Parkinson's Flashcards

(61 cards)

1
Q

What hormone is lost in parkinsons

A

Dopamine

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2
Q

What is the motor symptom triad

A

Bradykinesia
Muscle rigidity
Tremor

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3
Q

What are non motor symptoms of parkinsons

A

Depression
Fatigue
Anxiety
Constipation
Sweating
Dysphagia
Hypertension
bladder problems
sleep disturbance

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4
Q

Outline the 3 dopaminergic pathways

A

Motor –> nigrostriatal
Behavioural –> mesolimbic, mesocortical
Endocrine –> tuber hypophyseal

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5
Q

What is the main dopaminergic pathway for parkinsons

A

Nigrostriatal
affects motor movement

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6
Q

What are the characteristics of bradykinesia

A

Expressionless face
Shuffling gait
Soft voice
small handwriting

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7
Q

What are the characteristics of rigidity motor movements

A

Stooping posture
Muscle pain
Increased falls

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8
Q

What are the characteristics of tremor motor symptoms

A

Occurs at rest
improves on voluntary movement
One or both hands

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9
Q

What type of drugs can cause tremors?

A

Antiarrhythmics
antidepressants
mood stabilisers
bronchodilators
anti epileptics

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10
Q

What prescription drugs can cause Parkinson’s

A

Antipsychotics
antiemetics
Reserpine –> bp
tetrabenazine –> movement disorders

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11
Q

What physical factors can cause parkinson’s

A

Viral encephalitis
Brainstem injury

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12
Q

What genetic factors can increase the risk

A

Alpha-synuclein mutations
Lewy body formation
parkin gene

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13
Q

What is parkin

A

PARK2 gene
Has mitochondrial control
increases neuronal cell damage and death

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14
Q

How do antipsychotics contribute to parkinsons

A

Extra-pyramidal side effects
dose related
decrease dose = reduction in parkinsons symptoms

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15
Q

How do Reserpine and tetrabenazine contribute to parkinsons

A

Depletes MOA from pre-synaptic storage
Decrease in dopamine release

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16
Q

How do recreational drugs contribute to parkinsons

A

MPTP kills dopaminergic neurons
in substantia nigra
Irreversible

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17
Q

What can increase the risk of dementia pugilistica

A

Head ijuries
stroke

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18
Q

What is the first line therapy of parkinsons

A

Levodopa
+
Dopa decarboxylase inhibitors

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19
Q

What are the side effects of levodopa

A

Dyskinesia
Nausea
Hypotension
Sleep disturbances

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20
Q

What must you avoid 30-6- minutes after taking levodopa

A

Protein

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21
Q

What must you wait 2-3 hours to take after levodopa

A

Iron supplements

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22
Q

What are the risks of dopamine receptor agonists

A

Impulsive control disorders
Gambling
hypersexuality
binge eating
obsessive money spending/ shopping

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23
Q

What are the side effects of MOA-B inhibitors

A

Nausea
postural hypotension
dyskinesia
confusion

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24
Q

What is dyskinesia

A

Involuntary muscle movements

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25
When do we consider adjuvant therapy
When dyskinesia have wearing off episodes
26
What treatments do we use as adjuvant therapy
COMT inhibitor MOA-B inhibitor Dopamine agonists
27
Give an example of a dopamine agonist
Pramipexole ropinirole
28
Give an example of a COMT inhibitor
Entacapone
29
Give a example of a MOA-B inhibitor
Selegiline Safinamide
30
Give examples of DOPA decarboxylase inhibitor
Carbidopa Benserazide
31
Why are DOPA carboxylase inhibitors given alongside Levodopa
Levodopa converted to dopamine in periphery before it can reach the brain Dopamine cannot cross BB to exert therapeutic effect if in periphery DOPAC prevents conversion of levodopa in periphery and allows it to get into the brain before being converted
32
What should you do if a patient displays obsessive behaviours on a dopamine agonist
Reduce dosage Offer CBT if needed
33
What does amantadine do
Increase dopamine release
34
What are the side effects of amantadine
Psychological sleep disturbances Nausea vomiting weight loss dry mouth hypotension palpitations
35
What happens if patients miss a dose
Akinesia acute Inability to swallow Increased fall risk neuroleptic like malignant syndrome
36
Symptoms of neuroleptic like malignant syndrome
Fever rigidity hypoventilation altered consciousness
37
What causes neuroleptic like malignant syndrome
sudden reduction in dopamine activity
38
How do we treat depression in parkinsons
SSRI's
39
How do we treat dementia in parkinsons
Rivastigmine
40
How do we treat hallucinations in Parkinson's
Quetiapine
41
How do we treat constipation in parkinsons
Stimulant + softener
42
How do you treat postural hypotension in parkinsons
Midodrine fludrocortisone
43
How do you treat drooling in parkinsons
Glycopyrronium
44
How do you treat daytime sleepiness in Parkinson's
Modafinil
45
What drugs should you avoid when treating Parkinson's
OTC antihistamines OTC sympathomimetics with MOA-B inhibitors CCB
46
What is the precursor for dopamine synthesis
Tyrosine
47
What is the role of MOA-B in synthesis
Converts dopamine to inactive metabolite in pre synaptic terminal to regulate dopamine levels if needed
48
What transporter facilitates the reuptake of dopamine
DAT
49
What pathway des the D1 receptor take
GPCR G alpha S Activated DARPP-32 Inactivated PP1 PP1 cant dephosphorylate proteins so they can continue to have their downstream signalling effects
50
What does the D2 pathway dake
GPCR G alpha i Activates K+channels --> hyperpolarisation Beta/Gamma subunit inhibits Ca2+ cell entry --> Less excitability less neurotransmitter release
51
Where does the dopamine release start from in the nigra striatal pathway
Pars compacta in substantia nigra
52
Where are the D1 and D1 receptors found in the nigra striatal pathway
Corpus striatum
53
What role does dopamine play with acetylcholine
Releases it from the corupus striatum
54
What causes a tremor
Decrease in dopamine means increase in Ach in synapse Hyperactivity trremor
55
What protein are lewy bodies made from
Alpha-synuclein
56
What is the role of alpha-synuclein
Exocytosis in synaptic vesicles
57
How do lewy bodies form
Aggregation and plaque formation of alpha-synuclein
58
What causes mitochondrial damage
lots of energy required to allow dopaminergic neurons to work
59
How does mitochondrial damage cause cell death
Produces ROS oxidative stress
60
What genes are responsible for mitochondria turnover
Parkin PINK -1
61