Parkinson's disease is a neurodegenerative disorder that primarily affects individuals over 65. It results from the loss of dopaminergic neurons in the substantia nigra, leading to decreased dopamine levels and motor symptoms like tremors, rigidity, and bradykinesia. Levodopa is the most effective treatment for alleviating symptoms but its long-term use can cause dyskinesias and fluctuations. Other treatments include dopamine agonists, COMT inhibitors, MAO-B inhibitors, anticholinergics, and amantadine, each with their own benefits and side effects. Managing Parkinson's involves optimizing drug therapies to improve motor function while minimizing adverse effects.
Parkinsonism
It is an extra-pyramidal motor disorder characterized by rigidity, tremor and hypokinesia with secondary manifestations like defective posture and gait, mask-like face and sialorrhoea; dementia may accompany. If untreated the symptoms progress over several years to end-stage disease in which the patient is rigid, unable to move, unable to breathe properly; succumbs mostly to chest infections / embolism
BASIC PHARMACOLOGY REVISION NOTES BASED ON HIGH YEILD TOPIC AND LECTURE NOTES
ANTIPARKINSONIAN DRUGS
LEVODOPA DRUGS
PERIPHERAL DECARBOXYLASE INHIBITOR
COMT INHIBITOR
ENTACAPONE
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the presentation on anti parkinson drug contain their classification of drugs, mechanism of action. uses of drugs, side effect, causes, symptoms, additional symptoms, physiology, pathophysiology
Drugs used in Parkinsons Disease ( anti- Parkinson drugs) Ravish Yadav
detail and complete study on the topic of anti parkinson drug. the study is done under the guidance of faculty member. the learning content complete information of the topic
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Parkinsonism
It is an extra-pyramidal motor disorder characterized by rigidity, tremor and hypokinesia with secondary manifestations like defective posture and gait, mask-like face and sialorrhoea; dementia may accompany. If untreated the symptoms progress over several years to end-stage disease in which the patient is rigid, unable to move, unable to breathe properly; succumbs mostly to chest infections / embolism
BASIC PHARMACOLOGY REVISION NOTES BASED ON HIGH YEILD TOPIC AND LECTURE NOTES
ANTIPARKINSONIAN DRUGS
LEVODOPA DRUGS
PERIPHERAL DECARBOXYLASE INHIBITOR
COMT INHIBITOR
ENTACAPONE
TOLCAPONE
MAO B INHIBITORS
the presentation on anti parkinson drug contain their classification of drugs, mechanism of action. uses of drugs, side effect, causes, symptoms, additional symptoms, physiology, pathophysiology
Drugs used in Parkinsons Disease ( anti- Parkinson drugs) Ravish Yadav
detail and complete study on the topic of anti parkinson drug. the study is done under the guidance of faculty member. the learning content complete information of the topic
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2. Parkinson’s Disease (PD)
• Neurodegenerative disorder
• Primarily a disease of later life:
– ~1 -3% of individuals over age 65 and 0.3% of general
population
2
3. Parkinson’s Disease (PD) Development
• dopaminergic neurons in the substantia nigra that normally
inhibit the output of GABAergic cells in the corpus striatum
are lost
3
Decreased
Level of
dopamine Normal
level of Ach
(+)
(-) Normal
Motor
activity
Abnormal
motor
activity
4. Clinical Symptoms:
1. Bradykinesia: slowness and poverty of movement
2. Muscular rigidity: increased resistance to muscle stretch
3. Resting tremor: usually abates during voluntary movement
4. Postural instability leading to disturbances of gait and falling
• Parkinsonism: some symptoms of PD, but the pathology and causes
differ
4
5. Complications:
• inability to walk
• mask-like expression
• impairment of speech and skilled acts
• possible death (from immobility or falls)
• depression common and dementia may occur
Treatments alleviate symptoms, but do not alter the underlying course or
progression of the disease
5
7. Termination of action and catabolism:
• Reuptake (blocked by cocaine, amphetamine)
• Catabolism - COMT and MAO
Catabolic process may lead to the production of toxic free radicals
7
8. 1. Increase dopamine receptor activation:
a- Increase dopamine availability
b- Dopamine receptor agonists
2. Decrease cholinergic activity: Antimuscarinic
Treatment of PD
Decreased
amount of
dopamine
Normal
amount of Ach
Parkinsonism Treatment of
Parkinsonism
Increase
availability
of dopamine
Slow the loss
of dopamine
Reduce Ach
activity
8
10. Why don’t we use Dopamine for Parkinson’s disease?
• Dopamine cannot cross the blood brain barrier
• Dopamine has very short half life (around 1 min)
• Dopamine is given as IV infusion (inappropriate for chronic use)
• Dopamine can directly affect the cardiovascular system (direct
sympathomimetic)
10
11. Dopamine Precursor: Levodopa (L-DOPA)
• L-DOPA can slightly cross the blood brain barrier.
11
• Metabolic precursor of dopamine:
uptaken by brain dopaminergic
neurons and is conversed into
dopamine by “dopa decarboxylase”
enzyme
L-DOPA
12. Dopamine Precursor: Levodopa (L-DOPA)
• L-DOPA can also be uptaken by peripheral dopaminergic neurons
resulting in significant side effects.
• In early PD, it may almost completely alleviate the symptoms
• L-DOPA: most often prescribed
12
13. Dopa decarboxylase inhibitor
• Carbidopa
A peripheral dopa decarboxylase inhibitor.
It cannot cross the blood brain barrier
Normally added to L-DOPA
Reduce the peripheral conversion of L-DOPA to dopamine
Advantages:
Improve the bioavailability (reduce GI metabolism)
reduce the peripheral side effects
13
14. Fate of orally administered levodopa and the effect of
carbidopa
14
15. • The best results of levodopa treatment are obtained in the first few
years of treatment
• The daily dose of levodopa must be reduced over time to avoid side
effects at doses that were well tolerated at the outset.
• Some patients also become less responsive to levodopa, so that
previously effective doses eventually fail to produce any therapeutic
benefit.
• Responsiveness to levodopa may ultimately be lost completely, because
of the disappearance of dopaminergic nigrostriatal nerve terminals or
some pathologic process directly involving the striatal dopamine
receptors
Effects of L-dopa
15
16. Adverse effects of L-DOPA
Gastrointestinal:
• Without Carbidopa, anorexia and nausea and vomiting occur in about
80% of patients
• Vomiting has been attributed to stimulation of the chemoreceptor
trigger zone located in the brainstem but outside the blood-brain barrier
• With carbidopa, adverse gastrointestinal effects are less than in 20% of
cases
16
17. Adverse effects of L-DOPA
Cardiovascular:
• Cardiac arrhythmias
• may be reduced taken in combination with Carbidopa
17
18. Adverse effects of L-DOPA
Dyskinesias:
• Choreoathetosis of the face and distal extremities is the most
common presentation
• Occur in up to 80% of patients receiving levodopa therapy for long
periods.
• The form and nature of dopa dyskinesias vary widely among
patients but tend to remain constant in character in individual
patients.
18
19. Adverse effects of L-DOPA
Behavioral effects
• Depression, anxiety, agitation, insomnia, confusion, delusions,
hallucinations, nightmares and euphoria.
• More common with levodopa/Carbidopa combination, because
greater amounts of levodopa reach the brain.
19
20. Adverse effects of L-DOPA
Fluctuations in response
• Two possible causes:
Wearing-off reactions (end-of-dose akinesia)
On-off phenomenon: off-periods of akinesia alternate over the
course of a few hours with on-periods of improved mobility but
often marked dyskinesia
20
21. Possible causes of on-off phenomenon
• The inhibition of dopa decarboxylase is associated with compensatory
activation of COMT
• COMT increases plasma levels of 3-O-methyldopa (3OMD).
• 3OMD competes with levodopa for an active carrier mechanism that
governs its transport across the blood-brain barrier.
• Elevated levels of 3OMD have been associated with a poor therapeutic
response to levodopa
21
22. Dealing with on-off phenomenon
1. Drug Holidays
Discontinuance of the drug for (3–21 days) may temporarily improve
responsiveness to levodopa and alleviate some of its adverse effects
Disadvantages:
Of little help in the management of the on-off phenomenon.
It carries the risks of: aspiration pneumonia, venous thrombosis,
pulmonary embolism, and depression resulting from the immobility
accompanying severe parkinsonism
It is no longer recommended
2. Inhibition of COMT
22
23. COMT (catechol-O-methyltransferase) inhibitors
• Selective COMT inhibitors such as tolcapone and entacapone prolong the
action of levodopa by diminishing its peripheral metabolism.
• Levodopa clearance is decreased, and relative bioavailability of levodopa is
thus increased.
23
24. • Tolcapone: has longer duration of action, acts peripherally and centrally
• Entacapone: short duration of action (~2 hrs), mainly peripheral actions
• Therapeutic effect: often combined with L -DOPA when “on-off” becomes
a problem
COMT (catechol-O-methyltransferase) inhibitors
24
25. Side Effects of COMT inhibitors
• Related to increased levodopa exposure
Nausea and vomiting
Vivid dreams
Hallucinations
Confusion
Dyskinesias
Tolcapone may produce hepatotoxicity, therefore is used only in
patients that do not respond to other therapies
25
26. Dopamine receptor agonist
• Therapeutic Effect: mimic dopamine by binding to receptor
• Advantages:
1. Enzymatic conversion is not required and doesn’t depend on
functional capacity of nigrostriatal neurons
2. Does not compete for active transport across blood -brain barrier
3. Longer duration of action than levodopa
4. Less generation of free radicals
5. Lower incidence of response fluctuations and dyskinesias with long
term use
26
27. Older agonists (ergot derivatives):
• Bromocriptine
• Pergolide: more effective than Bromocriptine
Newer non-ergot agonists: Used as monotherapy or with L-DOPA
• Ropinirol: selective for D2 class
• Pramipexole: selective for D2 class, may also have neuroprotective actions
27
Dopamine receptor agonist
28. Side effects:
• Nausea
• Dyskinesias
• Confusion, hallucinations, delusions (reversible)
• Postural hypotension and arrhythmias
Contraindications dopamine receptor agonist:
- History of psychotic illness
- Recent myocardial infarction
- Active peptic ulceration
28
Dopamine receptor agonist
29. • Two forms of MAO:
– MAO-A:
• non-selective (DA, NE, 5-HT)
• more prevalent in periphery
– MAO-B:
• more DA -selective
• prevalent in brain
• does not inhibit peripheral catecholamine metabolism
MAO-B inhibitor : Selegiline
29
30. • Mechanism of Selegiline: increases dopamine levels and prolongs the
effects of L-DOPA
• Therapeutic Effect:
It is not therapeutically effective alone
Adjunct therapy with L -DOPA in patients with declining or fluctuating
response
MAO-B inhibitor : Selegiline
30
31. • Side Effects: nausea, headache, dizziness, confusion
• Dosing important: may also affect MAO-A at high concentrations
• Drug interactions: Not recommended for patients on Meperidine, Tricyclic
agents, Serotonin reuptake inhibitors
MAO-B inhibitor : Selegiline
31
32. • Trihexyphenidyl, Benztropine, Diphenhydramine
• Therapeutic Use: Modest anti-parkinsonian action
Early PD
as an adjunct to dopaminergic therapy
Extrapyramidal side effects of anti-psychotic drugs
• Improve tremor and rigidity with little effect on bradykinesias
• Side Effects: sedation, mental confusion, mood changes, blurred vision,
dry mouth, nausea, arrhythmias
Muscarinic Acetylcholine Antagonists (anti-cholinergic):
32
33. • Mechanism:
Antiviral agent; mechanism of anti-parkinsonian effect is not clear.
Its antagonist activity at NMDA receptors may augment dopamine
release
• Therapeutic Use: Modest effects, used only for mild PD or as adjuvant to
levodopa
• Benefits are short-lived, but it may improve bradykinesia, rigidity and
tremor
• Side effects:
CNS effects: depression, irritability, agitation, confusion, hallucinations
Amantadine
33
34. Treatment of side effects caused by anti-PD drugs:
• Domperidone
Therapeutic use: against nausea and vomiting (reduces peripheral
side effects of levodopa)
Mechanism: peripheral D2 antagonist
• Clozapine, Olanzapine:
Therapeutic use: treat hallucinations and psychotic symptoms of
levodopa
Mechanism: Atypical neuroleptic with minimal D2 blocking
properties
34
35. Drugs that may cause PD symptoms:
• Antipsychotics: haloperidol, chlorpromazine, thorazine
• Antiemetics: prochlorperazine and Metoclopramide
Mechanism: block dopamine receptors
35