Older Persons Mental Health Flashcards
(148 cards)
Delirium/acute confusional state: Predisposing factors and precipitating events
Predisposing factors include:
age > 65 years
background of dementia
significant injury e.g. hip fracture
frailty or multimorbidity
polypharmacy
The precipitating events are often multifactorial and may include:
infection: particularly urinary tract infections
metabolic: e.g. hypercalcaemia, hypoglycaemia, hyperglycaemia, dehydration
change of environment
any significant cardiovascular, respiratory, neurological or endocrine condition
severe pain
alcohol withdrawal
constipation
Presentation of delirium?
memory disturbances (loss of short term > long term)
may be very agitated or withdrawn
disorientation
mood change/personality changes
visual hallucinations
disturbed sleep cycle
poor attention
Causes of acute confusional state - DELERIUMS
D - Drugs and Alcohol (Anti-cholinergics, opiates, anti-convulsants, recreational)
E - Eyes, ears and emotional
L - Low Output state (MI, ARDS, PE, CHF, COPD)
I - Infection
R - Retention (of urine or stool)
I - Ictal
U - Under-hydration/Under-nutrition
M - Metabolic (Electrolyte imbalance, thyroid, wernickes
(S) - Subdural, Sleep deprivation
Delirium management
Optimise environment:
Provide a calm, quiet environment.
Keep inside lighting appropriate for the time of day.
Plan for uninterrupted periods of sleep at night.
Help the person keep a regular daytime schedule.
Encourage self-care and activity during the day.
TREATMENT OF UNDERLYING CAUSE
the 2010 NICE delirium guidelines advocate the use of haloperidol or olanzapine
Minimise risk of self harm or harm to others with appropariate supervision (1:1, 2:1)
Delerium management specifically in Parkinsons
management can be challenging in patients with Parkinson’s disease, as antipsychotics can often worsen Parkinsonian symptoms
careful reduction of the Parkinson medication may be helpful
use lorazepam rather than haloperidol
if symptoms require urgent treatment then the atypical antipsychotics quetiapine and clozapine are preferred
DSM 5 criteria for delerium
- Due to another medical condition
- Substance intoxication
- Substance withdrawal
- Delirium due to multiple eiteologies
- Medication related
Further specifiers:
Time: Acute - hours/days Persistent: weeks/months
Level of activity:
Hyperactive (increased psychomotor activity - e.g. myocolonus)
Hypoactive (psychomotor retardation)
Mixed (fluctuations between both
Highest prevelance of delirium
In increasing order:
Post repair of fractured hip
Post CABG
Nursing homes
ICU elderly
Terminally ill patients
Clinical course of delerium
Abrupt of acute onset - within days
Fluctuation in symptom severity:
Waxinag and waning, worse at night, may result in diagnostic uncertainty
Clinical course of delirium
Abrupt of acute onset - within days
Fluctuation in symptom severity:
Waxinag and waning, worse at night, may result in diagnostic uncertainty
Symptoms of hyperactive delrium?
Acting disorientated
Anxiety
Hallucinations
Rambling
Rapid changes in emotion
Restlessness
Cognitive defects
Symptoms of hyperactive delirium?
Acting disorientated
Anxiety
Hallucinations
Rambling
Rapid changes in emotion
Restlessness
Cognitive defects
Symptoms of hypoactive delirium?
Apathy
Decreased responsiveness
Flat affect
Laziness
Withdrawal
Cognitive defects
Delirium vs depression vs dementia
Delerium: abrupt, fluctuating, hours to weeks, alertness increased or decreased, activity increased or decreased, attention impaired, orientation impaired
Dementia: slow and incidious, usually stable daily course, lasts years, clear conciousnes, alertness normal, acitivty variable, attention usually normal and orientation is impaired
Depression: Variable onset, stable daily course, variable length, conciousness is clear, alertness normal, acitvity is variable, attention is usually normal, orientation is normal
How might you investigate an acute confusion?
Capillary Blood Glucose
CT head
FBC
LFT
TSH, B12, Folate
RPR
ABG
Levels of any drugs if appropriate (e.g. digoxin)
Urine dip +/- culture
MRI brain (focal neyroloigcal signs, head trauma, no clear cause found)
ECG
EEG (usually generalised slowing, low voltage fast activity in alcohol or sedative hypotonic withdrawal)
Cardiac enzymes
HIV
CXR
ANA RF CRP
Donepezil adverse effects?
is relatively contraindicated in patients with bradycardia
adverse effects include insomnia
Management of the non-cognitive symptoms of dementia?
NICE does not recommend antidepressants for mild to moderate depression in patients with dementia
antipsychotics should only be used for patients at risk of harming themselves or others, or when the agitation, hallucinations or delusions are causing them severe distress
Pharmacological management of Alzheimer’s disease?
First line: acetylcholinesterase inhibitors (donepezil, galantamine and rivastigmine) as options for managing mild to moderate Alzheimer’s disease
Second line: memantine (an NMDA receptor antagonist) - reserved for
- Pts with moderate Alzheimer’s who are intolerant of, or have a contraindication to, acetylcholinesterase inhibitors
- as an add-on drug to acetylcholinesterase inhibitors for patients with moderate or severe Alzheimer’s
- monotherapy in severe Alzheimer’s
Non-pharmacological management of Alzheimer’s disease
NICE recommend offering ‘a range of activities to promote wellbeing that are tailored to the person’s preference’
NICE recommend offering group cognitive stimulation therapy for patients with mild and moderate dementia
other options to consider include group reminiscence therapy and cognitive rehabilitation
What is Alzehimer’s disease?
Alzheimer’s disease is degenerative condition of the brain that leads to memory loss and ultimately global impairment of brain function.
Most common form of dementia
Risk factors for development of Alzheimer’s disease?
increasing age
family history of Alzheimer’s disease
(5% of cases are inherited as an autosomal dominant trait)
mutations in the amyloid precursor protein (chromosome 21), presenilin 1 (chromosome 14) and presenilin 2 (chromosome 1) genes are thought to cause the inherited form
apoprotein E allele E4 - encodes a cholesterol transport protein
Caucasian ethnicity
Down’s syndrome
Macroscopic pathological changes in Alzheimer’s?
widespread cerebral atrophy, particularly involving the cortex and hippocampus
Microscopic pathological changes in Alzheimer’s?
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
Biochemical pathological changes in Alzheimer’s?
there is a deficit of acetylcholine from damage to an ascending forebrain projection
Neurofibrillary tangles in AD
- paired helical filaments are partly made from a protein called tau
- tau is a protein that interacts with tubulin to stabilize microtubules and promote tubulin assembly into microtubules
- in AD are tau proteins are excessively phosphorylated, impairing its function