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B33CNS > Alzheimer's and other Dementias (Yvonne Mbaki) > Flashcards

Alzheimer's and other Dementias (Yvonne Mbaki) Flashcards

1
Q

Outline Vascular Dementia

A

Blood supply to the brain is blocked or interrupted by a blocked or diseased vascular system

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2
Q

What are the features/causes of VD?

A

Reduced cerebral perfusion (strokes), thromboembolism, small blood vessel disease in the brain, bleeding into the brain.

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3
Q

How is VD diagnosed?

A

Confirmed lesions that are caused by vascular disease using MRI or CT scans

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4
Q

How can VD be treated?

A

No approved treatments at present
Clinical trials; cholinergic stimulants, vasodilators, platelet aggregation inhibitors
Preventative measures to stop/prevent the initial blockage or interruption to cerebral blood flow

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5
Q

What is Dementia with Lewy Bodies? (DLB)

A

Prominence of alpha-synuclein in dopaminergic neurons of substantia nigra (a-synuclein is the protein that is found in the Lewy body)

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6
Q

How is DLB diagnosed?

A

Fluctuating cognition - varying attention/alertness
Visual hallucinations
Movement disorder
Dementia with Lewy Bodies is diagnosed at the same time as Parkinson’s disease or beforehand.

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7
Q

What is Parkinson’s Disease Dementia? (PDD)

A

Diagnosed after Parkinson’s disease already present in patients with existing movement disorder

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8
Q

What symptomatic treatment can be used to treat DLB and PDD?

A

Cognitive - cholinesterase inhibitors e.g. donepezil and rivastigmine OR NMDA receptor blockers such as memantine to block glutamate
Motor - levodopa
Psychiatric - antipsychotics are contraindicated
Non-pharmacological treatment
Memory prompts, education of caregivers, mobility aids etc

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9
Q

What is Fronto-temporal Dementia? Refer to the role of two lobes affected.

A

Frontal lobe ; reasoning, personality, judgement
- loss of emotional warmth, apathy, selfishness
Temporal lobe ; speech, language and memory
- declines in language

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10
Q

What is the cause of Fronto-temporal Dementia?

A

Mutation in tau protein

Disrupts normal cell processes leading to the death of nerves

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11
Q

How is Fronto-temporal Dementia diagnosed?

A

Neuropsychological evaluation

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12
Q

What is the pathophysiology of Alzheimer’s disease - beta amyloid plaques?

A

Normal function of alpha secretase alongside gamma secretase ensures that amyloid precursor protein is cleaved from the nerve cell membrane, to produce a harmless P3 protein fragment.
In an abnormal cell prone to Alzheimer’s, the alpha secretase is replaced by beta secretase (mutation?). When is cleaves the amyloid precursor protein it produces a beta-amyloid protein fragment. These fragments build up to form plaques that leads to neurodegeneration.

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13
Q

What is the pathophysiology of Alzheimer’s disease - neurofibrillary tangles?

A

Related to the tau protein mutation. Normally the tau protein is responsible for the stability of microtubules that maintain a stable cell and also regulate nutrients in the brain. When tau is phosphorylated the microtubule tangles, impeding nutrients and causing neurodegeneration.

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14
Q

What are cholinergic pathways involved in?

A

Cognition and memory

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15
Q

What is glutamate involved in?

A

Learning

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16
Q

What is serotonin (5-HT) involved in?

A

Psychoses and mood

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17
Q

What is GABA involved in?

A

Anxiety and lethargy

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18
Q

What is noradrenaline involved in?

A

Aggression

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19
Q

Are there genetic factors affecting the aetiology of Alzheimer’s?

A

Genetic factors
(Icelandic Study) - variant in amyloid precursor protein gene that protected elderly against Alzheimer’s.
Autosomal mutations in chromosome 14, 1 and 21 in families displaying the disease.
Late onset Alzheimer’s disease is linked to the gene apolipoprotein E (APOE) (allele 4) associated with lower cognitive performance and mild cognitive impairment that leads to dementia.

20
Q

What environmental factors can lead to Alzheimer’s disease?

A

Head trauma survivors have been found to overexpress amyloid precursor protein which can increase the risk of amyloid plaque formation.

21
Q

Can diet and malnutrition affect development of Alzheimer’s?

A

High cholesterol in rabbits lead to formation of amyloid plaques
Greater vitamin B12 deficiency in families with Alzheimer’s

22
Q

Symptoms of Mild AD?

A

Short term memory impairment and aphasia (inability ot communicate in speech)
Reversal changes i.e. previously social person becomes disinterested.
Depression
Acute episodes of confusion, disorientation, agitation and hallucination

23
Q

Symptoms of Moderate AD?

A

Poor retention of recent memories that can be triggered by cues
Chronological sequences of events become muddled
Language and comprehension impaired
Executive / decisive function diminshes
Reduced capacity for self care
Evidence of neurobiological changes to the brain
Serotonin, dopamine and noradrenaline implicated in aggression
Reduced function in frontal lobes determined by imaging
Sleep disturbances as a result of changes in the brain stem

24
Q

Which neurotransmitters are responsible for display of aggression in patients with moderate Alzheimer’s disease?

A

Serotonin, noradrenaline and dopamine

25
Q

Symptoms of Late AD?

A

Memory function is severely impaired, language skills are lost and speech is impoverished. Assistance is required with self-care and the patient is incontinent.
Challenge with swallowing
Mobility diminishes to person being chair bound or bed bound.
Aggression, agitation, sleep disturbances, psychoses, depression.

26
Q

Symptoms of Advanced AD?

A

Dependent, mute, swallow, incontinence, pneumonia, influenza, cardiac, stroke. Death

27
Q

What is MMSE?

A

Mini Mental State Examination (MMSE)

  • assesses mental impairment rather than diagnosing dementia
  • accuracy is influenced by education
28
Q

What are some sample questions of MMSE?

A

Orientation to time - ‘What is the date’
Registration - told three words to repeat again at end of conversation
Naming - ‘What is this’
Reading - ‘Please read this and do as it says’ i.e. close your eyes
Clock test drawing

29
Q

What medical diagnostic tests are carried out?

A

MRI and CT
Blood tests to eliminate organic disease state
Cell loss - enlarged ventricles or shrinking of the brain tissue on MRI or CT

30
Q

What is the aim of management?

A

Current drugs aim to improve symptoms rather than treating the underlying cause

31
Q

What are the challenges with treatment?

A

Hard to distinguish between different forms of dementias
Main side effect of drug treatment is further confusion
Delay in efficacy
Many drugs cause significant side effects before positive effect is observed and so are discontinued.

32
Q

How are cognitive symptoms treated?

A

Cholinesterase inhibitors: Donepazil (Aricept) - most suitable
Rivastigmine as a transdermal patch
Galantamine as extended release formulation.

33
Q

What are the side effects to Donepazil, Rivastigmine and Galantamine? (Cholinesterase inhibitors)

A 
GI disturbances (increased constipation)
Cardiac problems (reduced heart rate)
34
Q

How is the duration of treatment with CI’s determined in mild to moderate AD?

A

As long as benefits outweigh the side effects

Decline in function - consider a higher dose or swapping to an alternative

35
Q

What is Memantine and how does it act?

What are the side effects?

A

NMDA receptor blocker
Treats moderate to severe Alzheimer’s disease
Protects the brain nerve cells against glutamate that is released by damaged cells in Alzheimer’s disease.
GI disturbances, Hypertension and Dizziness are among the side effects of Memantine.

36
Q

What are ‘other’ treatments for Alzheimer’s?

A

Gingko biloba - chinese herbs improves circulation
Vitamin E - slows down progression (modest evidence)
Selegiline - treatment for Parkinson’s disease with evidence that t effects mood, behaviour, memory

37
Q

What are the ethical challenges with treating behavioural symptoms?

A

Legal consent is required, psychotropic drugs have a sedating affect. Are they being used for therapy or sedation?

38
Q

What are antipsychotic drugs used for in Alzheimer’s?

A

Treats aggressive behaviour, agitation and other behavioural symptoms

39
Q

What are the risks in elderly patients with using some psychotropic drugs?

A

Cerebrovascular stroke in the elderly increased risk when taking Risperidone and Olanzapine.
Best avoided in dementia with Lewy bodies due to induction of severe parkinsonism even at low doses.

40
Q

When are psychotropic drugs indicated? What kind of AD?

A

Lewy bodies Dementia - induces Parkinsonism

41
Q

How can depression in AD be treated?

A

CBT is the best option
There is generally little efficacy of antidepressants
SSRIs are fist choice - Citalopram due to fewest interactions
Venlafaxine may also be considered
If effective, prescription should be 6 months

42
Q

What drugs can be used to stabilise mood in AD?

A

In AD there is little or no evidence to show that Carbamazepine or Sodium Valporate can treat aggressive behaviour
Side effects ; sedation and liver dysfunction

43
Q

What role do hynotics and anxiolytics have in AD treatment?

A

Benzodiazepines - limited use due to oversedation

Sleep disturbances; short acting benzos Temazepam or Melatonin

44
Q

What non-pharmacological management can be used in AD that is mild?

A 
Memory training (diaries, memo books etc)
Cognitive stimulation therapy - NICE approved for mild Alzheimer's
45
Q

What non-pharmacological management can be used in AD that is moderate to severe?

A

Validation Therapy re hallucinations
Reminiscence Therapy - good at combatting depression
Multi-sensory stimulation
Physical therapy
Music therapy etc
No specific approach is deemed superior over the other

46
Q

What are some of the diagnostic tests and treatments of the future?

A

Diagnostic blood tests with biomarker for beta amyloid protein though translating changes in blood to brain ]Diagnostic CSF ; translatable to brain function
Beta amyloid protein decreased in patient’s CSF because used up in plaques
Tau protein increased in patient’s CSF
Structural neuroimagining

47
Q

What drugs are in clinical trials for the treatment of AD?

A

Secretase inhibitors - gamma or beta secretase enzymes involved in beta amyloid plaques
Beta amyloid vaccinations aim to increase the removal of beta plaques
Gene therapy of the future also

B33CNS (20 decks)

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