Dementia Flashcards
What is dementia? Who does it tend to affect? What are the types and how common are they?
It is an acquired, chronic and progressive cognitive impairment which is sufficient to impair ADLs
- > <65yo = early onset dementia
- > 5-10% population are over 65y, 20% are over 80yo
Types:
Alzheimers (70%)»_space;> Vascular Dementia»_space;> Dementia with Lewy-bodies
How may a patient with dementia present? What are some BPSD?
Sx:
1st - forgetfulness, either stepwise or progressive
2nd - disorientation (time -> place -> person) -> management problems
- Wandering
- Delusions + Hallucinations
- Calling out
- Sleep disturbance
- Inappropriate behaviour/aggression!
BPSD = behavioural and psychological symptoms of dementia
- Mood changes
- Abnormal behaviour
- Hallucinations/delusions
What Ix would you do for a patient with suspected dementia?
Ix:
- > Cognitive assessment
- Screening via AMTS (<7 suggests cognitive impairment), GPCOG
- Detailed via Addenbrooke’s (ACE-R - 100qs, MMSE - less used now but 30q - where 18-23 is mild cognitive impairment and <18 is severe, MoCA)
- > Dementia/delirium screen
- TFTs (hypothyroid can cause cognitive decline)
- LFTs (Korsakoff’s)
- U&Es and dipstick (infection, diabetes)
- HbA1c
- B12 and folate
+ Specific tests for each type of dementia
[Further tests]
- Alzheimers - FDG-PET, MRI (grey matter atrophy, wide ventricles and sulci, temporal lobe atrophy)
- Vascular - ECG (AF with emboli), MRI/CT
- Lewy-body - DaTScan; a tracer 123-I-FP-CIP used in single photon emission CT
- Frontotemporal - FDG-PET, perfusion SPECT, MRI (frontal lobe shrinkage)
AFTER GP: -> Memory Assessment Clinic Referral
- > Take collateral Hx and check bloods
- > Risk assess the patient
- > Cognitive assessment (MMSE)
- > Brain scan for organic pathology
- > Differentiate delirium vs dementia (confusion assessment method and observational scale of level of arousal - CAM + OSLA)
What is Alzheimers and what are the 3 theories regarding its pathophysiology?
Alzheimers is the most common form of dementia, with a steady progression (affects hippocampus first in pathophysiology)
Pathophysiology:
- Amyloid = Normally APP is cleaved by alpha-secretase to form sAPP-alpha and C83. C83 is degraded by gamma-secretase and removed. In AD, APP is cleaved by beta-secretase to form sAPP-beta and C99. C99 is digested by gamma-secretase to form beta-amyloid protein which forms toxic aggregates
- Tau = Tau is a soluble protein in axons used in assembly and neurone stability. Hyper-phosphorylation of Tau in AD makes it insoluble causing it to self-aggregate and form neurofibrillary tangles which cause microtubule instability and neurotoxic damage to the neurones.
- Inflammation = there are increased inflammatory mediators and cytotoxic proteins in AD, and therefore increased phagocytosis by the microglial cells (specialist CNS macrophages) which therefore reduces the levels of neuroprotective proteins
What are some risk factors for AD? [Think biopsychosocial]
RFs:
Bio:
- AGE = main RF, 1% at 60, and risk doubles every 5 years
- Genetics (8% of risk, 92% sporadic) - genes including APEN, APP, ApoE, Presenilin 1 gene (X14), Presenillin 2 gene (X1), APP (X21 - Coexistent Downs increases risk)
- Head injury
- Vascular RFs e.g. HTN
Psychosocial:
- Low IQ
- Poor educational level
How may a patient present with AD, and why do these symptoms occur?
Sx:
- Early = failing memory, wandering, irritability
- Middle = The 4A’s become apparent* - Amnesia, Aphasia, Agnosia and Apraxia
- Late = fully dependent, incontinence, primitive reflexes, extrapyramidal symptoms
- Other = BPSD - mood changes, abnormal behaviour and hallucinations/delusions
- Other = psychiatric symptoms such as depression, delusions, GAD, behavioural disturbances (note: patients with depression may do badly on MSE due to ‘depressive pseudodementia’)
** 4 As
Amnesia - Recent memories lost first, disorientation occurs early
Aphasia - finding correct words (Broca’s), speech muddled/disjointed
Agnosia - usually visual e.g. with faces (propagnosia)
Apraxia - usually with dressing, skilled tasks despite normal motor function
Causes of Sx due to atrophy, plaque and NF tangle formation and cholinergic loss
What investigations would you do in a patient with suspected AD?
Ix - same as dementia:
- > Cognitive assessment
- Screening via AMTS (<7 suggests cognitive impairment), GPCOG
- Detailed via Addenbrooke’s (ACE-R - 100qs, MMSE - less used now but 30q - where 18-23 is mild cognitive impairment and <18 is severe, MoCA)
- > Dementia/delirium screen
- TFTs (hypothyroid can cause cognitive decline)
- LFTs (Korsakoff’s)
- U&Es and dipstick (infection, diabetes)
- HbA1c
- B12 and folate
+ Specific tests for each type of dementia
[Further tests]
- Alzheimers - FDG-PET, MRI (grey matter atrophy, wide ventricles and sulci, temporal lobe atrophy)
- ECG pre-medication as QT prolongation, non-pacemaker treated heart block and HR<50 are contraindications!
- Also check co-morbid conditions for contraindications!!
DDx:
- Vascular - ECG (AF with emboli), MRI/CT
- Lewy-body - DaTScan; a tracer 123-I-FP-CIP used in single photon emission CT
- Frontotemporal - FDG-PET, perfusion SPECT, MRI (frontal lobe shrinkage)
AFTER GP: -> Memory Assessment Clinic Referral
- > Take collateral Hx and check bloods
- > Risk assess the patient
- > Cognitive assessment (MMSE)
- > Brain scan for organic pathology
- > Differentiate delirium vs dementia (confusion assessment method and observational scale of level of arousal - CAM + OSLA)
What are some good and bad prognostic factors for AD?
Good - female
Bad - male, depression, behavioural problems, severe focal cognitive deficit
How would you manage AD? What checks are important in f/u?
Biological: ‘start low, go slow’ aiming to raise ACh
- Anticholineserases (mild-moderate AD) such as Donepezil, Galantamine, Rivastigmine
- 2nd line (moderate or 1st line for severe AD) = Memantine, a partial NMDA receptor agonist
Psychological:
- 1st line = Structural group cognitive stimulation sessions (mild-moderate AD)
- Exclude depression or GAD
- Other = group reminiscence therapy, validation/reassurance therapy, multi sensory therapy
Social:
- Explain Dx and signpost support
- Optimise health in other areas such as hearing, visual aids
- Identify future wishes - advanced directives, lasting power of attorney
- F/u every 6m with patient and care manager (w care plan)
- Home + needs assessment: general social support such as dose boxes, changing gas to electricity, assistive house measures, identify and support any carers involved, meal supports and day centres
- CARER’s assessment!
- Legally required to inform DVLA and insurers for any form of dementia (review license yearly)
Other:
- Due to AChE you need to check ECG and SE (GI such as N+V, anorexia, dizziness, headaches, fatigue)
- Absolute CI to AChE are anticholinergics, B-blockers, NSAIDs, muscle relaxants, other relative CI are asthma/COPD, GI disease, bradycardia
What is Vascular dementia? What are some RFs?
Dementia which is caused by infarcts due to thromboembolism or narrowing of arteries due to HTN
RFs are same as CVD:
- HTN
- Male
- Obesity
- Smoking
- Sedentary/reduced exercise
- DM
- AF, Hx of stroke or TIA
How may a patient with vascular dementia present?
Sx:
- SUDDEN onset (may follow CVA, with STEPWISE deterioration
- 1st = emotional and minor personality changes (labile emotion so from tearful -> elation)
- 2nd = cognitive deficit
- Focal neurological signs (reflect site of infarct i.e. upward plantars, left arm, some cognition reserved)
- Co-morbid depression
- Relatively preserved personality (not like AD where “mum is not herself anymore” but just “different and not using arm as much”)
How would you investigate VD?
Ix (same as dementia):
- > Cognitive assessment
- Screening via AMTS (<7 suggests cognitive impairment), GPCOG
- Detailed via Addenbrooke’s (ACE-R - 100qs, MMSE - less used now but 30q - where 18-23 is mild cognitive impairment and <18 is severe, MoCA)
- > Dementia/delirium screen
- TFTs (hypothyroid can cause cognitive decline)
- LFTs (Korsakoff’s)
- U&Es and dipstick (infection, diabetes)
- HbA1c
- B12 and folate
+ Specific tests for each type of dementia
[Further tests]
- Alzheimers - FDG-PET, MRI (grey matter atrophy, wide ventricles and sulci, temporal lobe atrophy)
- Vascular - ECG (AF with emboli), MRI/CT
- Lewy-body - DaTScan; a tracer 123-I-FP-CIP used in single photon emission CT
- Frontotemporal - FDG-PET, perfusion SPECT, MRI (frontal lobe shrinkage)
AFTER GP: -> Memory Assessment Clinic Referral
- > Take collateral Hx and check bloods
- > Risk assess the patient
- > Cognitive assessment (MMSE)
- > Brain scan for organic pathology
- > Differentiate delirium vs dementia (confusion assessment method and observational scale of level of arousal - CAM + OSLA)
How would you Mx VD?
Mx:
Biological:
- Daily aspirin (if indicated due to CVA/AF risk)
- Reduce risk factors (increased exercise, stop smoking, treat HTN and AF, control DM)
Psychological:
- 1st line = Structural group cognitive stimulation sessions
- Exclude depression or GAD
- Other = group reminiscence therapy, validation/reassurance therapy, multi sensory therapy
Social:
- Explain Dx and signpost support
- Optimise health in other areas such as hearing, visual aids
- Identify future wishes - advanced directives, lasting power of attorney
- F/u every 6m with patient and care manager (w care plan)
- General social support such as dose boxes, changing gas to electricity, assistive house measures, identify and support any carers involved, meal supports and day centres
- Legally required to inform DVA and insurers for any form of dementia (review license yearly)
What is Dementia with LB? How is this different to Parkinson’s? What are some RFs?
Lewy bodies are alpha-synuclein with ubiquitin
Spectrum of diseases including Lewy-bodies from DLB —-> Parkinsons disease
- In Parkinson’s, LB are found in the brainstem
- In DLB, LB are found in the brainstem, cingulate gyrus and neocortex
RFs = Age, unknown
How may a patient with DLB present?
Sx (must be at least 2/+ out of 3, general gradual decline):
- Fluctuating confusion with marked variations in alertness levels (may resemble delirium) i.e. has some LUCID intervals unlike other dementias
- Vivid visual hallucinations (Lilliputian hallucinations) - of animals or humans
- Parkinsonism - shuffling gait, hypomimia, bradykinesia, rigidity [note anosmia is an early sign of PD]
- Frequent falls
- Co-morbid depression
