Geriatrics Flashcards
Delirium (acute confusional state)
clinical syndrome with acute onset, fluctuating change in mental status with inattention, disorganised thinking & altered levels of consciousness usually seen in >65y/o hospitalised pts
Characterised by high morbidity & mortality
Epidemiology of delirium
most common complication of hospitalisation in the elderly & high incidence in those with pre-existing cognitive impairment
↑ incidence with age
usually seen in those >65 y/o
Risk factors for delirium
age >65 yrs male sex pre-existing cognitive deficit e.g. dementia severe comorbidity previous delirium current severe illness/hip fracture ↑ pain drug use/dependence / substance misuse visual/hearing impairment poor mobility social isolation terminal illness ICU admission
Aetiology of delirium
Acute infections especially UTIs prescribed drugs e.g. benzos, analgesia (morphine), steroids, antiparkinson meds surgery/trauma urinary retention constipation sleep deprivation pain dehydration toxic substances (drugs/alcohol) neoplasia/malignancy
Subtypes of delirium
Hypoactive:
↓ psychomotor activity, apathy & quiet confusion
mostly seen in elderly pts
Hyperactive:
↑ psychomotor activity, agitation, delusions & disorientation
usually seen with substance abuse/withdrawal
Mixed delirium:
fluctuating psychomotor activity between hyper/hypoactive states
most common in general population
Presentation of delirium
usually acute presentation
fluctuating course throughout day
may be worse in evening (sundowning)
disorganised thinking, hallucinations (usually visual), cognitive deficits, impaired memory, emotional lability,, agitation, combativeness, disorientation, poor concentration, psychotic ideas (short duration & simple content)
Investigating delirium
Full physical examination Bloods (FBC/U&Es/LFTs/TFTs/Mg2+/Ca2+/creatinine/glucose) ECG Urine dip + MC&S CXR blood cultures ABG imagine/investigations for suspected cause
Management of delirium
treatment of underlying condition
Supportive care:
clear communication, reminders of day/time/location, familiar objects from home, involve family & carers
Environmental:
side room, control noise/lighting/temp
adequate nutrition
attention to continence / help with constipation
stop offending medication (e.g. benzos, morphine, warfarin, furosemide, lithium, TCAs, steroids)
Alzheimers dementia (AD)
a chronic neurodegenerative disease wait insidious onset & progressive but slow decline, may occur commonly with other types of dementia e.g. vascular
most common type of dementia
Characteristics of Alzheimer dementia (AD)
widespread cortical atrophy
extracellular senile/amyloid plaques made from beta amyloid
intracellular neurofibrillary tangles made from hyperposphorylated Tau
↓cholinergic function (acetylcholine deficiency)
Risk factors for Alzheimer dementia (AD)
caucasian heritage ↑ age hyperlipidaemia diabetes HTN smoking alcohol misuse Down's syndrome Genetics
Presentation of Alzheimer dementia (AD)
insidious onset & slow progression
short term memory impairment (episodic memory affected first)
disorientation (in time & place, subtle at first e.g. misplacing items/getting lost)
Presentation of Alzheimer dementia (AD)
insidious onset & slow progression
short term memory impairment (episodic memory affected first)
disorientation (in time & place, subtle at first e.g. misplacing items/getting lost)
nominal dysphasia
apathy
impaired ADLs
personality change / mood change
poor abstract thinking & judgement
psychiatric symptoms
agitation & irritability
impaired executive function (later on in disease)
Investigations for Alzheimer dementia (AD)
Bedside cognitive assessment (MMSE, MoCA, AMTS)
CT/MRI head (cortical atrophy)
Management of Alzheimer dementia (AD)
Person centred MDT care (memory assessment, memory enhancement strategies, therapies e.g. aroma/music therapy)
Pharmacological:
1st line: AChE inhibitors e.g. donepezil, galantamine, rivastigmine (for moderate AD)
2nd line: NMDA receptor antagonist e.g. memantine (if AChE contraindicated/as add on to AChE)
SSRIs as depression
Genetics of Alzheimer dementia (AD)
Amyloid precursor protein (APP)
Presenilin 1
Presenilin 2
ApoE4 (late onset)
NB ApoE3 = neutral & ApoE2 = portective
Vascular dementia (VD)
also know as multi infarct dementia, is a chronic progressive cognitive impairment caused by cerebrovascular disease leading to ischaemia / haemorrhage
2nd most common type of dementia
Sybtype of vascular dementia (VD)
its a spectrum of disease called vascular cognitive impairment of which vascular dementia is the worst
stroke related VD - multi/single infarct
subcortical VD - small vessel disease
mixed dementia - presence of both VD & AD
Inherited form of Vascular dementia
inherited as CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.
RARE
Risk factors for vascular dementia (VD)
↑ age history of stroke/TIA AF HTN Diabetes smoking obesity CHD
Investigation/Assessment of vascular dementia (VD)
cognitive impairment screening
MRI/CT (may show infarcts / white matter changes)
NINDS-AIREN for diagnosis of probably VD (presence of cognitive decline interfering with ADLs, presence of CVD, relationship between the 2 suspected)
Management of vascular dementia (VD)
Individualised person centred care (cognitive stimulation programmes, therapies, multi sensory stimulation)
consider AChE inhibitors or memantine if comorbid Alzheimers
Frontotemporal dementia
progressive neurodegenerative disease of the frontal and/or temporal lobe generally due to mutations of proteins leading to lobar atrophy
3rd most common type of dementia
Onset of Frontotemporal dementia
usually age <65yrs
i.e. earlier than other dementias
Presentation of Frontotemporal dementia
insidious onset relatively preserved memory & visuospatial skills personality change social conduct problems disinhibition inappropriate social behaviour loss of empathy/sympathy lack of insight may have difficulties with speech (hesitant, loss of vocabulary, ↓fluency)
Investigations/Assessment of Frontotemporal dementia
formal cognitive testing & dementia screen
MRI (atrophy of frontal and/or temporal lobe)
Management of Frontotemporal dementia
patient centred care (SALT, therapies, supportive therapy)
SSRIs = 1st line to modify behavioural symptoms
atypical antipsychotics = 2nd line
Hallmarks of the subtypes of frontotemporal lobar degeneration
Chronic progressive aphasia:
Non fluent speech with meaning
Semantic dementia:
fluent but empty speech
Pick’s disease (frontotemporal dementia)
personality change, disinhibition & inappropriate social conduct
Lewy body dementia (LBD)
clinical syndrome of progressive conginitve decline characterised by pathological alpha-synuclein cytoplasmic inclusion (Lewy bodies) in the substantial migration, paralimbic & neo cortical areas
~20% of all dementia
Lewy body dementia vs Parkinsons dementia
LBD:
onset of cognitive & motor symptoms within 1 year of each other
Parkinsons dementia:
if cognitive symptoms occur >1 year after onset of motor symptoms
Presentation of Lewy body dementia (LBD)
progressive cognitive impairment in contrast to Alzheimer’s, early impairments in attention and executive function
cognition may be fluctuating, in contrast to other forms of dementia
parkinsonism
visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)
Presentation of Lewy body dementia (LBD)
progressive cognitive impairment (memory loss, decline in problem solving ability, spatial awareness difficulties, impairment of executive function & attention)
conginiton may be fluctuation (fluctuating levels of attention & awareness)
Mild parkinsonism (tremor, rigidity poverty of facial expression, bradykinesia)
visual hallucinations
frequent falls
REM sleep disturbances
NB unlike AD there is early impairment of executive function & attention rather than just memory
Management of Lewy body dementia (LBD)
patient centred care (care plans, therapies, cognitive stimulation programmes)
Pharmacological:
AChE inhibitors & memantine can be used as in AD
Medication to avoid in Lewy body dementia (LBD)
Its very sensitive to antipsychotics
may cause them to develop irreversible parkinsonism & worsen the dementia
Osteoporosis
progressive systemic skeletal disease characterised by ↓ bone mass & micro-architectural deterioration of bone tissue leading to ↑ fragility of the bone & ↑ susceptibility to fractures
more common in women
↑incidence with age
Bone density assessment
Bone density is expressed as standard deviation in relation to a reference population
A Z-score compares bone density of an individual to normal at that age, with a score of -2 indicating bone density below the normal for that age
A T-score compares bone density of an individual to that of a young healthy population
Characterising bone density assessment
Normal:
T-score ≥ -1
Osteopenia:
T-score < -1 but > -2.5
Osteoporosis:
T-score ≤ -2.5
Severe osteoporosis:
T-score ≤ -2.5 + a fracture
Risk factors for osteoporosis
female sex ↑ age low BMI smoking alcohol misues prolonged immobilisation corticosteroid use menopause medications (PPIs, L-thyroxine, anticonvulsants, heparin, steroids) family history of osteoporosis / fragility fractures
Management of osteoporosis
For everyone: Vit D & Calcium supplementation
1st line: Bisphosphonates e.g. Alendronate (1st line) or risendronate (2nd line)
2nd line: denusomab (has increasing role as 2nd line), Raloxifene, strontium ranelate
NB if alendronate not tolerated try risendronate before moving onto 2nd line medication e.g. denusomab
Management of osteoporosis
For everyone: Vit D & Calcium supplementation
1st line: Bisphosphonates e.g. Alendronate (1st line) or risendronate (2nd line)
2nd line: denusomab (has increasing role as 2nd line), Raloxifene, strontium ranelate
NB if alendronate not tolerated try risendronate before moving onto 2nd line medication e.g. denusomab
Investigation / Assessment of osteoporosis
DEXA scan /plain X-rays
FRAX or Q-fracture scores to assess 10yr rick of pt developing frailty fracture
Ca2+ / Phosphate / PTH / Alkaline phosphatase (all normal)