Pharmacology Reporting-1

Antiseizure Drugs
Overview
• A seizure is a sudden, uncontrolled electrical disturbance in the brain.

It can cause changes in your behavior, movements or feelings, and in
levels of consciousness.
• There are many types of seizures, which range in symptoms and
severity. Seizure types vary by where in the brain they begin and how
far they spread.
• Generalized seizures
- Seizures that appear to involve all areas of the brain are called
generalized seizures.
• Focal seizures
- Focal seizures result from abnormal electrical activity in one area of
your brain. Focal seizures can occur with or without loss of
consciousness. Symptoms of focal seizures may be confused with other
neurological disorders, such as migraine, narcolepsy or mental illness.
• Generalized Seizures
- Absence seizures (“petit mal”}
- Tonic seizures
- Atonic seizures
- Clonic seizures
- Myoclonic seizures
- Tonic-clonic seizures (“grand mal”)
• Focal Seizures
- Focal seizure with awareness (“simple partial”)
- Focal seizure with impaired awareness (“complex partial”}
Antiseizure Drugs
• Drugs used for epileptic seizures are called antiseizure drugs,
anticonvulsants, or antiepileptic drugs (AEDs). Antiseizure
drugs stabilize nerve cell membranes and suppress the
abnormal electric impulses in the cerebral cortex. These
drugs prevent seizures but do not eliminate the cause or
provide a cure. Antiseizure drugs are classified as central
nervous system (CNS) depressants.
• Many types of antiseizure drugs are used to treat seizures,
including the hydantoins (phenytoin), long-acting
barbiturates (phenobarbital, primidone), succinimides
(ethosuximide), benzodiazepines (diazepam, clonazepam),
iminostilbanes (carbamazepine), and valproate (valproic
acid). Antiseizure drugs are not indicated for all types of
seizures. For example, phenytoin is effective in treating tonic-
clonic and partial seizures but is not effective in treating
absence seizures.
Pharmacophysiology: Action of Antiseizure Drugs
• Antiseizure drugs work in one of three ways: (1) by

suppressing sodium influx through the drug binding to the
sodium channel when it is inactivated, which prolongs the
channel inactivation and thereby prevents neuron firing; (2)
by suppressing the calcium influx, which prevents the electric
current generated by the calcium ions to the T type calcium
channel;
or (3) by increasing the action of GABA, which inhibits
neurotransmi ers throughout the brain. The drugs that
suppress sodium influx are phenytoin, fosphenytoin,
carbamazepine, oxcarbazepine, valproic acid, topiramate,
zonisamide, and lamotrigine. Valproic acid and ethosuximide
are examples of drugs that suppress calcium influx. Examples
of drug groups that enhance the action of GABA are
barbiturates, benzodiazepines, and tiagabine. Gabapentin
promotes GABA release.
Hydantoins
• Hydantoins inhibit sodium influx, stabilize cell
membranes, reduce repetitive neuronal firing, and
limit seizures. By increasing the electrical stimulation
threshold in cardiac tissue, it also acts as an
antidysrhythmic. It has a slight effect on general
sedation, and it is nonaddicting. However, this drug
should not be used during pregnancy because it can
have a teratogenic effect on the fetus.
Pharmacokinetics
• Phenytoin is slowly absorbed from the small intestine.
It is a highly protein-bound (90% to 95%) drug;
therefore a decrease in serum. Phenytoin is
metabolized to inactive metabolites and excreted in
the urine.
Pharmacodynamics
• The pharmacodynamics of orally administered
phenytoin include onset of action within 30 minutes
to 2 hours, peak serum concentration in 1.5 to 3
hours, and a duration of 6 to 12 hours. The onset of
action for intravenous (IV) administration is with
minutes, peak action is 10 to 30 minutes, and the
duration is up to 12 hours. The drug may be diluted in
saline solution.
Contraindications
• Hypersensitivity, heart block, bradycardia, Adams-
Stokes syndrome.
Caution: Hyponatremia, hypotension, hypoglycemia,

psychosis, suicidal ideation, myasthenia gravis,
hypothyroidism, alcoholism, cardiovascular disease,
diabetes mellitus, renal and hepatic impairment,
porphyria.
Therapeutic Effects/Uses
• To prevent tonic-clonic and partial seizures and status
epilepticus.
• Mechanism of Action: Reduces motor cortex activity

and alters ion transport by acting on sodium channels
on neuronal cell membranes
Side Effects and Adverse Reactions
• The adverse effects of hydantoins include psychiatric effects
such as depression, suicidal ideation, Stevens-Johnson
syndrome, ventricular fibrillation (irregular heartbeat), and
blood dyscrasias such as thrombocytopenia (low platelet
count) and leukopenia (low white blood cell count).
• Injection site reactions, such as purple glove syndrome
(swollen discolored, and painful extremities that may require
amputation), may occur. Patients on hydantoins for long
periods might have elevated blood glucose
(hyperglycemia) that results from the drug inhibiting
the release of insulin. Less severe side effects include
nausea, vomiting, gingival hyperplasia (overgrowth of
gums or reddened gums that bleed easily),
constipation, drowsiness, headaches, slurred speech,
confusion, and nystagmus (constant, involuntary,
cyclical movement of the eyeball).
References:
https://www.mayoclinic.org/diseases-conditions/seizure/symptoms-causes
https://basicmedicalkey.com/pharmacotherapy-of-the-epilepsies-3
Parkinsonism Drugs
What is Parkinson's disease?
• Parkinson’s disease is a
neurological disorder that
result in a progressive loss of
coordination and movement
Medicines for Parkinson’s disease
Medicines can help treat the symptoms of Parkinson’s by:
• Increasing the level of dopamine in the brain
• Having an effect on other brain chemicals, such as
neurotransmitters, which transfer information between brain cells
• Helping control non-movement symptoms
These drugs fall into five categories:
(1) anticholinergics
(2) dopaminergic
(3) dopamine agonists
(4) monoamine oxidase B (MAO-B) inhibitors
(5) catechol-O-methyltransferase (COMT) inhibitors
CARBIDOPA
DOPAMINE
BROMOCRIPTINE
DDC ROPINIROLE
PRAMIPEXOLE
LEVODOPA ANTICHOLONORGIC DRUGS
BENZTROPINE ROTIGOTINE
APOMORPHINE
COMT BIPERIDEN
PROCYCLIDINE
3-OMD
TRIHEXYPHENIDYL
ENTACAPONE
SELEGILINE
TOLCAPONE
RASAGILINE
TOLCAPONE
Pharmacokinetics
The absorption of L-dopa is rapid but is
delayed by food and also by certain amino
acids that compete for its transport in the GI
tract and transport from blood to the brain.
The concomitant administration of
carbidopa can decrease the peripheral
metabolism of L-dopa by up to 80 percent.
SIDE EFFECTS OF THE DRUGS
Levodopa & Selegiline & Entacapone & Dopamine Anticholinergic
Carbidopa Rasagiline Tolcapone agonist
Nausea Nausea Discoloration of Nausea Constipation
Urine, Sweat, or
Saliva
Loss of Appetite Insomnia Diarrhea Orthostatic Urinary retention
Hypotension Dyskinesia Hypotension Dry mouth
Mental Visual Mental Blurred vision

disturbances Hallucinations disturbances
Discoloration of Daytime
Urine, Sweat, or sleepiness
Saliva
CONTRAINDICATION
Dopamine Selegiline Anticholinergic
agonist
They are Should not be They are avoided

contraindicated in taken with TCAs, in patients with
Patients with SSRIs or the angle-closure
psychosis opioid glaucoma and
meperidine prostatic
because of hypertrophy
potential
development of a
“serotonin
syndrome”
Brand names
• Duopa®
• Rytary®
• Sinemet®
Brand names of combination products

• Stalevo® (containing Carbidopa, Entacapone, Levodopa)
Carbidopa reduces which of the following?
A. The activity of dopa-decarboxylase in the CNS
B. The L-dopa dose necessary to achieve a therapeutic effect
C. The severity of L-dopa-associated dyskinesias
D. The time to onset of L-dopa's therapeutic effects
Entacapone inhibits which of the following?
A. Dopamine D, receptors
B. COMT
C. Monoamine oxidase B
D. Muscarinic cholinoreceptors
Which of the following is the most common limiting adverse effect of L-dopa?
A. Depression
B. Dyskinesia
C. Nausea
D. Orthostatic hypotension
Reference:
https://www.nia.nih.gov/health/parkinsons-disease#:~:text=Parkinson's%20disease%20is%2
0a%20brain,have%20difficulty%20walking%20and%20talking
https://www.frontiersin.org/files/Articles/391669/fneur-09-00711-HTML/image_m/fneur-09
-00711-g001.jpg
https://www.labiotech.eu/trends-news/parkinsons-disease-proteins-therapy/
https://youtu.be/Z84iypHdftQ
Koller WC, Tolosa E, eds. Current and emerging drug therapies in the management of
Parkinson's disease. Neurology 1998:50(suppl 6):51. Frucht SJ. Parkinson disease: an update.
Neurologist 2004;10(4):185-94.
Nutt JG, Wooten GF. Diagnosis and initial management of Parkinson's disease. N
Engl J Med 2005:353:1021-7.
Alzheimer drugs
What is Alzheimer’s Disease?
Alzheimer disease is an incurable dementia illness characterized by
chronic, progressive neurodegenerative conditions with marked cognitive
dysfunction. Onset usually occurs between 45 and 65 years of age.
Pathophysiology
Many physiologic changes contribute to Alzheimer disease. Currently,
theories related to the changes that cause Alzheimer disease include the
following:
• Degeneration of the cholinergic neuron and deficiency in ACh
• Neuritic plaques that form mainly outside of the neurons and in the
cerebral cortex Apolipoprotein E, (apo E) that promotes formation of
neuritic
• plaques, which binds beta-amyloid in the plaques Beta-amyloid protein
accumulation in high levels that maycontribute to neuronal injury
• Presence of neurofibrillary tangles with twists inside theneurons
Acetylcholinesterase/Cholinesterase Inhibitors
The cure for Alzheimer disease is unknown. FDA-approved medications
to treat Alzheimer disease symptoms include acetylcholinesterase
(AChE) inhibitors. AChE is an enzyme responsible for breaking down
ACh and is also known as cholinesterase. The AChE inhibitors are
donepezil, memantine, galantamine, and rivastigmine, a drug that
permits more ACh in the neuron receptors. Rivastigmine has effective
penetration into the CNS; thus cholinergic transmission is increased.
These AChE inhibitors increase cognitive function for patients with mild
to moderate Alzheimer disease. A reversible AChE inhibitor used to
treat mild to moderate Alzheimer disease is galantamine.
Pharmacokinetics
Rivastigmine is absorbed faster through the GI tract without
food. It has a relatively short half-life and is given twice a day.
The dose is gradually increased. The protein-binding power is
average. It readily crosses the blood-brain barrier and is widely
distributed.
Pharmacodynamics
Rivastigmine has been successful in improving memory in mild
to moderate Alzheimer disease. The onset of action is 0.5 to 1.0
hour for topical application; peak action is 8 to 16 hours. When
given orally, the peak is 1 hour. This drug is contraindicated for
patients with liver disease because hepatotoxicity may occur.
Cumulative drug effect is likely to occur in older adults and in
patients with liver and renal dysfunction.
THANK
YOU!! :)
This is our reference

Pharmacology Reporting-1

Uploaded by

Copyright:

Available Formats

Pharmacology Reporting-1

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Pharmacology Reporting-1

Uploaded by

Copyright:

Available Formats

Antiseizure Drugs

• A seizure is a sudden, uncontrolled electrical disturbance in the brain.

• Antiseizure drugs work in one of three ways: (1) by

Caution: Hyponatremia, hypotension, hypoglycemia,

• Mechanism of Action: Reduces motor cortex activity

Hypotension Dyskinesia Hypotension Dry mouth

Mental Visual Mental Blurred vision

They are Should not be They are avoided

Brand names of combination products

You might also like