Elderly Flashcards
What is dementia?
Irreversible, chronic and progressive cognitive impairment which is sufficient to impair ADLs
Problems present for 6/12
Only proven post mortem with histological evidence
Differentials for dementia
Delirium
‘Reversible dementia’: present with cognitive impairment that may resolve if treated e.g subcutaneous haematoma, hypothyroidism and vitamin deficiency
Pseudodementia: memory problems in severe depression can resemble dementia
HIV-related cognitive impairment/dementia
MCI
Investigations for dementia
Bloods: FBC (infection/anaemia), U&Es (dehydration, renal failure, hyponatraemia)
Glucose
TFTs (hypothyroidism), LFTs (alcohol misuse)
MMSE
Collateral Hx
Septic screen: MSU, CXR, blood cultures, wound swabs, sputum/stool samples
CT head/MRI
Mx for dementia
Adaptations for patients: dosset boxes/blister packs to help medication compliance, reality orientation (visible clocks)
Social support: personal care, meal prep or med prompting
Support carers
Treat sensory impairment: glasses/hearing aids
Psychological therapies
Psychotropic meds
What psychotropic medications can be used in dementia?
Start low and go slow is golden rule
Acetylcholinesterase inhibitors (donepezil/rovastigimine) prevent acetylcholinesterase destroying acetylcholine - increasing neurotransmitter levels in synapses and compensating for overall cholinergic loss - not curative but slow process in AD and DLB
Sodium valproate and low dose BDZs or antipsychotics can also be used as a last resort if behavioural management
Aetiology of alzheimers
age is main risk factor
amyloid plaques and neurofibrillary tangles
accumulation of these leads to reduction in information and eventually death of brain cells
Genetics can cause early onset: autosomal dominant - Presenelin 1 (chromosome 14), Presenelin 2 gene (chromosome 1), beta-amyloid precursor protein (APP) gene (chromosome 21)
Pathology of Alzheimer’s
Atrophy: due to neuronal loss, hippocampus affected early, then temporal and parietal lobes, on CT sulci and ventricles may be enlarged (can be normal)
Plaque formation: APP can be abnormally cleaned into beta-amyloid which aggregates into insoluble lumps
Intracellular neurofibrillary tangles (NFTs)
Cholinergic loss
Risk factors for vascular dementia
older age
male sex
smoking
HTN
DM
Hypercholesterolaemia
AF
Pathology of vascular dementia
atherosclerosis, cortical ischaemia and infarction
Infarcts appear in CT as multiple lucencies
Presentation of vascular dementia
stepwise progression with each step representing a sudden deterioration as an infarct occurs
Many tiny infarcts causes a smoother more subtle deterioration
Sx reflect sites of lesions and may be ‘patchy’ and some areas of cognition spared
Neurological signs: hemiparesis or aphasia, episodes of confusion especially at night
Lewy Body dementia pathology
Lewy bodies are eosinophilic intracytoplasmic neuronal structures
Made of alpha-synuclein with uniquitin
PD found in brainstem but in DLB also seen in cingukate gurus and neocortex
Presentation of Lewy Body dementia
Fluctuating confusion with marked variation in levels of alertness
Vivid visual hallucinations
Spontaneous parkinsonism
Falls, syncope and TLOC
Short term memory is less affected
Can resemble delirium but don’t prescribe antipsychotics as extreme antipsychotic sensitivity in DLB can result in death
Aetiology of frontotemporal dementia
Neuron damage and death occurs in frontal and temporal lobes
Atrophy occurs due to deposition of abnormal proteins (often tau protein) within lobes
Clinical features of lewy body dementia
altered emotional responsiveness, apathy, disinhibition, impulsivity
progressive decline noted in interpersonal skills
changes on food preference, more childlike amusements
obsessions and rituals may be noted
progressive breakdown in output of language
speech takes effort and is not-fluent, apraxia or disorders of speech sound
impaired comprehension of sentences and impact on literacy skills
What is normal pressure hydrocephalus?
Occurs due to abnormal build up of cerebrospinal fluid in ventricles causing increased pressure, producing symptoms of cognitive impairment
Occur at any age
Risk factors for normal pressure hydrocephalus
head trauma
infection or inflammation of brain
tumours
subarachnoid haemorrhage
Sx of normal pressure hydrocephalus
progressively worsening memory lapses
personality and mood disturbances
difficulties with walking
dementia
urinary incontinence
Mx of normal pressure hydrocephalus
Ventriculoperitoneal (VP) shunt is used to drain excess CSF into abdomen, relieved pressure on brain
Prion protein diseases (CJD)
Infectious prion proteins cause diseases such as Creutzfeldt-Jakob disorder
can be sporadic or variant
sporadic CJD tends to affect under 40s
Variant CJD is caused by eating meat infected by bovine springform encephalopathy through infected cattle meat
Presentation of CJD
Initially minor memory lapses, mood disturbances and loss of interest
Progresses over weeks to unsteadiness and physical clumsiness
Then to stiffness, jerking movements, incontinence and aphasia
Death occurs within 6m of symptom presentation
Delirium
Acute transient state of global dysfunction with clouding of consciousness
Patient not aware of their environment
Sign of physical illness need to treat underlying cause
Risk factors for delirium
old age
pre-existing physical/mental illness
substance misuse
polypharmacy
malnutrition
Causes of delirium
Trauma: head injury, burns
hypoxia
infective
metabolic: electrolyte disturbances, end organ failure
hypoglycaemia
nutritional: Wernickes encephalopathy
raised ICP
Drugs and alcohol: intoxication/withdrawal
Medications: anticholinergics/opiates
Clinical presentation of delirium
sudden onset
fluctuating symptoms
often worse in evenings/night
usually disorientated and has poor attention/short term memory
mood changes
illusions and hallucinations
disorganised thinking and pressured/rambling speech
hypoactivity or hyperactivity