Geriatric Flashcards

1
Q

investigations done when originally diagnosing dementia

A

primary care:
blood tests to look for reversible causes

FBC, U&Es, LFTs, TFTs, glucose, calcium, vitamin B12 and folate, ESR/CRP

secondary care: neuroimaging
e.g. subdural haematoma, normal pressure hydrocephalus

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2
Q

role of acetylcholine

A

has a role in parasympathetic innervation
- smooth muscle contraction
- blood vessel dilation
- slows heart rate
- releases secretions

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3
Q

management of Alzheimer’s disease

A

non-pharmacological:
- offer a range of activities to promote wellbeing based on preference
- group cognitive stimulation therapy for patients with mild and moderate dementia
- to consider include group reminiscence therapy and cognitive rehabilitation

pharmacological:
acetylcholinesterase inhibitors
e.g. donepezil, galantamine, rivastigmine
for mild to moderate dementia

memantine = NMDA receptor antagonist
monotherapy in severe Alzheimer’s
add on drug to acetylcholinesterase inhibitors for patient’s with moderate/severe Alzheimer’s
moderate alzheimer’s where intolerance/contraindication to acetylcholinesterase inhibitors

NOT to recommend antidepressants
anti-psychotics used for patients at risk of harming themselves or others, or when agitation, hallucinations, delusions causing them severe distress

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4
Q

contraindications for donepezil

A

bradycardia
adverse effects include insomnia

should be started with caution in patients with conduction abnormalities or those already taking negatively chronotropic medications such as beta blockers, rate-limiting calcium channel blockers or digoxin

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5
Q

first line neuroimaging for diagnosing dementia

A

MRI

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6
Q

what is a Q risk score

A

identifies the 10 year risk of heart disease and who should be started on statins

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7
Q

role of STOPP tool

A

identifies medications where the risk outweighs the therapeutic benefits in certain conditions

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8
Q

what is frontotemporal dementia

A

form of dementia more common in those < 65yrs
various forms, where individuals can experience changes in personality & behaviour

e.g. primary progressive aphasia = inability to produce speech and loss of literacy skills

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9
Q

common features of frontotemporal lobar dementias

A

onset before 65yrs
insidious onset
relatively preserved memory & visuospatial skills
personality change & social conduct problems

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10
Q

what are the 3 types of frontotemporal lobar dementia

A

frontotemporal dementia (Pick’s disease)
chronic progressive aphasia/ progressive non-fluent aphasia
semantic dementia

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11
Q

what is Pick’s disease & its presentation

A

most common type of fronto-temporal dementia
characterised by personality change & impaired social conduct

hyperorality
disinhibition
increased appetite
perseveration behaviours

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12
Q

macro/microscopic changes seen in Pick’s disease

A

Focal gyral atrophy with a knife-blade appearance = characteristic

macroscopic: atrophy of the frontal and temporal lobes

microscopic:
pick bodies (spherical aggregations of tau protein, silver-staning)
Neurofibrillary tangles
gliosis
senile plaques

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13
Q

management of Pick’s disease

A

NICE do not recommend acetylcholinesterase inhibitors or memantine

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14
Q

presentation of chronic progressive aphasia

A

chief factor is non-fluent speech
short utterances that are agrammatic
comprehension relatively preserved

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15
Q

presentation of semantic dementia

A

speech is fluent but empty and conveys little meaning

unlike in Alzheimer’s memory is better for recent than remote events

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16
Q

predisposing factors to delirium

A

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

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17
Q

precipitating factors to delirium

A

infection: particularly UTIs
change of environment
constipation
severe pain
metabolic e.g. hypoglycaemia, dehydration, hypercalcemia
alcohol withdrawal
any significant condition

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18
Q

features of acute confusional state/delirium

A

memory disturbances
agitated
mood change
hallucinations
disorientation
disturbed sleep cycle
poor attention

19
Q

management of delirium

A

treat underlying cause
modification of environment

haloperidol 0.5mg
** can also use olanzapine

20
Q

management of delirium in those with Parkinson’s disease

A

antipsychotics can make symptoms worse

careful reduction of Parkinson’s medication may be useful
if need urgent treatment, atypical antipsychotics preferred e.g. quetiapine, clozapine

could use lorazpam

21
Q

characteristic pathological feature in Lewy body dementia

A

alpha synuclein cytoplasmic infusions (Lewy bodies) in the substantia nigra, paralimbic, and neocortical areas

22
Q

features of Lewy body dementia

A

progressive cognitive impairment
** in contrast to Alzheimer’s, early impairments in executive function & attention than memory loss
cognition may be fluctuating
usually develops before Parkinsonism

Parkinsonism

Visual hallucinations/delusions

23
Q

diagnosis of Lewy body dementia

A

mainly clinical
but can do a SPECT scan

24
Q

management of Lewy body dementia

A

acetylcholinesterase inhibitors & memantine

neuroleptics should be avoided
** these patients are sensitive to these and might develop irreversible parkinsonism
e.g. patient has deteriorated following the introduction of an antipsychotic agent

25
Q

what is a pressure ulcer

A

develops in patients unable to move parts of their body due to illness, paralysis, advancing age

typically develop over bony prominences e.g. sacrum, heel

26
Q

what predisposes someone to a pressure ulcer

A

malnourishment
incontinence
immobility (icl pain which might lead to immobility)

27
Q

screening tool used to screen for patients at risk of developing pressure sores

A

Waterlow score
**includes BMI, nutritional status, mobility, continence

28
Q

grading of pressure sores

A

grade 1 = non-blanchable erythema of intact skin, warmth, oedema, hardness

grade 2 = partial thickness skin loss involving epidermis or dermis, or both

grade 3 = full thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia.

grade 4 = Extensive destruction, tissue necrosis, or damage to muscle, bone or supporting structures with or without full thickness skin loss

29
Q

management of pressure ulcers

A

wound dressings, analgesia, nutritional assessment

need a moist wound environment to encourage healing - Hydrocolloid dressings and hydrogels
AVOID soap

DO NOT swab, antibiotics done on clinical findings e.g. cellulitis, systemically unwell, osteomyelitis

may need referral to tissue viability nurse/surgical debridement

30
Q

what 3 factors does normal gait involve?

A

neurological system e.g. basal ganglia
MSK - normal tone & strength
effective processing of the senses e.g. sight, sound, sensation

As individuals get older they are more likely to experience medical problems affecting these systems, which leads to gait abnormalities and increases the risk of falls

31
Q

risk factors that increase the risk of falls

A

lower limb weakness
vision problems
balance/gait disturbances e.g. diabetes, RA, parkinson’s
polypharmacy (>4 drugs)
incontinence
>65 yrs
arthritis in lower limbs
depression
postural hypotension
psychoactive drugs

32
Q

medications linked to increased risk of falls

A

drugs that cause postural hypotension:
diuretics
ACE-i
beta-blockers
nitrates
anti-cholinergic
antidepressants
Levodopa

other drugs:
benzodiazepines
opiates
codeine
antipsychotics
anti-convulsant
digoxin

33
Q

investigations of falls

A

bedside: BP, ECG, basic obs, urine dip, blood glucose

bloods: Full Blood Count, Urea and Electrolytes, Liver function tests and bone profile

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

34
Q

management of falls in the elderly

A

identify all individuals who have fallen in the last month & identify why
for those with a history of falls or at risk: complete ‘Turn 180° test’ or the ‘Timed up and Go test’.

Offer a multidisciplinary assessment by a qualified clinician to all patients over 65 with:
>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’

34
Q

management of falls in the elderly

A

identify all individuals who have fallen in the last month & identify why
for those with a history of falls or at risk: complete ‘Turn 180° test’ or the ‘Timed up and Go test’.

Offer a multidisciplinary assessment by a qualified clinician to all patients over 65 with:
>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’

35
Q

cut off level that suggests dementia in the mini mental state examination

A

24 or less

36
Q

factors favouring delirium over dementia

A

impairment of consciousness
fluctuation of symptoms e.g. worse at night, periods of normality
abnormal perception e.g. hallucinations
agitation, fear
delusions

37
Q

symptoms of digoxin toxicity

A

gastrointestinal disturbance (nausea, vomiting, abdominal pain)
dizziness
confusion
blurry or yellow vision
arrhythmias.

38
Q

side effects of anti-cholinergic drugs

A

dry mouth, dry eyes
hypotension
constipation
urinary retention
arrhythmias (QT interval prolongation)

39
Q

how should frailty be assessed?

A

evaluation of gait speed, self-reported health status, or the PRISMA-7 questionnaire

PRISMA-7 involves questions considering the age, sex, health problems, assistance required and walking aid use of the patient

40
Q

causes of dementia

A

common:
Alzheimer’s
vascular dementia
Lewy body dementia

rarer:
Huntington’s
CJD
Pick’s disease
HIV (50% of aids patients)

41
Q

reversible causes of dementia

A

hypothyroidism, Addison’s
folate/b12/ thiamine deficiency
syphilis
brain tumour
normal pressure hydrocephalus
subdural haematoma
depression
chronic drug use e.g. Alcohol, barbiturates

42
Q

pathophysiology of Alzheimer’s disease

A

progressive degenerative disease of the brain, accounting for majority of dementia in the UK

pathological changes:
macroscopic:
widespread cerebral atrophy, particularly involving the 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, impairing its function

biochemical:
deficit of acetylcholine from damage to an ascending forebrain projection