Geriatrics fifth yr Flashcards

1
Q

What is dementia?

A

irreversible, progressive decline and impairment of more than one aspect of higher brain function (concentration, memory, language, personality, emotion).

This occurs without impairment of consciousness

Biggest RF - increasing age

Can be proven post-mortem with histological evidence

Dx usually made clinically from Hx (pt and collateral), cognitive tests (10-CS, 6CIT), and formal neuropsychological assessment

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2
Q

Summary of Alzheimer’s dementia?

A

Most common cause of dementia in the UK - half of dementia diagnoses

F>M

Progresses steadily over time

Aetiology - amyloid plaques and neurofibrillary tangles (made from tau protein) accumulate - reduces information transmission, leading to death of brain cells, and abnormal deposits remain post-mortem

Macroscopic changes - widespread cerebral atrophy, particularly cortex and hippocampus
Microscopic - cortical plaques due to deposition of type A-Beta-amyloid protein and intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein
hyperphosphorylation of the tau protein has been linked to AD
Biochemical - deficit of acetylcholine from damage to an ascending forebrain projection

Features - >60 (early onset too), affects all areas of the brain (many functions/abilities impacted and lost)
Most common presenting Sx is memory loss - varying changes in planning, reasoning, speech and orientation

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3
Q

Summary of vascular dementia?

A

Second most common
M>F - due to increased risk of vascular disease
^ prevalence in those who have had a stroke

Step wise fashion - stability, decline, stability

Aetiology - subtypes - most common stroke related (multiple cerebrovascular infarcts), subcortical VD (small vessel disease), mixed dementia (presence of VD and Alzheimers)
most affected areas - white matter of cerebral hemispheres, grey nuclei, thalamus and striatum

RF - HTN, vascular RFs = smoking, DM, hyprelipidaemia, obesity, hypercholesterolaemia

Features - single infarct vascular disease presents with cognitive impairment following event, mood disturbances/disorders, psychosis, delusions, hallucinations, paranoia

Pts should be screened for depression and signs of psychomotor retardation. Emotional lability can be prominent

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4
Q

Summary of Lewy body dementia?

A

Pt > 50
M>F
Rapidly progressive - death common in first 7 years post-diagnosis

Aetiology - spherical Lewy body proteins deposited in brain. Also present in Parkinsons (mainly in substantia nigra) while in Lewy body dementia they are widespread

Features - visual hallucinations, Parkinsonism (if physical Sx precede cognitive decline by more than a year, Dx is Parkinson’s with superimposed cognitive decline)
problems multitasking and performing complex cognitive actions are primary issue (rather than memory)
sleep disorders
Fluctuations in cognitive ability

Dx - clinical, SPECT

Tx - both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer’s.
neuroleptics should be avoided in Lewy body dementia as patients are extremely sensitive and may develop irreversible parkinsonism.

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5
Q

Summary of frontotemportal dementia?

A

Less common
Responsible for Dx of dementia <65
Insidious onset
M=F
Average life expectancy is 8 years post-diagnosis
Several types, Frontotemporal dementia (Picks disease), progressive non fluent aphasia, semantic dementia

Aetiology - neutron damage and death in frontal and temporal lobes. Atrophy due to deposition of abnormal proteins within lobes. Genetic component in 1/4 cases

Features - one of 3 clinical pictures:
- behavioural - altered emotional responsiveness, apathy, disinhibition, impulsivity, progressive decline in interpersonal skills, changes in food preference, more childlike amusements, obsessions + rituals

  • semantic - progressive decline in understanding of words, speech fluent but difficulty in name-retrieval and use of less precise terms, unable to determine meanings of common words, develops to inability to recognise objects or familiar faces (prosopagnosia)
  • non-fluent prevention - progressive breakdown in output of language, speech takes effort and not fluent, speech apraxia, impaired comprehension of sentence and impact on literacy skills
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6
Q

Differential diagnoses for dementia?

A

Prion protein diseases - Creutzfeldt-Jakob disease

Sporadic CJD - over age of 40
Variant - eating meat infected by bovine spongiform encephalopathy

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7
Q

Differential diagnoses for dementia?

A

Prion protein diseases - Creutzfeldt-Jakob disease

HIV-related cognitive impairment/dementia - mild cognitive impairment, mood disturbance

Normal pressure hydrocephalus

Severe depression

Mild cognitive impairment - not severe enough to interfere with every day life. Yearly, 10-15% of people with mild cognitive impairment go on to develop form of clinical dementia. Causes - stroke, depression, stress, physical illness, drug SE

Huntingtons

Potentially treatable:
Hypothyroidism, Addisons, B12/folate/thiamine deficiency, syphilis, brain tumour, subdural haematoma, chronic drug use (alcohol, barbiturates)

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8
Q

Summary of normal pressure hydrocephalus?

A

Caused by abnormal build-up of CSF in ventricles - causing increased pressure and producing Sx of cognitive impairment

Occur at any age, but more common in elderly

RF - head trauma, infection or inflammation in brain, tumour and SAH

Features - progressively worsening memory lapses, personality and mood disturbances, difficulties with walking, dementia, urinary incontinence

Ix - imaging - hydrocephalus with ventriculomegaly in absence of, our out of proportion to, sulcal enlargement

Tx - ventriculoperitoneal shunt to drain excess CSF into abdomen

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9
Q

Ix for dementia?

A

Primary -
Blood (reversible causes) - FBC, U&E, LFTs, calcium, glucose, ESR/CRP, TFTs, vitamin B12, folate

Secondary -
Neuroimaging to exclude other reversible conditions (subdural haematoma, normal pressure hydrocephalus)

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10
Q

Management of Alzheimers disease?

A

Lifestyle - range of activities to promote wellbeing that are tailored to person’s preference, group cognitive stimulation

Pharmacological-
- acetylcholinesterase inhibitors (donepezil, galantamina, rivastigmine)
- donepezil - contraindicated in pt’s with bradycardia, SE = insomnia
- memantine (NMDA receptor antagonist) - second line

Managing non-cognitive Sx
- NICE don’t recommended antidepressants
- antipsychotics should only be used for patients at risk of harming themselves or others, or when the agitation, hallucinations or delusions are causing them severe distress

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11
Q

Summary of pellagra?

A

Caused by nicotinic acid (niacin) deficiency

Three D’s - dermatitis, diarrhoea, dementia

may occur as a consequence of isoniazid therapy (isoniazid inhibits the conversion of tryptophan to niacin) and it is more common in alcoholics.

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12
Q

Summary of Pick’s disease?

A

Frontotemporal dementia

Sx - personality change, impaired social conduct, hyperorality, disinhibition, increased appetite, perseveration behaviours

Focal gyral atrophy with knife-blade appearance

Macroscopic changes - Atrophy of the frontal and temporal lobes

Microscopic changes - Pick bodies (spherical aggregations of tau protein), gliosis, neurofibrillary tangles, senile plaques

Tx
NICE do not recommend that AChE inhibitors or memantine are used in people with frontotemporal dementia

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13
Q

Management of vascular dementia?

A

Address CVD RFs to slow progression

Non-pharmacological - cognition stimulation programmes, multi sensory stimulation, music/art therapy, animal therapy
managing challenging behaviours - address pain, avoid overcrowding, clear communication

Pharmacological - no specific Tx approved. Only consider AChE inhibitors or memantine for people with vascular dementia if they have suspected comorbid Alzheimer’s disease, Parkinson’s disease dementia or dementia with Lewy bodies.

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14
Q

Delirium vs dementia?

A

Factors favouring delirium over dementia:

acute onset
impairment of consciousness
fluctuation of symptoms: worse at night, periods of normality
abnormal perception (e.g. illusions and hallucinations)
agitation, fear
delusions

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15
Q

Depression vs dementia?

A

Factors suggesting diagnosis of depression over dementia:

short history, rapid onset
biological symptoms e.g. weight loss, sleep disturbance
patient worried about poor memory
reluctant to take tests, disappointed with results
mini-mental test score: variable
global memory loss (dementia characteristically causes recent memory loss)

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16
Q

Features of acute confusional state/delirium?

A

memory disturbances (loss of short term > long term)
may be very agitated or withdrawn
disorientation
mood change
visual hallucinations
disturbed sleep cycle
poor attention

17
Q

Predisposing factor for acute confusional state/delirium?

A

It affects up to 30% of elderly patients admitted to hospital.

Predisposing factors include:
age > 65 years
background of dementia
significant injury e.g. hip fracture
frailty or multimorbidity
polypharmacy

The precipitating events are often multifactorial and may include:
infection: particularly urinary tract infections
metabolic: e.g. hypercalcaemia, hypoglycaemia, hyperglycaemia, dehydration
change of environment
any significant cardiovascular, respiratory, neurological or endocrine condition
severe pain
alcohol withdrawal
constipation

18
Q

Management of delirium?

A

Treating underlying cause

Environment modification

haloperidol 0.5 mg as the first-line sedative. also olanzapine

management can be challenging in patients with Parkinson’s disease, as antipsychotics can often worsen Parkinsonian symptoms
careful reduction of the Parkinson medication may be helpful
if symptoms require urgent treatment then the atypical antipsychotics quetiapine and clozapine are preferred