Geriatric Flashcards
investigations done when originally diagnosing dementia
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
role of acetylcholine
has a role in parasympathetic innervation
- smooth muscle contraction
- blood vessel dilation
- slows heart rate
- releases secretions
management of Alzheimer’s disease
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
contraindications for donepezil
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
first line neuroimaging for diagnosing dementia
MRI
what is a Q risk score
identifies the 10 year risk of heart disease and who should be started on statins
role of STOPP tool
identifies medications where the risk outweighs the therapeutic benefits in certain conditions
what is frontotemporal dementia
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
common features of frontotemporal lobar dementias
onset before 65yrs
insidious onset
relatively preserved memory & visuospatial skills
personality change & social conduct problems
what are the 3 types of frontotemporal lobar dementia
frontotemporal dementia (Pick’s disease)
chronic progressive aphasia/ progressive non-fluent aphasia
semantic dementia
what is Pick’s disease & its presentation
most common type of fronto-temporal dementia
characterised by personality change & impaired social conduct
hyperorality
disinhibition
increased appetite
perseveration behaviours
macro/microscopic changes seen in Pick’s disease
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
management of Pick’s disease
NICE do not recommend acetylcholinesterase inhibitors or memantine
presentation of chronic progressive aphasia
chief factor is non-fluent speech
short utterances that are agrammatic
comprehension relatively preserved
presentation of semantic dementia
speech is fluent but empty and conveys little meaning
unlike in Alzheimer’s memory is better for recent than remote events
predisposing factors to delirium
age > 65 years
background of dementia
significant injury e.g. hip fracture
frailty/multimorbidity
polypharmacy
precipitating factors to delirium
infection: particularly UTIs
change of environment
constipation
severe pain
metabolic e.g. hypoglycaemia, dehydration, hypercalcemia
alcohol withdrawal
any significant condition
features of acute confusional state/delirium
memory disturbances
agitated
mood change
hallucinations
disorientation
disturbed sleep cycle
poor attention
management of delirium
treat underlying cause
modification of environment
haloperidol 0.5mg
** can also use olanzapine
management of delirium in those with Parkinson’s disease
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
characteristic pathological feature in Lewy body dementia
alpha synuclein cytoplasmic infusions (Lewy bodies) in the substantia nigra, paralimbic, and neocortical areas
features of Lewy body dementia
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
diagnosis of Lewy body dementia
mainly clinical
but can do a SPECT scan
management of Lewy body dementia
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
what is a pressure ulcer
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
what predisposes someone to a pressure ulcer
malnourishment
incontinence
immobility (icl pain which might lead to immobility)
screening tool used to screen for patients at risk of developing pressure sores
Waterlow score
**includes BMI, nutritional status, mobility, continence
grading of pressure sores
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
management of pressure ulcers
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
what 3 factors does normal gait involve?
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
risk factors that increase the risk of falls
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
medications linked to increased risk of falls
drugs that cause postural hypotension:
diuretics
ACE-i
beta-blockers
nitrates
anti-cholinergic
antidepressants
Levodopa
other drugs:
benzodiazepines
opiates
codeine
antipsychotics
anti-convulsant
digoxin
investigations of falls
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
management of falls in the elderly
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’
management of falls in the elderly
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’
cut off level that suggests dementia in the mini mental state examination
24 or less
factors favouring delirium over dementia
impairment of consciousness
fluctuation of symptoms e.g. worse at night, periods of normality
abnormal perception e.g. hallucinations
agitation, fear
delusions
symptoms of digoxin toxicity
gastrointestinal disturbance (nausea, vomiting, abdominal pain)
dizziness
confusion
blurry or yellow vision
arrhythmias.
side effects of anti-cholinergic drugs
dry mouth, dry eyes
hypotension
constipation
urinary retention
arrhythmias (QT interval prolongation)
how should frailty be assessed?
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
causes of dementia
common:
Alzheimer’s
vascular dementia
Lewy body dementia
rarer:
Huntington’s
CJD
Pick’s disease
HIV (50% of aids patients)
reversible causes of dementia
hypothyroidism, Addison’s
folate/b12/ thiamine deficiency
syphilis
brain tumour
normal pressure hydrocephalus
subdural haematoma
depression
chronic drug use e.g. Alcohol, barbiturates
pathophysiology of Alzheimer’s disease
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
