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Pathology > Neurodegenerative Disease > Flashcards

Neurodegenerative Disease Flashcards

0
Q

What is neurodegenerative disease a loss of

A

Cells in the brain and spinal cord

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1
Q

What does neurodegenerative disease affect

A

nerve cells and glial cells

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2
Q

List 4 diseases involving degeneration of CNS neurons

A
  1. Dementia
  2. Extrapyramidal disorders
  3. Ataxic disorders
  4. Motoneuron disorders
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3
Q

Give examples of dimentia

A
  • Alzheimer’s disease

- picks disease

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4
Q

What is the most common version of dementia

A

Alzheimer’s disease

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5
Q

Give examples of extrapyramidal disorders

A
  • Parkinson’s disease
  • Wilson’s disease
  • Huntington’s chorea
  • dystonia musculorum deformans
  • hallervorden-Spatz syndrome
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6
Q

Give examples of ataxic disorders

A
  • friedreich’s ataxia
  • cerebello-olivery atrophy
  • cerebellar atrophy
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7
Q

Give and example of motoneuron disorders

A

Motoneuron disease

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8
Q

In which part of the brain does dementia cause degeneration of neurones

A

Cerebral cortex

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9
Q

Which is the most common version of extrapyramidal disorders

A

Parkinson’s disease

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10
Q

Which sort of movements is involved in diseases from extrapyramidal disorders

A

Involuntary

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11
Q

Which sort of spinal disorder is linked with ataxic disorders

A

Cerebello spinal disorder

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12
Q

How many people does Parkinson’s affect

A

1 out of 750 people (common)

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13
Q

How many cases are there of Parkinson’s in the UK

A

100,000

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14
Q

Which other disease is Parkinson’s more common than

A

Multiple sclerosis

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15
Q

What does the prevalence of Parkinson’s increase with

A

Age

Reaching a max at about 70

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16
Q

Is Parkinson’s an age related disease

A

Yes

But can get when young (40) but rare

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17
Q

How many new cases of Parkinson’s are there each year in the UK

A

9000

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18
Q

List Parkinson’s disease symptoms

A
  • 4-8 Hz tremor of limbs
  • rigidity of muscle tone
  • difficulty initiating movement (akinesia)
  • movements slow
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19
Q

When is tremor of limbs at its worst

A

When anxious and resting

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20
Q

When does tremor of limbs stop

A

When asleep

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21
Q

Why don’t Parkinson’s disease px blink much

A

Due to rigidity of muscle tone

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22
Q

How to Parkinson’s patients appear due to difficulty initiating movement

A

Appear frozen

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23
Q

What do Parkinson’s disease symptoms result in

A
  • deadpan expression
  • stooped shuffling gait (increased muscle tone in back)
  • pill rolling (between fingers & forefingers)
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24
Q

What is the cause of Parkinson’s disease

A

It is idiopathic (don’t know what caused it)

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25
Q

Between which groups is Parkinson’s disease equal

A

Male & female

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26
Q

What is Parkinson’s disease characterised by a loss of

A

Dopamine producing cells in the substantia nigra of the basal ganglia

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27
Q

What is the substantia nigra

A

A black area visible on a cut section of the midbrain which produces dopamine

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28
Q

What does the substantia nigra produce

A

Dopamine

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29
Q

What is the basal ganglia

A

5 pairs of nuclei

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30
Q

Where is the basal ganglia located

A

In the thalamus

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31
Q

What region is involved in motor control

A

Substantia nigra of the basal ganglia

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32
Q

What is the appearance of the substantia nigra in Parkinson’s disease

A

Diminished (dark patch is reduced)

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33
Q

what is the aim of pharmacological treatments of parkinson’s disease

A

increase dopamine levels

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34
Q

what is L dopa

A

a smaller version of dopamine

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35
Q

what happens if you just try to inject more dopamine

A

it won’t work as it can’t go through the blood brain barrier

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36
Q

what is L dopa a precursor to

A

dopamine synthesis

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37
Q

what is the most common treatment for parkinson’s

A

administration of a precursor (L dopa) for dopamine synthesis (in the presence of a substance blocking its depletion outside the CNS)

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38
Q

what advantage has injecting L dopa instead of dopamine

A

L dopa has transporters that can go through the blood brain barrier

39
Q

what must you also give when giving L dopa to a px

A

an inhibitor of the AADC enzyme

40
Q

why must you give an inhibitor of the AADC enzyme when giving a px L dopa

A

so that the L dopa can go through the blood brain barrier from the periphery so that it can produce dopamine inside the brain

41
Q

what is the name of the inhibitor of the AADC enzyme

A

carbidopa

42
Q

what does carbidopa inhibit

A

it inhibits the enzyme which converts L dopa in dopamine

43
Q

what happens when you give L dopa & carbidopa at the same time

A

the dopamine isn’t produced in the periphery

44
Q

what ends up going through the blood brain barrier after L dopa & carbidopa are given at the same time

A

Ldopa

carbidopa stays behind

45
Q

what is the result of L dopa going through the blood brain barrier and carbidopa staying behind

A

the substantia nigra can produce dopamine with that L dopa

46
Q

what is the advantage of inhibiting the enzyme which produces dopamine in the periphery

A

you can use much smaller quantities of L dopa to relieve symptoms of parkinson’s

47
Q

does L dopa cure the symptoms of parkinson’s

A

no it only alleviates

48
Q

does L dopa have an ongoing effect

A

no it becomes less effective after 5-7 years

49
Q

name some other pharmacological ways of increasing dopamine levels

A
  • direct agonists of dopamine by latching onto dopamine receptors & stimulate the neurones can increase the release of dopamine
  • stop the destruction of dopamine as it is a monoamine so it can be destructed by monoamineoxidase therefore will have more dopamine around or it can stop the re uptake of dopamine
50
Q

what is the most powerful pharmacological way of increasing dopamine levels

A

increasing the availability of L dopa

51
Q

what side effects can pharmacological treatments for parkinson’s cause

A

ocular side effects

52
Q

list some non-pharmacological (therapies) used to treat parkinson’s

A
  • implantation of foetal tissue
  • implantation of modified fibroblasts
  • xenotransplantation
  • adult stem cell culture and implantation
  • glial derived neurotrophic factor (GDNF)
  • electrical stimulation of basal ganglia by implanted electrodes
  • gene therapy
53
Q

how does implantation of foetal tissue work as a therapy to treat parkinson’s

A

take parkinson cells from a baby and put into an adult brain but hasn’t worked well

54
Q

how does the implantation of modified fibroblasts work as a therapy to treat parkinson’s

A

can be genetically modified to produce dopamine and but into brain

55
Q

how does xenotransplantation work as a therapy to treat parkinson’s

A

transplantation from other species such as pigs

56
Q

how does adult stem cell culture and implantation work as a therapy to treat parkinson’s

A

re programme stem cells to produce dopamine and put into substantia nigra

57
Q

how does glial derived neurotrophic factor (GDNF) work as a therapy to treat parkinson’s

A

substances produced by glial cells which help neurones survive.
can implant a pump into the abdomen which have these glial derived neurotrophic factors and occasionally pump it into the brain and into the substantia nigra to keep dopamine producing cells going

58
Q

how does electrical stimulation of basal ganglia by implanted electrodes work as a therapy to treat parkinson’s

A

by implanting electrodes into basal ganglia and inject electricity through them to produce dopamine

59
Q

how does gene therapy work as a therapy to treat parkinson’s

A

genes are out into people to replace the defective gene by putting the gene into viruses which get into the dna to produce dopamine

60
Q

why are the effects of parkinson’s on vision likely to be retinal in origin

A
  • the basal ganglia are primarily motor
  • dopamine is a neurotransmitter/neuromodulator in retinal amacrine and interplexiform cells (so dopamine is found in retina)
  • in parkinson’s disease levels of retinal dopamine are decreased
  • parkinson’s disease is also associated with abnormal ERGs
61
Q

what is the basal ganglia involved in instead of vision

A

involved in movement so it won’t effect vision directly

62
Q

why is retinal activity changed in parkinson

A

due to lack of dopamine in the retina with parkinson’s disease

63
Q

name some visual deficits in parkinson’s disease

A
  • possibly decreased (low contrast) acuity
  • abnormal saccadic and smooth pursuit eye movements (increased latency & reduced speed)
  • decreased blinking
  • large light adapted pupil. possible anisocoria. speed and amplitude possibly decreased
  • longer latency and altered waveform of ERG and VEP - reduced temporal resolution
  • possible triton colour defect (in blue pathway so tritanopic, associated with Alzheimer’s)
64
Q

which sort of visual functions are unaffected in parkinson\s disease

A

visual fields

65
Q

how can akinesia (difficulty of movement) be alleviated

A
  • by placing visual stimuli infant of the feet so px has something to aim for when walking
67
Q

what can lead to akinesia (frozen movement)

A

irrelevent peripheral visual stimuli eg door frames inhibits movement

68
Q

at what age does Alzheimer’s disease usually occur

A

> 70 years old

69
Q

how many % of people over age 60 does alzheimer’s disease effect

A

2%

70
Q

how many % of people over age of 80 does alzheimer’s disease effect

A

20%

71
Q

what is alzheimer’s disease characterised by

A
  • loss of memory
  • severely impaired judgement
  • loss of emotional control
  • eventually complete breakdown of mental function
72
Q

how many phases does the progression of alzheimer’s have

A

three

73
Q

describe phase 1 of alzheimer’s

A
  • characterised by a slow deteriorating memory
  • a feeling of disorientation in time and space
  • inability to perform more complex tasks
  • may get mood swings
  • depression
  • restlessness
  • inability to sleep well
  • disease may not be obviously apparent
  • can last 5 years on average
  • lose memory from recent things but can remember old things
  • is not a bad stage when doing regular things e.g. making tea
74
Q

describe phase 2 of alzheimer’s

A
  • more rapid
  • deterioration of intellect and competence become more obvious
  • blunting of emotions and apathy
  • may get visual agonises (can’t recognise faces)
  • and dysphasia (use wrong words which are not understandable)
  • possibility of delusions and hallucinations
75
Q

describe phase 3 of alzheimer’s

A
  • represents the terminal stage
  • may get epileptic fits
  • general increase in muscle tone resulting in unsteady gait
  • eventually become bed ridden
  • and incontinent
  • complete loss of personality
  • patient fades away
76
Q

what can the total duration of alzheimer’s be

A

6-8 years

77
Q

what type of disease is alzheimer’s

A

terminal disease

so can end up dyeing from it

78
Q

which risk factor of alzheimer’s has a strong genetic component

A

family history of alzheimer’s disease 3.5%

79
Q

list the risk factors of alzheimer’s and state the relative risk in %

A
  1. family history of alzheimer’s 3.5
  2. family history of down’s syndrome 2.7
  3. previous head trauma
    males 2.67
    females 0.85
  4. family history of parkinson’s disease 2.14
  5. depression 1.82
  6. maternal age 40+ 1.7
  7. epilepsy 1.6
  8. encephalitis/meningitis 1.6
  9. herpes zoster/simplex 1.15
  10. general anaesthesis 1.0
  11. alcohol 1.0
  12. immune diorders, oesteoarthiritis, poliomyelitis, thyroid disease, headaches, smoking, solvent exposure, head injury, blood transfusion <1.0
80
Q

list the neuropathology of alzheimer’s

A
  • thinning of the cortex
  • sulci have widened
  • gyri have thinned
  • loss of tissue may be most severe in frontal and temporal lobes
  • brain has less bulk
  • ventricles are enlarged
  • deposition of amyloid beta-protein in the form of ‘senile plaques’ (5-200um)
  • and formation of neurofibrillary tangles
81
Q

what is the difference of brain mass from a normal individual to an individual with alzheimer’s

A

1350gms - 1000gms

82
Q

which levels of neurotransmitter are reduced in presynaptic in alzheimer’s

A

acetylcholine

83
Q

which neurotransmitter receptors are intact in postsynaptic region

A

acetylcholine receptors

84
Q

is there a proven drug therapy for alzheimer’s

A

no

85
Q

how does alzheimer’s affect the retina

A

reduction in retinal ganglion cells & thinning of nerve cell layer&lose magno cells

86
Q

how does alzheimer’s affect the optic disc

A
  • disc pallor
  • optic atrophy
  • disc cupping in the absence of open angle glaucoma in some patients
87
Q

how does alzheimer’s affect the optic nerve

A
  • decline in nerve axons

- preferentially affecting the large diameter axons (Magno cell pathway)

88
Q

how does alzheimer’s affect the lateral geniculate nucleus

A
  • accumulation of lipofuscin

- resistant to tangle (NFT) formation

89
Q

how does alzheimer’s affect the suprachiasmatic nucleus

A
  • degeneration reported in some patients

- has lot of tangles and plaques in alzheimer’s px so affects sleep patterns

90
Q

where is the suprachiasmatic nucleus found

A

just above the optic chiasm

91
Q

how does alzheimer’s affect the visual cortex

A
  • rarely atrophic
  • myelin reduced in outer laminae
  • loss of pyramidal cells
92
Q

how does alzheimer’s affect the B17 region

A

numerous cored senile plaques but few tangles

pre stiate cortex affected

93
Q

how does alzheimer’s affect the B18 region

A

numerous neuritic senile plaques and tangles

94
Q

what affect does the release of acetylcholine by the parasympathetic nervous system have on the iris sphincter muscle

A

constriction

95
Q

how do alzheimer patients’ pupils respond to light

A

it constricts less due to reduced levels of acetylcholine

96
Q

how does tropicamide affect an alzheimer’s px

A

they are more sensitive to it which can prove that they have less acetylcholine

97
Q

what other visual test is possible for early alzheimer’s identification

A
  • evidence indicates that in the early development of alzheimer’s, beta-amyloid protein gets deposited in the lens forming a cataract behind the iris
  • the level of amyloid proteins in the brain is reflected by the size of the lens deposit
  • the cataract is apparent a significant amount of times before dementia develops

Pathology (20 decks)

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