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MRCPsych Part B > Old Age Psychiatry > Flashcards

Old Age Psychiatry Flashcards

1
Q

Which anti-depressants are most likely to contribute to delirium?

A

Tricyclics - especially tertiary amine anti-depressants

Other notable medications include benzodiazepines (typically longer acting i.e. diazepam), opioids and anti-cholinergic medications

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2
Q

Outline the use of different cognitive drugs for dementia?

A

For Alzheimers:
- Donepezil, Rivastigmine & Galantamine –> mild to moderate Alzheimers

  • Memantine –> for moderate if unable to tolerate the above agents/contraindicated or add in for severe

For Dementia with Lewy Bodies:
- AchE-I (Rivastigmine or Donepezil) for mild - severe
- Galantamine if above not tolerated
- Memantine if AchE-I not tolerated/contraindicated

Only consider AchE-I or memantine for vascular dementia if Alzheimer’s, Parkinson’s or DLB present too

Do not offer AchE-I for frontotemporal dementia

Do not offer AchE-I for cognitive impairment due to multiple sclerosis

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3
Q

Outline the severity of dementia according to MMSE

A

Mild: 21 - 26

Moderate: 10 - 20

Severe: < 10

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4
Q

When is aspirin indicated in vascular dementia?

A

Only with established vascular disease - recent Cochrane review of RCTs showed that aspirin does not prevent vascular dementia in same way as it does in strokes, PVD and MI

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5
Q

Outline the mechanisms of Acetylcholine-esterase inhibitors?

A

Donepezil - selective and reversible –> metabolised through CYP2D6 and CYP3A4 (minor)

Rivastigmine - non-competitive and reversible (also works by inhibiting butlycholine-esterase) – > little involvement of CYP enzymes

Galantamine - competitive and reversible (also a nicotinic receptor antagonist) –> metabolised through CYP2D6 and CYP3A4

n.b memantine antagonises NMDA receptors (also 5HT3 antagonist) –> memantine is primarily metabolised by the kidneys

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6
Q

Name some risk factors for Charles Bonnet syndrome?

A

Advancing age
Social isolation
Visual impairment
Early cognitive impairment
Sensory deprivation

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7
Q

Outline the ICD-11 diagnosis for dementia?

A

Marked impairment in two or more cognitive domains relative to the expected level for their age and pre-morbid functioning

n.b commonly involves impairment of memory however it is not only this and other domains such as executive functioning, attention, language, psychomotor speed, visuoperceptual and visuospatial capabilities may be affected

Requires:
- Information from the informant, individual or clinical observation
- Substantial impairment in memory performance as demonstrated by neuropsychological testing

The symptoms result in impairment in personal, social or occupational functioning

The symptoms are not better accounted by disturbance of consciousness or altered mental state

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8
Q

What scale may be used to assess for depression in dementia?

A

Cornell scale - 30 minutes and involves and interview with the caregiver and the patient (not self-report)

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9
Q

How does the mneumonic DEMENTIA help to screen for reversible causes of dementia?

A

Drugs

Emotions (depressed)

Metabolic (hyper/hypothyroidism, hyper/hypoparathyroidism, Cushing’s,
Addison’s, Wilson’s disease, Hashimoto’s encephalitis)

Eyes or ears decline

Normal pressure hydrocephalus

Tumour

Infection (Syphillis,
Whipple’s disease,
sarcoidosis, AIDs, meningitis)

Anaemia (B12/Folate)

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10
Q

What is the first line agent recommended by NICE for use in delirium?

A

Haloperidol

  • note Maudsley guidelines recommend lorazepam if alcohol/hypnotic withdrawal otherwise to avoid as can worsen

Other agents not recommended by Maudsley are:
- Donepezil
- Rivastigmine
- Trazodone
- Sodium valproate

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11
Q

Outline the clinical features of normal pressure hydrocepalus?

A
  • Symmetrical broad based and mild high stepping gait
  • Urinary incontinence (late sign) - before this there may be urge, frequency and incontinence
  • Cognitive decline - slowness of mental processes and motor function (as it is a subcortical dementia there is difficulties in sustaining attention, switching attention and planning)
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12
Q

What are the causes of NPH?

A

50% identified cause with mechanical blockage - infection, trauma, subarachnoid haemorrhage

50% idiopathic

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13
Q

Name some investigations for NPH?

A

CT scan - increase in lateral ventricle size

CSF tap - withdraw 40-50ml then assess gait afterwards (low sensitivity and low predictive value)

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14
Q

What is the treatment of normal pressure hydrocephalus?

A

Ventriculo-peritoneal shunt

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15
Q

Name some features of chronic subdural haematoma?

A

Headache
Drowsiness
Altered GCS
Confusion

  • fluctuating picture similar to subcortical dementia
  • CT may be -ve in first 3-4 weeks
  • Treatment is neuro-surgery with burr hole or steroids (dexamethasone)
    –> risk of surgery is re-bleeding and seizures
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16
Q

What is the risk of getting Alzheimer’s in a first degree relative of a proband?

A

15 - 19%

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17
Q

Name some risk factors for the development of Alzheimer’s disease?

A

Protective:
- Apolipoprotein E2 allele
- NSAIDs
- Higher pre-morbid intelligence
- Oestrogen

Risk factors:
- Down’s syndrome
- Decline in

  • Genetics:
    –> Apolipoprotein E4 allele (chromosome 19) - one copy increases risk by 3 x // two copy increases risk by 8 x
    –> Presenilin 2 (chromosome 1) - associated with early onset
    –> Presenillin 1 gene (chromosome 14) - associated with early onset
    –> beta-APP gene (chromosome 21)
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18
Q

Name some neuroimaging findings seen in Alzheimer’s

A

CT - cortical atrophy particularly over parietal and temporal lobes, dilatation of the 3rd ventricles which correlates with cognitive impairment

MRI: Reduced grey matter, hippocampus, Amygdala and temporal lobe volumes

SPECT: Characteristic reduction in blood flow in temporal and parietal regions (SPECT could
distinguish specific features of dementia of Alzheimer type at early stages and frontal lobe
dementia)

PET: Reduced blood flow and metabolism in temporal and parietal regions

MRS: Abnormal synthesis of membrane phospholipids early in the disease

Amyloid PET imaging – shows deposition of beta amyloid even in preclinical stages of dementia

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19
Q

What language difficulties may be present in Alzheimer’s?

A

Expressive and receptive aphasia

Lexical anomia - word finding difficulty

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20
Q

Outline some symptoms of Alzheimer’s?

A

Apraxia - inability to perform coordinated motor tasks

Impaired executive function

Impaired visuospatial abilities

Amnesia - initially short term memory before long term events (disorientation particularly time)

Agnosia - inability to recognise peripheral sensory information, parts of the body or people

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21
Q

Which AchE-I is preferred in Parkinson’s dementia or Alzheimer’s with Parkinson’s disease?

A

Rivastigmine

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22
Q

How long is Donepezil’s half life?

A

70hrs - this means it can be taken as once daily dosing

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23
Q

When may AchE-I be contraindicate?

A

Severe cardiac conduction difficulties or severe asthma

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24
Q

Why is memantine termed a disease modifying drug?

A

Because due to its non-competitive antagonism of PCP site of NMDA receptor it is meant to stabilise neurotoxic glutamatergic transmission

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25
Q

What alternative treatments have been talked about for Alzheimer’s?

A

Gingko biloba - Cochrane review found evidence unconvincing

Tacrine - rarely used due to risk of hepatotoxicity

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26
Q

Name some poor risk factors associated with Alzheimer’s disease?

A

Male
Onset < 65 years
Parietal lobe damage
Depression
Cognitive deficits such as apraxia
Absence of misidentification syndromes

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27
Q

Name 3 types of vascular dementia?

A
  • Cognitive deficits following a single stroke (often with midbrain/thalamic infarcts)
  • Multi-infarct dementia: stepwise deterioration and may be stability between episodes (minor infarcts)
  • Progressive small vessel disease (Binswanger’s disease): multiple infarcts of small perforating vessels leads to lacunae formation (distinct infarcts) or leukoariasis
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28
Q

What is the Haschinki’s scoring system used for?

A

To try and identify likelihood of vascular dementia
- Scores > 7 means likely
- Scores < 4 unlikely

  • Abrupt onset (2)
  • Stepwise progression
  • Fluctuating course (2)
  • Normal confusion
  • Relative preservation of personality
  • Depression
  • Somatic complaints
  • Emotional incontinence
  • History of hypertension
  • History of strokes
  • Evidence of associated
    atherosclerosis
  • Focal neurological symptoms (2)
  • Focal neurological signs (2)
  • Unless marked, each item scores one
    point. Score < 4 unlikely, scores > 7
    likely to be vascular dementia
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29
Q

How does Biswanger’s present?

A

Biswanger’s disease - subcortical dementia: slowing of thought, slow intellectual decline, decreased short term memory, often gait disturbances and dysarthria. Aphasia and apraxia tend to only happen in complicated Biswanger’s

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30
Q

Is CADASIL autosomal dominant?

A

Yes

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31
Q

In Lewy Body Dementia where do Lewy Bodies tend to be found in the brain?

A

Brainstem
Subcortical Nuclei
Limbic Cortex (cingulate, enterohinal cortex, amygdala)
Neocortex (frontal, temporal, parietal)

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32
Q

What are the consensus criteria for the diagnosis of LBD?

A

Central - cognitive impairment sufficient to interfere with ADLs

Core features (two for probable, one for possible)
- Fluctuating cognition with profound variations in attention and alertness
- Well formed visual hallucinations that are recurrent
- Parkinsonism (seen in 70%)

Other supportive features:
- Repeated falls due to autonomic dysfunction
- Transient disturbances of consciousness
- Neuroleptic sensitivity (often worsens parkinson’s symptoms)
- Systematised delusions
- Hallucinations in other modalities

n.b short term memory may be relatively spared. Cognitive testing may reveal deficits in attention and visuospatial

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33
Q

What neuroimaging changes may be seen in LBD?

A

Relative sparing of medial temporal lobes

Enlargement of ventricles

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34
Q

What is drug treatment for LBD?

A

Choline-esterase inhibitors (Rivastigmine) treat cognitive symptoms as well as psychiatric delusions/hallucinations

35
Q

What are the 3M’s of subcortical diseases?

A

Movement
Mood
Mentation (cognition)

36
Q

When may a diagnosis of Parkinson’s dementia be given > LBD?

A

If Parkinson’s motor symptoms have been present > 12 months prior to the onset of dementia

37
Q

Name some typically observed cognitive deficits in Parkinson’s

A
  • Slowness of thought (bradyphrenia)
  • Executive deficits (planning, sequencing, set shifting)
  • Apraxia
  • Dysphasia

Less verbal memory impairment than Alzheimer’s

Alexia, agraphia, anomia and acalculia are also less pronounced.

38
Q
A
39
Q

Name some features associated with paraphrenias?

A

Women > Men
Socially isolated
Visual/hearing impairment
Less likely to be married
Less likely to have children
Associated with CVA changes on brain imaging

A paraphrenia is a late onset schizophrenia esque presentation that is not due to an organic illness

39
Q

How can SPECT scanning differentiate between Parkinson’s and LBD?

A

Parkinson’s dementia shows greater caudate involvement

40
Q

In Progressive Supranuclear Palsy how do individuals fall?

A

Backwards (tend to tilt their hips backwards - Parkinson’s individuals tend to fall forwards)

Other features are:
- Extra-pyramidal symptoms
- Cognitive dysfunction
- Supranuclear - vertical gaze dysfunction

It typically arises in the 6th decade of life and there are no cures

41
Q

What is a DAT scan also known as?

A

FP-CIT-Spect

42
Q

What one blood test should be conducted before and during Agomelatine treatment?

A

LFTs - has been linked to reports of hepatic failure

43
Q

How long should anti-depressants be continued in elderly patients?

A

At least 2 years

n.b SSRIs can increase the risk of falls

44
Q

Name some triggers for TGA?

A

Physical exertion
Pain
Stress
Cold weather
Sexual intercourse

45
Q

How do Lewy Body and Frontotemporal dementia differ on SPECT?

A

LBD - posterior deficits
Frontotemporal - anterior deficits

46
Q

What is the prevalence of Alzheimer’s dementia amongst the UK population?

A

1.3%

47
Q

What is the familial risk of Alzheimer’s?

A

3 - 4 x the background risk in those with a first degree relative

48
Q

At 6 months post-discharge what percentage of elderly patients have persistent delirium?

A

20%

49
Q

In post-65 year old UK population what is the proportion that are affected by dementia?

A

5% (out of over 80s it is 20%)

50
Q

What percentage of old age suicides visit their GP in the preceding week?

A

50%

51
Q

Atypical antipsychotics increase the risk of vascular events in the elderly by a factor of?

A

2

52
Q

The microtubule associated protein (MAPT) is located on which chromosome?

A

17 - this mutation has been linked to fronto-temporal dementia

53
Q

What is the ten year conversion rate of MCI to Alzheimer’s?

A

40%

For patients over the age of 75 - 10% may develop after a year

54
Q

How is schizophrenia categorised according to…

  • Early onset
  • Late onset
  • Very late onset
A

Early onset < 40 years
Late onset 40 - 60 years
Very late onset > 60 years

55
Q

Which personality disorders are associated with suicide in the elderly?

A

Avoidant and Ankastic

56
Q

In familial cases of Pick’s disease (occurs in 50%) what is the mode of inheritance?

A

Autosomal dominant
- May be through 17q21-22 or tau gene changes

57
Q

Name a scoring system that summarises performance on ADLs in the elderly?

A

Barthel index

58
Q

Outline some features of very late onset Schizophrenia?

A

Associated with:
- Social isolation
- Sensory impairment
- Female
- Visual hallucinations
- Higher likelihood of tardive dyskinesia

Less associated with:
- Affective blunting
- Thought disorder

59
Q

Outline the types of frontotemporal dementia?

A

Behavioural variant (Pick’s disease)
- Most common type
- Men > Women preponderance
- Onset 45 - 65 years
- Memory unaffected in early years
- Personality affected first includes: Emotional blunting; Coarsening of social behaviour; Disinhibition;
Apathy or restlessness; Aphasia (non-fluent aphasia)
- On CT and MRI changes includes frontal and temporal lobe atrophy with sparing of superior temporal gyrus “Knife blade atrophy”
- Pick cells are present on microscopy - swollen and pink on H and E staining

Semantic dementia (Semantic variant primary progressive aphasia/PPA)
- 9-12% of cases
- Anterior temporal lobe (L > R)
- Presents with fluent speech but word finding difficulties (anomia), speech comprehension impairment (single word and phrases), repetitive speech and reduced word comprehension

Non-fluent primary progressive aphasia
- 13-35%
- Slow effortful speech, apraxia of speech, word finding difficulties
- Spared single word comprehension
- Changes seen in dominant frontal operculum, premotor area, supplementary motor area, anterodorsal insula

60
Q

How common is depression in dementia?

A

Some studies estimate 25% prevalence

61
Q

Outline some features of vascular depression?

A

Less guilt and worthlessness
Apathy
Psychomotor retardation
Late age of onset
Poor executive functioning

62
Q
A
63
Q

Name some neurological signs of cerebrovascular disease

A

Rigidity, akinesia, brisk reflexes/clonus, pseudobulbar palsy

64
Q

Which depression scale is good for geriatric patients as it avoids somatic symptom questions?

A

Geriatric depression scale - score > 5 indicates depression

Takes 15 minutes to complete

65
Q

What depression scale may be able to be used in deaf patients?

A

BASDEC

Brief assessment schedule depression cards

  • Cards with true or false that patients answer to
  • Has been used in liaison psychiatry
66
Q

How may cognitive symptoms of depression differ in early onset compared to old age depression?

A

Early onset - episodic memory difficulties (temporal lobe)

Late onset - cognitive impairments commonly seen –> more frequent are difficulties of attention or executive functioning (frontal lobe tasks)

67
Q

How may pseudodementia differ from actual dementia?

A

Pseudodementia:
- Can often give onset of symptoms with more precision

  • More complaints or awareness of cognitive difficulties - in dementia patients may not notice or try to hide impairment
  • Attention and concentration less affected than in Dementia
  • No nocturnal accentuation of difficulties as seen in dementia
  • Faster progression
  • History of psychiatric impairment
  • Memory poor for both recent and remote events (only recent in dementia)
68
Q

What is the prevalence of late onset mania?

A

0.4%

1.4% in younger adults
More female preponderance 2F : 1M

69
Q

What dose of Lithium may be chosen for prophylaxis in old age bipolar disorder?

A

0.4 - 0.6 mmol/L

70
Q

For secondary mania from strokes which hemisphere typically causes infarcts?

A

Right side

71
Q

How does late-onset schizophrenia differ to early-onset schizophrenia?

A
  • Less negative symptoms
  • Less family history
  • Less thought disorder
  • More persecutory delusions
  • More visual hallucinations
  • Better pre-morbid functioning
  • Associated with sensory impairment
  • Associated with social isolation
  • Better response to antipsychotics
  • More likely to get tardive dyskinesia (5-6 x more likely)
72
Q

Name some contraindications for disulfiram?

A
  • Hypertension
  • Cardiovascular disease
  • Stroke
73
Q

When is grief delayed?

A

Avoidance of painful symptoms within 2 weeks of loss

74
Q

When is grief chronic?

A

If continued > 6 months

75
Q

Outline the phases of “normal” grief?

A

Normal grief reaction

Phase 1 - Shock and protest – includes numbness, disbelief and acute
dysphoria

Phase 2 Preoccupation – includes yearning searching and anger

Phase 3 – disorganization – includes despair and acceptance of loss

Phase 4 – resolution

76
Q

What are the common psychological changes seen in Huntington’s disease?

A

Apathy and irritability (apathy more common)

77
Q

Which antipsychotics have a high risk of orthostatic hypotension?

A

Risperidone + Clozapine

78
Q

What is tower of London/Hanoi test?

A

A frontal lobe and executive function test used in the elderly

Participants are required to move three cards in a set number of moves

79
Q

Gingko may increase the risk of…

A

increase the risk of bleeding

80
Q

Which patients may be at risk of progressive multifocal leukopathy?

A

If immunosuppressed - AIDS or long term immunosuppression for cancer, lymphoma or sarcoidosis

Symptoms are clumsiness, cognitive impairment, problems with coordination and visual impairment, speech disturbances and sometimes personality changes

Very quickly progressing to life threatening disability and death over weeks to months

81
Q

What are the EEG changes in…

a) Huntingtons
b) Hepatic encephalopathy
c) CJD
d) HSV encephalitis

A

a) loss of alpha then flattened trace
b) Triphasic waves against a background slowing
c) Generalised period 1-2hz sharp waves
d) Every 1-3 seconds discharges - with variable focal waves temporal areas

82
Q

Name some SE of memantine

A

Headache, confusion, somnolence, hypertension and rarely hallucinations and confusion

83
Q

Name some dementias that are

A) Cortical
B) Sub-cortical
C) Cortico-subcortical
d) Multi-focal

A

A) Alzheimers, Picks Disease, NPH
B) Huntington’s, Parkinson’s Disease, HIV-associated dementia, Binswanger’s disease
C) Lewy Body Dementia
D) CJD

MRCPsych Part B (13 decks)

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