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Phase 3a > Neurology > Flashcards

Neurology Flashcards

1
Q

What is dementia?

A

Not a disease, but a general term for the impaired ability to remember, think or make decisions that impacts everyday activities

An acquired, progressive cognitive impairment involving one or more cognitive functions

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2
Q

What is Alzheimer’s disease?

A

A neurodegenerative disease that leads to the symptoms characteristic of dementia

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3
Q

What does Amyloid Precursor Protein do?

A

Help the growth and repair of the neuron

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4
Q

What is the pathophysiology of plaques in Alzheimer’s?

A

Amyloid Precursor Protein should be broken down by alpha and gamma secretase.

If it is broken down by beta and gamma secretase it creates insoluble amyloid beta. This is sticky and creates plaques just outside the neurons.

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5
Q

How do plaques affect brain function?

A
  1. Plaques can get between neurons which can affect neuron signalling
  2. They can also trigger an immune response which can cause inflammation damage neurons
  3. They can also deposit on blood vessels (amyloid angiopathy) increased risk of rupture
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6
Q

What is the pathophysiology of tangles in Alzheimer’s?

A

Tau protein in microtubules triggers kinase to attach phosphate to tau protein

Tau protein changes shape and stops supporting microtubules. Joins together to make neurofibrillary tangles.

Cells can’t signal as well and undergo apoptosis.

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7
Q

What happens as neurons die in the brain?

A

Gyri get narrower and sulci widen

Ventricles get larger

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8
Q

What percent of Alzheimer’s is sporadic?

A

90-95%

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9
Q

What is sporadic Alzheimer’s?

A

Genetic and Environmental risk factors

Apolipoprotein E ^ risk

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10
Q

What percent of Alzheimer’s is familial (early onset)?

A

5-10%

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11
Q

What is familial / early onset Alzheimer’s?

A

Dominant gene speeds progression

PSEN-1 or PSEN-2 genes

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12
Q

What is the effect of PSEN-1 or PSEN-2 mutation?

A

These genes affect gamma secretase, so APP is broken down in a way that encourages plaques

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13
Q

What is a risk factor for early onset Alzheimer’s?

A

Trisomy 21 - the gene responsible for producing APP is located on chromosome 21

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14
Q

How does Alzheimer’s progress?

A

Gradual progression as plaques and tangles build up

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15
Q

What are the symptoms of Alzheimer’s?

A

Loss of short term memory
Loss of language and motor skills
Loss of long term memory
Disorientation
Bed-ridden

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16
Q

How can Alzheimer’s be diagnosed?

A

Memory and cognitive assessments

History / changes in behaviour

Imaging

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17
Q

What is the management of Alzheimer’s?

A

Rivastigmine - cholinesterase inhibitor
Supportive treatments and care

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18
Q

What is vascular dementia?

A

Progressive loss of brain function caused by long term poor blood flow to the brain (typically because of a series of strokes)

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19
Q

What is the pathophysiology of vascular dementia?

A
  1. Cerebral artery atherosclerosis
  2. Carotid artery / heart embolization
  3. Chronic hypertension -cerebral arterioles sclerosis
  4. Vasculitis
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20
Q

What are some risk factors for vascular dementia?

A

Smoking
HTN
Diabetes
Hyperlipidaemia
Hyperhomocysteinaemia

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21
Q

What are the features of vascular dementia?

A

Progressive, STEPWISE, cognitive function impairment (affected cortical area dependant)

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22
Q

What symptoms might a person with vascular dementia of the frontal lobe experience?

A

Executive dysfunction

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23
Q

What symptoms might a person with vascular dementia of the left parietal lobe experience?

A

Aphasia
Apraxia
Agnosia

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24
Q

What is apraxia?

A

Inability to perform movements or tasks, even when they are understood

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25
Q

What is agnosia?

A

Unable to recognize and identify objects, persons, or sounds using one or more of their senses despite otherwise normally functioning senses

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26
Q

What symptoms might a person with vascular dementia of the right parietal lobe experience?

A

Hemineglect
Confusion
Agitation
Visuospatial difficulty
Constructional difficulty

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27
Q

What symptoms might a person with vascular dementia of the temporal lobe experience?

A

Anterograde amnesia (can’t form new memories)

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28
Q

What deficits due to subcortical infarcts might be experienced in vascular dementia?

A
  1. Focal motor signs
  2. Gait disturbance
  3. Urinary frequency / urgency
  4. Personality / mood change
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29
Q

How can vascular dementia be diangosed?

A
  1. Neuropsychological testing to detect cognitive impairment and domains involved
  2. MRI/CT will show multiple cortical, subcortical infarcts
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30
Q

What is the management for vascular dementia?

A

No cure, so treatment is vascular risk factor control to try and prevent further infarcts

Cholinesterase inhibitors

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31
Q

Name some drugs that can be given as vascular risk factor conttrol

A
  1. Antihypertensives
  2. Anti diabetic agents
  3. Statins
  4. Antiplatelet agents
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32
Q

What is Lewy Body dementia?

A

A neurodegenerative disease characterised by the presence of Lewy bodies (abnormal deposits of a protein called alpha-synuclein)

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33
Q

What are some features of LBD?

A

Progressive, fluctuating cognitive function impairment

Attention, executive, visuospatial functions. Memory affected later

Visual hallucination

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34
Q

What can happen in the later stage of LBD?

A

Motor symptoms mimic Parkinson’s disease

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35
Q

What are some other clinical features of LBD?

A
  1. REM sleep behaviour disorder and other sleep disturbances
  2. Autonomic dysfunction (syncope, urinary incontinence, postural drop)
  3. Falls (Parkinsonism)
  4. Neuroleptic sensitivity
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36
Q

How can LBD be diagnosed?

A

Exclude other dementia causes

Neuropsychological testing

DaTSCAN to show dopamine perfusion

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37
Q

What is the treatment for LBD?

A

No cure, medications to alleviate symptoms

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38
Q

How can Acetylcholinesterase inhibitors help in the treatment of LBD?

A

Reduce cognitive symptoms

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39
Q

How can dopamine analogues help motor symptoms in LBD?

A

Reduce motor symptoms

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40
Q

How can atypical neuroleptic agents help in the treatment of LBD?

A

Reduce psychotic features and persistent disabling hallucinations

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41
Q

Name three cholinesterase inhibitors

A

Donepezil
Rivastigmine Galantamine

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42
Q

Name two atypical antipsychotics that can be used in LBD treatment

A

Quetiapine
Clozapine

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43
Q

What is frontotemporal dementia?

A

Neurodegenerative condition of the frontal and temporal lobes of the brain

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44
Q

What is Pick disease?

A

A subset of FTD, characterised by the presence of Pick bodies (tangles of tau protein)

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45
Q

What is the pathophysiology of FTD?

A

Tau protein hyperphosphorylation causes tangles of Tau proteins

Intracellular inclusions of Tau proteins causes loss of function or apoptosis

Brain atrophy

46
Q

What is the difference between Pick bodies and neurofibrillary tangles?

A

Pick bodies - 3R Tau isoforms only
Neurofibrillary tangles - 3R and 4R Tau isoforms

47
Q

What is the behavioural variant of FTD?

A

Frontal lobe atrophy - personality and behaviour changes

48
Q

What is semantic variant primary progressive aphasia in FTD?

A

Difficulty finding the right words

49
Q

What is nonfluent variant primary progressive aphasia?

A

Difficulty speaking while knowing the meanings of individual words

50
Q

How can FTD be diagnosed?

A

Brain imaging - frontal/temporal atrophy and brain enlargement

Mental status scale assessments

51
Q

How can FTD be treated?

A

No cure, symptom management

Antidepressants for severe behavioural symptoms

Antipsychotics can have significant side effects and no convincing evidence of benefit from cholinesterase inhibitors

52
Q

Features of PICK disease

A

Progressive degeneration of neurons
Intracytoplasmic Pick bodies
Cortical atrophy
Knife edge gyri

53
Q

What is the biggest risk factor for all forms of dementia?

A

Increasing age

54
Q

Causes of dementia

A

Diabetes
Ethanol
Medication
Environmental (CO poisoning)
Nutritional
Trauma
Infection
Alzheimer’s

55
Q

What isthe prevalence of different causes of dementia?

A

Alzheimer’s 60%
Vascular 15%
Mixed 10%
Lewy Body 10%
FTD 2%
PD 2%
Other 1%

56
Q

e

A

e

57
Q

What is Parkinson’s disease?

A

A neurodegenerative disorder of the dopaminergic neurons in the substantia nigra

58
Q

What is the basal ganglia?

A

A collection of brain regions that help to initiate and control movement through their connection to the motor cortex

59
Q

What are the two parts of the substantia nigra?

A

Pars reticulata and Pars compacta

60
Q

What does the Pars reticulata do?

A

Receive signals from the striatum (caudate nucleus and putamen)

Relay messages to the thalamus via neurons rich in the neurotransmitter GABA

61
Q

What is the function of the Pars compacta?

A

Relays messages to the striatum via neurons rich in the neurotransmitter dopamine

Helps to stimulate the cerebral cortex and initiate and fine tune movement

62
Q

What part of the substantia nigra is affected in Parkinson’s?

A

The pars compacta

63
Q

What are the hallmarks of Parkinson’s?

A
  1. Resting tremor (70%)
  2. Bradykinesia, Hypokinesia or Akinesia
  3. Rigidity
  4. Postural Instability
64
Q

What sort of tremor occurs in Parkinson’s?

A

Resting tremor that diminishes with intentional movement

“Pill-rolling tremor”

65
Q

What rigidity occurs in Parkinson’s?

A

Stiffness that can appear as cogwheel rigidity that has catches or stalls as a persons arms and legs are moved passively

66
Q

What are some other physical symptoms of Parkinson’s?

A

Hypomimia
Reduced arm swing
Micrographia
Dystonic cramp
Gait distrubance

67
Q

What are some non-motor symptoms of Parkinson’s?

A
  1. Depression / Low mood
  2. Dementia
  3. Sleep problems
  4. Anosmia
  5. Impulse control behaviours
  6. Daytime sleepiness
  7. Autonomic symptoms (constipation, postural drop, urinary incontinence)
68
Q

What are some pre-symptomatic warning signs of Parkinson’s?

A

REM sleep behaviour disturbance can be a PC 20 years before motor symptoms

69
Q

How can you differentiate between Parkinson’s and cerebellar disease?

A

Cerebellar disease gives an intention tremor

70
Q

How can you differentiate between Parkinson’s and diseases of the motor cortex or corticospinal pathway?

A

Parkinson’s does not cause weakness!!! Normal power, reflex, sensation

71
Q

What is the management for Parkinson’s?

A

Medication to help with symptoms (but none stop neurodegeneration)

72
Q

What is the first line treatment for Parkinson’s?

A

Levodopa, which is usually given with a dopa decarboxylase inhibitor

Co-beneldopa or Co-careldopa

73
Q

Why do we give the precursor Levodopa and not just dopamine?

A

Dopamine can’t cross the blood brain barrier

74
Q

What is the purpose of a dopa decarboxylase inhbitor?

A

Dopa decarboxylase converts levodopa to dopamine. It is found centrally and peripherally. The dopa decarboxylase inhibitor stops peripheral conversion and cannot cross the blood brain barrier

75
Q

What is Stavelo?

A

Co-careldopa and entacapone (COMT inhibitor, prevents breakdown of levodopa in the brain and periphery)

76
Q

What is Amantidine?

A

An antiviral medication that increases dopamine production. Helps with dyskinesia

77
Q

What are dopamine agonists?

A

Drugs that stimulate dopamine receptors to trick the brain into thinking there is more dopamine than there really is

78
Q

Name an ergot derivative dopamine agonist

A

Bromocriptine

79
Q

Name three non-ergot derivative dopamine agonists?

A

Ropinirole
Pramipexole
Rotigotine

80
Q

What are the advantages of dopamine agonists over levodopa?

A
  1. Less dyskinesia
  2. Longer acting
81
Q

What are the disadvantages of dopamine agonists over levodopa?

A

1.More risk of hallucinations and compulsive behaviour
2. Postural hypotension
3. Daytime sleepiness

82
Q

How do COMT inhibitors work?

A

Inhibit catecholamine O-methyltransferase to stop it from degrading dopamine and levodopa

83
Q

Name three COMT inhibitors

A

Entacapone
Tolcapone
Opicapone

84
Q

How do MAO-B inhibitors work?

A

Inhibit monoamine oxidase B to stop it from degrading dopamine and levodopa

85
Q

Name two MAO-B inhibitors

A

Selegiline
Rasagiline

86
Q

What is safinamide?

A

Used in combination with co-careldopa to treat adults with Parkinson’s who are having “off” episodes

87
Q

What is the mechanism of safinamide?

A

It has multiple mechanisms of action including as a MAO-B inhibitor

88
Q

What is apomorphine?

A

A strong type of dopamine agonist

89
Q

How can apomorphine be given?

A

Rescue treatment in pen form

Continuous daytime infusion (constant blood levels help smooth motor fluctuations)

90
Q

How often should Parkinson’s patients be reviewed?

A

Every 6- 12 months

91
Q

Who should Parkinson’s patients have access to?

A
  1. Physiotherapy
  2. Occupational therapy
  3. Speech and Language therapy
  4. Dietician
92
Q

What should Parkinson’s patients take?

A

Vitamin D

93
Q

What drug can be given to patients experiencing Parkinson psychosis?

A

Clozapine

94
Q

How should depression and anxiety be managed in Parkinson’s disease?

A

Current guidelines are same as rest of population

95
Q

What drugs can be given to patients experiencing mild to moderate Parkinson dementia?

A

Cholinesterase inhibitors

96
Q

What is deep brain stimulation?

A

Implantable device that sends signals directly to basal ganglia.

Used in late Parkinson’s when fluctuations become an issue and is no longer controlled by best medical therapy

97
Q

What problems can people experience with Parkinson medication?

A

“Wearing off phenomena”

People get “off” periods and need more frequent medications

98
Q

What is Parkinsonism?

A

Symptoms of Parkinson’s seen in other diseases or side effects from medication

99
Q

What are some causes of Parkinsonism?

A
  1. Lewy Body dementia
  2. WIlson disease
  3. Pick disease (FTD)
  4. Normal pressure hydrocephalus
  5. Vascular
  6. Iatrogenic (anti-psychotics and anti-emetics) Haloperidol and Metoclopramide
100
Q

What is an essential tremor?

A

A condition that affects the nervous system, causing involuntary and rhythmic shaking or trembling

101
Q

What part of the body is usually affected with essential tremor?

A

Hands, fingers, sometimes head, vocal cords

102
Q

What are the causes of essential tremor?

A

The exact cause is unknown, but it may be familial with an autosomal dominant inheritance pattern

103
Q

What sort of tremor is an essential tremor?

A

Rhythmic, symmetrical tremor

104
Q

What is the treatment for essential tremor?

A
  1. Beta blockers
  2. Anti-epileptics
  3. Benzodiazepines
  4. Botulinum toxin (Botox) (head tremors not responsive to medication
105
Q

What are some other interventions for essential tremor>

A
  1. Avoid nicotine and caffeine
  2. Get enough sleep
106
Q

How can alcohol affect essential tremor?

A

It can cause a short term benefit and reduce the tremor

107
Q

How does an essential tremor differ from a Parkinson tremor?

A
  1. Essential tremor is symmetrical
  2. Essential tremor is on movement / posture
  3. Essential tremor is higher frequency
  4. Parkinson’s tremor affects hands, legs, chin
108
Q

e

A
109
Q
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110
Q
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111
Q
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112
Q
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