understanding the parkinson's disease
DESCRIPTION
parkinson's disease pathophysiology, treatment...TRANSCRIPT
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Parkinson’s disease
by Syed Baseeruddin Alvi (09)
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INTRODUCTION• Parkinsonism is a clinical syndrome comprising
combinations of motor problems—namely, bradykinesia,
resting tremor, rigidity, flexed posture, “freezing,” and loss
of postural reflexes.
• Studied and discovered by James
Parkinson (1817) which he called the shaking palsy
and by the Latin term paralysis agitans.
• Pathology shows loss of neuromelanin-containing
monoamine neurons, particularly dopamine (DA) neurons
in the substantia nigra pars compacta.
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• Examinations reveals the presence of cytoplasmic
eosinophilic inclusions Lewy bodies in monoamine
neurons.
• The loss of DA content in the nigrostriatal neurons
accounts for many of the motor symptoms which is due
to neuronal degradation
• Six cardinal clinical features of parkinsonism:Tremor at rest Bradykinesia Loss of postural
reflexes
Rigidity Flexed posture of neck, trunk, and limbs
Freezing phenomenon
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Concept on pathogenesis of Parkinson’s disease.
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The five stages of parkinson’s disease:
Stage 1:Unilateral involvement only with minimal or no functional impairment
Stage 2:Bilateral or midline involvement, without balance impairment
Stage 3:Impairment of righting reflex
Stage 4:Fully developed and severely disabling
Stage 5:Confinement to bed or wheel chair.
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Pathogenesis of PD:
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Pathogenesis of PD:
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Pathogenesis of PD:
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Drugs used in treatment of PD:
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Dopamine precursor:
Levodopa (L-DOPA, LARODOPA, L-3,4
dihydroxyphenylalanine), the metabolic precursor of
dopamine, is the single most effective agent in the
treatment of PD .
It is inert both therapeutic & adverse effects are due
to decarboxylation , central and peripheral respectively .
In practice it is always administered in combination
with peripherally acting inhibitor of aromatic L-amino acid
decarboxylase ( carbidopa , benserazide)
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Site of action:
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Adverse reactions:
Involuntary muscular twitching of the limbs or facial
muscles
muscular spasms most often affecting the tongue, jaw,
eyes, and neck
mental changes, such as depression, psychotic
episodes, paranoia, and suicidal tendencies.
less serious adverse reactions include anorexia,
nausea, vomiting, abdominal pain, dry mouth, difficulty
in swallowing, increased hand tremor, headache, and
dizziness.
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Anticholinergic drugs:
Drugs with anticholinergic activity inhibit acetylcholine
(a neurohormone produced in excess in Parkinson’s disease)
in the CNS. Drugs with anticholinergic activity are generally
less effective than levodopa.
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Adverse reactions:
Dry mouth, blurred vision, dizziness, mild nausea, and
nervousness.
Other adverse reactions may include skin rash, urticaria
urinary retention, tachycardia, muscle weakness,
disorientation, and confusion.
COMT inhibitors:
These drugs prolong the effect of levodopa by blocking
(COMT). When given with levodopa, the COMT inhibitors
increase the plasma concentrations and duration of action
of levodopa.
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Adverse reactions:
Disorientation, confusion, light-headedness, dizziness,
dyskinesias, hyperkinesias, nausea, vomiting, hallucinations,
and fever
Other adverse reactions are orthostatic hypotension,
sleep disorders, excessive dreaming, and muscle cramps
Dopamine receptor agonists (non ergot):
It is thought that these drugs act directly on
postsynaptic dopamine receptors of nerve cells in the
brain, mimicking the effects of dopamine in the brain.
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Adverse reactions:
Nausea, dizziness, postural hypotension, hallucinations,
somnolence, vomiting, confusion, visual disturbances,
abnormal involuntary movements, and headache.
Selective MAO-B Inhibitors:
By interfering with one of the enzymes that break
down dopamine (monoamine oxidase, or MAO-B),
they can enhance and prolong the effect of each
dopamine molecule.
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Treatment:
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Surgical Therapy:
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