Palliative and end of life care

Question 1

Acute confusional state

Answer 1

Acute confusional state is also known as delirium or acute organic brain syndrome. It affects up to 30% of elderly patients admitted to hospital.

Question 2

Predisposing factors of delirium

Answer 2

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

Question 3

Precipitating events for delirium

Answer 3

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

Question 4

Presentation of delirium

Answer 4

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may be very agitated or withdrawn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

Question 5

Management of delirium

Answer 5

treatment of the underlying cause
modification of the environment
recommended haloperidol 0.5 mg as the first-line sedative
advocate the use of haloperidol or 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

Question 6

Alzheimer’s disease

Answer 6

Alzheimer’s disease is a progressive degenerative disease of the brain accounting for the majority of dementia seen in the UK

Question 7

Non-pharmacological management of Alzheimer’s

Answer 7

NICE recommend offering ‘a range of activities to promote wellbeing that are tailored to the person’s preference’
NICE recommend offering group cognitive stimulation therapy for patients with mild and moderate dementia
other options to consider include group reminiscence therapy and cognitive rehabilitation

Question 8

Pharmacological management of Alzheimer’s

Answer 8

the three acetylcholinesterase inhibitors (donepezil, galantamine and rivastigmine) as options for managing mild to moderate Alzheimer’s disease
memantine (an NMDA receptor antagonist) is in simple terms the ‘second-line’ treatment for Alzheimer’s, NICE recommend it is used in the following situation reserved for patients with
moderate Alzheimer’s who are intolerant of, or have a contraindication to, acetylcholinesterase inhibitors
as an add-on drug to acetylcholinesterase inhibitors for patients with moderate or severe Alzheimer’s
monotherapy in severe Alzheimer’s

Question 9

Managing non-cognitive symptoms of Alzheimer’s

Answer 9

NICE does not recommend antidepressants for mild to moderate depression in patients with dementia
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

Question 10

Donepezil

Answer 10

is relatively contraindicated in patients with bradycardia
adverse effects include insomnia

Question 11

Risk factors of Alzheimer’s disease

Answer 11

increasing age
family history of Alzheimer’s disease
5% of cases are inherited as an autosomal dominant trait
mutations in the amyloid precursor protein (chromosome 21), presenilin 1 (chromosome 14) and presenilin 2 (chromosome 1) genes are thought to cause the inherited form
apoprotein E allele E4 - encodes a cholesterol transport protein
Caucasian ethnicity
Down’s syndrome

Question 12

Macroscopic pathological changes in Alzheimer’s

Answer 12

widespread cerebral atrophy, particularly involving the cortex and hippocampus

Question 13

Microscopic changes in Alzheimer’s

Answer 13

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

Question 14

Biochemical changes due to Alzheimer’s

Answer 14

there is a deficit of acetylcholine from damage to an ascending forebrain projection

Question 15

Neurofibrillary tangles

Answer 15

paired helical filaments are partly made from a protein called tau
tau is a protein that interacts with tubulin to stabilize microtubules and promote tubulin assembly into microtubules
in AD are tau proteins are excessively phosphorylated, impairing its function

Question 16

Delirium vs dementia

Answer 16

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

Question 17

Dementia features

Answer 17

diagnosis can be difficult and is often delayed
assessment tools recommended by NICE for the non-specialist setting include: 10-point cognitive screener (10-CS), 6-Item cognitive impairment test (6CIT)
assessment tools not recommended by NICE for the non-specialist setting include the abbreviated mental test score (AMTS), General practitioner assessment of cognition (GPCOG) and the mini-mental state examination (MMSE) have been widely used. A MMSE score of 24 or less out of 30 suggests dementia

Question 18

Management of Alzheimer’s

Answer 18

in primary care, a blood screen is usually sent to exclude reversible causes (e.g. Hypothyroidism). NICE recommend the following tests: FBC, U&E, LFTs, calcium, glucose, ESR/CRP, TFTs, vitamin B12 and folate levels. Patients are now commonly referred on to old-age psychiatrists (sometimes working in ‘memory clinics’).
in secondary care, neuroimaging is performed* to exclude other reversible conditions (e.g. Subdural haematoma, normal pressure hydrocephalus) and help provide information on aetiology to guide prognosis and management

Question 19

Types of dementia

Answer 19

• Alzheimer’s
• vascular
• Lewy body dementia
  -Conditions may coexist

Question 20

Common causes of dementia

Answer 20

Alzheimer’s disease
cerebrovascular disease: multi-infarct dementia (c. 10-20%)
Lewy body dementia (c. 10-20%)

Question 21

Rarer causes of dementia

Answer 21

Huntington’s
CJD
Pick’s disease (atrophy of frontal and temporal lobes)
HIV (50% of AIDS patients)

Question 22

Differentials for dementia

Answer 22

hypothyroidism, Addison’s
B12/folate/thiamine deficiency
syphilis
brain tumour
normal pressure hydrocephalus
subdural haematoma
depression
chronic drug use e.g. Alcohol, barbiturates

Question 23

Risk factors for the elderly falling

Answer 23

Lower limb muscle weakness
Vision problems
Balance/gait disturbances (diabetes, rheumatoid arthritis and parkinson’s disease etc)
Polypharmacy (4+ medications)
Incontinence
>65
Have a fear of falling
Depression
Postural hypotension
Arthritis in lower limbs
Psychoactive drugs
Cognitive impairment

Question 24

What medications cause postural hypotension

Answer 24

Nitrates

Diuretics

Anticholinergic medications

Antidepressants

L-Dopa

Angiotensin-converting enzyme inhibitors - (ACE) inhibitors

Question 25

Medications associated with falls due to other mechanisms

Answer 25

Benzodiazepines

Antipsychotics

Opiates

Anticonvulsants

Codeine

Digoxin

Other sedative agents

Question 26

Bedside tests for falls

Answer 26

Basic observations,
blood pressure
blood glucose
urine dip
ECG

Question 27

Blood tests to consider falls

Answer 27

Full Blood Count
Urea and Electrolytes
Liver function tests and bone profile

Question 28

Imaging to consider when patient falls

Answer 28

X-ray of chest/injured limbs,
CT head and cardiac echo

Question 29

When should an MDT be carried out for an elderly patient

Answer 29

> 2 falls in the last 12 months
A fall that requires medical treatment
Poor performance or failure to complete the ‘Turn 180° test’ or the ‘Timed up and Go test’

Question 30

Normal gait assessment in the elderly

Answer 30

The neurological system - basal ganglia and cortical basal ganglia loop.
The musculoskeletal system (which must have appropriate tone and strength).
Effective processing of the senses such as sight, sound, and sensation (fine touch and proprioception).

Question 31

Frontotemporal lobar degeneration (FTLD)

Answer 31

Frontotemporal dementia (Pick’s disease)
Progressive non fluent aphasia (chronic progressive aphasia, CPA)
Semantic dementia

Question 32

Common features of frontotemporal lobar dementias

Answer 32

Onset before 65
Insidious onset
Relatively preserved memory and visuospatial skills
Personality change and social conduct problems

Question 33

Picks disease

Answer 33

This is the most common type and is characterised by personality change and impaired social conduct

Other common features include hyperorality, disinhibition, increased appetite, and perseveration behaviours.

Focal gyral atrophy with a knife-blade appearance is characteristic of Pick’s disease.

Question 34

Macroscopic changes seen in Pick’s disease include

Answer 34

Atrophy of the frontal and temporal lobes

Question 35

microscopic changes in Pick’s disease

Answer 35

Pick bodies - spherical aggregations of tau protein (silver-staining)
Gliosis
Neurofibrillary tangles
Senile plaques

Question 36

Semantic dementia

Answer 36

Here the patient has a fluent progressive aphasia. The speech is fluent but empty and conveys little meaning. Unlike in Alzheimer’s memory is better for recent rather than remote events.

Question 37

Lewy body dementia

Answer 37

The characteristic pathological feature is alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas.

Question 38

Features of Lewy body dementia

Answer 38

progressive cognitive impairment
typically occurs before parkinsonism, but usually both features occur within a year of each other. This is in contrast to Parkinson’s disease, where the motor symptoms typically present at least one year before cognitive symptoms
cognition may be fluctuating, in contrast to other forms of dementia
in contrast to Alzheimer’s, early impairments in attention and executive function rather than just memory loss
parkinsonism
visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)

Question 39

Diagnosis of Lewy body dementia

Answer 39

usually clinical
single-photon emission computed tomography (SPECT) is increasingly used. It is currently commercially known as a DaTscan. Dopaminergic iodine-123-radiolabelled 2-carbomethoxy-3-(4-iodophenyl)-N-(3-fluoropropyl) nortropane (123-I FP-CIT) is used as the radioisotope. The sensitivity of SPECT in diagnosing Lewy body dementia is around 90% with a specificity of 100%

Question 40

Management of Lewy body dementia

Answer 40

both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer’s. NICE have made detailed recommendations about what drugs to use at what stages. Please see the link for more details
neuroleptics should be avoided in Lewy body dementia as patients are extremely sensitive and may develop irreversible parkinsonism. Questions may give a history of a patient who has deteriorated following the introduction of an antipsychotic agent

Question 41

Risk factors for multimorbidity

Answer 41

Increasing age
Female sex
Low socioeconomic status
Tobacco and alcohol usage
Lack of physical activity
Poor nutrition and obesity

Question 42

Grade 1 pressure ulcers

Answer 42

Non-blanchable erythema of intact skin. Discolouration of the skin, warmth, oedema, induration or hardness may also be used as indicators, particularly on individuals with darker skin

Question 43

Grade 2 pressure ulcers

Answer 43

Partial thickness skin loss involving epidermis or dermis, or both. The ulcer is superficial and presents clinically as an abrasion or blister

Question 44

Grade 3 pressure ulcers

Answer 44

Full thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia.

Question 45

Grade 4 pressure ulcers

Answer 45

Extensive destruction, tissue necrosis, or damage to muscle, bone or
supporting structures with or without full thickness skin loss

Question 46

Management of pressure ulcers

Answer 46

a moist wound environment encourages ulcer healing. Hydrocolloid dressings and hydrogels may help facilitate this. The use of soap should be discouraged to avoid drying the wound
wound swabs should not be done routinely as the vast majority of pressure ulcers are colonised with bacteria. The decision to use systemic antibiotics should be taken on a clinical basis (e.g. Evidence of surrounding cellulitis)
consider referral to the tissue viability nurse
surgical debridement may be beneficial for selected wounds

Question 47

Factors which predispose to develop pressure ulcers

Answer 47

malnourishment
incontinence: urinary and faecal
lack of mobility
pain (leads to a reduction in mobility)

Question 48

Waterlow score

Answer 48

screen for patients who are at risk of developing pressure areas. It includes a number of factors including body mass index, nutritional status, skin type, mobility and continence.

Question 49

Vascular dementia

Answer 49

second most common form of dementia after Alzheimer disease.

It is not a single disease but a group of syndromes of cognitive impairment caused by different mechanisms causing ischaemia or haemorrhage secondary to cerebrovascular disease.

Vascular dementia has been increasingly recognised as the most severe form of the spectrum of deficits encompassed by the term vascular cognitive impairment (VCI). Early detection and an accurate diagnosis are important in the prevention of vascular dementia.

Question 50

VD epidemiology

Answer 50

VD is thought to account for around 17% of dementia in the UK

Prevalence of dementia following a first stroke varies depending on location and size of the infarct, definition of dementia, interval after stroke and age among other variables. Overall, stroke doubles the risk of developing dementia.

Incidence increases with age

Question 51

Main subtypes of VD

Answer 51

Stroke-related VD - multi-infarct or single-infarct dementia
Subcortical VD - caused by small vessel disease
Mixed dementia - the presence of both VD and Alzheimer’s disease

Question 52

Risk factors of VD

Answer 52

History of stroke or transient ischaemic attack (TIA)
Atrial fibrillation
Hypertension
Diabetes mellitus
Hyperlipidaemia
Smoking
Obesity
Coronary heart disease
A family history of stroke or cardiovascular

Question 53

Patients with VD present with

Answer 53

Several months or several years of a history of a sudden or stepwise deterioration of cognitive function.

Focal neurological abnormalities e.g. visual disturbance, sensory or motor symptoms
The difficulty with attention and concentration
Seizures
Memory disturbance
Gait disturbance
Speech disturbance
Emotional disturbance

Question 54

Diagnosis of VD dependant on…

Answer 54

A comprehensive history and physical examination
Formal screen for cognitive impairment
Medical review to exclude medication cause of cognitive decline
MRI scan - may show infarcts and extensive white matter changes

Question 55

NINDS-AIREN criteria

Answer 55

Presence of cognitive decline that interferes with activities of daily living, not due to secondary effects of the cerebrovascular event
established using clinical examination and neuropsychological testing

Cerebrovascular disease
defined by neurological signs and/or brain imaging

A relationship between the above two disorders inferred by:
the onset of dementia within three months following a recognised stroke
an abrupt deterioration in cognitive functions
fluctuating, stepwise progression of cognitive deficits

Question 56

Non-pharmacological management of VD

Answer 56

Tailored to the individual
Include: cognitive stimulation programmes, multisensory stimulation, music and art therapy, animal-assisted therapy
Managing challenging behaviours e.g. address pain, avoid overcrowding, clear communication

Question 57

Pharmacological management of VD

Answer 57

There is no specific pharmacological treatment approved for cognitive symptoms
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.
There is no evidence that aspirin is effective in treating patients with a diagnosis of vascular dementia.
No randomized trials found evaluating statins for vascular dementia