236 - Dementia Flashcards

1
Q

what is the diagnostic criteria for dementia?

A

acquired memory impairment for at least 6m plus impairment in one or more cognitive domains:

  • executive functioning - abstract thinking, judge, reason
  • language - expressive and receptive
  • praxis - learned motor tasks
  • gnosis - ability to recognise objects, faces, sensory info
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2
Q

what is the prevalence of dementia?

A

5% of >65s but 22% of 85-90 - 20 million worldwide

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3
Q

name some differentials for dementia?

A
  • depression - low mood, worthlessness, guilt, suicide, anhedonia, appetite change, sleep disturb, fatigue, conc - also pseudodementia (aware of memory loss)
  • delirium - acute confusion sudden onset and fluctuating. associated with physical illness (infection, drugs, alcohol)
  • vitamin deficiency. vit B1 (thiamine) >wernickes, B12, folate
  • hypothyroidism - depression
  • hepatic/renal impairment
  • normal pressure hydrocephalus -abnormal CSF resorption - enlargement of ventricles and compression
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4
Q

what is the difference between dementia and mild cognitive impairment?

A

does not interfere with activities of daily living

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5
Q

who does alzheimers affect?

A
  • > 50% of dementias
  • > 70s and more females 2:1
  • family hx - apolipoproteins E-4 allele and Presenilin
  • down’s syndrome
  • head injuries
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6
Q

what is thought to cause alzeimers?

A
  • neurofibrillary tangles - changes to Tau proteins that act as glue to hold neuron microfobrils together
  • senile plaques - extracellular deposits of amyloid in grey matter between neurons or cerebral blood vessel walls. Especially in hippocampus (memory area)
  • cerebral cortex atrophy - association regions and medial temporal lobe
  • overactivation of NMDA receptors by glutamate. deficiencies in reuptake by astroglial cells in synaptic cleft
  • leads to cholinergic dysfunction and cholinergic input to hippocampus and amigdala from basal forebrain
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7
Q

what is the difference between alzheimers and vascular dementia?

A
  • AD - dementia with insidious onset and progressive gradual decline.
  • VD - Abrupt onset, stepwise deterioration, fluctuating cognitive performance, gait and incontinence, neuro signs (focal deficits/stroke), evidence of vascular disease on brain imaging
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8
Q

who does vascular dementia affect and what causes it?

A
  • 20-25% of dementias
  • > 60s, more male than female, hypertensives and those with cardiovascular risk factors
  • either focal (2ndry to thrombtic or embolic vascular occlusion - affects white matter or cerebrum and deep grey nuclei of thalamus and striatum) r difuse (2ndry to HTN or stenosis of vessels)
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9
Q

what is dementia with Lewy bodies?

A
  • 10-15% of dementias
  • Lewy bodies are intracellular aggregates of alpha-synuclein protein causing disruption to dopaminergic and cholinergic systems of brain
  • criteria - dementia plus one of: visual hallucinations, parkinsonism, reduced alertness plus one of: REM behaviour disorder or non specific neuro signs. If symptoms soon after parkonism then DLB
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10
Q

what is fronto-temporal dementia?

A
  • picks disease
  • fronto-temporal atrophy
  • early onset, more males, behavioural changes (personality and inappropriate behaviour), loss of speech with memory and skills intact, FH
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11
Q

how could a patient with dementia be assesed?

A

*mini mental exams
- Addenbrookes Cognitive Exam (ACE III)
- Montreal Cognitive Assessment (MoCA)
6 item CIT (Kingshill)
*Clock drawing test
*CT to exclude other path
*MRI - regional atrophy and cerebrovascular disease

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12
Q

how would you manage mild to mod alzheimers and DLB?

A
  • Aceytlcholinesterase Inhibitors eg donepezil, rivastigimine, galantamine
  • inhibit ACh breakdown and incr conc in synaptic cleft
  • gastric irritation and ulceration, bradycardia, epilespy, asthma, prostatism
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13
Q

how would you manage advanced alzeimers or mild AD when unresponsive to ACh-esterase?

A
  • NMDA receptor antagonists eg memantine

* inhibits glutamate by blocking NMDA receptors - reduces glutamate’s excitotoxic effects

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14
Q

how would you treat vascular dementia?

A

aspirin, statin, BP management and glucose management, lifestyle change

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15
Q

what is neurodegeneration and what causes it?

A
  • chronic, progressive neuronal loss
  • genes and toxins by:
  • apoptosis
  • autophagia
  • necrosis by:
  • infarction, neuroinflammation
  • misfolded proteins > plaques and hyperphosphrylated Tau (tangles)
  • oxidative stress
  • glutamate release after cell death> cycle
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16
Q

what types of memory are there?

A
  • short term memory
  • long term memory - short term made perm
  • working memory - held for mins to complete task
  • declarative (explicit) - semantic memories (concepts) and episodic (autobiographical) - stored in medial temp lobe, thalamus and hypothalamus
  • non-declarative (implicit) - procedural memory/skills/habits in striatum, motor learning in cerebellum and emotional conditioning in the amygdala
17
Q

what types of amnesia are there?

A
  • retrograde
  • anterograde
  • transient global amnesia - both retro and antero
18
Q

how is memory created?

A

sensory input > cortical association areas (identify stimulus, make sense and plan) > parahippocampal /rhinal cortices (storage of long term memory > hippocampus (consolidation of short term/working memory into long term) > mamilary bodies (hypothalamus) and thalamus (recognition, smell, emotion)

19
Q

what do the hippocampus and amygdala do?

A
  • hippocampus - learning of newinfo, consolidation to long term memory with cortex communication, place memory
  • amygdala - emotional info learning and its consolidation
20
Q

what is affected in korsakoffs syndrome

A
  • irreversible damage to medial thalamus and maillary bodies - caused by thiamine (vit B1) deficiency - may also cauuse Wernickes encephalopathy
  • causes antero/retrograde amnesia and cofabulation (cannot distinuish between imagination and memory)
21
Q

what does each lobe of the brain do?

A
  • occipital - visual cortex
  • parietal - attending to stimuli (where is it)
  • temporal - identify nature of stimuli (what is it)
  • frontal - planning appropriate response (what should I do about it)
22
Q

what is the parietal cortex responisible for?

A
  • integration of visual, auditory and somatosensory information
  • damage causes sensory neglect, conceptual neglect, motor neglect and hemiasomatognosia (denial that part of body is theirs) on contralateral side of body
23
Q

what is apraxia/

A

inability to carry out a motor task in response to a spoken command

24
Q

what is the temporal cortex responsible for?

A
  • identifying nature of stimuli
  • damage causes agnosia (loss of knowledge)
  • inf temp cortex - visual agnosia (cant identify objects)
  • fusiform gyrus (med temp occipital) - prosopagnosis (cant identify faces)
  • middle temp cortex - movement agnosia (cant tell between stationary and moving)
25
Q

what is the frontal cortex responsible for?

A
  • mediates behaviour - restraint, intiative and order
  • damage causes inability to plan sequence of events, loss of thought flexibilty, perservation, loss of focus, passivity, apathy, expressive aphasia
26
Q

what are wernickes and brocas areas responsible for/

A
  • wernickes- understanding speech

* brocas - makes speech

27
Q

what are wernickes and brocas aphasia?

A
  • wernickes - inability to understand language - fluent speech but makes no sense (little repetition but good syntax and grammar)
  • brocas - ability to understand language but inability to produce own halting speech - repetitive, disordered syntax and grammar