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33 Cards in this Set

  • Front
  • Back

triad of diseases with overlapping symptoms

dementia


delirium


depression

delirium




dementia




depression


dementia

complex and progressive




syndrome: a collection of signs and symptoms caused by a number of diseases




dementia starts with cognitive and behavioural changes




and progress to affect the person more globally

demntia stage one vs two vs three

stage 1 impairment in changes in memory




stage 2 further impairment of memory




stage 3 complication of ommobility

pathology of dementia

alzheimers disease


lwey body disease


frontotemporal dementia


vascular dementia

alzheimers

60-70 percent cases of dementia in older people likely to be Alzheimer's disease




progressive


loss of ability to form new memories


loss of higher order human capabilities


difficulty with orientation time and place


language difficulties; expression and sometimes comprehension


personality changes

alzheimers cerebral cortex

Alzheimer's disease tends to rob people of higher brain functions and many of these are locked in the cerebral cortex.




Specific parts of the cerebral cortex become damaged, shrinks and atrophy




Specifically the Frontal, Temporal and Parietal lobes

Alzheimer's specific pathophysiology

beta amyloid plaques




happens outside nerve cells




beta amyloid proteins form filaments which self combine to form the actual plaque like structures




cant diagnose someone with Alzheimer's just from this one thing, will also need neurofibrillary tangle

neurofibrillary tangle

Occur inside the nerve cell




Tau Proteins undergo abnormal changes and form tangles




The neurofibrillary tangles cause the nerve cell to die




because as they are insoluble they are left in the brain after the nerve cell has gone




then they are called tombstone tangles

hippocampus and alzheimer's

within the temporal lobes




Tangles form in the hippocampus first




Hippocampus has a role in processing sensory info for memories so the tangles disrupt this process




this is why they cant make new memories

Summary Alzheimer's disease

Amyloid plaques and neurofibrillary tangles are key pathological changes in Alzheimer's




There are variations in genes that are linked to relative risk of dementia




The hippocampus and memory formation are affected very early on




Alzheimer's disease starts in the brain many years before symptoms are expressed.




This is known as the 'preclinical' phase of the disease

FTD - behavioral Variant

FTD - behavioural Variant




personality and behavioural changes




impaired planning and judgement




apathy




loss of empathy




disinhibition




diet

FTF - speech variant

primary progressive aphasia (inablity to comprehend language)




inability to understand speech




inability to produce speech

Frontotemporal dementia

often thought of as an early onset of dementia

Frontal temporal dementia pathophysiology

Protein Tau and TDP-43 cause clumps or aggregates




Where: inside the cell , axon, oligodendrocytes



TDP-43 PROTEIN

is aggregated in some cases of frontotemporal dementia




plays a role in motor neuron disease




15% of people who have motor neuron disease may go on to develop frontotemporal dementia VIA VERSA

Frontotemporal dementia summary

Characterized: atrophy of frontal cortex and front parts of temporal cortex




There are several disease that cause frontotemporal dementia




Two forms of frontotemporal dementia - BEHAVIOURAL and SPEECH




Two key proteins: Tau and TDP-43 which abnormally accumulate in neural cells




Strong genetic predisposition




Frontotemporal dementia and motor neuron disease are related and one may cause the other

Lewy body disease vs Alzheimer's

different to alzheimers because cognitive changes from degeneration in cortex FLUCTUATE. good or bad days





Lewy body disease changes

visual.spatial awareness




sleep disorder




Parkinson's type features

Lewy body protein does what

lewy body proteins form spherical structures within neurons




Main protein present in Lewy Body is ALPHA-SYNUCLEIN




Form in the substantia nigra



Summary of Lewy Body disease

aka know as lewy body dementia or dementia with lewy bodies




characterised by: prescence of spherical bodies in the nerve cells in the cortex call 'lewy bodies'




Main protein is ALPHA-SYNUCLEIN




Features of disease include: sleep/wake, visual/spatial, parkinsons type features

Vascular dementia symptoms

step-wise pattern of degeneration




problems in gait and executive functions




problems in mood/behaviour




small vessel disease

Therapeutic goals

symptom management




disease modification




neuroprotection

risk factors dementia




non modifiable

older age




inheritance of genes

risk factors dementia




potentially modifiable

smoking




high cholesterol




obesity




type 2 diabetes




hypertension




sedentary lifestyle

increase quality of life by

early diagnosis




5 years from diagnosis to death




The earlier diagnosis, more time for medical trials to delay symptom onset




time to talked to family about values and what to do before loss of ability to do so

Four strategies dementia prevention

keeping mind active




keeping body active




acessing apropriate suport




managing health conditions and nutrition

Medical management of dementia

medications careful considerations




protection of brain




treating symptoms caused by dementia




providing comfort end of life




can have unwanted side effect


can make dementia worse

Medications for dementia

Cholinesterase inhibitors




symptoms control meds




avoid meds that make worse eg:


opiate anagesia, anti cholinergics





non pharmacological therapy

cognitive and physical activity interventions




music




reminiscence




aroma




massage




assistive technology

BPSD what

behavioral


psychological


symptoms of


dementia

BDSP is caused by

untreated pain

BDSP ss

calling out




agitation




restlessness