Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

2nd year > Parkinson's > Flashcards

Parkinson's Flashcards

1
Q

what type of movement disorder is Parkinson’s?

A

akinetic rigid syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

types of parkinson’s related disease

A

drug induced parkinsonism
Parkinson’s disease
Parkinson’s plus disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the cardinal features of parkinson’s?

A

rest tremor - disappears on movement
rigidity
bradykinesia - slow movements
postural instability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

pathophysiology of parkinson’s

A

diminished/ loss of dopaminergic neurones in substantia nigra
lewi bodies form in brain - substantia nigra
downward movement control is lost as less dopamine is produced by dopaminergic neurones of substantia nigra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

imaging for Parkinson’s

A

DaTscan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

DaTscan findings

A

asymmetric
loss of tail on substantia nigra dopamine
minimal dopamine secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

diagnosis of parkinson’s

A

clinical features
exclude other syndromes
DaT scan
trial L-dopa or apomorphine to see if it helps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

apomorphine

A

quicker effect than L-dopa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does L dopa work?

A

replaces what is lost

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

treatments for parkinson’s

A

Levodopa
dopamine agonists
surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

dopamine agonists e.g.

A

apomorphine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

risk of dopamine agonists

A

can cause dopamine dysregulation syndrome
changes behaviour
hypersexuality
gabbling addiction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

levodopa

A

becomes less effective as disease progresses
resistance develops
symptoms then worsen
therapeutic zone can be very specific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

too much levodopa

A

dyskinesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

surgery for parkinson’s

A

destructive lesion
chronic stimulation
reconstruction of lost circuitry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

destructive lesions

A

create lesion in brain to treat the parkinson’s symptoms
use injections or gamma-knife
lesion in basal ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

chronic stimulation

A

electrode inserted into areas of the brain

deep brain stimulation into subthalamic nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are the risks of chronic stimulation/ deep brain stimulation

A

risk of temporary blindness due to proximity of optic nerve
risk of damage to swallowing areas
to avoid these risks electrodes are inserted while patient awake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

reconstruction of host circuitry

A

stem cell transplant
differentiation into dopaminergic neurones
insert into basal ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what drugs can cause parkinsonism?

A

antiemetics

antipsychotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

antiemetics that cause parkinsonism

A

cyclizine

metoclopramide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

antipsychotics that cause parkinsonism

A

haloperidol
clozapine
deplete dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is parkinson’s plus syndrome?

A

parkinson’s features as well as additional features

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

examples of parkinson’s plus syndromes

A

PSP
MSA
Wilson’s disease
CBD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

PSP

A

progressive supranuclear palsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

PSP

A 
parkinsonism 
supranuclear gaze palsy 
pseudobulbar palsy 
dystonic rigidity of neck and trunk 
dysarthria 
dementia 
poor response to L dopa 
midbrain degeneration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

supranuclear gaze palsy

A

unable to look up or down voluntarily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

pseudobulbar palsy

A

very extreme mood swing type behaviour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

MSA

A

multiple system atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

multiple system atrophy symptoms

A 
parkinsonism 
autonomic failure
cerebellar degeneration - poor balance 
pyramidal signs - spastic paraparesis and weakness 
sighs for no reason 
sleep apnoea
31
Q

multiple system atrophy pathogenesis

A

area affected around pons
relay of all tracts is the area affected
hot cross bun appearance on MRI of midbrain

32
Q

treatment for MSA

A 
no response to L dopa 
treatments often unlikely to be beneficial 
anticholinergics 
BP support 
elastic stockings 
bed head up 
fludrocortisone
33
Q

mean age of onset of PD?

A

45-60
0.5-1% of over 60s
2nd most common neurodegenerative disease

34
Q

risk factors for PD?

A 
genetics
pesticides/ herbicides
pollution
age
men more at risk 
drugs
35
Q

symptoms of PD?

A 
tremor at rest - 4-7Hz 
rigidity 
bradykinesia 
bilateral signs 
no sensory loss 
power is normal 
shuffling steps gait 
stooped gait with reduce arm swinging and narrow base
slow, monotonous and slurred speech 
plain face/ facial stare 
reduced blinking rate 
depression
dementia 
hallucinations 
greasy and sweaty skin 
heartburn 
dribbling dysphagia 
weight loss 
constipation
36
Q

investigations/ diagnosis

A 
clinical 
MRI will be normal 
dopamine transporter imaging = unreliable and expensive 
handwriting 
anosmia 
violent dreams 
no lab tests 
DaT scan 
trial of levodopa/ apomorphine
37
Q

lewy bodies

A

can be seen throughout the brain

often cause co-existing dementia

38
Q

dopamine and ACh in PD

A

dopamine is normally inhibitory at corpus striatum
normally dopamine inhibits ACh release in corpus striatum but in Parkinson’s too much ACh is released
there is cell death by excitotoxcity, oxidative stress and apoptosis

39
Q

progression of PD

A

no remission
usual course = 10-15 years
doesn’t directly cause death
puts strain on the body, increasing susceptibility to infection
progression is unique to each person and rate of progression is variable

40
Q

what is the main cause of death in PD?

A

bronchopneumonia as a result of dysphagia

41
Q

how many stages of PD are there?

A 
1 - mild symptoms
2 - worsening symptoms
3 - mid-stage
4 - severe and limiting symptoms
5 - advanced and debilitating
42
Q

stage 1 of PD

A

tremor and unilateral movement symptoms

changes in posture, walking and facial expressions

43
Q

stage 2 of PD

A 
tremor
rigidity 
bilateral movement symptoms
walking problems
poor posture
able to live alone but daily tasks are challenging
44
Q

stage 3 of PD

A

loss of balance
bradykinesia
falls more common
impaired daily activities

45
Q

stage 4of PS

A

able to stand unassisted but walked required

need support with daily activities and unable to live alone

46
Q

stage 5 of PD

A 
unable to stand or walk due to stiffness
wheelchair needed or bed ridden 
constant nursing required
hallucinations and delusions
motor and non-motor symptoms
47
Q

rating PD scales

A

Hoehn and yahr stages

unified parkinson’s disease rating scale

48
Q

Hoehn and yahr stages

A

monitor motor symptoms and progression

49
Q

Unified parkinson’s disease rating scale

A

accounts for motor and non-motor symptoms, mental functioning, mood and social interaction
accounts for cognitive difficulties, ability to carry out daily activities and treatment complications

50
Q

other causes of Parkinsonism/ differentials

A 
alzheimers
multi-infarct dementia
repeated head injury
drugs 
vascular events, orthostatic hypotension with atonic bladder, dementia, wilson's disease, apraxic gait 
parkinson's plus syndrome 
multi-system atrophy
progressive supranuclear palsy
51
Q

what drugs can cause parkinsonism?

A

neuroleptics

dopamine reducing drugs - dopamine antagonists

52
Q

what are the treatments for PD?

A

Dopamine agonists
L-dopa
drugs that release dopamine
MAO-B inhibitors

53
Q

Dopamine agonists mechanism of action

A

bind to dopamine receptors and mimic the effects of dopamine

54
Q

L dopa mechanism of action

A

dopamine precursor so increases the amount of dopamine in CNS - can cross BBB

55
Q

MAO-B inhibitors

A

selective inhibition of monoamine oxidase B which metabolises dopamine
therefore increasing dopamine levels in the brain

56
Q

L-dopa downsides

A

efficacy decreases over time

on-off effect

57
Q

side effects of L-dopa

A 
nausea
GI upset
dyskinesia - unwanted movements
psychosis
impulse control disorders 
hypotension
arrhythmia
confusion
disorientation
insomnia
nightmares
58
Q

impulse control disorders

A 
compulsive eating
compulsive shopping
hypersexuality
punding 
pathological gambling
59
Q

side effects of MAO-B inhibitors

A

postural hypotension
atrial fibrillation
can be very serious

60
Q

anticholinergic side effects

A 
dry mouth
dizziness
urinary retention
anxiety
confusion
tachycardia
hallucinations
insomnia
memory problems
61
Q

contraindications for anticholinergics

A

urinary retention
acute glaucoma
GI obstruction
prostate problems

62
Q

psychological effects of PD

A 
depression and anxiety are most common 
hallucinations
memory problems
dementia
psychosis
delusions
impulse control disorders
apathy
sleep disorders
panic attacks 
lonliness
63
Q

what is apathy?

A

diminished motivation and goal directed behaviour

64
Q

progressive supranuclear palsy symptoms

A 
falls 
balance problems
paralysis
vertical gaze
parkinsonism
cognitive impairment
progressive and varying course
65
Q

age of onset of progressive supranuclear palsy

A

60-65

7 years survival on average

66
Q

treatment for progressive supranuclear palsy

A

poorly responds to L-dopa

67
Q

symptoms of multi-system atrophy

A 
parkinsonism
cerebellar problems 
autonomic problems - postural hypotension
akinesia
rigidity
68
Q

treatment for multi-system atrophy

A

responds poorly to L-dopa

69
Q

what is multi-system atrophy?

A

degenerative neurological disorder

70
Q

symptoms of Wilson’s disease

A 
parkinsonism
liver failure
renal failure
wide neurological problems
parkinsonism
chorea
akinesia
tremors
rigidity 
personality and behavioural problems
cognitive impairment
71
Q

Wilson’s disease age of onset

A

6-20

72
Q

treatment of wilson’s disease

A

Penicillamine

treat early and can be very well controlled

73
Q

pathogenesis of wilson’s disease

A

autosomal recessive condition

causes problems with copper metabolism so copper is deposited in the liver, basal ganglia, cornea and kidneys

74
Q

what happens to the direct and indirect pathways in PD?

A

loss of activation of direct and loss of inhibition of indirect pathways

2nd year (48 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions