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Questions and Answers
What is the primary mechanism of action for Amantadine in treating Parkinson's disease?
What is the primary mechanism of action for Amantadine in treating Parkinson's disease?
- Direct stimulation of dopamine receptors
- Inhibition of acetylcholinesterase
- Release and reuptake of dopamine (correct)
- Release and reuptake of serotonin
Why are anticholinergics considered less effective for treating bradykinesia in Parkinson's disease?
Why are anticholinergics considered less effective for treating bradykinesia in Parkinson's disease?
- They enhance motor neuron excitability
- They only alleviate tremor and rigidity (correct)
- They have sedative effects that impair movement
- They primarily target serotonin pathways
What is a significant side effect associated with the use of Amantadine?
What is a significant side effect associated with the use of Amantadine?
- Cognitive decline
- Urinary retention (correct)
- Severe hypertension
- Severe hallucinations
Which statement about Rasagiline is true?
Which statement about Rasagiline is true?
What condition should be avoided when prescribing Amantadine?
What condition should be avoided when prescribing Amantadine?
What is the primary reason neurodegenerative diseases are often difficult to treat?
What is the primary reason neurodegenerative diseases are often difficult to treat?
Which of the following is NOT one of the cardinal motor features of Parkinson’s disease?
Which of the following is NOT one of the cardinal motor features of Parkinson’s disease?
Which neurotransmitter is primarily involved in regulating muscle movement in Parkinson’s disease?
Which neurotransmitter is primarily involved in regulating muscle movement in Parkinson’s disease?
Which of the following describes a characteristic pathway of dopaminergic neurons?
Which of the following describes a characteristic pathway of dopaminergic neurons?
What is a non-motor symptom associated with Parkinson’s disease?
What is a non-motor symptom associated with Parkinson’s disease?
Excessive excitotoxicity in the central nervous system is primarily caused by which substance?
Excessive excitotoxicity in the central nervous system is primarily caused by which substance?
Which age group is primarily affected by Parkinson’s disease?
Which age group is primarily affected by Parkinson’s disease?
Which process is NOT a cause of neuronal damage in neurodegenerative diseases?
Which process is NOT a cause of neuronal damage in neurodegenerative diseases?
What is a common central side effect of levodopa therapy?
What is a common central side effect of levodopa therapy?
Which of the following is a known peripheral side effect of levodopa?
Which of the following is a known peripheral side effect of levodopa?
What medication is commonly used to manage levodopa-induced nausea?
What medication is commonly used to manage levodopa-induced nausea?
Which receptor type is primarily overstimulated in the development of dyskinesia due to levodopa?
Which receptor type is primarily overstimulated in the development of dyskinesia due to levodopa?
How does long-term levodopa use affect dopamine receptors in the brain?
How does long-term levodopa use affect dopamine receptors in the brain?
What is the primary risk associated with the use of tolcapone?
What is the primary risk associated with the use of tolcapone?
Which atypical antipsychotic is mentioned as being used to treat levodopa-induced psychosis?
Which atypical antipsychotic is mentioned as being used to treat levodopa-induced psychosis?
What is the primary reason a D2 blocker like metoclopramide is not used for levodopa-induced nausea?
What is the primary reason a D2 blocker like metoclopramide is not used for levodopa-induced nausea?
What characterizes Primary Parkinson’s Disease?
What characterizes Primary Parkinson’s Disease?
Which of the following is a form of Secondary Parkinsonism?
Which of the following is a form of Secondary Parkinsonism?
What is the primary goal of Parkinson's treatment?
What is the primary goal of Parkinson's treatment?
Why does levodopa require large doses for effectiveness?
Why does levodopa require large doses for effectiveness?
How does carbidopa benefit the treatment of Parkinson’s disease?
How does carbidopa benefit the treatment of Parkinson’s disease?
What does the presence of oxidative stress correlate with in Parkinson’s Disease?
What does the presence of oxidative stress correlate with in Parkinson’s Disease?
Which treatment specifically targets tremors and rigidity in Parkinson's disease?
Which treatment specifically targets tremors and rigidity in Parkinson's disease?
What is a significant challenge in using levodopa for treatment?
What is a significant challenge in using levodopa for treatment?
What is a significant advantage of dopamine receptor agonists over levodopa?
What is a significant advantage of dopamine receptor agonists over levodopa?
Which of the following is an adverse effect associated with dopamine receptor agonists?
Which of the following is an adverse effect associated with dopamine receptor agonists?
In what scenario is apomorphine predominantly used?
In what scenario is apomorphine predominantly used?
Which is true about the MAOB inhibitor deprenyl?
Which is true about the MAOB inhibitor deprenyl?
What is a potential drug-disease interaction with bromocriptine?
What is a potential drug-disease interaction with bromocriptine?
Which statement about the effects of dopamine receptor agonists is correct?
Which statement about the effects of dopamine receptor agonists is correct?
Which medication is taken orally as a dopamine receptor agonist?
Which medication is taken orally as a dopamine receptor agonist?
What is a common side effect of deprenyl?
What is a common side effect of deprenyl?
What is the physiological effect of D1 receptor stimulation in renal blood vessels?
What is the physiological effect of D1 receptor stimulation in renal blood vessels?
What phenomenon describes the gradual fading of improvement from levodopa medication before the next dose?
What phenomenon describes the gradual fading of improvement from levodopa medication before the next dose?
How can high protein diets affect the absorption of L-dopa?
How can high protein diets affect the absorption of L-dopa?
Which strategy can not help overcome the on-off phenomenon of levodopa?
Which strategy can not help overcome the on-off phenomenon of levodopa?
What effect does Vitamin B6 (pyridoxine) have on the efficacy of L-dopa?
What effect does Vitamin B6 (pyridoxine) have on the efficacy of L-dopa?
What is a potential risk of combining levodopa with nonselective MAO inhibitors?
What is a potential risk of combining levodopa with nonselective MAO inhibitors?
Which side effect may occur in patients taking anti-psychotics that block D2 receptors?
Which side effect may occur in patients taking anti-psychotics that block D2 receptors?
What condition should cardiac patients be monitored for when using dopaminergic drugs?
What condition should cardiac patients be monitored for when using dopaminergic drugs?
Flashcards
Parkinson's Disease
Parkinson's Disease
Progressive neurological disorder affecting muscle movement, characterized by slowness of movement (bradykinesia), muscle rigidity, resting tremor, and abnormal gait. In late stages, it can lead to akinesia, where the patient is immobile.
Akinesia
Akinesia
A state of complete or almost complete loss of movement.
Bradykinesia
Bradykinesia
A decrease in the ability to move quickly and smoothly
Muscle Rigidity
Muscle Rigidity
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Resting Tremor
Resting Tremor
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Abnormal Gait
Abnormal Gait
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Neurodegenerative Disease
Neurodegenerative Disease
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Apoptosis
Apoptosis
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What is Primary Parkinson's disease?
What is Primary Parkinson's disease?
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What is Secondary Parkinson's disease?
What is Secondary Parkinson's disease?
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What is the treatment goal for PD?
What is the treatment goal for PD?
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How does Levodopa (L-dopa) work?
How does Levodopa (L-dopa) work?
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Why are large doses of Levodopa needed?
Why are large doses of Levodopa needed?
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What is the purpose of Carbidopa and Benserazide?
What is the purpose of Carbidopa and Benserazide?
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What is 'Wear-off phenomenon' in Parkinson's treatment?
What is 'Wear-off phenomenon' in Parkinson's treatment?
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What is the 'On-Off phenomenon' in Parkinson's treatment?
What is the 'On-Off phenomenon' in Parkinson's treatment?
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How does levodopa affect the pupils?
How does levodopa affect the pupils?
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How does protein intake affect levodopa absorption?
How does protein intake affect levodopa absorption?
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What is the mechanism of action of levodopa?
What is the mechanism of action of levodopa?
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How does levodopa cross the blood-brain barrier?
How does levodopa cross the blood-brain barrier?
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How does vitamin B6 affect levodopa's efficacy?
How does vitamin B6 affect levodopa's efficacy?
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Why are non-selective MAO inhibitors problematic with levodopa?
Why are non-selective MAO inhibitors problematic with levodopa?
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What are MAOB inhibitors?
What are MAOB inhibitors?
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What is Rasagiline?
What is Rasagiline?
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What is Amantadine?
What is Amantadine?
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What are anticholinergic drugs?
What are anticholinergic drugs?
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Give examples of anticholinergic drugs used to treat Parkinson's disease.
Give examples of anticholinergic drugs used to treat Parkinson's disease.
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Peripheral dopa decarboxylase inhibitors
Peripheral dopa decarboxylase inhibitors
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COMT inhibitors
COMT inhibitors
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Dyskinesia
Dyskinesia
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Central side effects of L-dopa
Central side effects of L-dopa
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Nausea, vomiting, and anorexia due to L-dopa
Nausea, vomiting, and anorexia due to L-dopa
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Domperidone
Domperidone
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Tachycardia, arrhythmia, and postural hypotension
Tachycardia, arrhythmia, and postural hypotension
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Tolcapone
Tolcapone
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What are dopamine receptor agonists and how do they work?
What are dopamine receptor agonists and how do they work?
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When are dopamine receptor agonists used in Parkinson's disease?
When are dopamine receptor agonists used in Parkinson's disease?
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What are the common side effects of dopamine receptor agonists?
What are the common side effects of dopamine receptor agonists?
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What are the specific risks associated with bromocriptine?
What are the specific risks associated with bromocriptine?
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How is apomorphine used in Parkinson's Disease treatment?
How is apomorphine used in Parkinson's Disease treatment?
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What are the different forms and uses of non-ergot dopamine receptor agonists?
What are the different forms and uses of non-ergot dopamine receptor agonists?
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How does Deprenyl affect dopamine levels?
How does Deprenyl affect dopamine levels?
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How is Deprenyl used in treating Parkinson's Disease?
How is Deprenyl used in treating Parkinson's Disease?
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Study Notes
Drugs Affecting the Central Nervous System
- Neurodegenerative diseases involve neuronal damage in specific brain areas.
- Neuronal damage is caused by excitotoxicity (excess glutamate acting on NMDA receptors), stroke, head trauma, oxidative stress (free radicals like OH), and apoptosis (programmed cell death).
- Neurodegenerative diseases like Parkinson's, Alzheimer's, Huntington's, and Multiple sclerosis are challenging to treat due to the inability of CNS neurons to regenerate once damaged. Treatment focuses on symptom management rather than disease progression.
Antiparkinsonian Drugs
- Dopamine (DA) is a precursor to norepinephrine and a neurotransmitter in major dopaminergic pathways (nigrostriatal, mesolimbic-mesocortical, tuberoinfundibular, and chemoreceptor trigger zone).
- The nigrostriatal pathway regulates movement (kinesis).
- The mesolimbic-mesocortical pathway regulates cognitive functions and sensory perceptions.
- The tuberoinfundibular pathway regulates prolactin.
- Dopamine pathways in the brain's substantia nigra are damaged in Parkinson's disease.
Parkinson's Disease
- Parkinson's Disease (PD) is a progressive neurological disorder affecting muscle movement, characterized by four cardinal motor features: bradykinesia (slow movement), rigidity, resting tremor, and abnormal posture/gait (shuffling gait).
- Non-motor symptoms include depression, dementia, and sleep disturbances.
- PD most commonly affects individuals over 65.
- The etiology involves a balance imbalance between inhibitory dopaminergic (DA) neurons and excitatory cholinergic (Ach) neurons.
Classification of Parkinson's Disease
- Primary (Idiopathic) PD: Degeneration of greater than 80% of DA neurons, often linked to oxidative stress and aging.
- Secondary (Atypical) PD has multiple causes: Vascular Parkinsonism caused by multiple small strokes affecting movement control areas, Post-Traumatic Parkinsonism (repeated head injuries), Toxin-induced Parkinsonism (exposure to certain toxins), Infectious Parkinsonism (brain infections), and Drug-induced Parkinsonism (use of dopamine blockers, such as antipsychotics).
Treatment for Parkinson's Disease
-
The goal of treatment is to increase DA and decrease Ach.
-
Dopaminergic drugs and anticholinergic drugs are used.
- Dopamine receptor agonists also help.
- Levodopa (L-dopa), a dopamine precursor, is the most commonly used treatment.
- Large doses of Levodopa are needed, but most is converted to dopamine in the periphery and not the brain causing unwanted effects.
- Carbidopa is added to levodopa to decrease peripheral conversion.
- Entacapone and Tolcapone are COMT inhibitors that increase the availability of levodopa to the CNS.
-
Anticholinergic drugs (Benztropine, Trihexyphenidyl, procyclidine,) reduce Ach effects, but primarily treat tremor and rigidity.
Adverse Effects of Levodopa
- Central adverse effects include dyskinesias (involuntary movements) potentially occurring within 4-10 years after treatment start due to dopamine receptor overstimulation.
- Central adverse effects also include psychosis (delusions, hallucinations, mood changes, anxiety). Low doses of certain atypical antipsychotics can be helpful in this instance.
- Peripheral effects can include nausea, vomiting, postural hypotension, and brown saliva, sweat, and urine, due to higher levels of dopamine in the body. Wearing-off phenomenon (end-of-dose deterioration) occurs because symptomatic improvement from a levodopa dose wears off between doses. This can be mitigated through more frequent administrations, sustained release formulations or combination treatments.
- High protein foods decrease L-dopa absorption. L-dopa absorption can improved by taking it 30 minutes before a meal.
- Fluctuations in plasma concentrations of levodopa create "on-off" periods, where the symptoms return. This can be mitigated through adjustments to medication dosing or by adding other medications.
- Levodopa interacts with other drugs including vitamin B6,MAOIs and antipsychotics.
- Amantadine is an antiviral that also increases dopamine release and is used as an adjunct to levodopa.
Dopamine Receptor Agonists
- Dopamine receptor agonists stimulate dopamine receptors, and their use is effective in patients who do not respond to levodopa as they reduce motor fluctuations and dyskinesias. These may be less effective than levodopa alone, but are better tolerated in the long term.
- Bromocriptine is an ergot-derived dopamine receptor agonist. A serious side effect is worsening of peripherial vascular disease from alpha receptor and serotonin receptor stimulation..
- Non-ergot drugs (Apomorphine,Pramipexole, Ropinirole and Rotigotine) have slightly different side effect profiles and usages, and are usually taken orally or by patch.
MAO-B Inhibitors (Selegiline and Rasagiline)
- These drugs inhibit MAO-B; a critical enzyme for dopamine metabolism. They have a free radical scavenging effect, preserving DA neurons in brain tissue and increasing L-dopa effects, thus reducing the dosage required.
- Selegiline can be metabolized to amphetamine or methamphetamine, which can cause insomnia or anxiety.
- Rasagiline does not have this side effect. It is more potent and can be used in early stages of Parkinson's.
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Description
Test your knowledge on the mechanisms and side effects of key medications in Parkinson's disease treatment. This quiz covers Amantadine, anticholinergics, and Rasagiline, focusing on their efficacy and associated risks. Perfect for students and professionals in medical and health fields.