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“Solution-Pharmacy”
Drug Acting on Central Nervous System
Model ANSWER- Parkinson disease
B.Pharmacy- 4th Semester (New PCI Syllabus)
Note- This model answer is made by “Solution-Pharmacy” to give a brief idea
about- How to solve any question of short and long answer type. Although it’s
based on our opinion but please be prepared for your exams.

Section 02- Long answer type questions


(1) Explain Parkinson disease in short and classify anti-Parkinson drugs along with mechanism
of action for any one drug in detail. (10 Marks)
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Explanation-
As you can see that there is 03 section in the above question. Let’s see each section separately.
Section 01- Explain Parkinson Disease. 05 Marks
Section 02- Classify Anti-Parkinson drugs. 02 Marks
Section 03- Give mechanism of action of any one drug. 03 Marks

Special Instruction- It’s not necessary that question will ask you to make a diagram, but it’s
really a good practice to make a diagram or flow chart in question.

Answer of section 01, 02 and 03


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Parkinson's disease is a progressive nervous system disorder that affects movement. Symptoms
start gradually, sometimes starting with a barely noticeable tremor in just one hand. Tremors
are common, but the disorder also commonly causes stiffness or slowing of movement. In
Parkinson's disease, certain nerve cells (neurons) in the brain gradually break down or die.
Many of the symptoms are due to a loss of neurons that produce a chemical messenger in your
brain called dopamine. When dopamine levels decrease, it causes abnormal brain activity,
leading to symptoms of Parkinson's disease. Dopamine plays a role in sending messages to the
part of the brain that controls movement and coordination. Low dopamine levels can make it
harder for people to control their movements.

Parkinson's signs and symptoms may include:

1. Tremor. A tremor, or shaking, usually begins in a limb, often your hand or fingers.
You may a rub your thumb and forefinger back-and-forth, known as a pill-rolling
tremor. Your hand may tremor when it's at rest.

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2. Slowed movement (bradykinesia). Over time, Parkinson's disease may slow your
movement, making simple tasks difficult and time-consuming. Your steps may become
shorter when you walk. It may be difficult to get out of a chair. You may drag your feet
as you try to walk.

3. Rigid muscles. Muscle stiffness may occur in any part of your body. The stiff muscles
can be painful and limit your range of motion.

4. Impaired posture and balance. Your posture may become stooped, or you may have
balance problems as a result of Parkinson's disease.

5. Loss of automatic movements. You may have a decreased ability to perform


unconscious movements, including blinking, smiling or swinging your arms when you
walk.

6. Speech changes. You may speak softly, quickly, slur or hesitate before talking. Your
speech may be more of a monotone rather than with the usual inflections.

7. Writing changes. It may become hard to write, and your writing may appear small.
Reference- https://www.mayoclinic.org/diseases-conditions/parkinsons-disease/symptoms-causes/syc-20376055

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Diagram- Classification of antiparkinson drug

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Mechanism of action of Levodopa and Carbidopa

Levodopa is converted to dopamine via the action of a naturally


occurring enzyme called DOPA decarboxylase. This occurs both in the peripheral circulation
and in the central nervous system after levodopa has crossed the blood brain barrier. Activation
of central dopamine receptors improves the symptoms of Parkinson's disease; however,
activation of peripheral dopamine receptors causes nausea and vomiting. For this reason
levodopa is usually administered in combination with a DOPA decarboxylase inhibitor
(DDCI), in this case carbidopa, which is very polar (and charged at physiologic pH) and cannot
cross the blood brain barrier, however prevents peripheral conversion of levodopa to dopamine
and thereby reduces the unwanted peripheral side effects of levodopa. Use of carbidopa also
increases the quantity of levodopa in the bloodstream that is available to enter the brain.

As the substantia nigra degenerates in Parkinson's disease (PD), the nigrostriatal pathway is
disrupted, reducing striatal dopamine and producing PD symptoms. Although dopamine does
not readily cross the blood-brain barrier, its precursor, levodopa, does. Levodopa is absorbed
in the small bowel and is rapidly catabolized by aromatic-L-amino-acid decarboxylase
(AADC) and catechol-O-methyltransferase (COMT). Because gastric AADC and COMT
degrade levodopa, the drug is given with inhibitors of AADC (carbidopa or benserazide), and
inhibitors of COMT will also enter clinical use. Although the exact site of decarboxylation of
exogenous levodopa to dopamine in the brain is unknown, most striatal AADC is located in
nigrostriatal dopaminergic nerve terminals.

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