Geriatrics Flashcards
Features acute confusional state (delirium)
- Memory disturbance
- Agitation or withdrawn
- Disorientation
- Mood change
- Visual hallucinations
- Disturbed sleep cycle
- Poor attention
Management acute confusional state
Treatment of underlying cause
Modification of environment
Consider haloperidol or olanzapine
Management acute confusional state in Parkinsons
Consider careful reduction of Parkinson medication
If symptoms require urgent treatment then atypical antipsychotics such as quetiapine and clozapine
Non-pharmacological management Alzheimer’s
- Group cognitive stimulation therapy with mild and moderate dementia
- Group reminiscence therapy and cognitive rehabilitation
First line pharmacological management Alzheimer’s disease
Acetylcholinesterase inhibitors:
- Donepezil
- Galantamine
- Rivastigmine
Second line treatment Alzheimer’s disease
Memantine (NMDA receptor antagonist)
When is memantine used
- Moderate Alzeimer’s who are intolerance of, or contraindication to, acetylcholinesterase inhibitors
- Add on drug to acetylcholinesterase inhibitors for patients with moderate-severe asthma
- Monotherapy in severe asthma
Use of anti-psychotic medications in Alzheimer’s
Only used for patients at risk of harming themselves or others, or when agitation, hallucinations, or delusions causing severe depression
CI’s donepezil
Bradycardia (relative)
Adverse effects donepezil
Insomnia
Dementia assessment tools in non-specialist setting recommended by NICE
10-point cognitive screener (10-CS)
6 item cognitive impairment test (6CIT)
Investigation in primary care for suspected dementia
Blood screen to exclude reversible causes - FBC, U&E, LFTs, calcium, glucose, ESR/CRP, TFTs, vitamin B12, folate
Investigation in secondary care for suspected dementia
Neuroimaging to exclude reversible conditions, e.g. subdural haematoma, normal pressure hydrocephlaus
Types of frontotemporal lobar degeneration
Frontotemporal dementia (Pick’s disease)
Progressive non-fluent aphasia
Semanic dementia
Common features of frontotemporal lobar dementias
Onset before 65
Insidious onset
Relatively preserved memory and visuospatial skills
Personality change and social conduct problems
Features frontotemporal dementia (Picks disease)
- Personality change
- Impaired social conduct
- Hyperorality
- Disinhibition
- Increased appetite
- Perseveration behaviours
CT changes frontotemporal dementia
Focal gyral atrophy with knife-blade appearance
Microscopic changes frontotemoral dementia
Pick bodies - spherical aggregations of tau protein
Gliosis
Neurofibrillary tangles
Senile plaques
Features chronic progressive aphasia
Non fluent speech
Short utterances that are agrammatic
Comprehension relatively preserved
Presentation semantic dementia
Fluent progressive aphasia - speech fluent but empty and conveys little meaning
Memory better for recent rather than remote events
Macroscopic changes Alzheimers
Widespread cerebral atrophy, particularly involving cortex and hippocampus
Microscopic changes Alzheimer’s
Cortical plaques due to deposition of type A-beta-amyloid protein and intraneuronal neurofibrillary tangles causes by abnormal aggregation of tau protein
Hyperphosphorylyation of tau protein
Characteristic pathological feature of Lewy body dementia
Alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic, and neocortical areas
Features Lewy body dementia
Progressive cognitive impairment
Parkinsonism
Visual hallucinations
Features of cognitive impairment in Lewy body dementia
Typically occurs before parkinsonism, but usually both features occur within a year of each other
Congition may be flucutating
Early impairments in attention and executive function rather than just memory loss
Diagnosis Lewy body dementia
Usually clinical
SPECT increasingly used
Management Lewy body dementia
Acetylcholineterase inhibitors and memantine as in Alzheimer’s
Neuroleptics in Lewy body dementia
Should be avoided - patients extremely sensitive and may develop irreversible Parkinsonism
What is vascular dementia
Group of syndromes of cognitive impairment caused by different mechanisms causing ischaemia or haemorrhage secondary to cerebrovascular disease
Presentation vascular dementia
Several months/years of history of sudden or stepwise deterioration of cognitive function
Focal neurological abnormalities, e.g. visual disturbance, sensory or motor symptoms
Difficulty with attention and concentration
Seizures
Memory disturbance
Gait disturbance
Speech disturbance
Emotional disturbance
MRI findings vascular dementia
May show infarcts and extensive white matter changes
Non-pharmacological management options in vascular dementia
Cognitive stimulation programmes
Multisensory stimulation
Music and art therapy
Animal-assisted therapy
Pharmacological management vascular dementia
Only consider AChE inhibitors or memantine if suspected comorbid forms of dementia that respond
No evidence of effectiveness of aspirin or statins
