-
carbamezapine
- targets sodium channels
- This is a first choice for treating partial seizures and tonic-clonic seizures.
- The inactivated state of Na+ channels is prolonged, leading to decrease in repetitive action firing.
-
Lamotragine
- targets sodium channels
- This is a first choice for treating partial seizures and tonic-clonic seizures.
- The inactivated state of Na+ channels is prolonged, leading to decrease in repetitive action firing.
-
Pregablin
- targets high voltage calcium channels
- Used to treat partial seizures in those with impaired hepatic function (cleared by the kidneys).
- It is designed as a structural analog of GABA, and inhibits voltage-gated Ca+ channels.
-
valproic acid
- targets sodium channels, T-type calcium channels, and GABAergic signaling Targets sodium channels in the inactivated state and prolongs this to decrease rapid firing.
- Targets T-type calcium channels by blocking them to stop absence seizures.
- They target GABAergic signaling by increasing the levels of GABA.
-
ethosuximide
- targets T-type calcium channels
- Blocks the T-type calcium channels that cause absence seizures.
- Ethosuximide is only effective in treating absence seizures.
-
phenobarbital
- targets GABAergic signaling
- Used as an alternative treatment for partial and tonic-clonic seizures (is ineffective against absence seizures).
- Its anti-seizure properties are due to the action at the GABA-induced influx of chloride via GABA-A receptors.
- Sometimes AMDPA receptors are blocked also. Not all experience maximum effects at doses that also produce hypnosis—it needs to act only at GABA-A receptors. Phenobarbital acts more like a general anesthetic, which targets the AMPA receptors. It is also used in lethal injections because it profoundly depresses the CNS.
-
clonazepam
- targets GABAergic signaling
- Clonazepam is a benzodiazepine. It acts at the GABA-induced influx of chloride via the GABA-A receptor.
- It is useful in treating partial, tonic-clonic, and also absence seizures. Clonazepam is also able to inhibit T-type calcium channels. These are safer than barbiturates.
- They aid in returning surround inhibition. Profound tolerance results from repeated administration.
-
diazepam
- targets GABAergic signaling
- Diazepam is a benzodiazepine. It acts at the GABA-induced influx of chloride via the GABA-A receptor. It is useful in treating partial and tonic-clonic seizures.
- Diazepam is safer than barbiturates. They aid in returning surround inhibition. Profound tolerance results from repeated administration.
-
rufinamide
- targets Glutamatergic signaling
- Rufinamide blocks the metabotropic glutamate receptors (mGluR5) and also prolongs Na+ channel activation.
- Glutamate underlies almost every signal in the brain, so need drugs that are selective for certain types of receptors and that have limited binding capabilities.
-
morphine
- prototypical opioid analgesic
- poor oral bioavailability (25%)
-
fentanyl
- opioid full agonist
- more lipophilic (faster acting)
- transdermal application for chronic pain
-
codeine
- higher bioavailability than morphine following oral administration
- analgesic prodrug
- 1/10th affinity of morphine
- 10% converted into morphine
- effective antitussive
-
tramadol
- opioid full agonist
- racemic mixture
- one enatiomer is a prodrug of a weak opioid
- another increases synaptic NE/50HT levels by inhibiting their reuptake and promiting release
- serotonin syndrome
- fewer morphine like side effects
-
nalbuphine
- opioid mixed partial agonist
- agonist at kappa opioid receptors
- antagonist at mu opioid receptors
- still produces analgesia but not euphoria
-
naltrexone
- antagonist at mu opioid receptors
- reverses full agonist adverse effects, such as respiratory depression
- shorter half-life of most full agonists
-
methylnaltrexone
- antagonist of opioid receptors
- incapable of penetrating the BBB
- would not reverse any central mediated side effects, but still reduces peripheral side effects
-
aspirin
- eg sodium salicylate and acetylsalicylic acid
- covalently modifies COX1 and 2 resulting in an irreversible inhibition of COX activity
- more selective for COX1
-
ibuprofen
- propinoic acid derivative
- less effective in reducing platelet aggregation
- often used in place of chronic aspirin therapy in the treatment of inflammatory disorders
- less likely to produce GI side effects compared to aspirin
-
ketorolac
- femanate
- potent analgesic, poor anti-inflammatory effects
- oral doses of ketorolac 10 mg more effective than aspirin 650 mg or acetaminophen 600 mg in reducing postoperative pain
- moderate to severe pain
- SIDE EFFECTS: acute renal failure
-
rofecoxib
- Vioxx
- COX2 selective drug
- effective against inflammation, pain, fever
- 50-60% decrease in serious GI complications
- can result in renal complications
- increased cardiovascular risk
- associated with higher incidence of thrombotic cardiovascular events than placebo
-
acetaminophen
- inhibition of central COX
- lower levels of peroxide, COX3
- does not inhibit inflammation or platelet aggregation
- no GI side effects
- adverse effects confined to acute overdose
-
duloxetine
- SNRI
- inhibition of NE and serotonin uptake
- treats depression and neuropathic pain
- augment activity of descending pathways
-
gabapentin
- increases GABA levels
- antiseizure agents
- prolong the inactive state of voltage-dependent Na+ channels
-
ketamine
- NMDA R antagonist
- inhibits central sensitization by decreasing calcium-mediated activation of kinase
- can prevent phosphorylation of AMPA Rs
- reduce chronic and postoperative pain
- SIDE EFFECTS: psychtominmetric effects
-
tricyclic antidepressants
- they will block either NE transport alone (secondary amine) or 5-HT/NE transporter (tertiary amine)
- Antidepressant
- They block a lot of other things that you wouldn't get with an SNRI (muscarinic, histamine, and adrenergic receptors)
- SIDE EFFECTS: nausea, vomiting, dry mouth, blurred vision, tachycardia, sedation, weight gain, orthostatic hypotension, drowsiness, dizziness
- ACUTE TOXICITY: coma, respiratory depression, delirium, seizures, cardiac arrhythmias
- POTENTIALLY FATAL
-
selective serotonin reuptake inhibitors
- antidepressant
- selective blockade of serotonin (5-HT)
- SIDE EFFECTS: nausea/vomiting, headaches, sexual dysfunction, insomnia, nonfatal acute toxicity)
- DRUG INTERACTIONS: MAO inhibitors, serotonin syndrome, can occur weeks after SSRI administration due to half-life of active metabolites
-
monoamine oxidase inhibtors
- inhibition of monoamine oxidase A (5-HT and NE) and B
- ADVERSE REACTIONS: sleep disturbances, weight gain, high risk of postural hypotension
- ACUTE TOXICITY: agitation, hallucinations, convulsions, potentially fatal
- acts in cytosol
-
serotonin-norepinephrine reuptake inhibitors
- blockade of NE and 5-HT transporters
- SIDE EFFECTS: nausea, constipation, dry mouth, headache, insomnia, sweating, anxiety, sexual dysfunction
- DRUG INTERACTIONS: MAO inhibitors, serotonin syndrome
-
ketamine
- NMDA receptor antagonist
- immediate effects
-
-
-
-
-
-
imipramine
tricyclic antidepressant (tertiary)
-
amoxapine
tricyclic antidepressant (secondary)
|
|
