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Medicine Phase 2a Neuro > Dementia > Flashcards

Dementia Flashcards

1
Q

6CIT: 6 questions to asses brain function

A 
What year is it?
What month is it?
Give an address with 5 parts (John, Smith, 42, High, St, Bedford)
Count 20-1
Say months of year in reverse
Repeat address
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2
Q

Diagnostic tests of Alzheimer’s disease

A

Structure (MRI or CT)
Pathology - non-invasive (amyloid and tau imaging)
Function-brain networks

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3
Q

Define dementia

A

A syndrome caused by a number of brain disorders (e.g. Alzheimer’s) which cause memory loss, difficulties with thinking, problem-solving or language as well as difficulties with activities of daily living

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4
Q

Revision question:

How would you make a clinical diagnosis of epilepsy

A

From history, there needs to be at least 2 unprovoked seizures occurring > 24hrs apart to DIAGNOSE EPILEPSY

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5
Q

Types of dementia

A

Alzheimers (50%)
Vascular (25%)
Lewy-body (17%)
Fronto-temporal

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6
Q

What is the most common cause of dementia

A

Alzheimers disease

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7
Q

Pathophysiology of Alzheimers disease

A

Accumulation of beta-amyloid peptide, a degradation product of amyloid precursor protein, results in progressive neuronal damage, neurofibrillary tangles, increases in the number of amyloid plaques and the loss of ACh.
Degenration of the cerebral cortex (with cortical atrophy)

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8
Q

Risk factors of Alzheimers

A 
Down's syndrome due to increased APP gene load
Familial gene associations
Hypothyroidism
Previous head trauma
Family history of Alzheimer's disease
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9
Q

Examples of familial gene associations for Alzheimer’s disease

A

Amyloid precusor protein (APP) - chromosome 21
Presenilin-1 (chromosome 14)
Presenilin-2 (chromosome 1)
Apolipoprotein E4 (ApoE4) alleles - chromosome 19

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10
Q

Signs and symptoms of Alzheimers disease

A 
Amnesia
Disorientation
Changes in personality
Decreasing self care
Apraxia
Agnosia
Aphasia
Lexical anomia
Paranoid delusions
Depression
Wandering
Aggression
Sexual disinhibition
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11
Q

Investigations of Alzheimers disease

A

Mini Mental State Examination
Addenbrooke’s Cognitive Examination (ACE-III)
Bloods - FBC, U&Es, LFTs, TFTs, CRP, ESR, glucose, magnesium, phosphate, VDRL, HIV, serology, vitamin B12 and folate levels, blood culture
ECG, lumbar puncture, CXR, CT scan, MRI scan, SPECT
Histology

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12
Q

3 main findings on histology of Alzheimers

A

BAT
Beta amyloid plaques
decreased Acetylcholine
neurofibrillary Tangles

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13
Q

Complications of Alzheimers

A 
Amnesia
Increased risk of infection
Dysphagia
Urinary incontinence
Increased risk of falls
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14
Q

Treatment of Alzheimers

A

Memantine
Donepezil
Rivastigmine

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15
Q

How does Memantine work?

A

inhibits glutamate by blocking N-methyl-D-asparate (NMDA) receptors

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16
Q

How does Donepezil work?

A

Acetylcholinesterase inhibitor

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17
Q

How does Rivastigmine work?

A

Acetylcholinesterase inhibitor

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18
Q

What is second most common cause of dementia

A

Vascular dementia

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19
Q

Aetiology of Vascular dementia

A

Caused by infarcts of small and medium sized vessels in the brain
Brain damage due to cerebrovascular disease (major stroke, multiple unrecognised strokes or chronic changes in smaller vessels)
Genetic association with cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL) on chromosome 19

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20
Q

Vascular dementia - follows a deteriorating stepwise progression. What are the 3 types

A

Vascular dementia following stroke
Multi-infarct dementia following multiple strokes
Binswanger disease following microvascular infarcts

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21
Q

Signs and symptoms of vascular dementia

A 
Follows a deteriorating stepwise progression
Amnesia
Disorientation
Changes in personality
Decreasing self care
Depression
Signs of UMN lesions e.g. brisk reflexes
Seizures
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22
Q

Investigations of vascular dementia

A

Mental state examination ACE-III
Bloods - FBC, U&Es, LFTs, TFTs, CRP, ESR, glucose, calcium, magnesium, phosphate, VDRL, HIV serology, vitamin B12 and folate levels, cholesterol levels, vasculitis screen, syphilis serology, ECG, lumbar puncture, CXR, CT scan, MRI scan, SPECT

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23
Q

Treatment of vascular dementia

A

Dietary advice
Smoking cessation
Treat DM and hypertension
Aspirin

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24
Q

Complications of vascular dementia

A

Significant co-morbidity e.g. cardiovascular disease and renal disease

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25
Q

What is the third most common cause of dementia

A

Lewy-body dementia

26
Q

Which dementia is associated with Parkinsons

A

Lewy-body dementia

27
Q

Causes of Lewy-body dementia

A

Associated with Parkinson’s disease

Avoid antipsychotic drugs in these patients

28
Q

Signs and symptoms of Lewy-body dementia

A

Triad of:

  1. Parkinsonism - bradykinesia, gait disorder
  2. Hallucinations - predominantly visual hallucinations, usually of animals and people
  3. Disease process follows a fluctuating course
29
Q

Investigations of Lewy-body dementia

A

Mental state examination ACE-III
CT scan, MRI scan, SPECT scan
Histology

30
Q

What is found on histology of Lewy-body dementia

A

ApoE genotype Lewy bodies
Ubiquitin proteins
Alpha-synuclein

31
Q

Treatment of Lewy-body dementia

A

AVOID ANTIPSYCHOTICS - causes hypersensitivity to neuroleptics
Levodopa - may be used to treat Parkinson’s symptoms but these may worsen psychotic symptoms

32
Q

Complications of Lewy-body dementia

A 
Neuroleptic hypersensitivity
Autonomic dysfunction
Fluctuating blood pressure
Arrhythmias
Urinary incontinence
Dysphagia
Increased risk of falls
33
Q

What is Fronto-temporal dementia

A

Specific degeneration/atrophy of the frontal and temporal lobes of the brain
Mixed dementia
Parkinsons dementia*

34
Q

Causes of fronto-temporal dementia

A

Genetic association with chromosome

17q21-22 and tau 3 gene mutations

35
Q

Signs and symptoms of fronto-temporal dementia

A 
Amnesia
Disorientation
Changes in personality
Decreasing self care
Mutism
Echolalia
Overeating
Parkinsonism
Disinhibition
36
Q

Investigations of fronto-temporal dementia

A

Mini Mental state examination
ACE-III
CT scan, MRI scan, SPECT scan
Histology (depends on subtype)

37
Q

Subtypes of fronto-temporal dementia

A

Microvascular type - microvacuolation
Motor neurone disease type - histological changes like MND
Pick type - widespread gliosis, no microvacuolation

38
Q

Treatment of fronto-temporal dementia

A

Currently none

Only supportive treatment avaliable

39
Q

Complications of fronto-temporal dementia

A

Increased risk of falls

Increased risk of infection

40
Q

Other less common types of dementia

A 
Huntingtons dementia
Creutzfeldt-Jakob disease (CJD)
HIV
Vit B12 deficiency
Syphilis
Wilsons disease
Dementia pugilistica (seen in boxers)
41
Q

What is Wilsons disease

A

Autosomal recessive condition where copper accumulates within the tissue

42
Q

Cause of Huntingtons dementia

A

Complication of Huntington’s disease (an autosomal dominant condition where theres a defective gene on chromosome 4)
Causes uncontrollable choreiform movements and dementia

43
Q

Signs and symptoms of Huntingtons dementia

A 
Uncontrollable choreiform movements
Depression
Irritability
Anxiety
Psychosis
Obsessive compulsive behaviour
44
Q

Investigations of Huntingtons dementia

A

Genetic testing (diagnostic)

45
Q

Treatment of Huntingtons dementia

A

No cure
Treat symptoms:
Chorea - an atypical antipsychotic agent
Obsessive compulsive thoughts and irritability - selective serotonin reuptake inhibitors (SSRIs)

46
Q

Complications of Huntingtons dementia

A

Dysphagia

Increased risk of falls and/or infection

47
Q

What is Creutzfeldt-Jakob disease (CJD)

A

Caused by prions
Progressive and without cure
(Also variant Creutzfeldt-Jakob disease (vCJD) which has earlier death)

48
Q

Signs and symptoms of Creutzfeldt-Jakob disease (CJD)

A 
Rapidly progressive dementia (4-5 months)
Amnesia
Disorientation
Changes in presonality
Depression
Psychosis
Ataxia
Seizures
49
Q

Investigations of Creutzfeldt-Jakob disease (CJD)

A

EEG - triphasic spikes seen
Lumbar puncture (LP) - for 14-3-3 protein
CT scan
MRI scan

50
Q

Treatment of Creutzfeldt-Jakob disease (CJD)

51
Q

Complications of Creutzfeldt-Jakob disease (CJD)

A

Increased risk of infection
Coma
HF
Respiratory failure

52
Q

Prevention of dementia

A

Healthy behaviours
Smoking cessation, good diet, physical activity and low alcohol
Engaging in more than 6 leisure activities lowers risk of dementia
Education, occupation, premorbid IQ and mental activities decreases risk

53
Q

Support avaliable in treatment of dementia

A
  • Socially active - talking to family and friends
  • Cognitively active - cognitive stimulation programmes, board games etc.
  • Specialist memory service
54
Q

Medication that could be given in dementia

A

Acetylcholinesterase inhibitor in Alzheimer’s to increase ACh e.g. ORAL DONEPEZIL or ORAL RIVASTIGMINE
Blood pressure control to reduce further vascular damage, particularly in vascular dementia such as ACE-inhibitors e.g. RAMIPRIL

55
Q

Differential diagnosis of dementia

A

Substance abuse, hypothyroidism, space-occupying intracranial lesions, Huntington’s

56
Q

Clinical presentation of Alzheimers

A

Insidious onset with steady progression over years
Short-term memory loss is usually the most prominent early symptom
Subsequently there is slow disintegration of the personality and intellect, eventually affecting all aspects of cortical function
Decline in:
language (difficulty naming and in understanding what is being said)
visuospatial skills
apraxia (impaired ability to carry out skilled motor tasks)
agnosia (failure to recognise objects e.g. clothing, people and places)

57
Q

Clinical presentation of Vascular dementia

A
  • Stepwise deterioration with declines followed by short periods of stability
  • History of TIA’s and or strokes
  • Evidence of artheropathy
58
Q

Clinical presentation of Lewy-body demetia

A
  • Fluctuating cognition with pronounced variation in attention and alertness
  • Prominent or persistent memory loss may not occur in the early stages
  • Impairment in attention, frontal, subcortical and visuospatial ability is often prominent
  • Depression and sleep disorders occur
  • Visual hallucinations
  • Parkinsons e.g. slowing and rigidity is common
  • Loss of inhibitions
59
Q

What are Lewy-bodies

A

Abnormal aggregates of protein that develop inside nerve cells, contributing to Parkinson’s disease (PD)

60
Q

Describe the MMSE

A

Mini Mental State Examination (MMSE) commonly used to screen for cognitive function:
Score of 25 or above out of 30 is normal, 18-24 = mild/moderate impairment
Score of 17 or below indicates serious impairment

61
Q

Diagnosis - generally

A

History - assess cognitive function by asking various questions
MMSE
Exclusion of rare treatable causes of dementia (substance abuse, vitamin
B12 deficiency, hypothyroidism) should be considered Blood tests: FBC, liver biochemistry, thyroid function tests and vitamin B12 and folate measurement
Neuropsychology
Brain CT in younger patients or those with atypical presentation MRI - to see extent of atrophy
Brain function can be assessed:
Energy and blood supply via PET & SPECT scanning
Brain networks via functional MRI

Medicine Phase 2a Neuro (28 decks)

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