ANTONIO, CHARISMA J.

BS – PHARMACY 2-1

CASE STUDY 1
A 66-year-old man comes in to your office for evaluation of
a tremor. He has noticed a progressively worsening tremor in his hands for the
past 6 months. The tremor is worse when he is resting and improves a little
when he reaches for an object or is using his hands. He has also noticed that
it is harder to “get started” when he stands up to walk. He takes several
small, “shuffling” steps before he can reach his full stride. He has no
significant medical history and takes only an aspirin a day. On examination you
note that his face is fairly expressionless, he has a pill-rolling-type tremor
of his hands at rest and has cogwheel rigidity of his arms. You diagnose him
with Parkinson disease and prescribe a combination of levodopa (L-dopa) and
carbidopa.

Questions:
1. What is the most common cause of the symptoms of idiopathic
Parkinson disease?
• The most common symptoms of idiopathic Parkinson's are tremor, rigidity and slowness of movement.
• TRAPS ( Tremors, Rigity , Akinesia, Postural Instability, Shufling gait. )
REF:
https://www.parkinsons.org.uk/information-and-support/types-parkinsonism
Notes nyo po galing yung TRAPS.

2. What is the mechanism of action of L-dopa?

• Levodopa, a precursor of dopamine, crosses the blood-brain barrier and is converted to dopamine by striatal
enzymes, thereby relieving the symptoms of Parkinson's disease.
• Levodopa is in a class of medications called central nervous system agents. It works by being converted to
dopamine in the brain. Carbidopa is in a class of medications called decarboxylase inhibitors. It works by
preventing levodopa from being broken down before it reaches the brain.
REF: https://www.mims.com/philippines/drug/info/levodopa?mtype=generic

3. Why is L-dopa usually given in combination with carbidopa?

• Without the carbidopa, the levodopa would be broken down in the body before it got a chance to make it into
the brain. The carbidopa acts to inhibit the enzyme that breaks down levodopa.
• Carbidopa is a drug that blocks conversion of levodopa to dopamine outside of central nervous system (CNS)
and thus inhibits unwanted side effects of levodopa on organs located outside of CNS during management of
Parkinson’s Disease (PD). PD is associated with increased expression of inflammatory genes in peripheral and
central nervous system (CNS), infiltration of immune cells into brain, and increased numbers of
activated/memory T cells. Animal models of PD have shown a critical role of T cells in inducing pathology in
CNS.
REF: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5595290/

CASE STUDY 2
An 18-year-old man is brought to the emergency department by paramedics
after a series of grand mal seizures. He required repeated doses of IV
lorazepam to finally control the episode. A family member with him states that
he has had epilepsy since childhood. He is supposed to take phenytoin, but
often forgets or refuses. His last seizure was about 3 months ago. In the emergency room he is confused and
combative but has an otherwise normal neurologic examination. Blood tests show an undetectable phenytoin
level.
Questions:

1. What is the mechanism of action of phenytoin?

• Phenytoin is often described as a non-specific sodium channel blocker and targets almost all voltage-gated
sodium channel subtypes. More specifically, phenytoin prevents seizures by inhibiting the positive
feedback loop that results in neuronal propagation of high frequency action potentials.
• Blocks sodium channels and inhibits the generation of action potentials.
REF: https://go.drugbank.com/drugs/DB00252

2. How is phenytoin metabolized?

• Phenytoin is metabolized by cytochrome P450 (P450) enzymes primarily to 5-(p-hydroxyphenyl-),5-
phenylhydantoin (HPPH), which may be further metabolized to a catechol that spontaneously oxidizes
to semiquinone and quinone species that covalently modify proteins.
REF:
https://pubmed.ncbi.nlm.nih.gov/10901705/#:~:text=Phenytoin%20is%20metabolized%20by%20cytochrome,spec
ies%20that%20covalently%20modify%20proteins.

CASE STUDY 3
A 61-year-old man is noted to have increased intraocular pressure on a routine
eye examination. The visual acuity is normal in both eyes. The dilated eye
examination reveals no evidence of optic nerve damage. Visual field testing
shows mild loss of peripheral vision. He is diagnosed with primary open-angle
glaucoma and is started on pilocarpine ophthalmic drops.

Questions:
1. What is the action of pilocarpine on the muscles of the iris and cilia?
• When used as a miotic agent, pilocarpine is available in the form of ophthalmologic eye drops. This dose
form will result in ciliary contraction (a contraction of the iris), which will increase aqueous humor
outflow, miosis, and accommodation. CONSTRICTION OF THE MUSCLES

2. What receptor mediates this action?

• Muscarinic receptors are involved in the transduction of cholinergic signals in the central nervous
system, autonomic ganglia, smooth muscles, and other parasympathetic end organs .

3. Is pilocarpine the appropriate first-line drug for treatment of primary open-angle glaucoma?
• NO…
Pilocarpine is a second-line drug for the treatment of chronic open-angle glaucoma, in which it lowers
intraocular pressure by increasing the outflow of aqueous humor.
Pilocarpine is a muscarinic acetylcholine agonist that is effective in the treatment and management of acute
angle-closure glaucoma and radiation-induced xerostomia. Although not a first-line treatment for glaucoma,
it is useful as an adjunct medication in the form of ophthalmic drops. Pilocarpine is app roved for use as an
agent to decrease intraocular pressure (IOP) in glaucoma cases, as well as in the management of xerostomia
resulting from radiation exposure and Sjogren disease

• Timolol, a beta blocker, is the most commonly prescribed first line therapy in the treatment of primary
open angle glaucoma.
REF:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4740613/#:~:text=Introduction,of%20primary%20open%20angle
%20glaucoma.