lewy body dementia is around 90% with a specificity of 100%

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12
Q

How is Lewy body dementia managed?

A

both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer’s. NICE have made detailed recommendations about what drugs to use at what stages. Please see the link for more details
neuroleptics should be avoided in Lewy body dementia as patients are extremely sensitive and may develop irreversible parkinsonism. Questions may give a history of a patient who has deteriorated following the introduction of an antipsychotic agent

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13
Q

which kind of dementia presents in stepwise deterioration?

A

vascular dementia

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14
Q

what are the subtypes of vascular dementia?

A

Stroke-related VD - multi-infarct or single-infarct dementia

Subcortical VD - caused by small vessel disease

Mixed dementia - the presence of both VD and Alzheimer’s disease

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15
Q

what are the risk factors for vascular dementia?

A

History of stroke or transient ischaemic attack (TIA)
Atrial fibrillation
Hypertension
Diabetes mellitus
Hyperlipidaemia
Smoking
Obesity
Coronary heart disease
A family history of stroke or cardiovascular

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16
Q

What are the symptoms of vascular dementia?

A

Focal neurological abnormalities e.g. visual disturbance, sensory or motor symptoms
The difficulty with attention and concentration
Seizures
Memory disturbance
Gait disturbance
Speech disturbance
Emotional disturbance

17
Q

What criteria is used to make a diagnosis of vascular dementia ?

A

NINDS-AIREN

Presence of cognitive decline that interferes with activities of daily living, not due to secondary effects of the cerebrovascular event
established using clinical examination and neuropsychological testing

Cerebrovascular disease
defined by neurological signs and/or brain imaging

A relationship between the above two disorders inferred by:
the onset of dementia within three months following a recognised stroke
an abrupt deterioration in cognitive functions
fluctuating, stepwise progression of cognitive deficits

18
Q

What are the 3 types of frontotemporal lobar dementia?

A

Frontotemporal dementia (Pick’s disease)
Progressive non fluent aphasia (chronic progressive aphasia, CPA)
Semantic dementia

19
Q

What are the common features of frontotemporal lobar dementias?

A

onset before 65
insidious onset
relatively preserved memory and visuospatial skills
personality change and social conduct problems

20
Q

What is Pick’s disease?

A

most common type of frontotemporal dementia

21
Q

what is Pick’s disease characterised by?

A

characterised by personality change and impaired social conduct. Other common features include hyperorality, disinhibition, increased appetite, and perseveration behaviours.

22
Q

what are the macroscopic and microscopic changes seen in Pick’s disease?

A

Focal gyral atrophy with a knife-blade appearance is characteristic of Pick’s disease.

Macroscopic changes seen in Pick’s disease include:-
Atrophy of the frontal and temporal lobes

Microscopic changes include:-
Pick bodies - spherical aggregations of tau protein (silver-staining)
Gliosis
Neurofibrillary tangles
Senile plaques

23
Q

what is semantic dementia?

A

Here the patient has a fluent progressive aphasia. The speech is fluent but empty and conveys little meaning. Unlike in Alzheimer’s memory is better for recent rather than remote events.

24
Q

what are the risks factors for Alzheimer’s ?

A

increasing age
family history of Alzheimer’s disease
5% of cases are inherited as an autosomal dominant trait
mutations in the amyloid precursor protein (chromosome 21), presenilin 1 (chromosome 14) and presenilin 2 (chromosome 1) genes are thought to cause the inherited form
apoprotein E allele E4 - encodes a cholesterol transport protein
Caucasian ethnicity
Down’s syndrome

25
Q

What are the pathological changes in Alzheimer’s?

A

macroscopic:
widespread cerebral atrophy, particularly involving the cortex and hippocampus
microscopic:
cortical plaques due to deposition of type A-Beta-amyloid protein and intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein
hyperphosphorylation of the tau protein has been linked to AD
biochemical
there is a deficit of acetylcholine from damage to an ascending forebrain projection

Neurofibrillary tangles
paired helical filaments are partly made from a protein called tau
tau is a protein that interacts with tubulin to stabilize microtubules and promote tubulin assembly into microtubules
in AD are tau proteins are excessively phosphorylated, impairing its function