Dementia Flashcards

1
Q

define dementia

A

syndrome due to a disease of the brain usually chronic and progressive present for more than 6 months

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2
Q

what functions of the brain can be affected in dementia?

A

multiple higher cortical functions including memory, thinking, orientation comprehension, learning capicty, language and judgment

ESPECIALLY:
o Memory - especially learning and retrieval of new info
o Cognitive abilities - deterioration in judgement, thinking and language
o Emotional control - emotional lability, apathy, irritability, wandering, disinhibition

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3
Q

if you suspect dementia but there is clouding of consciousness, what is it?

A

delerium

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4
Q

what are the differentials for dementia?

A
D rugs/delirium
E motions/depression (pseudodementia)
M etabolic disorder (glucose or thyroid)
E eye/ear problems (e.g. deafness)
N utritional disorders (e.g. B12/folate deficiency)
T umours, toxins, trauma
I nfections
A lcohol, arteriosclerosis
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5
Q

In what order do you get symptoms in alzheimers?

A
memory loss
impaired thinking
language impairment
deterioration in personal functioning
disturbed personality and behaviour
perceptual abnormalities
motor impairments
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6
Q

How is memory affected in alzheimers?

A

short-term > long-term

leads to impaired learning and disorientation (time first, then place and person)

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7
Q

How is thinking impaired in alzheimers?

A

poor judgement, decreased fluency, concrete thinking and impaired abstraction, lack of ability to plan, delusions

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8
Q

how is language impaired in alzheimers?

A

expressive and receptive aphasia and dysphasia

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9
Q

how is personal functioning affected in alzheimers?

A

deterioration in occupational and social functioning and AoDL/ self-care

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10
Q

how is personality and behaviour affected in alzheimers?

A

euphoria and lability or apathy and irritability. disinhibition which can lead to aggressive and inappropriate behaviour, inattention and distractibility, obsessive and stereotyped behaviours.

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11
Q

How are perceptions altered in alzheimers?

A

visual and auditory agnosia, visuospatial difficulties, body hemineglect, prosopagnosia (can’t recognise faces), illusions, hallucinations, cortical blindness

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12
Q

how is the motor function altered in alzheimers?

A

Apraxia, spastic paresis, urinary incontinence

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13
Q

What are primary causes of dementia?

A

Alzheimer’s disease (most common)
Dementia with Lewy bodies and PD
Pick’s disease and other frontotemporal dementias
Huntington’s disease

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14
Q

what are secondary causes of dementia?

A
Vascular
Infective (AIDs, lyme disease)
Inflammatory (SLE)
Neoplastic
Metabolic (cardiac, hepatic and renal failure)
Endocrine (thyroid)
Toxic (alcohol)
Traumatic
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15
Q

What investigations should you do in dementia?

A
  • A physical examination should be carried out to identify any underlying causes of dementia and any complications of dementia such as malnutrition, burns, or falls.
  • Baseline bloods as standard. Other investigations on case by case basis
  • Detailed neurocognitive testing by a clinical psychologist can be helpful in identifying cognitive impairments and in confirming a diagnosis.
  • Dr Ostler scans anyone under 75 or if something Hx raises a question  MRI/CT and can use PET scan
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16
Q

What neurocognitive testing can you do?

A

o MMSE/AMTS/MOCA for screening and monitoring
 MMSE <24 = suggestive of dementia
 Only need to know AMTS!
o Addenbrooke’s Cognitive Exam (ACE – III) is what they use in memory clinics (<88/100)

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17
Q

What blood tests should you do in a confusion screen and why?

A

• FBC
o Infection, anaemia, increased MCV (macrocytic anaemia caused by B12/folate deficiency)
• LFTs
o Liver failure, alcohol abuse
• U&Es
o Kidney failure can cause cognitive impairment?
• INR
o If on warfarin and concerned about bleeds from fall/head injury
• TFTs
o Confusion more common in hypothyroid states
• Calcium
o Hypercalcaemia can cause confusion/delirium (bones, moans, psychotic groans
• B12/folate  can cause confusion (alcohol use, leukaemias, dietary deficiency/ malabsorption)
• Glucose
o Hypoglycaemia = common cause of confusion
• Syphilis
o Not often necessary, rare but overlooked
• HIV
o Dementia common in AIDS

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18
Q

what other investigations should you do in a confusion screen?

A

CT HEAD – stroke, lesion, bleeds from fall/trauma, cerebral atrophy, widening of the sulci or gyri, dilated ventricles (could be hydrocephalus), atrophy of medial temporal lobe in Alzheimer’s
(MRI recommended by NICE but CT usually sufficient)

CXR – as part of sepsis screen – rule out pneumonia, bronchial CA w/cerebral mets

BLOOD CULTURES – if appropriate

URINE DIPSTICK/CULTURE – v common cause in elderly, but positive dipstick w/o clinical signs is not enough to diagnose urosepsis as a cause of delirium (look this up)

URINE DRUG TEST – if illicit drugs considered possible cause of confusion/psychosis

EEG – characteristic 3Hz ‘spike and wave’ in prion disease

LP – normal pressure hydrocephalus, herpes encephalitis

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19
Q

What is the very general management in dementia?

A
  • Secondary dementias may be reversible
  • But usually aim of management is to improve/maintain QOL for patient and carer(s).
  • This involves treating the SYMPTOMS AND COMPLICATIONS of dementia, addressing FUNCTIONAL problems, addressing SOCIAL problems, and providing EDUCATION and SUPPORT for carers.
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20
Q

What are important considerations in the MDT approach in treating dementia? (general info)

A

• Personal hygiene & nutrition
• Functional abilities can be maintained and even improved by a regular daily routine, environmental modifications, and graded assistance.
• The patient should be reoriented and reassured, and encouraged to partake in physical and mental activity.
• Memory aids such as clocks, calendars, notebooks, and photographs, and reality orientation and reminiscence therapies may also be helpful, particularly in the early stages of the disease.
• To aid sleep, sleep hygiene, Horlicks or milky drinks, sedation at night, sedative antidepressants e.g. trazadone (may increase risk of falls), change to another AChEi, try NDMA blocker e.g. memantine.
• Telecare to stop wandering.
• If dementia is diagnosed must inform DVLA
• Social problems:
o Isolation, accommodation (?specialist home)
o Financial/legal matters e.g. power of attorney
• Carer education and support

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21
Q

What classes of drug can you use in dementia?

A

Acetylcholinesterase inhibitors
NMDA receptor antagonist (memantine)
Other possible drugs (use sparingly and infrequently - benzos, SSRIs, Antipsychotics (quetiapine)

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22
Q

Whats the most common cause of dementia?

A

• AD = most common cause of dementia - over 50% of all cases (850,000 people in UK)

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23
Q

what is the neuropathology of alzheimers?

A

• Selective neuronal and synaptic loss leads to neurochemical abnormalities (notably decreased ACh) and symmetrical cortical atrophy that is initially more pronounced in the medial temporal and parietal lobes.
• Extracellular senile plaques and intracellular neurofibrillary tangles are seen in normal ageing, but they are more numerous in AD and they are closely related to the degree of cognitive impairment.
• Senile plaques consist of a core of beta-amyloid surrounded by filamentous material.
• Neurofibrillary tangles consist of coiled filaments of abnormally phosphorylated microtubule-associated protein tau (note that tau is also found in Pick bodies)
• Decreased ACh
o Due to degeneration of the cholinergic neurons of the basal forebrain
• Other histopathological findings include glial proliferation, granulovascular degeneration, and Hirano inclusion bodies (intracellular aggregates of actin).

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24
Q

What are risk factors for alzheimers?

A
Age
Female sex (2:1)
FH
Down’s syndrome
Head injury
Dialysis (aluminium containing dialysis fluids)
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25
Q

what are protective factors for alzheimers?

A
Healthy and engaged lifestyle
High educational achievement (does this just delay
diagnosis?
NSAIDs
HRT
Vit C Vit E
Statins
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26
Q

what is the genetic link in alzheimers?

A

• E4 allele of apolipoprotein E
o Chromosome 19
o Risk factor for common, sporadic, late-onset form
• E2 is protective
• APP (amyloid precursor protein) mutations
o Chromosome 21
o AD inherited, early onset
• PSEN1/PSEN2 also associated with familial presenile dementia

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27
Q

what is the life expectancy after diagnosis of alzheimers?

A

8 years

28
Q

what are the 5 As of alzheimers?

A
  • AMNESIA
  • APHASIA
  • AGNOSIA
  • APRAXIA
  • ASSOC BEHAVIOUR
29
Q

What is the medication therapy for alzheimers?

A

o Mild/moderate = AChEi - donepezil, galantamine, rivastigmine
o Severe AD = memantine monotherapy
o For patients already on AChEi consider adding memantine if progresses
• Pharmacological therapy should only be given by specialist of GPs with special expertise

30
Q

What is the second most common form of dementia?

A

vascular dementia

31
Q

what is mixed dementia?

A

evidence of both AD and vascular dementia

32
Q

what is the neuropathology of vascular dementia?

A
  • Focal disease may result from single, or more commonly, from multiple thrombotic or embolic infarcts.
  • Note that focal and diffuse disease often co-exist.
33
Q

What are the risk factors in vascular dementia?

A

• CV disease and risk factors
o Older age, male, smoking, DM, HTN, hypercholesterolaemia, valvular disease, hypercoagulation disorders, alcohol)
• Cardiovascular disease
• Cerebrovascular disease

34
Q

what are the signs and symptoms and differences to alzheimers in vascular dementia?

A

• Vascular dementia classically has an abrupt onset and step wise progression.
• Clinical features are variable and depend on the location of the infarcts, but commonly:
o Personality changes
o Labile mood
o Preserved insight (until late)
• UNEQUAL DISTRIBUTION of defectits (some v affected, others spared)
• Significant comorbidity leads to a shorter mean life expectancy than in Alzheimer’s disease

35
Q

What is the treatment in vascular dementia?

A

• Lifestyle changes to reduce CV risk factors (prevent further decline)
• Social care/support, OTs,
• ANTICOAGULATE to prevent further CVAs
• Statins for high cholesterol
• Antiplatelet e.g. aspirin, clopidogrel
• Ensure diabetes is under control
• AChEi or memantine will not affect cognitive decline in vascular dementia!
o But can be used if suspected comorbid AD/PD/DLB

36
Q

what is the epidemiology of lewy body dementia?

A

overlaps with Alzheimer’s disease and parkinsonian dementia.
• It is the third commonest cause of dementia, and accounts for about 10-15% of all cases.
• Onset 50-85
• Slightly more M>F
• Lewy bodies = abnormal aggregates of protein that develop inside nerve cells

37
Q

What is the neuropathophysiology in LBD?

A

• Both subcortical and cortical structures involved
• Associated neuronal loss leading cholinergic deficit and other chemical abnormalities
o Only minimal cortical atrophy
• Senile plaques may be present but nurofibrilliary tangles are not are marked fearutre
• Aetiology (cause) unclear

38
Q

What is the difference between LBD and PD?

A

• Lewy bodies present in both
• PD – lewy bodies are in basal ganglia
• DLB – lewy bodies are in cortical areas
o Esp cortical layers V and VI of temporal lobe, cingulate gyrus and insular cortex
• If parkinsons symptoms present first its parkinson’s dementia, if memory symptoms appear first then parkinsons Sx, it is DLB

39
Q

What is the classical triad of symptoms in LBD?

A

o Marked fluctuations in cognitive impairment and alertness.
o Vivid visual hallucinations and other psychotic symptoms (70/80%)
o Parkinson-like movement symptoms e.g. rigidity & lack of spontaneous movement

40
Q

What are other symptoms in LBD?

A

• REM sleep disorder  vivid dreams w/body movement
• Frequent faints, falls, dizziness
• Neuroleptic sensitivity
o Severe neuroleptic sensitivity affects up to 50% of the LBD patients who are treated with traditional antipsychotic medications
o Characterized by worsening cognition, sedation, increased or possibly irreversible acute onset parkinsonism, or symptoms resembling neuroleptic malignant syndrome
o Can be fatal
• Memory loss may not be a marked feature in early stages
• Life expectancy from diagnosis = 6 years

41
Q

what is the investigations for parkinsonian dementia?

A

formally diagnosed by a DaT scan (Ioflupane I 123 injection). Dopamine transporter scan (used in diagnosis of PD)

42
Q

what is the treatment for PD?

A

• Not going to cure but may help managing symptoms (shock)
• Before drug treatment
o Evaluate physical health problems that could be provoking behavioural disturbance
o Look at current medications
• Drug treatment
o AChEi
 Rivastigmine or donepezil
 Only consider galantamine if others not tolerated
o Memantine
 If AChEi not tolerated/CI
o Antipsychotics
 Avoid unless absolutely necessary (NEUROLEPTIC SENSITIVITY)
 Quetiapine (atypical) preferred, or clozapine
 Traditional (e.g. haloperidol) should be avoided

43
Q

What is the epidemiology of frontotemporal dementia?

A

5% of all cases of dementia.
• F>M
• peak age of onset = 45–60 years
• Aetiology unclear. Familial forms exist and are more common in people of Scandinavian descent.

44
Q

what is frontotemporal dementia also called?

A

Pick’s disease

45
Q

What is the neuropathology of FTD?

A

selective, often asymmetrical, ‘knife-blade’ atrophy (radiology feature) , neuronal loss, and gliosis affecting the frontal and temporal lobes.
• There are characteristic ‘ballooned’ neurons called Pick cells and tau-positive neuronal inclusions called Pick bodies.
• There are, however, no senile plaques or neurofibrillary tangles as in Alzheimer’s disease.

46
Q

What are the typical signs and symptoms of FTD?

A

o early and prominent personality/behaviour changes
 early decline in social interpersonal conduct, emotional blunting, regulation of personal conduct – social disinhibition, neglect of responsibilities, loss of interest in personal hygiene
o eating disturbances
o mood changes
o early loss of insight
o expressive dysphasia
o cognitive impairment, language abnormalities, and motor signs.
 See everything as “black & white” – can’t see the grey
• All concrete thinking, struggle with abstract
• Can appear bit like autism
 Problems with problem solving
• Executive impairment = the range of symptoms of frontal lobe damage
o early preservation of episodic memory and spatial orientation, disinhibiton, hyperorality, stereotyped behaviour and emotional unconcern.

47
Q

What is the treatment for FTD?

A

• Stop drugs which may be exacerbating memory problems or confusion (anticholinergics, CNS drugs).
• SSRIs may be helpful
o For loss of inhibitions, compulsions and overeating
• Atypical antipsychotics used occasionally where there are severe behavioural problems such as agitation and psychosis.
• Levodopa/carbodopa may be tried when there are Parkinsonian symptoms.
• AChEi may worsen so do not use

48
Q

What is the prevalence and onset of huntingtons disease?

A
  • 5-10 per 100 in caucassions

* Onset 30s-40s but in some cases it can be in childhood or old age

49
Q

What is the neuropathology in huntingtons?

A

• Abnormal Huntington protein leads to the degeneration of the neurons, notably in the caudate nucleus and putamen in the cerebral cortex
• Degeneration in the caudate nucleus and putamen leads to movement dsorders
o Degeneration in the cerebral cortex leads to dementia
• Due to anticipation each generation age of onset increases
o For mcq, cause = more than 36 repeats of CAG in hungtington gene chromosome 4

50
Q

What are the classical signs and symptoms of huntingtons?

A
  • Choreiform (dance like movements)
  • Schizophrenia like psychosis
  • Early depression and behavioural disturbances
  • Insight often retained to until late - suicide rate high 10%
51
Q

Give other dementias and amnesic syndromes.

A
normal pressure hyrdocephalus
HIV related dementia
Hypothyroidism
chronic subdural haematoma
neurosyphillis 
CJD
52
Q

How does normal pressure hydrocephalus present?

A

o Accumulation of CSF = large ventricles, ut no increases in ICP
o Triad = gait disturbance and ataxia, dementia, urinary incontinence (in that order)

53
Q

How does CJD present?

A

o Neurodgenerative disease which result from deposition of prion protein in the form of amyloid sheets
o Sx  rapidly progressive dementia, myoclonic jerks, constellation of pyriamidal, extrapyrimaldal and cerebellar signs
o EEG changes  3Hz ‘spike and wave’

54
Q

What is the epidemiology of delerium?

A
  • Delirium (acute confusional state or acute brain syndrome) is common in hospitalised patients and particularly in young children/the elderly.
  • It occurs in ~40% of >65s during hospitalisation.
55
Q

What is the definition of delerium?

A

an aetiologically non-specific syndrome characterised by concurrent disturbances of consciousness and attention, perception, thinking, memory problems, psychomotor behaviour, emotion, and the sleep wake cycle, that is of transient and fluctuating intensity

56
Q

what is the onset like in delerium?

A

quick - hours to days

57
Q

What do you need for a definite diagnosis of delerium?

A
  1. IMPAIRED CONSCIOUSNESS, difficulty focusing and inattention
  2. GLOBAL DISTURBANCE OF COGNITION:
    a) Impairment of abstract thinking and comprehension and in some cases transient delusions
    b) Impairment of immediate recall and recent memory, with remote memory being relatively spared
    c) Disorientation in time and, if severe, in place and person
    d) Perceptual abnormalities including distortions, illusions and hallucinations (usually visual)
  3. PSYCHOMOTOR DISTURBANCES - Hyper/hypo-activity and unpredictable shifts from one to the other
  4. Disturbance and in severe cases, reversal of SLEEP-WAKE CYCLE
  5. EMOTIONAL DISTURBANCES e.g. depression, anxiety or fear, irritability, euphoria, apathy
58
Q

What are possible causes of delerium?

A

PINCH ME
• Pain
• INfection
o Any, but commonly UTI - Remove unnecessary catheters ( top 3 - UTI, pneumonia and cellulitis)
• Constipation
• Hydration/hypoxia
o Dehydration
o Urinary retention
o Electrolyte imbalance – esp hyponatraemia and hypercalcaemia
o Renal/hepatic failure
• Medication
o Commonest cause
o Alcohol, opiates, sedatives, anticholinergics, diuretics, steroids, digoxin, anticonvulsants, lithium, TCAs, levodopa, polypharmacy
o Also WITHDRAWAL from alcohol, benzos or others
• Environment
o Confusion from unfamiliar/distressing surroundings

Other = hypoglycaemia, DKA, hypo/hyperthyroidism, Cushings, stroke, head injury, stress, sleep deprivation, urinary retention, encephalitis, bleed, tumour

59
Q

What are the questions in an AMTS?

A
  1. Age
  2. DOB
  3. 42 West Street
  4. Year
  5. Time (nearest hour)
  6. Place
  7. Identify two people
  8. Dates of WW1
  9. Current monarch
  10. Count back from 20
  11. Recall address
60
Q

What are your differentials in delerium?

A
  • Delirium superimposed on dementia
  • Dementia
  • Substance misuse
  • Affective disorder
  • Psychotic disorder
61
Q

What investigations should you do in delerium?

A
  • Daily assessment of cognitive and mental status
  • If delirium suspected  full psych hx, MSE, physical exam, delirium screen and COLLATERAL Hx
  • Confusion screen  as above
62
Q

How can you prevent delerium?

A

 Routine cognitive assessment
 Rationalising the drug chart
 ORIENTATE PATIENT - ensure sensory aids e.g. spectacles and hearing aids are in place.
o Also clocks, calendars, familiar items
 Encouraging fluids and nutrition and correcting any electrolyte imbalances and nutritional deficiencies.
 Encouraging mobilisation.
 Encouraging family members to spend time at the bedside.
 Nursed in consistent, comfortable and familiar environment

63
Q

When should tranquilisers be used in delerium and what is the drug of choice?

A

extreme agitation or psychosis

 Haloperidol is the drug of choice (except if the delirium is caused by alcohol or benzodiazepines, in which case it is a benzodiazepine) because of its minimal anticholinergic side
(remember stroke risk in dementia patients)

Doses should be kept to a minimum to avoid precipitating alternating episodes of agitation and sedation and stopped as soon as it is felt no longer indicated

64
Q

What are possible complications of delerium?

A
o	Prolonged hospital stay and increased risk of nosocomial (hospital) infections.
o	Accelerated cognitive decline.
o	Aspiration pneumonia. 
o	Fluid and electrolyte imbalance.
o	Malnutrition.
o	Falls.
o	Injuries.
o	Decreased mobility
o	Pressure sores
65
Q

What is the mortality in delerium?

A

high, both in hospital and after discharge  one year mortality has been estimated to be as high as 50%.