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medicine year 2 > Week 236 - Dementia > Flashcards

Week 236 - Dementia Flashcards

1
Q

Name at least two other types / causes of dementia besides Alzheimer’s and Vascular?

A

Lewy Body Dementia (DLBT) or Parkinson’s dementia
Fronto-temporal e.g. Pick’s

Also rarer forms e.g. Huntington’s dementia, CJD, HIV and alcohol

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2
Q

What is the main difference between Parkinson’s dementia and Lewy Body dementia (both Parkinson’s related dementia)?

A

Parkinson’s dementia: prominent motor features which pre-date dementia by at least 6months
Lewy Body dementia: mild motor symptoms, onset of cognitive and motor Sx similar (time-wise)

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3
Q

How does Alzheimer’s Disease present?

A

Insidiously with gradual deterioration

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4
Q

What neuropathic changes occur typically in AD?

A
  • Formation of neurofibrillary tangles and amyloid plaques

- Cholinergic transmission deficit

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5
Q

What changes are you likely to see in a CT head of a patient with Alzheimer’s Disease?

A

Widening of sulci
Enlargement of ventricles
Atrophy / shrinking of brain

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6
Q

What are the risk factors for Alzheimer’s?

A 
Age
Female gender
Genetics
Head injury
Environmental e.g. Oxidative stress
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7
Q

What are the two most common forms of dementia?

A

Alzheimer’s Diease followed by Vascular Dementia

Common to have a mixed diagnosis of the two

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8
Q

How does vascular dementia present?

A

Sudden onset
Stepwise deterioration
Mood/behaviour changes
Insight preserved

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9
Q

What neuropathological changes occur in Vascular Dementia?

A

Atherosclerosis
Single or multiple thrombotic or embolism enfarcts
Small vessel disease

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10
Q

What are the risk factors for vascular dementia?

A 
Smoking 
Diabetes
High cholesterol
HTN 
Male gender
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11
Q

How does Lewy Body Dementia (DLB) present?

A 
Fluctuating cognition
Vivid visual hallucinations
Mild Parkinsonian features
Repeated falls
Memory loss (may not be marked early in disease!)
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12
Q

What neuropathological changes are seen in DLB?

A

Lewy Bodies: abnormal aggregate of protein (synuclein fibrils) develop inside nerve cells

a) Classical - brainstem: round, brown, eosinophilic cytoplasmic inclusion with halo of radiating fibrils
b) Cortical: still made of alpha-synuclein fibrils but lacks halo

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13
Q

How does Fronto-temporal Dementia (such as Pick’s Disease) present?

A

Apathy; reduced motivation; self-neglect
Disinhibition; reduced social awareness, lack of judgement
Personality changes and social inappropriateness
Memory loss is variable but language difficulties are prominent
More common in men, with onset

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14
Q

What are the main differentials for dementia?

A

Secondary dementia due to underlying illness
Mild cognitive impairment (MCI)
Depression
Acute confusional state / delirium

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15
Q

What is the prevalence of mod/severe dementia >65 and >80 in the UK?

A 
>65 = 5%
>80 = 20%
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16
Q

What are the three key features of dementia?

A

1) Global impairment of higher cortical function
2) Occurring in clear consciousness
3) Progressive and present for >6 months

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17
Q

What five main areas of cognition are important to assess according to the ICD 10 Diagnostic Criteria?

A

Memory
Executive functioning (abstract thinking, judgement, reasoning)
Motor skills (Praxis)
Language (expressive and receptive)
Gnosis (ability to recognise objects, faces, sensory information)

18
Q

What is the key difference between dementia and MCI?

A

Dementia: global impairment of intellect, memory and personality resulting in impaired performance in activities of daily living

MCI: cognitive decline >expected for age and edu level but does not notably interfere with activities of daily living

19
Q

What pharmacological options should be considered for Alzheimer type dementia and Lewy Body dementia ?

A
  • Mild-Mod consider anti-cholinesterase meds

- Mod-Advanced consider Memantine (NMDA antagonist)

20
Q

What treatment options should be considered for Vascular Dementia?

A

Consider: low dose aspirin; statin
Appropriate BP and blood glucose management
Life-style advice re smoking, low fat diet

21
Q

Name 3 anti-cholinesterases

A

Aricept - Donepezil
Exelon - Rivastigmine
Reminyl - Galantamine

22
Q

How do anti-cholinesterases work?

A

Increase concentration of acetylcholine (neurotransmitter) at synaptic cleft by reducing aceytylcholine breakdown

23
Q

How do NMDA antagonists work? (E.g. Memantine)

A

Blocks the effects of pathologically high levels of glutamate by uncompetitively binding to NMDA receptors (on which glutamate acts a remember glutamate is the major excitatory neurotransmitter in the CNS)

24
Q

Name 3 genes associated with early onset Alzheimer’s Disease

A

Presenilin 1 and Presenilin 2

Beta amyloid precursor protein gene (APP)

25
Q

On which chromosome is each of the 3 genes assoc with Early onset AD found?

A

Presenilin 1 - Ch 14
Presenilin 2 - Ch 1
APP - Ch 21

26
Q

Which gene is associated with late onset AD (onset >65) and on which chromosome is it found?

A

Apolipoprotein E gene (apoE4) found on Ch 19

27
Q

Why would antidementia meds not be worthwhile prescribing in Parkinson’s Dementia?

A

Because they act on either blocking NMDA receptors on neurones (Memantine) or increasing acetylcholine availability in the synaptic cleft (acetylcholinesterase inhibitors such as Aricept (Donepezil))
Parkinson’s ‘Dementia’ is caused by a lack of dopamine production in the substantia nigra so levodopa +/- carbidopa is the correct treatment

28
Q

What are the 4 primary symptoms that occur as a result of dopamine in Parkinson’s?

A

Tremor (trembling arms, legs, face, jaw)
Rigidity
Slow movement AKA Bradykinesia
Postural instability (impaired balance and co-ordination)

29
Q

What is declarative memory?

A

AKA “explicit” memory - the long-term retention of facts and concepts (semantic) and events (episodic) that can be drawn upon when necessary

30
Q

What is non-declarative memory?

A

The learned skills and activities that are committed to memory

31
Q

What parts of the brain are associated with declarative memory?

A

Hypothalamus
Thalamus
Medial temporal lobe (hippocampus and hippocampal region)

32
Q

What parts of the brain are associated with non-declarative memory?

A

Motor - cerebellum

Emotional conditioning - amygdala

33
Q

What is retrograde amnesia?

A

A loss of memories before trauma or specific event

34
Q

What is antegrade amnesia?

A

An inability to form new memories

35
Q

What is Korsakoff syndrome and what commonly causes it?

A

A deficiency in Vit B1 (thiamine) due to inability to absorb it
Often due to chronic alcoholism
Causes irreversible damage to medial thalamus and mammillary bodies resulting in anteretrograde and retrograde amnesia

36
Q

Damage to Brodmann’s areas results in what? Where is it located?

A

‘Neglect’ of incoming sensory information

Posterior parietal area

37
Q

Damage to the temporal cortex is associated with what?

A

Agnosia (non-knowledge or a loss of knowledge)

38
Q

What does prosopagnosia mean?

A

The inability to recognise people from their faces

39
Q

Damage to the frontal lobe is associated with what sorts of signs?

A

Inability to plan a sequence of events
Loss of flexibility in thought
Emotional lability (instability) / personality change
Passivity / apathy
Socially inappropriate behaviour Expressive aphasia

40
Q

Explain the difference between aphasia and dysarthria

A

Aphasia is difficulty with naming objects (producing speech) and understanding speech as a result of brain damage

Dysarthria is difficulty with muscle movements within the face and tongue to form words and mediate speaking

41
Q

Describe the effects of damage to Wernicke’s area? Where is it located?

A

Temporal lobe (left in most)
Wernicke’s aphasia results - unable to understand language
- able to form speech fluently but it makes no sense

42
Q

Describe the effects of damage to Broca’s area? Where is it located?

A

Frontal lobe (left in most)
Damage results in Broca’s aphasia:
- able to understand language
- not able to construct own speech (result = disordered syntax and grammar, repetitive and halting speech)

medicine year 2 (28 decks)

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