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CPT 1 > Parkinson's > Flashcards

Parkinson's Flashcards

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0
Q

What impact do the main symptoms of Parkinson’s have on the patient?

A 
Postural instability
Stooped posture
Hard to start/stop movements
Speech problems
Expressionless face
Depression
Writing problems
Difficulty swallowing
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1
Q

What are the most common symptoms of Parkinson’s disease?

A

Tremor, shaking
Rigidity - no smooth movements, broken down into smaller jerky parts
Bradykinesia - slowness of movement. Short shuffling steps

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2
Q

What factors can produce Parkinsonian symptoms, and is this the same as Parkinson’s disease?

A

Having a stroke, certain infections and certain drugs can all induce Parkinsonian symptoms, but this is not the same as Parkinson’s disease. When they cause is removed, the symptoms should clear.

Parkinson’s disease is currently unknown as to what causes it.

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3
Q

How common is Parkinson’s disease and how does it progress with age?

A

Most common neuro degenerative disease after Alzheimer’s.

It progresses with age, with higher likelihood as age increases.

Slightly higher instances in men than women.

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4
Q

What is happening in Parkinson’s disease?

A

Progressive loss of dopamine neurons in the substantia nigra which is a small part of the brain involved in motor control. ( located in the basal ganglia).

This means there is a reduction of dopamine in the striatum, which causes the symptoms.

Loss of 70-80% of neurons before symptoms begin to show.

There are some other pathways that are responsible for the lack of symptoms until the disease has progressed so far, that help the brain carry out normal function.

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5
Q

What is the substantia nigra?

A

Dark matter in the brain located in the basal ganglia.

Contains dopamine neurons.

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6
Q

What is the nigrostriatal pathway?

A

It controls motor control, and is responsible for 75% of brain dopamine. Released from substantia nigra into the striatum.

Cell bodies are in the substantia, neurons end in the striatum.

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7
Q

Are the dopamine neurons in the substantia nigra the only dopamine neurons?

A

No, we have other dopamine neurons in other locations that control diffent functions, such as emotional and behavioural control, and endocrine function.

In Parkinson’s it is the substantia nigra dopamine neurons that are preferentially affected in Parkinson’s.

Because of this it is important to realise that by increasing dopamine we can affect the other aras and produce side effects.

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8
Q

How would dopamine usually work in a nonparkinsons patient?

A

In this pathway dopamine is inhibitory, so it would normally reduce acetycholine which is excitatory.

Because of this the increased acetycholine in Parkinson’s patients there is over activity, which can cause involuntary muscle contractions.

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9
Q

What causes the death of dopamine neurons in Parkinson’s?

A 
There is no simple genetic test as only a small number of cases are thought to be genetic. In the rest of the cases it is not known what the cause is, it is believed that these neurones are particularly sensitive to certain abnormalities, such as:
Change in metabolism
Problem with mitochondrial activity
Calcium signalling
Abnormal deposition of protein
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10
Q

What environmental factors can cause Parkinsonian symptoms, and are these reversible?

A

Drugs - antipsychotics, calcium channel blockers.
Toxins - designed drugs
Pesticides and fungicide

If the neurones are damaged, they cannot be replaced.

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11
Q

How is Parkinson’s disease diagnosed?

A

Clinical observation
Detailed history
Difficult to diagnose because may diseases have similar symptoms.
Symptoms

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12
Q

What medical tests can be used to help support a diagnosis of Parkinson’s disease?

A

SPECT and MRI can be used to exclude leisions.

PET not recommended.

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13
Q

Apart from medication, what other support might a Parkinson’s patient need?

A 
Speech therapy
Physiotherapy
Dietician
Specialist nurse
Surgery
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14
Q

What is the aim of treatment in Parkinson’s disease?

A 
There is no cure.
Medication treats the symptoms, not the cause of neuro degeneration
Improve qualify of life
Minimise deterioration
Have minimal side effects
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15
Q

What are the two ways Parkinson’s patients can be targeted for in terms of medication?

A

Increase dopaminergic activity

Reduce cholinergic activity.

Both aim to restore the pathway balance in the basal ganglia.

16
Q

What drugs are avalible for patients who are diagnosed with early Parkinson’s?

A

Levodopa is a precursor of dopamine, and will be administered with a dopa decarboxylase(DDC) inhibitor.

Dopamine agonists

Mono amine oxidase b (MAO-B) inhibitors, which reduces how much dopamine is broken down.

Anti cholinergic drugs should not be used as 1st line treatment

17
Q

What is L dopa and why is it used?

A

It is a precursor to dopamine.

Dopamine cannot cross the blood brain barrier, so giving it as treatment would be ineffective.

18
Q

What is the dopamine uptake pathway?

A

Dopamine is a neurotransmitter.
It is manufactured in several steps from tyrosine.

Initially, tyrosine is convert to dopa( or L dopa) by tyrosine hydroxylase.
Ldopa is then decarboxylased by dopa decarboxylase, which yells dopamine.

In certain cells where there is the presence of specific enzymes, this can then be converted to noradrenaline, and then further converted to adrenaline.

19
Q

What is the degradation pathway for dopamine?

A

Dopamine is broken down by monoamine oxidase(MAO) into dihydroxyphenylacetic acid(DOPAC)

DOPAC is further broken down into homovanillic(HVA) by catechol-o-methyl-transferase (COMT).

These can also be targets of drug therapy.

20
Q

Why is it beneficial for diagnosis and treatment to start earlier in Parkinson’s?

A

Levodopa is taken up by the remaining dopaminergic neurons, and convert to dopamine by neuronal DDC.

This is why it is important for treatment to start as early as possible, as it requires remaining neurones to have an effect.

21
Q

What happens to oral Ldopa?

A

Good absorption, 98% in GI tract, but only In the early tract.

Unfortunately lots of DDC and MAO in Gi and liver, so 70-90% metabolised immediately. (Important to note this could also be converted into NA/A side effects )

The remaining Ldopa enters the systemic circulation, where there are more DDC and COMT break down all but 1%.

Only this 1% passes through the BBB

22
Q

What improvements will be seen with Ldopa treatment alone in Parkinson’s?

A

Improvement in initiating and stoping movement.
Smooth and faster more controlled movement.
Improved speech
Reduced tremor.

MUST be some neuronal DDC left for improvement to occur or there is no conversion.

23
Q

What are the side effects of giving Ldopa on its own in Parkinson’s?

A

Because there is a lot of dopamine released into the systemic circulation there are a lot of serious side effects.
Cardiac arrhythmia
Hypotension
Gi bleeding

24
Q

What could be given with Ldopa to prevent these peripheral side effects?

A

Levodopa should be given with a peripheral dopa decarboxylase inhibitor (DDCI)
This will not cross the BBB, and will only affect Ldopa in the peripheral

Examples carbidopa or benserazide.

Reduced side effects and increases specificity.

25
Q

How does administering a DDCI with levodopa affect dosing?

A

As less is broken down in the gut and liver, more reaches the systemic system. In the systemic system less is broken down and so more crosses the BBB.

This reduced the required dose three to four fold.

It also increases its half life by 50%

Also reduces side effects.

26
Q

What are examples of Parkinson’s drugs and what are the doses?

A

Sinemet and madopar.

Many different doses and combinations, tweaking needed throughout treatment.

27
Q

What drugs can interact with Parkinson’s drugs?

A 
Anaesthetics
Antidepressants
Hypnotics
Antipsychotics
Vitamin b6
28
Q

What form is levodopa supplied in?

A

Oral only main used so far.
Sustained release does not work as it only absorbed in the start of the gut.
Because of this skin nasal and rectal also ineffective.
Gel does work but very expensive so not used.

29
Q

What is the recommended treatments for Parkinson’s?

A

First line levodopa combination.
Dopamine agonists
MAOI b
2nd line b antagonists or anti cholinergic - can be first line in young people who only have tremor.

30
Q

What is important when ceasing or changing Parkinson’s medication?

A

Do not with draw abruptly, or allow to fail when absorption in patient is impaired.

High risk of neuroleptic malignant syndrome.

Make sure that patients can self manage medication even when in hospital, as the times they need to take it will be different in each patient, and when changed the Parkinson’s may become badly controlled.

31
Q

What are the two main classes of dopamine agonists, and what is an example?

A

Ergot derivatives vs non ergot derivative. Non preferred.

Ergot - cabergoline
Non ergot - ropinerole

32
Q

What are side effects expected with dopamine agonists for Parkinson’s?

A

Sleepiness with complications for driving.
Nausea and vomiting - can be given
Hallucination

33
Q

What is a rare condition that can develop in Parkinson’s patients, particularly in young patients?

A

Dopamine dysregulation syndrome.

Causes hyper sexuality, pathological gambling. Problem because dopamine feeds the reward system, so can be hard to reverse.

34
Q

What additional care should be taken with ergot derivative dopamine agonists?

A

Not suitable if patient has risk of heart value problems.

Must take regular ECG, blood test, echocardiogram and chest X-rays.

35
Q

What side effects do anti muscarinics have when given for Parkinson’s?

A 
Anti muscarinics block the parasympathetic system, so we expect is effects related to this.
Dry mouth
Constipation
Confusion
Hallucinations

Use with caution in patients with cv disease

36
Q

What is the long term problems with Parkinson’s treatment?

A

Progressive decline as treatment does not stop the death of the neurons.
Drugs become less effective as less neurons, and CNS becomes less sensitive to the dopamine that is there.

5/10 years into treatment it tends not to be working anymore, and the drug therapy can also now cause additional symptoms on top of additional Parkinson’s symptoms.

Increased psychiatric complications

37
Q

What is MOA-B and its use in Parkinson’s?

A

Monoamine oxidase b inhibitors work by reducing the breakdown of dopamine.
Can be used individually or in combination with l-dopa.

Causes hallucinations,confusion,insomnia.

CPT 1 (12 decks)

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