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integrated studies in mental health > parkinsons Mastered version > Flashcards

parkinsons Mastered version Flashcards

1
Q

What are the four clinical symptoms of Parkinson’s disease?

A

Bradykinesia, rigidity, tremor, and postural instability.

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2
Q

What is the definition of Parkinson’s disease?

A

Parkinson’s disease is a neurodegenerative, progressive disease primarily involving the dopamine generating neurones in the substantia nigra, characterized by bradykinesia, rigidity, tremor, and postural instability.

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3
Q

Who first described Parkinson’s disease and what did he call it?

A

British doctor James Parkinson first described Parkinson’s disease and called it “the shaking palsy.”

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4
Q

What was the major breakthrough in Parkinson’s disease research in the 1960s?

A

The major breakthrough was the link between the disease and the loss of cells that produce dopamine (DA), leading to the development of DA replacement therapies which still remain the mainstay of treatment to this day.

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5
Q

What is the epidemiology of Parkinson’s disease?

A

PD occurs in about 1% of the population aged 60 years and in about 4% at 80 years. There are also familial cases of early onset PD (age range 21–40 years) and a rarer form of juvenile onset PD (younger than 21 years of age).

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6
Q

What are some causes of Parkinsonism?

A

DRUGS – Anti psychotics, metaclopramide, TCA, MPTP, vascular disease, Parkinson plus syndromes (multiple system atrophy, progressive supranuclear palsy, corticobasal degeneration, Lewy-body dementia), and trauma.

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7
Q

What are the core diagnostic symptoms of Parkinson’s disease?

A

The core diagnostic symptoms are bradykinesia, rigidity, and tremor.

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8
Q

What are some initial symptoms of Parkinson’s disease?

A

Initial symptoms include persistent mild fatigue, handwriting might become “shaky,” the person might feel unbalanced or have difficulty performing sit-to-stands, agitation, irritability, & depression, lack of affect (masked face phenom), and initial symptoms can go on for years.

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9
Q

What are some motor symptoms of Parkinson’s disease?

A

Motor symptoms include hand tremors, rigidity or resistance to movement, spontaneous movements becoming progressively slower and may actually cease (bradykinesia), and impaired balance and coordination (postural instability).

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10
Q

What is rigidity in Parkinson’s disease?

A

In PD, both sets of muscles remain engaged and contracted, leading to rigidity.

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11
Q

What is postural instability in Parkinson’s disease?

A

Postural instability in PD refers to patients leaning unnaturally backward or forward, head down and stooped stance, and becoming vulnerable to falls.

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12
Q

What are some non-motor symptoms of Parkinson’s disease?

A

Non-motor symptoms include depression, emotional changes (irritable, pessimistic, fearful, become dependent or isolated), memory loss (slower thought processes) leading to dementia with Lewy Bodies (DLB), swallowing difficulties, speech problems, bladder/bowel disorders, excessive sweating, and sleep disturbance.

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13
Q

What is Parkinsonism?

A

Parkinsonism refers to a neurological syndrome characterized by tremor, bradykinesia, and rigidity.

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14
Q

What is bradykinesia?

A

Bradykinesia is slowness of movement and is a core diagnostic symptom of Parkinson’s disease.

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15
Q

What is tremor in Parkinson’s disease?

A

Tremor in PD is a rhythmic back-and-forth motion of the thumb, and is a core diagnostic symptom of the disease

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16
Q

What is the classic triad of symptoms in Parkinson’s disease?

A

The classic triad of symptoms in Parkinson’s disease includes
bradykinesia (slowness),
rigidity (stiffness/increased tone),
and tremor (pill rolling/resting), along with postural instability.

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17
Q

What are some non-motor symptoms of Parkinson’s disease?

A

Non-motor symptoms of Parkinson’s disease can include depression, emotional changes (irritable, pessimistic, fearful, become dependent or isolated), memory loss leading to dementia with Lewy Bodies (DLB), swallowing difficulties, speech problems, bladder/bowel disorders, excessive sweating, and sleep disturbance.

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18
Q

What is the core pathology of Parkinson’s disease?

A

A: The degeneration of pigmented neurons in the pars compacta of the substantia nigra.

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19
Q

What are Lewy bodies, and what do they contain?

A

A: Lewy bodies are aggregates that contain a protein called alpha-synuclein (AS).

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20
Q

What is the function of alpha-synuclein in a healthy brain?

A

A: Alpha-synuclein is expressed in presynaptic terminals and controls neurotransmitter release.

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21
Q

How does increased expression of alpha-synuclein lead to Parkinson’s disease?

A

A: Increased expression of alpha-synuclein leads to AS aggregation which are lewy bodies that these lewy bodies causes death of SN neurons, and vulnerability to developing PD.

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22
Q

Is there a link between normal aging and Parkinson’s disease?

A

A: Yes, normal aging is associated with increased expression of alpha-synuclein, which can increase inherent vulnerability to developing PD.

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23
Q

What brain regions are involved in motor control, cognitive processing, and emotional regulation?

A

A: The basal ganglia, cerebellum, thalamus, brainstem, spinal cord, premotor and cerebral cortex association, and limbic cortex.

8

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24
Q

What is the role of the basal ganglia in movement?

A

A: The basal ganglia is responsible for the initiation, control, and modulation of movement.

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25
Q

How does Parkinson’s disease disrupt the parallel organization of the basal ganglia?

A

A: Parkinson’s disease impairs the balance between the direct and indirect pathways of the basal ganglia, leading to the characteristic motor symptoms of the disease.

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26
Q

What is the function of the thalamus in the brain?

A

A: The thalamus relays sensory and motor information to the cortex.

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27
Q

What is the role of the limbic cortex in Parkinson’s disease?

A

A: Dysfunction in the limbic cortex can lead to emotional and behavioral disturbances, such as depression and anxiety.

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28
Q

What is disrupted in the parallel organization in Parkinson’s disease?

A

A: The loss of dopamine-producing neurons in the substantia nigra disrupts the balance between the direct and indirect pathways of the basal ganglia.

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29
Q

How does the loss of dopamine in the direct pathway affect movement in Parkinson’s disease?

A

A: The loss of dopamine in the direct pathway impairs the ability to initiate movement, resulting in bradykinesia.

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30
Q

How does the overactivity of the indirect pathway contribute to motor symptoms in Parkinson’s disease?

A

A: The overactivity of the indirect pathway leads to excessive inhibition of movement, resulting in rigidity, tremor, and other motor symptoms.

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31
Q

What other neurotransmitters can be affected by the loss of dopamine in Parkinson’s disease?

A

A: The loss of dopamine can lead to changes in the activity of other neurotransmitters, such as acetylcholine and serotonin, which can contribute to some of the non-motor symptoms of the disease.

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32
Q

What other brain regions can be affected by Parkinson’s disease?

A

A: Parkinson’s disease can also affect other brain regions, such as the thalamus, which can contribute to some of the other motor symptoms of the disease, such as freezing of gait.

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33
Q

What is the substantia nigra, and what neurotransmitter does it produce?

A

A: The substantia nigra is a region of the midbrain that produces dopamine, a neurotransmitter critical for the regulation of movement.

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34
Q

What is the globus pallidus, and what is its function within the basal ganglia?

A

A: The globus pallidus is a nucleus within the basal ganglia that receives input from the striatum and sends inhibitory signals to the thalamus.

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35
Q

What is the subthalamic nucleus, and what is its function within the basal ganglia?

A

A: The subthalamic nucleus is a nucleus within the basal ganglia that receives input from the cortex and sends excitatory signals to the globus pallidus.

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36
Q

What is the striatum, and what is its function within the basal ganglia?

A

A: The striatum is a nucleus within the basal ganglia that receives input from the cortex and the substantia nigra pars compacta. it relays this information to the other structures in the basal ganglia

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37
Q

What is the substantia nigra pars compacta, and what neurotransmitter is primarily produced there?

A

A: The substantia nigra pars compacta is a subregion of the substantia nigra that contains dopamine producing neurons.

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38
Q

What is the substantia nigra pars reticulata SNr, and what is its function within the basal ganglia?

A

A: The substantia nigra pars reticulata is a subregion of the substantia nigra that sends inhibitory signals to the thalamus.

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39
Q

Globus Pallidus Externa (GPe) what pathway is it part of and what is its function in the basal ganglia?

A

it is Part of the indirect pathway. It receives inhibitory signals from the striatum and sends inhibitory signals to the STN and to the GPi/SNr through the indirect pathway.

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40
Q

Subthalamic Nucleus (STN): what pathway is it part of and what is its function in the basal ganglia?

A

Subthalamic Nucleus (STN) is Involved in the indirect pathway. It receives inhibitory signals from the GPe and sends excitatory signals to the GPi and SNr.

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41
Q

what is the thalamus and what is its function in Parkinson’s? what modulates its activity?

A

Thalamus: A relay station in the brain that sends excitatory signals to the cerebral cortex. The activity of thalamic neurons is modulated by inhibitory signals from the GPi and SNr.

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42
Q

Motor Cortex: what is the function in relation to parkinsons?

A

Receives excitatory input from the thalamus and sends motor commands to the muscles.

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43
Q

What are D1 receptors, and where are they primarily located within the basal ganglia?

A

A: D1 receptors are a subtype of dopamine receptors that are primarily located in the direct pathway of the basal ganglia.

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44
Q

What is substance P, and where is it released in the basal ganglia?

A

A: Substance P is a neuropeptide that is released by striatal neurons in the direct pathway of the basal ganglia.

45
Q

What is GABA, and where is it released in the basal ganglia?

A

A: Gamma-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the brain and is released by striatal neurons in the indirect pathway of the basal ganglia.

46
Q

What are D2 receptors, and where are they primarily located within the basal ganglia?

A

A: D2 receptors are a subtype of dopamine receptors that are primarily located in the indirect pathway of the basal ganglia.

47
Q

What is the direct pathway of the basal ganglia, and how is it normally activated by dopamine?

A

Direct Pathway (facilitates voluntary movement):
1. Dopamine from substantia nigra pars compacta (SNc) binds to D1 receptors on Medium Spiny Neurons (MSNs) in the striatum, activating them.
2. Activated MSNs release GABA, inhibiting the globus pallidus interna (GPi) and substantia nigra pars reticulata (SNr).
3. This inhibition (“disinhibition”) of the GPi and SNr results in reduced inhibitory signals to the thalamus.
4. The thalamus, now disinhibited, sends excitatory signals to the motor cortex, facilitated by the neurotransmitter glutamate.
5. The motor cortex responds by sending commands to the muscles to initiate movement.

48
Q

How does the loss of dopamine from the substantia nigra affect the direct pathway in Parkinson’s disease?

A

Direct Pathway: Normally, dopamine acts on D1 receptors in this pathway to promote movement. With less dopamine, there’s less stimulation of D1 receptors on the medium spiny neurons (MSNs) in the striatum. This results in less inhibition of the globus pallidus interna (GPi) and the substantia nigra pars reticulata (SNr), the output nuclei of the basal ganglia. As a result, these structures send more inhibitory signals to the thalamus. This, in turn, means less excitation of the motor cortex and less initiation of movement. So overall, the effect of reduced dopamine in the direct pathway is less facilitation of movement, contributing to the motor symptoms seen in Parkinson’s disease (bradykinesia)

49
Q

What is the indirect pathway of the basal ganglia, and how is it normally inhibited by dopamine?

A

Indirect Pathway (inhibits and modulates movements):
1. Dopamine from substantia nigra pars compacta (SNc) binds to D2 receptors on MSNs in the striatum, inhibiting them.
2. Inhibited MSNs release less GABA, reducing the inhibition of the globus pallidus externa (GPe).
3. Reduced inhibition of GPe increases the input of excitation (glutamate) in the GPi via the STN
4. Increased excitatory input to GPi results in increased inhibitory output to the thalamus.
5. The thalamus sends fewer excitatory signals to the motor cortex due to increased inhibition.
6. The motor cortex responds by sending fewer commands to the muscles, thus suppressing or modulating unnecessary movements.

50
Q

How does the loss of dopamine from the substantia nigra affect the indirect pathway in Parkinson’s disease?

A

Medium Spiny Neurons (MSNs) in the striatum will not be inhibited by dopamine. These neurons are inhibitory in nature, meaning they release inhibitory neurotransmitters, particularly GABA (gamma-aminobutyric acid), when they are activated.

With MSNs not inhibited by dopamine, they become more active and release more GABA onto the neurons in the external segment of the globus pallidus (GPe).

This increased inhibition reduces the activity of the GPe. As the GPe normally inhibits the subthalamic nucleus (STN), this leads to more activity in the STN.

The STN, in turn, sends excitatory signals to the internal segment of the globus pallidus (GPi) and the substantia nigra pars reticulata (SNr), increasing their activity.

The GPi and SNr send inhibitory signals to the thalamus. With their activity increased, they send more inhibitory signals, which reduces the activity of the thalamus.

The thalamus sends fewer excitatory signals to the motor cortex, resulting in decreased motor activity.

51
Q

What is the overall effect of the disruption of the balance between the direct and indirect pathways in Parkinson’s disease?

A

A: The disruption of the balance between the direct and indirect pathways in Parkinson’s disease leads to the characteristic motor symptoms of the disease, such as bradykinesia, rigidity, and tremor.

52
Q

What is the main target of dopamine produced by SN neurons in the basal ganglia? what is another name for the striatum?

A

A: The main targets of dopamine produced by SN neurons are the caudate nucleus and putamen (striatum), which are involved in the regulation of movement.

53
Q

What is the extrapyramidal motor system, and how is it involved in the regulation of movement?

A

A: The extrapyramidal motor system is a network of neural pathways in the brain that is involved in the regulation of movement, particularly movements that are not under conscious control, such as reflexes and automatic movements. The basal ganglia pathway is a key component of the extrapyramidal motor system.

54
Q

What happens when cells of the substantia nigra degenerate in Parkinson’s disease?

A

A: When cells of the substantia nigra degenerate in Parkinson’s disease, the neurons of the striatum are no longer well regulated, resulting in loss of control of movements and the characteristic symptoms of Parkinson’s disease.

55
Q

Which brain region is affected by locus coeruleus degeneration, and what non-motor symptoms can result from this?

A

A: Locus coeruleus degeneration can occur in Parkinson’s disease, resulting in emotional changes, anxiety, and stress.

56
Q

Which brain region is affected by degeneration of the Nucleus Basalis of Meyenert, and what non-motor symptoms can result from this?

A

A: The Nucleus Basalis of Meyenert can degenerate in Parkinson’s disease, leading to memory and cognitive impairments.

57
Q

What role does the enteric nervous system play in Parkinson’s disease, and what non-motor symptoms can result from its dysfunction?

A

A: The enteric nervous system, which regulates the gastrointestinal tract, can be affected in Parkinson’s disease, leading to symptoms such as constipation, difficulty swallowing, and drooling.

58
Q

What is idiopathic PD, and what percentage of cases fall under this category?

A

A: Idiopathic PD refers to cases of Parkinson’s disease where the cause is unknown. The majority of cases of Parkinson’s disease fall under this category.

59
Q

How can genetics play a role in the development of Parkinson’s disease?

A

A: Genetics can play a role in the development of Parkinson’s disease, particularly mutations in the alpha-synuclein gene.

60
Q

What environmental factor has been linked to Parkinson’s disease, and how does it lead to cell death?

A

A: Toxins such as MPTP have been linked to Parkinson’s disease, as they can induce oxidative stress and impair energy regulation, leading to cell death.

61
Q

How does oxidative stress contribute to the development of Parkinson’s disease?

A

A: Oxidative stress can contribute to the development of Parkinson’s disease by impairing energy regulation and leading to cell death.

62
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.

63
Q

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

A

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

64
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.

65
Q

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

A

Bradykinesia and rigidity.

66
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.

67
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).

68
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.

69
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.

70
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

71
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.

72
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.

73
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.

74
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.

75
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.

76
Q

How do dopamine receptor agonists act on dopamine receptors?

A

Dopamine receptor agonists act directly on selected dopamine receptors.

77
Q

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

A

Psychiatric side effects such as impulse control and pathological gambling.

78
Q

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

A

Bromocriptine.

79
Q

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

A

Pergolide.

80
Q

What potential side effect is associated with Pergolide?

A

Valvular heart disease.

81
Q

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

A

Pramipexole.

82
Q

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

A

Ropinirole.

83
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.

84
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.

85
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.

86
Q

What is rasagiline and how does it differ from selegiline?

A

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

87
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.

88
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.

89
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.

90
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.

91
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.

92
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.

93
Q

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

A

Rasagiline is a more potent MAO-B inhibitor than selegiline

94
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.

95
Q

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

A

Benzotropine and Orphenadrine.

96
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.

97
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.

98
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.

99
Q

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

A

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

100
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.

101
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.

102
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.

103
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.

104
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.

105
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.

106
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.

107
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.

108
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.

integrated studies in mental health (20 decks)

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