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mental health modified > parkinsons Mastered version > Flashcards

parkinsons Mastered version Flashcards

1
Q

What is the mainstay of first-line therapy for PD?

A

DA replacement, using levodopa (L-DOPA) which is converted to dopamine in the brain.

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2
Q

Why can’t dopamine be administered directly for PD treatment?

A

Dopamine itself cannot cross the blood-brain barrier (BBB).

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3
Q

How is L-DOPA administered to ensure it reaches the brain?

A

A preparation containing L-DOPA and a peripheral dopa decarboxylase inhibitor (e.g. Benzerazide or Carbidopa) is used to prevent degradation of L-DOPA by dopa decarboxylase in the periphery, which effectively extends the duration of drug action and minimises peripheral side effects.

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4
Q

What are the common motor symptoms of PD that L-DOPA can effectively treat?

A

Bradykinesia and rigidity.

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5
Q

What is the ON/OFF phenomenon related to L-DOPA treatment?

A

It refers to the marked improvement in mobility (ON) and marked akinesia (OFF) that can occur after 4-6 years and in most patients within 10 years of treatment.

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6
Q

What are some early side effects of L-DOPA treatment?

A

Gastrointestinal side effects, cardiovascular side effects, orthostatic or postural hypotension, behavioral side effects, and abnormal involuntary movements (dyskinesia).

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7
Q

How does the effectiveness of L-DOPA treatment change over time?

A

Although initially effective, its effectiveness diminishes with time and long-term use can lead to motor fluctuations, which are related to the timing of L-DOPA intake.

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8
Q

What is the mechanism of action of dopamine replacement therapy in Parkinson’s disease (L-DOPA)?
Answer:

A

The mechanism of action involves replacing the lost dopamine in the brain using a precursor amino acid called levodopa, which can cross the blood-brain barrier and be converted to dopamine in the brain.

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9
Q

Why are peripheral dopa decarboxylase inhibitors used with levodopa? WHAT DRUG IS IN THIS CLASS?
Answer:

A

Levodopa is susceptible to degradation by the enzyme dopa decarboxylase, which is also present in the periphery. Peripheral dopa decarboxylase inhibitors such as carbidopa or benzerazide are used to effectively extend the duration of drug action and minimize peripheral side effects. carbidopa or benzerazide

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10
Q

What is the role of dopamine receptor agonists in treating motor symptoms of Parkinson’s disease?
Answer:

A

Dopamine receptor agonists can activate dopamine receptors and improve motor symptoms of Parkinson’s disease.

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11
Q

What are the side effects of antimuscarinic drugs?
Answer:

A

Antimuscarinic drugs can improve tremor and rigidity, but they may cause cognitive side effects.

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12
Q

How can the breakdown of dopamine be prevented to prolong its effects?
Answer:

A

Monoamine oxidase inhibitors and catechol-O-methyl transferase inhibitors can prevent the breakdown of dopamine and prolong its effects.

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13
Q

What is the mechanism of action of Amantadine in Parkinson’s disease?

A

Amantadine acts by releasing dopamine from intact dopamine terminals in the striatum.

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14
Q

Why are dopaminergic agonists potentially useful as a first-line treatment option for early PD?

A

Dopaminergic agonists delay the onset of motor fluctuations and dyskinesia and have longer half-lives than L-DOPA, reducing peaks and troughs and preventing motor complications.

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15
Q

How do dopamine receptor agonists act on dopamine receptors?

A

Dopamine receptor agonists act directly on selected dopamine receptors.

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16
Q

What are some potential side effects associated with dopamine receptor agonists?

A

Psychiatric side effects such as impulse control and pathological gambling.

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17
Q

Which dopamine receptor agonist is widely used for PD and endocrine disorders and is an agonist at D2 receptors?

A

Bromocriptine.

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18
Q

Which dopamine receptor agonist is an agonist at D1 & D2 receptors and potentially more effective than Bromocriptine?

A

Pergolide.

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19
Q

What potential side effect is associated with Pergolide?

A

Valvular heart disease.

20
Q

Which dopamine receptor agonist is an agonist at D3 receptors and may lessen affective symptoms of PD?

A

Pramipexole.

21
Q

Which dopamine receptor agonist is a selective agonist at D2 receptors and effective in “smoothening” the response to L-Dopa?

A

Ropinirole.

22
Q

What is the mechanism of action of Apomorphine in advanced cases of PD?

A

Apomorphine is a potent dopamine receptor agonist administered s.c under specialist conditions and can be helpful in advanced cases unresponsive to other therapies for refractory motor fluctuations.

23
Q

What is the mechanism of action of monoamine oxidase inhibitors (MAOIs) in Parkinson’s disease?

A

MAOIs inhibit the breakdown of dopamine by MAO-B, leading to an increase in the amount of dopamine in the brain.

24
Q

What is selegiline and how is it used in the treatment of Parkinson’s disease?

A

Selegiline is an irreversible inhibitor of MAO-B, which prolongs the antiparkinsonian effect of L-dopa by preventing dopamine breakdown. It is used as adjunctive therapy with declining effects of L-dopa in later stages.

25
Q

What is rasagiline and how does it differ from selegiline?

A

Rasagiline is a more potent MAO-B inhibitor than selegiline.

26
Q

What is the mechanism of action of catechol-O-methyl transferase (COMT) inhibitors?

A

COMT inhibitors such as entacapone and tolcapone prolong the activity of L-dopa by preventing its peripheral breakdown, leading to more L-dopa reaching the brain.

27
Q

How are COMT inhibitors used in the treatment of Parkinson’s disease?

A

COMT inhibitors are used as adjunct therapy to L-dopa in patients experiencing end-of-dose off symptoms.

28
Q

What are the two types of MAO in the brain and what do they metabolize?

A

The two types of MAO in the brain are MAO-A, which metabolizes noradrenaline and serotonin, and MAO-B, which metabolizes dopamine.

29
Q

What is entacapone and how does it differ from tolcapone?

A

Entacapone and tolcapone are both COMT inhibitors, but entacapone is a peripheral inhibitor only, whereas tolcapone is a central and peripheral inhibitor.

30
Q

What is the main benefit of using MAOIs or COMT inhibitors in the treatment of Parkinson’s disease?

A

The main benefit of using MAOIs or COMT inhibitors is to prolong the effect of L-dopa and reduce fluctuations in motor function.

31
Q

What is the role of COMT inhibitors in the management of end-of-dose off symptoms?

A

COMT inhibitors can be used as adjunct therapy to L-dopa in patients experiencing end-of-dose off symptoms.

32
Q

What is the difference between selegiline and rasagiline in terms of potency?

A

Rasagiline is a more potent MAO-B inhibitor than selegiline

33
Q

What is the mechanism of action of antimuscarinic drugs in Parkinson’s disease?

A

Antimuscarinic drugs block muscarinic cholinergic receptors to alleviate the imbalance caused by the lack of inhibitory effect of dopamine and over-excitation by cholinergic neurons in the striatum.

34
Q

Which drugs are classified as antimuscarinic drugs for Parkinson’s disease?

A

Benzotropine and Orphenadrine.

35
Q

What non-motor symptoms are associated with Parkinson’s disease?

A

Depression, psychosis, dementia, sleep disorders, restless legs syndrome, periodic limb movements of sleep, REM sleep behaviour disorder, falls, autonomic disturbance, urinary dysfunction, weight loss, dysphagia, constipation, erectile dysfunction, orthostatic hypotension, excessive sweating, and sialorrhoea.

36
Q

Which types of non-motor symptoms are associated with Parkinson’s disease sleep disorders?

A

Restless legs syndrome, periodic limb movements of sleep, and REM sleep behaviour disorder.

37
Q

Which drugs can be used to treat non-motor symptoms in Parkinson’s disease?

A

Clonazepam, movicol, citalopram, quetiapine, clozapine, acetylcholinesterase inhibitors, oxybutynin, and tolterodine.

38
Q

What non-medical treatments are available for Parkinson’s disease?

A

Brain grafts and stem cell therapy, and deep brain stimulation.

39
Q

What is the purpose of deep brain stimulation in Parkinson’s disease?

A

Deep brain stimulation is used to alleviate the motor symptoms of Parkinson’s disease by providing electrical stimulation to specific regions of the brain.

40
Q

What are the side effects associated with antimuscarinic drugs for Parkinson’s disease?

A

Antimuscarinic drugs may cause cognitive and autonomic side effects, such as urinary dysfunction, constipation, erectile dysfunction, orthostatic hypotension, excessive sweating, and sialorrhoea.

41
Q

What non-motor symptom of Parkinson’s disease can be treated with clonazepam?

A

Clonazepam can be used to treat sleep disorders in Parkinson’s disease.

42
Q

What non-motor symptom of Parkinson’s disease can be treated with movicol?

A

Movicol can be used to treat constipation in Parkinson’s disease.

43
Q

What non-motor symptom of Parkinson’s disease can be treated with citalopram?

A

Citalopram can be used to treat depression in Parkinson’s disease.

44
Q

What non-motor symptoms of Parkinson’s disease can be treated with quetiapine and clozapine?

A

Quetiapine and clozapine can be used to treat psychosis and dementia in Parkinson’s disease.

45
Q

What non-motor symptom of Parkinson’s disease can be treated with acetylcholinesterase inhibitors?

A

Acetylcholinesterase inhibitors can be used to treat cognitive impairment in Parkinson’s disease.

46
Q

What non-motor symptoms of Parkinson’s disease can be treated with oxybutynin and tolterodine?

A

Oxybutynin and tolterodine can be used to treat urinary dysfunction and excessive sweating in Parkinson’s disease.

47
Q

WHAT IS THE FIRST LINE TREATMENT FOR NON MOTOR SYMPTOMS?

A

There is no specific first-line treatment for non-motor symptoms in Parkinson’s disease because the choice of treatment depends on the particular symptom and the individual patient. Treatment options include medications such as antidepressants, antipsychotics, and acetylcholinesterase inhibitors, as well as non-pharmacological interventions such as cognitive-behavioral therapy and physical therapy. The selection of treatment depends on the specific non-motor symptom and the individual patient’s needs and preferences.

mental health modified (11 decks)

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