Barbituates instructor
INTRODUCTION TO BARBITURATES (BTS)
Barbiturates (BTS) are a class of drugs that were initially used for various medical purposes.
INITIAL USES OF BARBITURATES
BTS emerged for four distinct applications:
Surgical Anesthetics:
Example: Sodium thiopental
Note: Not analgesics (pain relievers).
Anxiolytics:
Example: Phenobarbital
Hypnotics:
Examples: Amytal, Seconal
Antiepileptics:
Example: Phenobarbital
Important Question: Is sedation synonymous with targeted treatment for the specific condition being addressed?
PHARMACOKINETICS OF BARBITURATES
BTS are grouped based on structural similarities but have different pharmacokinetics.
Absorption and Distribution:
Rapidly absorbed and effectively distributed via bloodstream.
Classified into Ultrashort Acting and Normal Classes.
Blood-Brain Barrier (BBB):
Lipid-soluble ultra-short-acting barbiturates quickly cross BBB, inducing immediate effects (e.g., sodium pentothal induces total sedation 20 seconds post-injection).
Water-soluble forms cross BBB more slowly, leading to delayed effects.
Global Action: Barbiturates impact overall bodily functions; for example, one cannot experience anxiety reduction without sedation.
Clearance and Metabolism:
Primarily cleared by the liver; metabolic tolerance can develop.
Pharmacodynamic Tolerance:
Emerges quickly in higher brain regions (sedation effects) and slower in brainstem (respiration drive).
Results in a diminishing therapeutic index.
MECHANISMS OF ACTION FOR BARBITURATES
Barbiturates, akin to ethanol, function through at least two primary actions:
Action #1: Reduce the conductance (ionic movement) of Na+ ions.
Consequence: Prevents excitatory postsynaptic potentials (EPSPs) at the axon hillock, effectively inhibiting the “on” signal.
Action #2: Reduce Ca++ inflow at presynaptic membranes, which decreases neurotransmitter release.
Primary Action:
Barbiturates mimic GABA (γ-aminobutyric acid), acting as agonists:
Promote Cl- influx, hyperpolarizing neurons (inducing inhibitory postsynaptic potentials or IPSPs), making it harder to reach action potential thresholds at the axon hillock.
Specific examples, such as pentobarbital, effectively open Cl- channels independently, resulting in potent sedation (potentially toxic).
EFFECTS OF BARBITURATES
Induce global inhibition similar to the effects of ethanol:
May result in disinhibition, leading to transient euphoria and potential for abuse.
Pharmacodynamic Tolerance:
Can escalate the effective dose (ED50) by as much as 600%, indicating a higher risk of dependence and abstinence syndrome.
Mortality Data:
In the 1970s, estimates indicated 10 billion doses of BTS produced in the U.S.; not all were used medically.
Associated with approximately 1,500 deaths and 10,000 non-lethal overdoses annually during the '70s to '90s.
Cause of death often rooted in respiratory drive suppression, analogous to opiate overdoses (Telling comparison: 80,000 opiate deaths in 2023 and 178,000 ethanol deaths in 2021).
CONTRIBUTION OF PHARMACOKINETICS TO DEPENDENCE
It is commonly asserted that drugs with rapid onset and offset are typically more addictive:
Barbiturates, with variable onset speeds, serve as a test for this claim.
Pentobarbital: Ultrashort-acting, with a very brief half-life.
Barbital: Long-acting, longer half-life.
Experimental Result: Upon reversing their half-lives:
Pentobarbital: Changed from 5 hours to 27 hours.
Barbital: Changed from 30 hours to 7 hours.
Observations: Changes in withdrawal severity were noted, reinforcing the role of the half-life in addictive potential predictions.
QUIZ QUESTIONS ON BARBITURATES
Quiz Question 1: Barbiturate (BTS) abuse appears most associated with:
a. ultrafast acting BTS
b. more potent BTS
c. BTS with longer half-lives
d. BTS that operate on the GABA receptor
Quiz Question 2: Shortening the half-life of barbital results in:
a. reduced ED50
b. reduced LD50
c. reduced therapeutic margin
d. increased severity of withdrawal
NON-BARBITURATE SEDATIVES
Non-BT sedatives are seldom used today due to their replacement with safer drugs that have superior dose-response functions.
Example: Meprobamate (Miltown)
From 1955 to 1960, it gained popularity as an accessible sedative (nicknamed "mother’s little helper").
Historical Reference: Meprobamate was widely discussed in the following publication:
Ramchandani, D., López-Muñoz, F., & Alamo, C. (2006).
HISTORY OF METHAQUALONE
Methaqualone was discovered as an antimalarial drug with sedative and anxiolytic properties, approved initially as Schedule 5 (low potential for abuse) in 1965.
It was sold as Quaalude.
Evolving regulations: Moved to Schedule 2 in 1980 due to abuse potential, and ultimately to Schedule 1 in 1983.
Current status: Most Quaaludes available today are either foreign or contain alternative ingredients.
GENERAL ANESTHETICS
Example: Propofol (Diprovan)
Used for rapid onset general anesthesia and provides amnesiac effects via GABA site occupancy, inducing global inhibition and sedation.
Case Study: Michael Jackson's cause of death was attributed to propofol overdose in June 2009.
Administration caution: Administering 20 mg IV every 10 seconds until onset (1-1.5 mg/kg) is recommended, avoiding rapid bolus to mitigate risks of cardiorespiratory depression, hypotension, and airway obstruction.
Example Calculation: For a 110 kg patient:
Total dose: 165 mg
Timing: Administering 165 mg at a rate of 20 mg every 10 seconds takes approximately 82.5 seconds.
PHARMACOKINETIC PROPERTY OF PROPOFOL
Notes the timeline of effects:
Infusion → drug enters heart → circulation goes to lungs → back to the heart → to the brain → sedation begins.
KETAMINE AS A RECENT ANTIDEPRESSANT
November 2023 case: Matthew Perry's death during ketamine treatment for resistant anxiety and depression, with overdose exceeding his recognized effective dose (ED).
Mechanism of Action: Works as a noncompetitive antagonist at NMDA receptor complex, blocking Na+ channels and blocking voltage-sensitive K+ and Ca++ channels.
Reference: Schnoebel et al. (2005).
Recent Findings: Ketamine can effectively mitigate treatment-resistant depression (various studies presented).
Notably contradictory: Ketamine acts as a depressant yet increases AMPA receptor activity after NMDA blockade, yielding an arousal effect that alleviates depression.
Reference studies showing antidepressant effects:
Zarate et al. (2006), Berman et al. (2000), Liebrenz et al. (2007).
QUIZ QUESTION ON KETAMINE
Question 3: Ketamine’s antidepressant effect is due to:
a. blocked serotonin reuptake
b. excess release of GABA
c. pharmacodynamic changes in glutamate receptors
d. improved sleeping
ANTIEPILEPTIC MEDICATIONS
Epilepsy: Referring to a spectrum of neurological disorders, including absence and grand mal seizures.
Localized epilepsy involves two phases:
1. Large synchronous depolarization, potentially “kindling” a seizure.
2. Rebound hyperpolarization, rendering focal neurons unresponsive.
Mechanism suggested: GABA may hyperpolarize neurons, minimizing excitation and preventing massive depolarization.
Introduction of GABA deficit theory.
GABA DEFICIT THEORY EVIDENCE
Supporting data for the GABA deficit theory includes:
1. Blocking GABA receptors increases seizure likelihood.
2. Inhibiting GABA metabolism corresponds to seizure reduction.
3. Enhancing GABA actions using various agents (BTS, BDZs, ethanol) mitigates seizures.
4. Common antiepileptic medications like phenobarbital function as GABA agonists.
Other medications such as Valproic acid (Depakote) have speech variations in actions including:
Augmenting GABA synthesis.
Blocking sodium channels (phenytoin and carbamazepine).
Lamictal (Lamotrigine) performs similarly.
NEUROMODULATORS IN TREATMENT
Many antiepileptic medications fall under a newly recognized category called "neuromodulators," potentially employed for treating bipolar disorder as well.
QUIZ QUESTION ON EPILEPSY
Question 4: One major theory suggests seizures are due to:
a. excessive serotonin
b. excessive GABA
c. lack of glutamate
d. lack of GABA
ANTIEPILEPTIC MEDICATIONS AND TERATOGENICITY
Teratogenesis: Defined as birth defects induced by an external factor during pregnancy.
Common examples include ethanol, smoking (CO), and malnutrition.
Antiepileptic medications present a unique challenge.
Increased risk of birth defects in mothers using AEDs: approximately double compared to the general population.
Research indicates a two- to threefold risk of major malformations associated with AEDs, influenced by dosage and polytherapy.
Notable findings:
Lamotrigine emerged as a preferred AED during pregnancy, though it has been associated with an increased risk for cleft palate.
RESEARCH ON AEDs AND PREGNANCY OUTCOMES
Study (Mawer, G. et al., 2010):
Included 277 women with epilepsy (WWE) vs. 315 control women.
Results indicated:
45% of WWE faced obstetric complications compared to 33% in controls (p = 0.01).
Normal vaginal delivery rates were comparable (63% WWE vs. 61% control).
Major congenital malformations (MCM) occurred more often in WWE (6.6%) versus controls (2.1%) (p = 0.02).
Fetal/infant deaths: WWE (2.2%) vs. controls (0.3%) (p = 0.09).
MCM prevalence highest with Valproate (11.3%).
Lamotrigine (5.4%) and Carbamazepine (3.0%) did not significantly differ from controls.
SPECIFIC FINDINGS ON LAMOTRIGINE
A subset of the study involving lamotrigine showed five cases of isolated cleft lip/palate arising from 564 women treated with lamotrigine alone, resulting in a prevalence of 8.9 per 1000 cases.
This prevalence is significantly higher than the controls but remains below 1%.
Important Note: Women on lamotrigine are advised to consult healthcare providers upon pregnancy considerations, weighing risks
Manufacturer’s statement: "Lamictal should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus."