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Pharmacy Semester 2 > Parkinson's Disease > Flashcards

Parkinson's Disease Flashcards

1
Q

What is Parkinson’s disease?

A

A degenerative condition caused by the loss of dopamine-secreting neurons in the midbrain area of the substantia nigra causing tremor and impairment.
It is progressive due to death of dopaminergic neurones as well as presence of Lewy Bodies

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2
Q

What are the main functions of DA?

A

Memory
Movement
Motivation
Mood
Learning
Sleep
Attention
Good behaviour
Thinking

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3
Q

What is the purpose of Lewy Bodies?

A

Disruption of neurotransmitter balance and loss of connection between nerves and ultimately destruction of dopamine.

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4
Q

If something attacks substantia nigra what are the symptoms?

A

Tremors and moto impairment

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5
Q

Where is DA released/contained from?

A

Substantia nigra

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6
Q

DA released from nucleus accumbens and hippocampus normally functions with?

A

Pleasure

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7
Q

DA released from substantia nigra normally functions as?

A

Motor function & memory

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8
Q

What are the three areas that DA can be released from?

A

Substantia nigra, nucleus accumbens & hippocampus

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9
Q

If DA drops then ACh what?

A

Increase vice versa

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10
Q

3 Functions of DA?

A

Voluntary movement
Produces Neurotransmitter DA
Regulates mood

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11
Q

What are motor and non-motor symptoms of parkinsons?

A

Motor - Bradykinesia - slow movement
Hypokinesia - delayed action
Stiffness & rigidity
Rest tremor due to increase of ACh

Non-motor - Depression - DA = pleasure - decrease will decrease happiness
Also due to reduced movement which is depressing
Reduced cognitive impairment

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12
Q

Diagnose parkinsons?

A

Take a med history and physical examination

Within examination monitor motor function and also if there was a positive response to Levodopa

CT & PET - not useful
Biomarkers in urine, blood and CSF - not useful

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13
Q

Is PD linked to aging?

A

No

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14
Q

What is the ideal of clinical management for PD?

A

To restore DA & ACh levels
No cure so aim to slow deterioration

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15
Q

What are 4 drug functions used to manage PD?

A

Replace DA
Inhibit ACh
Mimic role of DA
Prevent destruction of DA/ Allow reuptake of DA

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16
Q

What are the three main treatments of early stages of PD? & THEIR DRUG TYPE

A

Levodopa - precursor of dopamine
Oral/transdermal NON ERGOT dopamine agonists - stimulate release of DA from substantia nigra
Monoamine-oxidase-B inhibitors - ACh inhibitor

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17
Q

What is the cheese interaction?

A

Patient on MAOI means increased levels of tyramine which is vasoconstrictive. Cheese contains tyramine resulting in hypertensive crisis

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18
Q

Why don’t you start pt on Levodopa?

A

Can develop resistance so preserve this as another stage of treatment (most effective treatment)
Start with DA Agonist

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19
Q

Why can Levodopa cross BBB?

A

Lipophilic & small

20
Q

Why is levodopa given as a combo rather than on its own?

A

Levodopa can cross BBB. It is a prodrug meaning it needs activation - we require these to be in the brain not the periphery.
These enzymes are - Dopa decarboxylase - breakdown levodopa to da in the peripheral system meaning they can’t cross BBB and work in CNS.

Combination of levodopa and enzyme inhibitors to inhibit peripheral metabolism of levodopa to dopamine & allow levodopa to cross BBB and be converted to DA in central. It also means you are giving pt lowest dose - reduces adverse effects & increase therapeutic effect

21
Q

What are the three LD enzymes that breakdown L-dopa to DA?

A

COMT -p&c
DD - DOPA DECARBOXYLASE - p&c
MAO- c only

22
Q

What does carbidopa do?

A

Protective enzyme which acts on DD and allows DA to cross BBB

23
Q

What are the two main examples of peripheral dopa-decarboxylase inhibitors? When are these given?

A

Carbidopa & Benserazide
Later stage treatments

24
Q

Why is a lower dose of Levodopa administered when in conjunction with carbidopa or benserazide?

A

These inhibit peripheral conversion of Levodopa to DA - therefore more can cross BBB

25
Q

What happens to levodopa once it crosses the BBB?

A

Broken down by dopa decarboxylase into DA and stored in nigrostriatal nerve terminals

26
Q

What is Levodopa with Benserazide?

A

Co-Beneldopa = Madopar

27
Q

What is Levodopa with Carbidopa?

A

Co-Careldopa = Sinemet

28
Q

Symptoms of DA in periphery

A

Vomiting Nausea & postural hypertension

29
Q

What is the first line treatment of Parkinson’s?
Examples

A

Dopamine agonists - Non ergot derived (specifically)
Non-Ergot - Pramipexole, Ropinirole & Rotigotine

30
Q

Why are Ergot Derived Dopamine agonists not used?

A

Severe side effects in lungs and hrt
- Cabergoline & Pergolide

31
Q

Which to start with DA agonist or Levodopa in early stages?

A

DA Agonist as Levodopa can improve symptoms rapidly but also causes resistance in prolonged use. This causes a rapid improvement followed by a rapid decline. By constantly increasing the dose of L-dopa - side effects increase.

DA Agonists have many advantages as they act directly on DA receptors
They don’t require conversion to form the active product - no issue with metabolic enzymes
DA Agonists have a longer half life
DA Agonists are associated with less motor side effects such as dyskinesias
topical or patches

32
Q

Side effects of ergot derived DA

A

Pleural fibrosis
Two fold to four fold increased risk for cardiac valve fibrosis when compared to non-ergot derived

33
Q

What is the Mechanism of action and examples of MAO-B inhibitors?
Side effects & Withdrawal symptoms?

A

They promote reuptake of DA by decreasing the breakdown of DA in the striatum.
Examples - Selegiline and Rasagiline
Considered a first line treatment
Selegiline has side effects - hallucinations, insomnia & confusion
Selegiline when during withdrawal = causes deteriorated motor function

33
Q

What is the Mechanism of action and examples of MAO-B inhibitors?
Side effects & Withdrawal symptoms?

A

They promote reuptake of DA by decreasing the breakdown of DA in the striatum.
Examples - Selegiline and Rasagiline
Considered a first line treatment
Selegiline has side effects - hallucinations, insomnia & confusion
Selegiline when during withdrawal = causes reduced motor function

34
Q

What are the MAO of COMT inhibitors?
What line of treatment?

A

Prevent the conversion of L-dopa to DA in periphery.
Second line therapy. Must be given alongside L-dopa
Example - Tolcapone

35
Q

What is a side effect of tolcapone?

A

Hepatotoxicity

36
Q

Why are antimuscarinics used in Parkinson’s

A

Younger patients with severe tremor and dystonia which is painful muscle movements
Work by inhibit ACh level restoring DA balance
Late stage
Procycline

37
Q

Why would amantadine be coprescribed?

A

An antiviral to help aid L-dopa induced dyskinesia - cuncontrolled muscle twitching
Works by facilitating presynaptic DA release
Blocking DA reuptake - anticholinergic effect

38
Q

What are last line therapy for parkinson’s?

A

Pallative care - Duodopa
Apomorphine
Deep brain stimulation - to still function substantial nigra cells to promote DA release

39
Q

What is a risk of interrupting therapy for parkinson’s?

A

Neuroleptic Malignant Syndrome - if therapy is stopped
Tachycardia
Epileptic Seizures

40
Q

As parkinson’s disease progresses?

A

Increase drug dose
Shorten intervals between doses
Drug combinations

41
Q

Look at slide 66

A
42
Q

What is drug induced parkinsons disease?

A

When a patient has been on a drug for prolonged period of time and it has caused muscular rigidity
A pronounced tremor in limbs and jaw
Difficulty walking - Not due to permanent damage so may last for 2 yrs

43
Q

What drugs can induce Parkinson’s

A

Antipsychotics - Chlorpromazine
Anti-emetics - cyclizine

44
Q

What are two surgery methods to treat parkinsons?

A

Pallidotomy - Help with dyskinesia - destroys internal globus pallidus
Thalamotomy - Treat severe tremor - destroys thalamus

Pharmacy Semester 2 (12 decks)

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