Ageing: AD, VD, LBD, FTD, PD, ET, MSA, PSP Flashcards

1
Q

Alzheimers
-epidemiology
-genetic, environmental risk factors
-pathophysiology

A

MOST COMMON DEMENTIA
Genetic
-sporadic, late - APOE4
-inherited - APP, PSEN1, 2
-Downs

Environment
-brain/SC injury, CVA
-drugs, alcohol, vitamin deficiency, hypoglycemia
-HIV, HSV, syphilis

Pathophysiology
-cerebral atrophy, esp hypothalamus - wide sulci, narrow gyri, large ventricles
-extracellular AMYLOID PLAQUE, intracellular TAU TANGLES

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2
Q

Alzheimers
-presentation
-management specific to AD
-drugs to avoid

A

Gradual cognitive decline
-poor short term memory
-confusion, increased anxiety

Later
-agnosia, aphasia, apraxia, amnesia
-hallucinations, depression, delusions, disinhibition

NORMAL GAIT, POSTURE

Drug
1st line - cholinesterase inh
-donepezil, rivastigmine, galantamine
2nd line - NMDA ant
-memantine

Avoid antidepressants
Antipsychotics only to be used if risk to self/others

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3
Q

Vascular dementia
-epidemiology
-pathophysiology
-risk factors

A

2nd most common dementia
-CV risk factors damage brain => synergy with AD

Vascular risk factors
-stroke, TIA, AF, CVD
-HTN. DM, high cholesterol, smoking

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4
Q

Vascular dementia
-presentation
-investigations. diagnosis

A

Stepwise progression in cognitive decline
-focal neuro deficits
-attention, concentration
-memory, gait, speech, emotional disturbances

Diagnostic criteria
-presence of cognitive decline that interferes with ADLs, confirmed with clinical neuropsych exam
-CV disease - confirmed with neuro signs/brain imaging
-relationship between decline and CVD - onset of dementia within 3 months of stroke/abrupt or fluctuating stepwise decline

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5
Q

Vascular dementia
-management
-supportive

A

If comorbid with AD/LBD - same as AD

Vascular optimisation to slow progression

Tailored to individual
-cognitive stimulation programmes, music/arts therapy
-home adaptations
-physio for movement difficulties
-SALT input for speech and swallow

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6
Q

Differentials you want to rule out in cognitive decline

A

Drugs
-medication review (BZ, opioids, anticholinergic, antipsychotics, antidepressants, alcohol)

Endocrine
-hypothyroid, Addisons

Mental
-depression

Nutritional
-B12 (ataxia, memory loss, gait abnormalities)
-Thiamine (Wernicke’s enceph, Korsakoff psychosis)

Trauma
-SDH

Malignancy
-brain tumour

Infection
-syphilis

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7
Q

Lewy body dementia
-epidemiology
-pathophysiology
-presentation
-diagnosis, investigation
-management

A

3rd most common dementia
-ASYNUCLEIN in SNPC

Fluctuating cognitive impairment => Parkinsonian
-visual hallucinations
-falls, gait instability
-incontinence, constipation. RBD

Clinical diagnosis - confirm with DATSCAN

Management - same as AD
-avoid neuroleptics
Poor response to Parkinsonian meds

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8
Q

Frontotemporal dementia
-epidemiology
-pathophysiology
-types, presentation

A

Most common in U65
-atrophy of FTL, neurofibrillary tangles

50% - Behavioural variant - execuctive cognitive dysfunction
-early disinhibition, loss of empathy, impulsivity
-hyperorality, dietary change
-other cognitive areas

50% - Language variant
Semantic dementia - problems with matching names to objects
Non fluent aphasia - slow hesitant speech
-difficulty finding right words
-grammatical errors, difficulty understanding complex sentences

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9
Q

Frontotemporal dementia
-management

A

Do not use cholinesterase inh (memantine)

Pharmacological management when conservative measures have failed
-irritability - lorazepam
-compulsions - SSRI (citalopram)

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10
Q

Parkinsons Disease
-epidemiology
-genetic, encironmental risk factors

A

Men, 65+
Most idiopathic
Genetic - PARK1 gene overexpressed
Environmental - unclear

Degeneration of dopaminergic neurons in SNPC => Lewy body formation

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11
Q

Parkinsons Disease
-presentation (prediagnosis)

A

Constipation
Autonomic dysfunction => OH, urogenital dysfunction
Anosmia, visual changes
REM behaviour disorder
Depression+anxiety
Face-like mask
Micrographia

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12
Q

Parkinsons Disease
-presentation (early and late)

A

Early - classic unilateral triad
-bradykinesia - shuffling. difficulty initiating mv, reducing arm swing
-cogwheel rigidity
-pillrolling resting tremor - worse when stressed/tired, improves with voluntary mv

Advanced - on off dyskinesia
-flexed posture, dystonias, freezing
-gait instability, falls
-dysarthria, dysphagia
-dementia
-psychosis, hallucinations

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13
Q

Basal ganglia thalamocortical loop
D1
D2

How does dopamine relate to the resting tremor

A

D1 => activation promotes mv via direct path
D2 => activation inhibits mv inhibitions via indirect path

Low D => inactivity of D1, overactivity of D2
Increased ACh => resting tremor

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14
Q

Parkinsons Disease
-diagnosis, investigations
-differentials you want to rule out

A

CLinical diagnosis but can be confirmed by DATSCAN

Degenerative
-MSA, PSP

Reversible
-drug induced (metoclopramide, haloperidol, prochlormethazine)
-acute onset motor, rigidity and resting tremor not common => improved with procyclidine
-stroke, head trauma, encephalitis, Wilsons

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15
Q

Parkinsons Disease
-management

A

1st line if motor symptoms affecting QOL
-levopoda + carbidopa/benserazide
-progression => levepoda induced freezing/chorea or dystonia

Adjuncts
-dopamine agonists - bromocriptine, cabergoline, ropinrole
-MAOBinh - selegiline
-COMTinh - entecapone
-domperidone/ondasetron - antiemetic

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16
Q

SE of
-levepoda
-dopamine agonist

A

Dyskinesia
Psychosis, sedation
Impulsive behaviour
Dry mouth, palpitations, postural hypotension

DA
-hallucinations, impulse control issues, sedation

17
Q

Essential tremor
-epidemiology
-presentation
-how does this differ from PD
-management

A

40+ progressive common neurological condition
-bilateral postural tremor - worse when arms outstretched
-improved with alcohol and rest
-intention tremor worse on voluntary mv, stress
-tremulous voice, head tremor
Mx - propanolol

PD
-unilateral symptoms
-resting tremor improved with voluntary mv, worse with stress/fatigue
-no change with alcohol
-no head tremor
-low pitched voice

18
Q

Multiple system atrophy
-pathophysiology
-presentation

A

Alpha synuclein in multiple brain regions

Parkinsonism
Cerebellar signs
AUTONOMIC FAILURE
-erectile dysfunction
-postural hypotension
-atonic bladder

No definitive tests exist
Bloods
-FBC, U&E, CRP, LFT - infection/metabolic
-HIV, syphilis serology
-Copper study - Wilsons

MRI

NOT RESPONSIVE TO LDOPA
Midodrine for orthostatic hypotension
Desmopressin for incontinence

19
Q

Progressive supranuclear palsy
-pathophysiology
-presentation

A

Tau aggregation in multiple areas

Parkinsonism
Cognitive impairment
Postural instability and falls
IMPAIRMENT OF VERTICAL GAZE

Poor response to LDOPA

20
Q

Normal pressure hydrocephalus
-pathophysiology
-presentation
-investigations
-manegement

A

Reversible cause of dementia
-reduced CSF absorption

Gradual onset of
-Urinary incontinence
-Dementia
-Gait abnormality

Hydrocephalus with ventriculomegaly without/out of proportion to sulcal enlargement

Ventriculoperitoneal shunting