M pharmacy pharmacology

1. Parkinson’s Disease
Submitted By: Ayodhya Tanaji Paradhe Submitted To: Dr. Mandade Sir
M Pharm 1st Year ( Pharmacology) ( Pharmacology Department)
Sudhakar Rao Naik Institute Of Pharmacy Pusad

2. Contents:
 Introduction
 Etiology of Parkinson’s
 Pharmacology of antiparkinson’s

3. Introduction
 Parkinson’s disease (PD) is a chronic, progressive, motor
neurodegenerative disorder is named after James Parkinson who in
1817 wrote a classic “shaking palsy” PD is characterized by
tremors, rigidity, and bradykinesia
 PD is caused by the degeneration of nerve cells in a part
of the brain called the substantia nigra which controls
movement these nerve cells die or become impaired,
thus loss of the ability to produce an important chemical called
Dopamine

4. Sign & Symptoms:
 Depression, sleep disorder
Excessive salivation,
Respiratory problems,
Constipation, increased sweating

5. Etiology:
 Imbalance between inhibitory dopamine and excitatory acetylcholine in basal ganglia
 Destruction of dopaminergic neurons at the substantia nigra region of the brain
 Basal ganglia- control movement
step 3 neostriatum Ach neuron
step 1
inh. DA inh. GABA neuron
Neuron
substantia nigra
step 2

6. Destruction of DA neuron
Loss of dopamine release in substantia nigra
Less inhibitory dopamine
More production of acetylcholine
Trigger abnormal signals
Impaired motility
Parkinson’s Disease

8. PHARMACOLOGY
Classification of Antiparkinson’s disease drugs:
A. By increasing brain’s dopaminergic levels
a) Dopamine precursor- Levodopa
b) DDC inhibitors- carbidopa
c) Dopaminergic agonist- bromocriptine
d) MAO-B inhibitors- selegiline, rasagiline
e) Dopamine facilitator- amantadine
f) COMT inhibitors- entacapone, tolcapone
B. By reducing the brain’s cholinergic levels
a) Central anticholinergic- procyclidine
b) Antihistamine- promethazine

10. Pharmacology of Levodopa drug
 most commonly used in the treatment of PD
 It is L- tyrosine derivative
 Mechanism of action:
Levodopa crosses the blood-brain barrier
where it is converted to dopamine
by decarboxylation in the presynaptic
terminals of dopaminergic neurons.

11.  Pharmacokinetics:
• Absorption- absorbed rapidly from the small intestine,70% oral inhaled
bioavailability when given in combination with carbidopa
half-life: 50 minutes, given with carbidopa increase to 1.5 hours
• Distribution- distributed in the gut, liver, kidney gastric and intestinal wall,
brain
• Metabolism- peripheral dopamine metabolized in the liver by Dopa
decarboxylase (DDC) in GIT and blood vessels
• Excretion- mainly excreted in urine after conjugation

12. Uses:
 Dopamine acts on areas of the brain to give a feeling of pleasure, and
motivation
 Controlling memory, mood, sleep, learning, movement, and other body
functions
 Control of Parkinson’s disease
 Used to treat low blood pressure, low heart rate, and cardiac arrest

13. Adverse effect:
 GIT: anorexia, nausea and vomiting
 CVS: tachycardia, hypertension
 Lethargy, Dyskinesia, decreased prolactin level
 Orthostatic hypotension
 Confusion, hallucination, palpitation etc.
Drug interaction:
 vit, B6 reduces the beneficial effects of levodopa by enhancing its extracerebral metabolism
 MAO inhibitors- hypertensive crises due to increased catecholamines i.e. dopamine
potentiate toxicity
 Phenothiazine and metoclopramide decrease the therapeutic Effect of levodopa by blocking the
DA receptors
 Contraindicated in psychosis, narrow-angle glaucoma, melanoma, cardiac arrhythmias

14. References:
1. Essential of medical pharmacology 8th edition KD Tripathi
2. http://pdcenter.neutrology. Ucsf.edu/patients-guide/overview-Parkinson’s disease
3. https://www.webmd.com/parkinsons-desease/ default.htm

15. THANK YOU