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Questions and Answers
What is required before reproducing any part of the publication?
What is required before reproducing any part of the publication?
What should readers do to ensure they have the most accurate medical information?
What should readers do to ensure they have the most accurate medical information?
What does the publisher state about their association with products mentioned in the book?
What does the publisher state about their association with products mentioned in the book?
What is the responsibility of practitioners in relation to the information provided in the book?
What is the responsibility of practitioners in relation to the information provided in the book?
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What is implied by the statement about medical knowledge and practice?
What is implied by the statement about medical knowledge and practice?
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Which of the following is not mentioned as a part of the publisher's contact information?
Which of the following is not mentioned as a part of the publisher's contact information?
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What should practitioners ensure before administering any products mentioned in the book?
What should practitioners ensure before administering any products mentioned in the book?
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What caution does the publisher express regarding their liability?
What caution does the publisher express regarding their liability?
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Which of the following drugs is an example of a high extraction ratio drug?
Which of the following drugs is an example of a high extraction ratio drug?
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What effect does Quinidine have on digoxin?
What effect does Quinidine have on digoxin?
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What type of pharmacodynamic interaction occurs when two drugs with similar mechanisms of action are combined?
What type of pharmacodynamic interaction occurs when two drugs with similar mechanisms of action are combined?
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Which combination is an example of an antagonistic interaction?
Which combination is an example of an antagonistic interaction?
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Which drug is known to inhibit CYP3A4 and significantly reduce the clearance of midazolam?
Which drug is known to inhibit CYP3A4 and significantly reduce the clearance of midazolam?
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In drugs with low extraction ratio, which metabolic activity is rate limiting?
In drugs with low extraction ratio, which metabolic activity is rate limiting?
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What effect does sodium bicarbonate have on bupivacaine?
What effect does sodium bicarbonate have on bupivacaine?
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What is a characteristic of synergistic interactions?
What is a characteristic of synergistic interactions?
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Which of the following anesthetic combinations exemplifies an additive pharmacodynamic interaction?
Which of the following anesthetic combinations exemplifies an additive pharmacodynamic interaction?
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Which combination of agents can lead to serotonin syndrome when used together?
Which combination of agents can lead to serotonin syndrome when used together?
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Which of the following is a drug with a low extraction ratio?
Which of the following is a drug with a low extraction ratio?
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What is the effect of neostigmine on ester local anesthetics?
What is the effect of neostigmine on ester local anesthetics?
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What is one of the effects of reduced hepatic blood flow?
What is one of the effects of reduced hepatic blood flow?
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What is a consequence of MAO inhibitors in relation to indirect sympathomimetics?
What is a consequence of MAO inhibitors in relation to indirect sympathomimetics?
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Which enzyme is inhibited by etomidate, resulting in reduced synthesis of cortisol?
Which enzyme is inhibited by etomidate, resulting in reduced synthesis of cortisol?
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Which of the following is an enzyme inducer that can affect drug metabolism?
Which of the following is an enzyme inducer that can affect drug metabolism?
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What happens to the elimination of phenobarbital in acidic urine?
What happens to the elimination of phenobarbital in acidic urine?
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What is the mechanism by which probenecid affects penicillin?
What is the mechanism by which probenecid affects penicillin?
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Which food product can cause hypertensive crises due to tyramine when consumed with MAO inhibitors?
Which food product can cause hypertensive crises due to tyramine when consumed with MAO inhibitors?
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Which sympathomimetic agent's effects are enhanced by MAO inhibitors but only to a lesser extent?
Which sympathomimetic agent's effects are enhanced by MAO inhibitors but only to a lesser extent?
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What is a common consequence of prolonged propofol infusion exceeding 48 hours in pediatric patients?
What is a common consequence of prolonged propofol infusion exceeding 48 hours in pediatric patients?
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Which condition is NOT associated with the risk factors for hyperkalemia?
Which condition is NOT associated with the risk factors for hyperkalemia?
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Which early marker would likely indicate complications from high dose propofol prior to renal failure?
Which early marker would likely indicate complications from high dose propofol prior to renal failure?
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What is a recommended prevention method to mitigate the effects of propofol infusion?
What is a recommended prevention method to mitigate the effects of propofol infusion?
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Which substance is specifically mentioned as being avoided to prevent complications of hyperkalemia from propofol use?
Which substance is specifically mentioned as being avoided to prevent complications of hyperkalemia from propofol use?
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What crucial intervention should be taken immediately upon detection of complications from high-dose propofol?
What crucial intervention should be taken immediately upon detection of complications from high-dose propofol?
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Which of the following best describes the pathophysiology of effects related to propofol in relation to cardiac function?
Which of the following best describes the pathophysiology of effects related to propofol in relation to cardiac function?
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What potential adverse effect is associated with catecholamines and corticosteroids in the setting of sedation?
What potential adverse effect is associated with catecholamines and corticosteroids in the setting of sedation?
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What lab investigation might reveal the earliest signs of adverse effects from prolonged propofol infusion?
What lab investigation might reveal the earliest signs of adverse effects from prolonged propofol infusion?
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Which receptor does ketamine act upon to produce its bronchodilator effect?
Which receptor does ketamine act upon to produce its bronchodilator effect?
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Which is true regarding the potency of the S (+) isomer of ketamine compared to the R (–) isomer?
Which is true regarding the potency of the S (+) isomer of ketamine compared to the R (–) isomer?
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What is the primary difference in the metabolism of the S (+) isomer compared to the R (–) isomer?
What is the primary difference in the metabolism of the S (+) isomer compared to the R (–) isomer?
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Which statement correctly describes the emergence reactions of the two isomers?
Which statement correctly describes the emergence reactions of the two isomers?
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What is the effect of ketamine on salivation as seen between its two isomers?
What is the effect of ketamine on salivation as seen between its two isomers?
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What is a significant pharmacokinetic characteristic of ketamine?
What is a significant pharmacokinetic characteristic of ketamine?
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How does the S (+) isomer of ketamine affect EEG suppression compared to the R (–) isomer?
How does the S (+) isomer of ketamine affect EEG suppression compared to the R (–) isomer?
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Which statement describes the neurovascular effect of ketamine administration?
Which statement describes the neurovascular effect of ketamine administration?
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Study Notes
Anesthesia Review - Drug Interactions and Mechanisms
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Sodium bicarbonate: Reduces bupivacaine solubility, causing precipitation. Inactivates catecholamines.
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Neostigmine: Increases ester local anesthetic effects (procaine, cocaine, tetracaine).
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Etomidate: Inhibits cytochrome P450 17α hydroxylase and 11β hydroxylase, reducing cortisol and aldosterone synthesis.
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MAO inhibitors: Increase indirect sympathomimetics (ephedrine, amphetamine) effects. Potentially cause hypertensive crises with tyramine-containing foods (aged cheese, wine). Increase direct sympathomimetics (epinephrine, norepinephrine) effects to a lesser extent. When given with meperidine, it can cause serotonin syndrome (excitation, hyperpyrexia, HTN, diaphoresis, rigidity, seizures, coma, death).
Hepatic Biotransformation
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High extraction ratio (ER ≥ 0.7): Rate-limiting is blood flow to liver (metabolism at max). Lidocaine, Propranolol. Reduced hepatic blood flow (reduced cardiac output) and vasopressors (isoproterenol, noradrenaline) increase lidocaine concentration.
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Low extraction ratio (ER ≤ 0.3): Rate-limiting is enzyme activity, enzyme induction can increase metabolism. Diazepam, mepivacaine, alfentanil.
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Competitive inhibition: Midazolam and fentanyl compete with CYP3A4. Propofol inhibits CYP3A4 and reduces midazolam clearance by 37%.
Elimination
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Ion trapping: Phenobarbital (weak acid) excretion increases in acidic urine.
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Ion secretion: Probenecid inhibits penicillin secretion. Quinidine reduces digoxin volume of distribution and clearance.
Pharmacodynamic Interactions
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Additive interactions: Combining drugs with similar mechanisms (rocuronium + vecuronium; 2 volatile anesthetics + nitrous oxide).
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Antagonistic interactions: SCH + non-depolarizing muscle relaxant (NDMR); Neostigmine + NDMR; Flumazenil + benzodiazepines; Naloxone + opioid; Butorphanol + midazolam (increased sedation, less amnesia).
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Synergistic interactions: Small doses of two drugs producing a larger effect (opioid potentiation by NSAIDs; NDMR potentiation by volatile anesthetics; aminosteroid + benzylisoquinoline NDMR).
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Hyperkalemia; Hyperlipidemia/hypertriglyceridemia associated risks: acute refractory bradycardia, sinus arrest, asystole, cardiomyopathy, cardiac failure, hypotension, fatty liver, hepatomegaly, skeletal myopathy, rhabdomyolysis, acute renal failure.
Propofol
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Increased incidence: More common in children, prolonged infusion (>48 hours), or sedation in patients with TBI, sepsis, or respiratory issues.
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Risk factors: Pediatric age, Cumulative dose (>75 µg/kg/min; >4 mg/kg/hr), duration of infusion (>48 hrs), severe inciting illness (CNS origin/TBI, sepsis), catecholamines/corticosteroid supplementation, inadequate carbohydrate intake, subclinical mitochondrial disease.
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Early markers: Unexplained metabolic acidosis, elevated serum lactate, elevated creatinine kinase, elevated myoglobin levels, hyperlipidemia, ECG changes (ST elevation in V1-V3).
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Prevention: Avoid high doses, minimize infusion duration, avoid infusion in children or individuals with mitochondrial disease, adequate carbohydrate intake, avoid lipid overload, high index of suspicion-serum triglyceride 2 days post-continuous infusion.
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Treatment: Mainly supportive: stop propofol infusion, start alternative sedation, maintain hemodynamic stability (IV crystalloids/colloids, vasopressors/inotropes, transvenous pacing), provide nutritional support (avoid additional lipids, add dextrose to IV fluids, 4-8 mg/kg/hour glucose). Renal support (dialysis, continuous renal replacement therapy), maintain oxygenation.
Ketamine
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Introduction: Phencyclidine derivative for induction, two optical isomers (S(+) and R(-)), widely used.
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Chemistry: Phencyclidine derivative, racemic mixture.
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Pharmacodynamics: Positive modulation of GABA receptors (lower GABA needed); allosteric agonism (high doses); disinhibitory effects (extrapyramidal pathways, myoclonus); central nervous system (decreased CMRO2, cerebral blood flow, intracranial pressure, increased cerebral perfusion pressure); cardiovascular (minimal, hemodynamic stability); respiratory (minimal, does not usually cause apnea, hyperventilation). endocrine (transient cortisol/aldosterone inhibition). Analgesia more potent with S+ isomer; potency differences in isomers.
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Pharmacokinetics: Rapid onset (high lipid solubility, vasodilatation, increased drug delivery), redistribution, onset 30-60 seconds. Less protein bound; large volume of distribution; rapid hepatic biotransformation; recovery - differences in isomers; salivation/EEG suppression; apoptosis effects - differences in isomers. Inhaled agents affect.
Etomidate
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Introduction: Phencyclidine derivative, induction of anesthesia, short-term sedation, hemodynamically unstable patients, neurosurgical procedures, trauma.
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Mechanism of Action: Positive modulation of GABA receptors (lower GABA needed), allosteric agonism, disinhibitory effects (extrapyramidal pathways); central nervous system (decreased CMRO2, cerebral blood flow, intracranial pressure); cardiovascular system (minimal, hemodynamic stability). respiratory, endocrine. adrenal suppression up to 72 hours.
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Clinical uses: Induction (especially if poor cardiovascular reserve); neurosurgery; trauma (questionable intravascular volume status). Short term sedation for hemodynamically unstable patients.
Midazolam
- Introduction: Common short-acting benzodiazepine.
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Description
This quiz explores the critical drug interactions and mechanisms in anesthesia. This includes the effects of various anesthetics and their interactions with other medications. Ideal for students and professionals looking to deepen their understanding of pharmacology in anesthesia.
