CNS Drugs Flashcards
(106 cards)
Name the Inhibitory neurotransmitters of CNS:
GABA
Glycine
Name the Excitatory Neurotransmitters of the CNS:
Acetylcholine Norepinephrine Dopamine Serotonin Glutamate
What is etiology of Parkinson’s Disease?
In Parkinson’s disease there is a loss of dopamine-containing neurons that project from the substantia nigra to the striatum where they inhibit cholinergic (ACh) neurons. Normally the striatum is connected to the substantia nigra by neurons that secrete the inhibitory transmitter GABA at their termini in the substantia nigra. In turn, substantia nigra sends neurons back to the striatum, secreting the transmitter dopamine to the termini. This mutual inhibitory pathway normally maintains balance. Destruction of cells of substantia nigra results in overproduction of Acetylcholine which triggers a chain of abnormal signaling, resulting in loss of control of muscle movements.
What types of drug therapies are available for Parkinson’s?
Dopamine Replacement Therapy
Dopamine Receptor Agonist Therapy
Anticholinergic Therapy
Anti-Parkinson Drugs: Dopamine Replacement Therapy
- **Levodopa (L-dopa)
- **Carbidopa (Lodosyn)
- **Selegiline
- **Amantidine
Anti-Parkinson Drugs: Dopamine Replacement Therapy –> Levadopa
***Levadopa (L-dopa) - dopamine replacement therapy for Parkinson’s
Levadopa is a metabolic precursor of dopamine. Decarboxylated to dopamine in brain. DA does not cross brain barrier.
Carbidopa and Levodopa are used today in combination. This is a prime example of a beneficial drug interaction that is logical based on the mechanism of action. Sinemet is the combined drug
Anti-Parkinson Drugs: Dopamine Replacement Therapy –> Carbidopa
Carbidopa (Lodosyn): Diminishes decarboxylation of L-dopa in peripheral tissies thereby prevents its peripheral biotransformation. Decreased required dose of L-dopa by about 75%.
Carbidopa and Levodopa are used today in combination. This is a prime example of a beneficial drug interaction that is logical based on the mechanism of action. Sinemet is the combined drug.
Anti-Parkinson Drugs: Dopamine Replacement Therapy –> Selegiline
***Selegiline (Deprenyl), is an inhibitor of monoamine oxidase - B (MAO - B), the enzyme that metabolizes dopamine in the CNS
Anti-Parkinson Drugs: Dopamine Replacement Therapy –> Amantidine
***Amandtidine (Symadine): in an antiviral drug effective in the Tx of influenza. It also enhances the synthesis, release and reuptake of dopamine from the surviving neurons.
Anti-Parkinson Drugs: Dopamine Receptor Agonist Therapy MOA:
DA Agonists can be used in Parkinson’s disease because although the dopamine-releasing neurons have disappeared, the postsynaptic dopamine receptors are still present and functional. Adminstration of dopamine agonists to stimulate these receptors should therefore restore the balance of inhibition and excitation in the basal ganglia.
Anti-Parkinson Drugs: Dopamine Receptor Agonist Therapy –>
- **Bromocriptine (Parlodel): Powerful dopamine receptor agonist
- **Ropinirole (Requip)
Anti-Parkinson Drugs: Dopamine Receptor Agonist Therapy –> Bromocriptine
Bromocriptine (Parlodel): powerful dopamine-receptor agonist
Anti-Parkinson Drugs: Dopamine Receptor Agonist Therapy –> Ropinirole
Ropinirole (Requip)
Anti-Parkinson Drugs: Anticholinergic Therapy MOA
These are muscarinic antagonists used in Parkinson’s disease. They reduce ACh: dopamine imbalance in the striatum. Side effects of these drugs include dry mouth, constipation, urinary retention, and confusion.
Anti-Parkinson Drugs: Anticholinergic Therapy - side effects
Side effects of these drugs include dry mouth, constipation, urinary retention, and confusion
Which Anti-Parkinson drug is also an anti-viral?
Amantidine is an antiviral drug effective in treating of influenza.
What is MOA of Anti-Alzheimer Drugs?
Alzheimer’s disease (AD) has been found to involve a number of systems in the brain. There is evidence for a decrease in choline acetyltransferase (that catalyzes the transfer of the acetyl group of acetyl CoA to choline, forming acetylcholine) and other markers of cholinergic neuron activity. Eventually cholinergic nuerons die or destroyed. Treatment has focused on increasing the amount of acetylcholine in the synapse by inhibiting the breakdown of acetylcholine. The most recent drug is an antagonist of N-methyl-D-aspartane (NMDA) receptor (Glutamate receptor), Overstimulation of these receptors may be a mechanism for neurodegenerative process in AD.
Anti-Alzheimer Drugs:
Cholinesterase Inhibitors - Donezepil (Aricept)
NMDA antagonists - Memantine: Appears to slow the progression of AD (slows the rate of memory loss).
Anti-Alzheimer Drugs - Cholinesterase Inhibitors - Donezepil
Donezepil (Aricept)
Anti-Alzheimer Drugs - NMDA Antagonist - Memantine
Memantine - Appearst to slow the progression of AD (slows the rate of memory loss).
What are Anxiolytic and Hypnotic Drugs?
These drugs are used for a variety of purposes, including treatment of anxiety and epilepsy, sleep induction and anesthesia. They are often called sedative-hypnotics or just anxiolytics. Cross tolerance occurs between all the CNS sedatives including the barbituates, benzodiazepines (BZDs) and ethanol.
How to classify Anxiolytics and Hypnotic drugs?
Barbituates
Benzodiazepines
And Other
What is MOA of Barbiturates?
Barbiturates enhance the fx of y-aminobutyric acid (GABA) in the CNS by enhancing the duration of chloride channel openings. This action hyperpolarizes the cell, and causes an increase in inhibition of CNS.
- -Barbiturates produce sedation at low doses. At high doses, it can cause hypnosis, coma, death…
- -Suppress respiration by inhibiting hypoxic and CO2 responses to chemoreceptors.
- -Induce the LV P-450 system; so the metabolism of other drugs will be altered in its presence.
- -Physical dependence occurs after chronic use.
- -Symptoms of withdrawal in a person dependent on barbiturates include anxiety, nausea & vomiting, hypotension, seizures and psychosis. CV collapse may develop leading to death.
What does the duration of action of barbiturates depend on?
lipid solubility