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Class: antiepileptic
Mechanism: reduces high frequency firing and enhancing GABAnergic transmission
Pharmokinetics: well absorbed from gut, 50% plasma bound, eliminated 25% kindey, 75% liver. Half life 90 hrs.
Side Effects: sedation, fatigue, tolerance
Indications: tonic-clonic, cortical focal with phenytoin, status epilepticus
Barbituate site and mechanism of action, metabolism, and tolerance
Ultra short (redistribution), short and intermediate(hepatic), and long-acting (hepatic and renal excretion).
Act as a Cl ionophore of GABA receptor, widespread CNS depression which increases with dose.
Tolerance within a few nights (decreasing TI), cross tolerance to other drugs is a significant problem
Barbituate dependence and side effects
There is drug and physical dependence with continued use. EEG abnormalities, REM rebound, rebound insomnia, tonic-clonic seizures, delirium. Long-acting barbituates show less tendency for withdrawl. Some side effects: daytime hangover, cross tolerance, severe CNS depression when taken with alcohol. respiratory depression, paradoxical excitement.
Barbituate poisoning and clinical use
Frequent use for suicide, depression of the medulla leads to respiratory depression and hypotension.
Clinical Use: ultrashort used as IV anesthetics, Phenobarbital for seizures
Class: Ultra short acting barbituate
Mechanism: May act as Cl channel of GABA receptor.
Kinetics: Elim- redistribution and metabolism, induces CYP450, TI decreases with tolerance
Side Effects: Dependence, withdrawl, and basic side effects of barbituates
Use: IV anesthetics
Class: Intermediate Acting barbituate
Mechanism: Cl channel for GABA receptor
Kinetics: Elim- hepatic, induces CYP450, densensitization occurs, decreased TI with tolerance
Side Effects: Dependence, withdrawl, basic barbituate side effects
Use: hypnotic
Class: intermediate barbituate
Mechanism: Cl channel for GABA receptor
Kinetics: Elim-hepatic, Induces CYP450, desensitization occurs, and TI decreases with tolerance
Use: Hypnotic
Class: Antiepileptic
Mechanism: Reduces high frequency firing by increasing Na inactivation
Kinetics: Slowly absorbed from gut, 90% bound to albumin. Elim-hepatic, 1st order at low conc., zero order at high conc.
Side Effects: Sedation, ataxia, nystagmus, nausea, gingivial hyperplasia
Use: 1st line for tonic clonic, cortical focal, and psychomotor seizures. Used in status epilepticus as well
Class: Antiepileptic
Mechanism: Reducing high frequency firing by increasing Na inactivation.
Side Effects: Sedation, possible serious liver, kidney, bone marrow problems
Uses: Psychomotor, Cortical Focal, Tonic-clonic seizures. 1st line for trigeminal neuralgia
Misc: Doesn't cause gingivial hyperplasia
Class: Antiepileptic
Mechanism: Reduces slow frequency, pacemaker driven repetitive firing by blocking Ca T-channels
Kinetics: Absorbed from gut, eliminated by hepatic metabolism to inactive compound
Side effects: nausea, lethargy, ataxia, serious side effects unlikely
Uses: 1st line for the absence seizures (petit mal)
Valproic Acid
Class: Antiepileptic
Kinetics: Rapid uptake from gut, eliminated hepatically, short half-life
Side Effects: Less likely than other antiepileptics.
Uses: Cortical Focal, Absence, Tonic-Clonic seizures
Class: Benzodiazepine
Kinetics: IV admin
Side Effects:
Uses: Status Epilepticus
Class: Benzodiazepine
Side Effects:
Uses: Status Epilepticus
Class: New Antiepileptics
Mechanism: Inhibits neuronal and glial uptake of GABA
Side Effects:
Uses: Cortical Focal and Psychomotor (complex partial seizures)
Class: New Antiepileptics
Mechanism: GABA analog with unknown mechanism
Side Effects:
Uses: Partial Seizures
Class: New Antiepileptics
Side Effects:
Uses: Partial and Tonic Clonic
Principles of Antiepileptic Treatment
Start and stop treatment gradually, monitor plasma concentration of drug when starting treatment, use multi-drug therapy only when monotherapy is clearly insufficient
Other uses for antiepileptic drugs (AEDs)
Neuropathic pain (phenytoin, carbamezapine, gabapentin)
Migraines (valproate)
Movement disorders and trigeminal disorders (carbamazepine)
Psychiatric disorders like bipolar and schizophrenia, though reasons for effectiveness unclear
What are two distinctive characteristics of opioid-induced analgesia?
1. very effective without loss of consciousness
2. reduction in suffering disproportinate to reduction in pain perception
Describe the ascending pain pathway.
A-delta (fast pain) and C (slow pain) primary sensory fibers synapse on projection neurons in the spinal cord. Project from there to thalamus and regions involved in processing information and regulating autonomic responses. Amygdala, Prefrontal Cortex, Hypothalamus.
Describe the descending pain pathway.
The periaqueductal gray receives inputs from spinal cord, prefrontal cerebral cortex, hypothalamus, and amygdala. PAG projects to rostral ventral medulla. This projection inhibits SC projection neurons via local inhibitory interneurons that use the opioid transmitter, enkephalin
List the receptor type and site of action for:
nausea, vomitting
decreased respiration
psychotomimesis, dysphoria
supraspinal (u1,k3,d)
spinal (u2,k1,d2)
bowel (u2)
postrema of medulla (u)
parasym innervation of pupil (u,k)
respiratory center medulla (u2)
cough center (u)
brainstem DA neurons (u)
DA neurons (k)
What is the structure and mechanism of action of opioid receptors?
7 transmembrane GPCR. That inhibits adenlyl cyclase, increase K conductance, and inhibits Ca conductance
List the endogenous opoids
enkephalins, B-endorphins, dynorphins, alpha-neoendorphin
List the opioid agonists.
mophine, methadone, meperidine, fentanyl, pentazocine, butorphanol
List the mixed opioids.
nalbuphine and buprenorphine
List the opioid antagonists
naloxone and naltrexone
Describe the general characteristics of endorphins
B-endorphin is the most potent endogenous opioids, derived from proteolytic processing from POMC. High affinity for mu and delta receptors. Found in the arcuate nucleus of hypothalamus which projects to the PAG
Describe the general characteristics of enkephalins
Leu- and met-enkephalins. Derived from proenkephalin. Bind well to mu and delta receptors. Important in inhibitory interneurons in dorsal horn of spinal cord also in PAG
Describe the general characteristics of dynorphins
Dynorphins A, B, and alpha-neoendorphin. Derived from pordynorphin. High affinity for kappa receptor. Dynorphin A also binds well to mu receptor. In spinal cord and PAG
Class: Strong analgesic; opiate
Mechanism: Acts on mu receptor
Kinetics: well absorbed via all routes, considerable first pass hepatic metabolism w/ oral admin, undergoes hepatic glucoronidation into active and inactive metabolites. Morphine conjugate excreted in kindney.
Side Effects: nausea, drowsiness, inability to concentrate, euphoria, depressed respiration, miosis, constipation, flushed skin
Uses: analgesia, reduction in suffering with pain, better with dull pain
Class: Strong Analgesic; Opiate
Mechanism: mu receptor, demethylated to morphine
Kinetics: Less 1st pass effect than morphine. Higher oral potency
Uses: antitussive (binding mu receptor and non-opioid receptor). Get effects without substantial respiratory depression.
Misc: use in combo w/ non-opioid to increase potency w/o side effects
Class: Strong Analgesic
Methadone: Mu receptor binding
Kinetics: Slow onset and long duration of action, no rush, little high
Uses: Treatment of opioid addiction and severe chronic pain. Has less withdrawl symptoms
Meperidine (Demerol)
Class: Strong Analgesic; Opioid Agonist
Mechanism: Mu receptor binding
Kinetics: More rapid onset and shorter duration than morphine.
Side Effects: Contraindicated for patients using MAOIs
Uses: analgesic for labor due to less respiratory depression than morphine. Less constipation as well
Class: Strong Analgesic; Opioid agonist
Mechanism: Mu receptor binding
Kinetics: Rapid and brief action
Uses: General anesthesia and for post-op pain. Less constipation than morphine
Class: Strong Analgesic; opioid agonist
Mechanism: Binds to kappa receptor; partial agonist at mu receptor
Side Effects: Psychotomimetic at high doses
Uses: analgesic, less respiratory depression than morphine at high doses.
Class: Strong Analgesic, mixed agonist/antagonist (derived from thebaine)
Mechanism: potent mu receptor partial agonist, and kappa receptor antag.
Side Effects: Reduce the effects of morphine, induces abstinence syndrome
Class: Strong Analgesic; opiate (related to codiene)
Mechanism: binding to non-opioid receptors
Uses: Antitussive action , no analgesic activities
Class: Strong Analgesic, antagonist
Mechanism: competitive mu and kappa receptor blocker
Kinetics: Admin parenterally; rapid effect
Uses: diagnose and treat opioid overdose
Class: Strong Analgesic; antagonist
Mechanism: Competitive mu and kappa receptor blocker
Kinetics: higher oral efficacy and longer lasting than naloxone
Uses: Treat opioid addiction
Class: Strong Analgesic, opiate
Mechanism: Mu receptor binding
Kinetics: Penetrates BBB much more rapidly causing big rush
Uses: Drug of addiction
Misc: replaces hyroxyl groups of morphine with uncharged acetyl groups
Class: Strong Analgesic
Mechanism: mu receptor binding
Kinetics: Relatively high oral/parenteral ratio of potency
Uses: Pain, used in combination with aspirin and acetaminophen
Class: Antiparkinson
Mechanism: DA precursor decarboxylation by AAAD yields DA
Kinetics: absorption in proximal small bowel. Stomach controls emptying and therefore absorption. Cmax: 30min, halflife: 1-2 hrs. Not protein bound
Side effects: confusion, somnolence, nausea, hypotension, hallucinations
Uses: restore movement in patients with Parkinson's
Class: Antiparkinson
Mechanism: AAAD inhibitor thus preventing the conversion of levadopa to DA in periphery
Kinetics: absorption in proximal small bowel. Stomach controls emptying and therefore absorption. Cmax: 30min, halflife: 1-2 hrs. Not protein bound
Side effects: confusion, somnolence, nausea, hypotension, hallucinations
Uses: restore movement in patients with Parkinson's
Class: Antiparkinson
Mechanism: D2, D3 receptor binding. Direct stimulation of DA receptors eliminates complications imposed by a degenerating population of DA neurons and pool of AAAD
Kinetics: half-life is 6-8 hrs.
Side Effects: St. Anthony's fire, orthostatic hypotension, ankle edema, hallucinations, nausea
Uses: early in PD; rarely effective after three years
Class: Antiparkinson; Dopamine agonist, non-ergot derivative
Mechanism: D3>D2 receptor binding. eliminates complications imposed by degenerating pop. of neurons and pool of AAAD
Kinetics: Half-life 6-8hrs
Side effects: orthostatic hypotension, ankle edema, hallucinations, nausea
Uses: early in PD, rarely effective after 3 years
Class: Antiparkinson
Mechanism: Augments DA release in amphetamine like manner; also an NMDA blocker which is thought to mediate it's effectiveness at controlling levadopa
Kinetics: Cmax 1-4 hours, half-life: 15-24 hrs. Excreted almost essentially unchanged. Dossage 100mg BID (2x) or TID (3x)
Side effects: ankle edema, lived reticularies, anticholinergic effects
Use; Early in PD w/ mild symptoms and for control of tremor, also during advanced PD for control of levodopa induced side effects
Class: MAOI w/ antiparkinson effects
Mechanism: Selective MAOB irreversible inhibitor
Kinetics: well absorbed from gut, highly lipophilic enters BBB quickly, undergoes hepatic metabolism, higher doses produce effects of non-selective MAOI
Side Effects: Nightmares, insomnia, impotence, worsening of levodopa dyskinesias
Class: COMT inhibitor w/ antiparkinson effects
Mechanism: Prevents DA metabolism in periphery
Kinetics: rapidly absorbed, half-life: 2hrs. 100% protein bound, undergoes hepatic metabolism
Side effects: diarrhea, discoloration of urine, increase in levadopa related side effects
Use: Management of motor complications from prolonged L-dopa therapy. Increase half-life of L-dopa and AUC increases with no change to Cmax or Tmax
Class: COMT inhibitor w/ anti parkinson
Mechanism: Inhibits DA metabolism in periphery.
Kinetics: rapidly absorbed, half-life: 2hrs.
Side effects: hepatotoxicity
Use: Management of motor complications from prolonged L-dopa therapy

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