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Year 3 > Memory Impairments: Dementia, Delirium And Old Age Psychiatry > Flashcards

Memory Impairments: Dementia, Delirium And Old Age Psychiatry Flashcards

1
Q

What is dementia?

A

Syndrome characterised by progressive irreversible global cognitive deficits that impact on activities of daily living , which are divided into degenerative, intracranial and infective causes.

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2
Q

What are the common clinical features of dementia?

A

Behaviours fall into cognitive, psychiatric or behavioural:
-> Cognitive impairment initially affecting episodic short term memory that progresses to apraxia, agnosia and dysphasia

-> Personality change, characterised by social withdrawal, disinhibition and loss of executive functioning and self-care. There is rigid and stereotyped routines, loss of adaptability and an overreaction to minor stresses (Catastrophic reaction)

-> Anxiety, depression, Hallucinations and delusions.

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3
Q

What worsens progression of dementia?

A

PINCH ME acronym:
Pain
Infection
Constipation
Hydration
Medication
Environmental changes

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4
Q

Which medication is licensed for the alleviation of agitation?

A

Risperiodne
-> Ideally limited

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5
Q

What is sundown syndrome?

A

Most commonly occurs in Alzheimer’s disease where there is increased confusion, agitation and confusion at night time that can lead to issues sleeping.

To manage this, a regular routine and time spent outdoors in daylight hours is best and keeping the home well-lit at night with reduced stimulation from screens.

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6
Q

What are the common principles of managing dementia?

A

->Assessment of the diagnosis of dementia, and the individual’s social function
->Improving cognitive enhancement through pharamcological treatments
->Addressing anxiety, depression and insomnia
Improving functional management through ->maximising mobility, aiding communication and encouraging independence
->Social management through accommodation arrangement and financial matters like power of attorney and health executor

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7
Q

What is part of the normal ageing process?

A

Reduction in short-term episodic memory, with psychomotor slowing however verbal comprehension is maintained. There is a reduction in performance IQ.

The brain undergoes a reduction in size and increase in subarachnoid space and ventricualr size. Neurofibrilary tangles form but are confined to the hippocampus and Lewy bodies to the substantia nigra.

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8
Q

What is mild cognitive impairment?

A

Decline in one or more cognitive domains which is subjectively and objectively observable and cannot be attributed to psychiatric conditions, however this does not impair an individual’s activities of daily living. There is a higher risk of dementia,

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9
Q

What is the screening for dementia?

A

->Excluding and treating any reversible causes of cognitive impairment
->Ruling out depression
->Taking a history from both the patient, family and carers
->Completing a mental state examination and cognitive assessment
->Blood test
->CT scan
->Functional assessment of ADL, ideally within the home
-> Social assessment of home, need for care

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10
Q

What is assessed in a blood test for dementia?

A

Full blood count
Biochemical screen
Blood glucose
B12 and folate levels

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11
Q

Which drugs can induce a pseudodementia?

A

Benzodiazepines
Opiates
Anticholinergic medication is the most commonly prescribed

-> These drugs cause a degree of cognitive impairment that is significant in vulnerable individuals or those with brain pathology

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12
Q

Which psychiatric causes can be mistaken for dementia?

A

Depression
Psychosis
Schizophrenia

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13
Q

What is the clinical presentation of depression in the elderly to differentiate from dementia?

A

Shorter presenting history with a previous Hx of depression
Patient will complain of memory problems
Worse symptoms in the morning
Mental state examination highlights concentration problems, unattempted questions and a variable performance

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14
Q

What is the history for dementia compared to depression?

A

Longer and progressive insidious history with no precipitating event
Less likely to report memory problems
Presents with worse symptoms in the evening
Mental state examination will show mood swings, consistent performance and an attempt to answer all questions

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15
Q

Which metabolic causes can be mistaken for dementia?

A

Uraemia
Electrolyte imbalance, such as Calcium or magnesium
Hepatic encephalopathy

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16
Q

Which endocrine causes can be mistaken for dementia?

A

Hypothyroidism
Hyperthyroidism
Cushing’s disease
Addison’s disease

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17
Q

Which vitamin deficiencies can mimic dementia?

A

B12
Folate
Thiamine (B3)

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18
Q

What is the most common form of dementia?

A

Alzheimer’s disease is a degenerative disease of the brain with an onset of 7-10 years characterised by:
-> Extracellular amyloid senile plaques in the hippocampus, amygdala and cerebral cortex

-> Neurofibrillary tangles with a buildup of phosphorylated tau protein in the cortex, hippocampus and substantia nigra

-> Cerebral atrophy in the medial temporal lobes

-> Reduction in acetylcholine due to a deficiency of Chat

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19
Q

What are the features of early Alzheimer’s disease?

A

Failing memory, disorientation in time and reduced efficiency in ADL and changes in behaviour

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20
Q

What are the features of middle stage Alzheimer’s disease?

A

Intellectual deterioration with aphasia/apraxia/agnosia
Impaired visuospatial skills and executive dysfunction
Depression/aggression

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21
Q

What are the features of late-stage of Alzheimer’s disease?

A

Fully dependent on family/carers
Physical deterioration with incontinence, gait abnormalities and extra-pyramidal signs, spasticity and seizures
Bedridden

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22
Q

What are the risk factors for Alzheimer’s disease?

A

-> Increasing age
-> Women
-> Caucasian
->Head injury
->Vascular risk factors like smoking and hypertension and diabetes
->Down’s syndrome
->Apolipoprotein E4 allele
->Social isolation

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23
Q

What is the epidemiology of Alzheimer’s disease?

A

Risk increases in old age
Incidence is the same for men and women
Mean survival is 4-8 years old

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24
Q

What is the management of Alzheimer’s disease?

A

Occupational therapy to address ADL
Cognitive rehabilitation
Providing carer support
Pharmacological therapies to slow rate of progression

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25
Q

What is the intervention for mild to moderate Alzheimer’s disease?

A

Acetylcholinesterase inhibitors
->Donepezil and rivastigmine

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26
Q

What is the intervention for severe Alzheimer’s disease?

A

Memantine is recommended, which is a partial NMDA receptor antagonist that protects from glutamate-mediated excitotoxicity

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27
Q

What is Lewy Body dementia?

A

Progressive dementia characterised by alpha-synuclein deposits in the neocortex, substantia nigra and hippocampus and there is associated neuronal loss. It is characterised by:
-> Fluctuating cognition
-> Visual hallucinations
-> Parkinsonian features like bradykinesia, rigidity, must start at the same time as cognitive symptoms.

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28
Q

What are the supportive features of Lewy-Body dementia?

A

Sensitivity to antipsychotics

Reduction in dopamine in SPECT imaging

REM sleep disturbances

Orthostatic hypotension, falls, syncope, and incontinence

29
Q

What is the epidemiology for Lewy body dementia?

A

Affects more men than women
Age is 50-83 years old, with age of death being 68-92 years old

30
Q

What are the investigations for Lewby Body dementia?

A

CT scan shows relative sparing of medial temporal lobe and deep white matter lesions

Temporal lobe is relatively preserved

Reduced levels of presynaptic dopamine transporter

31
Q

What is the management for Lewy-Body dementia?

A

Acetylcholinesterase inhibitors used for treatment of non-cognitive symptoms like apathy and agitation

Avoid the use of antipsychotics which will worsen Parkinson’s symptoms

32
Q

What is Vascular dementia?

A

Second most common dementia, characterised by sudden stepwise deterioration due to small vessel disease which is typically caused by cerebral ischaemia, with deficits dependent on the affected region.

It is associated with risks for cardiovascular disease and affects men more than women, typically those aged 60-70 years old.

33
Q

What are the clinical features of vascular disease?

A

Sudden stepwise progression
Onset occurs often a stroke and has associated motor symptoms
Impairments occur in emotions, personality an dlanauage
Neurological impairments with rigidity, akinesia

34
Q

What is the intervention for vascular dementia?

A

-> Establish causative factors for disease
-> Medication such as aspirin and anticoagulants
->Screening for cardiovascular disease factors such as cholesterol, clotting, vasculitis and autoimmune conditions like rheumatoid factor
->ECG, Carotid artery Doppler ultrasound and MRI
->Establish causative factors
->Promote lifestyle changes

35
Q

What is frontotemporal dementia?

A

Second most common dementia with an age of onset after 53 that causes degeneration of the the frontal and temporal lobe involving tau proteins and the DNA binding protein TDP-43. There is stereotypical and repetitive and compulsive behaviour. Memory and visuospatial functioning is preserved in the early stages.

There is a significant family history and associated with autosomal dominant mutation.

36
Q

What is the most common subtype of frontotemporal dementia?

A

Behavioural variant caused by intracellular accumulation of tuna protein to form Pick bodies, which causes a progressive deterioration of behaviour and cognitive symptoms which include:
-> Disinhibition in food and sex, loss of social empathy,
-> Preference for sweet food
-> Compulsions and rituals
-> Cognitive symptoms of poor attention and executive dysfunction with decisions
-> Imaging will show assymetrical abnormalities of the contralateral temporal lobes

37
Q

What is primary progressive aphasia?

A

Disease of the temporal lobe affecting Wernicke’s area where there is fluent speech but impaired language function for meaning of words and finding words, and with disease progression behavioural variant dementia emerges.

38
Q

What is progressive non-fluent aphasia?

A

Effortful speech that is non fluent, caused by atrophy in Broca’s area.

39
Q

What is semantic dementia?

A

Fluent speech but loss of concept and meanings, and there is atrophy of the left temporal lobe over the right temporal lobe

40
Q

What is the management of frontotemporal dementia?

A

Occupational therapy
Physiotherapist
Speech and language therapy
Structured daily routine

41
Q

What is AMTS?

A

Abbreviated Mental Test score (AMTS) is a 10-point test for rapidly assessing elderly patients for the possibility of dementia.

42
Q

What is delirium?

A

A fluctuating disturbance of consciousness, global impairment of cognitive function and perception which develops acutely and is associated with behavioural abnormalities such as a disturbed sleep-wake cycle.

43
Q

What is the epidemiology of delirium?

A

Most common acute disorder in hospitals affecting in patients. Tends to affect high risk groups such as:
Elderly
Pre-existing dementia
Blind/deaf patients
Post-operative patients, especially cardiac
Burn victims
Alcohol and Benzodiazepine dependent

44
Q

What does NICE recognise as at risk groups for delirium?

A

Those aged over 65 years old
Pre-existing cognitive impairment
Current hip fracture
Existing severe illness that is at risk of deterioration

45
Q

Why does a hip fracture increase the incidence of delirium?

A

Prolonged surgery with a high risk of intraoperative trauma and blood loss that may induce hypoxia in brain cells.

46
Q

Which patient groups are at higher risk of delirium?

A

Stroke patients
Critical care patients
Hip fracture
Vascular surgery
Poly pharmacy
Renal impairment
Immobile patients

47
Q

What is the course of delirium?

A

Acute onset but gradual resolution of symptoms, that is slower in the elderly. Patchy amnesia may occur and there is a high risk of mortality and development of dementia.

48
Q

What are the clinical features of hyperactive delirium?

A

Global impairment of cognition and attention with disorientation in recent memory
->Psychomotor agitation
->Visual or auditory hallucinations
-> Changes in mood and behaviour
->Paranoid delusions
->Rambling or incoherent speech
-?Sleep deprivation and nocturnal worsening of symptoms, which is a modifiable risk factor for prevention of delirium

49
Q

What are the clinical features of hypoactive delirium?

A

Lethargic
Reduced mobility
Reduced appetite
Loss of interest in activities
Quiet and withdrawn

50
Q

What is the cause of delirium?

A

Multi factorial and includes:
-> Infective
-> Metabolic
-> Intracranial
-> Endocrine

51
Q

What are the infective causes of delirium?

A

UTI
Chest infection
Abscess
Endocarditis
Subacute bacterial endocarditis

52
Q

What are the metabolic causes of delirium?

A

Electrolyte disturbances, especially Ca2+ and Mg2+
Hepatic encephalopathy due to buildup of toxins
Uraemia
Cardiac failure
Hypothermia

53
Q

What are the intracranial causes of delirium?

A

Raised intracranial pressure from:
Head injury
Encephalitis
Metastatic tumour

54
Q

What are the endocrine causes of delrlium?

A

Vitamin deficiencies of B12, folate, B3 and B2
Diabetes
Hypoglycaemia
Disease of adrenal gland, pituitary, thyroid and parathyroid

55
Q

Which drugs can cause delirium?

A

Diuretics
Antihypertensives
Anticonvulsants
Digoxin
NSAIDs
Hypoxia

56
Q

What is the initial investigation for delirium?

A

Take history from patient and any family/carer for behaviour, drug use, oral intake and precipitating factors

Examine drug history since hospital admission

Check patient vital signs e.g blood pressure, heart rate, blood glucose and temperature

General multi-system examination

Focused investigation such as urinalysis, blood tests, sputum culture, thyroid function, chest x-ray

57
Q

What is the treatment for delirium?

A

Identify and treat underlying cause
Ensure effective communication and reorientation
De-escalation for distressed patients and if necessary, low dose short treatment with haloperidol

58
Q

What should be avoided in the treatment of delirium?

A

Avoid sedation unless necessary to mitigate risk to patient and help facilitate investigation and treatment

Antipsychotics should ideally be atypical quetiapine and avoid typical like haloperidol at the lowest possible dose

Reduce unnecessary noise in the environment

Antipsychotics in the elderly increase the risk of cardiac and neurological side effects

59
Q

What is the management for delirium?

A

Provide environmental and supportive measures
Create a stimulating environment with lighting, reducing unnecessary noise, correcting sensory impairment and mobilising patients
Optimise patient for hydration, nutrition, urination and pain control

60
Q

What are the clinical features of somatisation

disorder?

A
61
Q

What are the clinical features of depression in the elderly?

A

-> Severe psychomotor retardation and agitation
-> Cognitive impairment, especially with effortful tasks
-> Cotard’s syndrome, where they believe they do not exist, dead and are rotting
-> Depressive delusions about poverty and physical illness that are nihilistic in nature

Patient may present with somatic, anxiety or hypochondriacal complaints.

First line treatment is SSRIs at a low starting dose with gradual increases. For severe illness, ECT is reccomended as it does not present as a contraindication with dementia

62
Q

What are the features of pseudo dementia?

A

Exaggerated symptoms
Depressed mood with previous history of sepsis on
Low effort on relatively easy tasks
Effective response to anti-depressant medication

63
Q

What are the clinical features of somatisation disorder in the elderly?

A

Commonly associated with depression, neurotic personality and existing psychiatric illness.
Persistent thoughts/behaviours associated with the somatic symptom which generates a high level of anxiety

64
Q

What are the clinical features of anxiety in the elderly?

A

Patients in this group are less likely to report classical symptoms and this presents as:
Insomnia
Palpitations
Irritability
Loss of appetite
Fatigue
Muscle tension

65
Q

How does aging affect the pharmacokinetics of drug treatment?

A

Older people are more likely to engage with poly pharmacy due to co-morbidity which increases the risk of side effects and drug interactions and associated physiological changes so lower dose is required:

->There is an increased free drug levels and half life due to reduced body mass and lower albumin.
->There is reduced blood flow to the liver reducing drug metabolism
->There is reduced renal clearance that prolongs the cumulative effects of drugs and risk of toxicity
-> There is a reduced drug absorption due to lower gastric pH and mesenteric blood flow and motility

66
Q

How does the pharmacodynamics of drugs affect the CNS?

A

Reduction of
-> Cholinergic receptors in the brain
-> Dopapminergic cells in the basal ganglia
-> Noradrenaline levels
-> Increased sensitivity to sedatives due to fewer receptors

67
Q

What are the centres of support for older patients?

A

Primary care services such as GPs, health visitors and community nurses
Specialised old age psychiatry units
Outpatient mental health units or psychiatric day hospitals
Community psychiatric nurses that assess patients on referral from GPs and home support
Informal carers
Voluntary organisations such as charities
Residential and nursing care provided by local authorities such as nursing homes

68
Q

How is capacity assessed in older adults?

A

Mental capacity should always be presumed in adults regardless of indivudal factors like dementia diagnosis.
However it is important to assess the patient’s capacity for a specific procedure and to make personal welfare decisions. The patient’s capacity should be based on their ability to understand the information relevant, weigh it up, retain the memory and communicate their choice. The presence of a psychiatric illness should be evaluated for the influence on their decision.

Finally, it is important to gather information about the patient’s views when they had capacity or if they have a relative wit surrogate decision-making.

Year 3 (22 decks)

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