Pharmacology From PPT Flashcards

Question

What is the role of neurokinin 1 receptor antagonists like aprepitant?

Answer 1

Suppressing activity at the NST to prevent emesis.

Answer 2

0.625 to 1.25 mg IV

Answer 3

Aprepitant (Emend), fosaprepitant, netupitant/palonosetron (Akynzeo), and rolapitant (Varubi) ## Footnote They suppress activity at the NST, where vagal afferents from the GI tract converge with inputs from the brain that initiate emesis.

Answer 4

Aprepitant ## Footnote Others are approved for CINV.

Answer 5

Long half-life ## Footnote This makes it effective for PONV.

Answer 6

Extrapyramidal side effects ## Footnote It is contraindicated in Parkinson's disease.

Answer 7

FDA warnings about QT interval prolongation ## Footnote This raised safety concerns.

Answer 8

1-2 mg ## Footnote It has antiemetic properties at low doses.

Answer 9

Blocking cholinergic impulses ## Footnote It prevents nausea and vomiting.

Answer 10

Sedation, blurred vision, dizziness, dry mouth ## Footnote These side effects can affect patient comfort.

Answer 11

Significant antiemetic effect ## Footnote It decreases dopamine's emetic effect in the chemoreceptor trigger zone. decreases serotonin release by binding to the GABA receptor complex.

Answer 12

Greater than 20 mg ## Footnote It has a mild dopamine receptor blocking effect.

Answer 13

Short half-life of 30-45 minutes ## Footnote This limits its utility if administered at the beginning of surgery.

Answer 14

Multimodal PONV and PONV prophylaxis ## Footnote Combination therapy is advised.

Answer 15

Combination therapy using a 5-HT3 antagonist and a second drug ## Footnote This approach enhances prophylaxis effectiveness.

Answer 16

Do not give a repeat dose of the prophylactic antiemetic ## Footnote Rescue therapy should be from a different therapeutic class.

Answer 17

Achieve a state of unconsciousness and prepare the patient for surgery. ## Footnote This phase is crucial for ensuring that the patient is adequately anesthetized before surgical procedures begin.

Answer 18

Administering anesthetic agents, either intravenously or via inhalation. ## Footnote The choice of method depends on various factors including the patient's condition and the type of surgery.

Answer 19

Close observation of vital signs to ensure adequate anesthesia depth. ## Footnote Vital signs include heart rate, blood pressure, and respiratory rate.

Answer 20

Managing potential complications like hypotension or airway obstruction. ## Footnote These complications can arise from the anesthetic agents used or the patient's pre-existing conditions.

Answer 21

Maintain a steady state of anesthesia and ensure patient comfort and safety. ## Footnote This phase is critical for the duration of the surgical procedure.

Answer 22

Adjusting anesthetic dosage and using a combination of agents for optimal effect. ## Footnote The combination helps in achieving effective anesthesia while minimizing side effects.

Answer 23

Safely bring the patient out of anesthesia. ## Footnote This phase marks the transition from unconsciousness to alertness.

Answer 24

Gradual reduction of anesthetic agents, allowing the patient to regain consciousness. ## Footnote This process must be carefully managed to avoid complications.

Answer 25

Managing airway and ensuring pain control while avoiding complications like nausea or delirium. ## Footnote These challenges require careful monitoring and intervention.

Answer 26

Providing care in the recovery room, assessing for return of reflexes, and ensuring patient stability. ## Footnote Post-anesthesia care is crucial for monitoring the patient's recovery from anesthesia.

Answer 27

Dexmedetomidine hydrochloride is the S-enantiomer of medetomidine, chemically described as (-) -4-[1-(2,3-dimethylphenyl)ethyl]-1H-imidazole monohydrochloride.

Answer 28

Dexmedetomidine is freely soluble in water, with a pKa of 7.1.

Answer 29

The partition coefficient (n-octanol/water) at pH 7.4 is 2.89.

Answer 30

Onset of action with loading infusion is 10 to 20 minutes, and the duration of action after the infusion is stopped is 10 to 30 minutes.

Answer 31

Dexmedetomidine exhibits linear kinetics in the dosage range of 0.2 to 0.7 µg/kg/hour when administered by intravenous infusion for up to 24 hours.

Answer 32

The loading dose is 1 µg/kg infused over 10 minutes followed by maintenance infusions of 0.2 to 0.7 µg/kg/hour.

Answer 33

Dexmedetomidine is widely used for sedation in critical care and for nonintubated patients requiring sedation for short-term surgical procedures.

Answer 34

Dexmedetomidine produces dose-dependent sedation resembling natural sleep without causing respiratory depression.

Answer 35

The main cardiovascular effects are hypotension and bradycardia, occasionally transient hypertension with rapid initial loading doses.

Answer 36

Respirations are maintained, with normal brain respiratory responsiveness to CO2 and preserved airway patency.

Answer 37

Dexmedetomidine maintains respirations and normal brain respiratory responsiveness to CO2. Airway patency and reflexes are present or only slightly diminished. It completely blocked histamine-induced bronchoconstriction in dogs and appears beneficial in decreasing airway reactivity in patients with chronic obstructive pulmonary disease or asthma.

Answer 38

Dexmedetomidine has a mild diuretic effect mediated via a2-receptor stimulation. It also exhibits renal, gastroprotective, and anti-inflammatory effects. It is thought to decrease the incidence of emergence delirium after general anesthesia in pediatric patients.

Answer 39

Dexmedetomidine does not interfere with neurologic monitoring, making it suitable for procedures requiring wake-up tests and does not change cerebral metabolism. Its effects on intracranial pressure are not clinically significant.

Answer 40

The main cardiovascular effects of dexmedetomidine are hypotension and bradycardia, resulting from CNS a-receptor stimulation and systemic vasodilation. Transient profound hypertension can occur when using certain drugs to treat dexmedetomidine-induced bradycardia in children.

Answer 41

• Dexmedetomidine is an az-receptor agonist that results in central sympatholysis. • Dexmedetomidine sedation allows for an arousable patient to ascertain neurologic status. • Dexmedetomidine does not interfere with neurologic monitoring. • Hypotension and bradycardia are the most frequent cardiovascular adverse effects. • Respirations are maintained. • It may reduce postoperative agitation and emergence reactions.

Answer 42

Etomidate is a carboxylated imidazole derivative, synthesized in 1965 and introduced to European anesthesia practice in 1972. It has two isomers, but only the (+) isomer possesses hypnotic properties.

Answer 43

Etomidate is supplied as a 2-mg/ml preparation, containing 35% propylene glycol as a solvent. It has a pH of 8.1 and a pKa of 4.2.

Answer 44

Etomidate produces dose-dependent CNS depression within one arm-brain circulation time, decreases cerebral blood flow and cerebral metabolic rate of oxygen consumption, acts as a GABA-mimetic, and does not release histamine.

Answer 45

Etomidate is rapidly metabolized in the liver by hepatic microsomal enzymes and plasma esterases, primarily through ester hydrolysis, forming inactive carboxylic acid metabolites.

Answer 46

Approximately 10% of the drug is excreted unchanged in the urine. The terminal half-life is 2 to 5 hours, and awakening typically occurs 5 to 15 minutes after bolus administration.

Answer 47

Etomidate is primarily used in compromised patients where the use of other intravenous anesthetics may be problematic. Its major advantage is minimal cardiorespiratory depression.

Answer 48

The induction dose of Etomidate is typically 0.2-0.3 mg/kg.

Answer 49

Etomidate produces dose-dependent CNS depression, decreases cerebral blood flow, and affects electroencephalogram (EEG) patterns and auditory evoked potentials (AEPs).

Answer 50

Etomidate offers hemodynamic stability upon induction, making it a preferred choice in patients with compensated heart conditions. It does not significantly affect cardiac dysrhythmias.

Answer 51

Etomidate causes dose-dependent respiratory depression, but to a lesser extent than propofol. It may cause brief periods of apnea following induction.

Answer 52

Etomidate can cause pain on injection, thrombophlebitis, nausea, and vomiting. The current formulation containing propylene glycol results in burning and pain on injection in up to 90% of patients. The incidence of subsequent venous sequelae up to 7 days postoperatively is 50%. Myoclonia during onset is common with etomidate use.

Answer 53

Etomidate inhibits the enzyme 11ß-hydroxylase, essential in the production of corticosteroids and mineralocorticoids, leading to clinically significant reductions in steroid production even with a single dose.

Answer 54

Etomidate is contraindicated in patients with known sensitivity, adrenal suppression, and acute porphyrias.

Answer 55

Etomidate contributes to cardiovascular stability by acting as an agonist at a1B-adrenoceptors, mediating an increase in blood pressure. This effect helps maintain myocardial oxygen supply and demand balance.

Answer 56

Etomidate is used in compromised patients when the use of other intravenous anesthetics may be problematic. The major advantage of etomidate is minimal cardiorespiratory depression. Etomidate reduces intracranial pressure, cerebral blood flow, and CMRO2. The mechanism of action of etomidate appears to be GABA-mimetic. Involuntary movements or myoclonia during onset is common. Etomidate frequently causes burning on injection. Etomidate increases postoperative nausea and vomiting. The induction dose is 0.2-0.3 mg/kg.

Answer 57

Ketamine enhances opioid-induced analgesia and prevents hyperalgesia.

Answer 58

The primary pathway for ketamine metabolism by the cytochrome P-450 system is demethylation to form the metabolite norketamine.

Answer 59

Hydroxylation of norketamine occurs at one of two positions in the cyclohexone ring to form hydronorketamine metabolites.

Answer 60

These metabolites form a glucuronide derivative via conjugation, producing a more water-soluble compound that is eliminated primarily via renal excretion.

Answer 61

Ketamine is used for induction of anesthesia, especially in high-risk patients, and is effective in obstetric and pediatric anesthesia, as well as for analgesia in combination with other agents.

Answer 62

Ketamine produces a dissociative state of anesthesia, characterized by catalepsy, open eyes, reactive pupils, intact corneal reflexes, and horizontal nystagmus.

Answer 63

Ketamine acts as a circulatory stimulant, increasing systemic blood pressure, heart rate, cardiac contractility and output, and central venous pressure.

Answer 64

Ketamine increases cerebral blood flow, cerebral metabolic rate, and intracranial pressure. It is a moderate analgesic with a preference for skin, bone, and joint pain.

Answer 65

Ketamine is a potent bronchodilator, preserving airway reflexes and increasing secretions. It maintains respirations and airway reflexes, although initial apnea may occur with high doses and rapid administration.

Answer 66

Emergence phenomena, including vivid dreams, floating sensations, and delirium, can occur after ketamine administration. These are more common in adults than children and are reduced by benzodiazepine or other sedative administration.

Answer 67

Ketamine is used in obstetrics for analgesia or anesthesia. It is highly lipid-soluble and readily crosses the placenta, producing rapid anesthesia without compromising uterine tone, uterine blood flow, or neonatal status at delivery.

Answer 68

There is a controversy regarding anesthetic neurotoxicity caused by ketamine. Neuroapoptosis has been noted in several animal models when ketamine is used in the developing brain, with implications for human use still being researched.

Answer 69

Ketamine usually increases intraocular pressure (IOP), but the effect appears to be dose-dependent. It blocks oculocardiac reflex-induced arrhythmias better than propofol during sevoflurane anesthesia for strabismus surgery.

Answer 70

A benzodiazepine such as midazolam is administered if patient status allows. An antisialagogue may also be given to decrease secretions.

Answer 71

Ketamine 15-45 mcg/kg/min (1-3 mg/min) by continuous IV infusion or 0.5-1.0 mg/kg supplemental IV doses as needed.

Answer 72

Ketamine 2-4 mg/kg IV, or 4-6 mg/kg IM (oral dose is 10 mg/kg).

Answer 73

Ketamine 0.2-0.8 mg/kg IV (over 2-3 min) followed by a continuous ketamine infusion (5-20 mcg/kg/min). 10-20 mg may produce preemptive analgesia.

Answer 74

The NMDA receptor, where it inhibits glutamate as a noncompetitive antagonist.

Answer 75

Ketamine produces an anesthetic state referred to as dissociative anesthesia.

Answer 76

The onset of effect is relatively slow compared to other induction drugs (2-5 min).

Answer 77

Ketamine produces a rise in cerebral perfusion pressure.

Answer 78

Ketamine is a bronchodilator, preserves airway reflexes, and increases secretions.

Answer 79

Ketamine is an indirect sympathomimetic, releasing catecholamines, which accounts for the cardiac stimulation and bronchodilation.

Answer 80

Ketamine is a moderate analgesic and is used preoperatively as an analgesic.

Answer 81

Propofol is a 2,6-diisopropylphenol.

Answer 82

It consists of 10% soybean oil, 2.25% glycerol, and 1.2% purified egg lecithin.

Answer 83

The pH of Propofol ranges from 7 to 8.5, and its pKa is 11.

Answer 84

Propofol's unique vehicle is particularly susceptible to bacterial contamination.

Answer 85

Diprivan contains disodium edetate (EDTA) as a preservative.

Answer 86

They contain sodium metabisulfite or benzyl alcohol, depending on the manufacturer.

Answer 87

It interacts with the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) and the GABA_A glycoprotein receptor complex.

Answer 88

Rapid distribution occurs within 2 to 4 minutes.

Answer 89

The elimination half-life is 1 to 2 hours.

Answer 90

The induction dose is typically 1-2 mg/kg.

Answer 91

The maintenance infusion is 100-200 µg/kg/min.

Answer 92

It produces a rapid and pleasant loss of consciousness and reduces cerebral blood flow.

Answer 93

It usually results in a mild to moderate transient decrease in blood pressure.

Answer 94

Propofol causes transient respiratory depression, commonly leading to apnea.

Answer 95

It is used for induction of general anesthesia, intravenous sedation, and in electroconvulsive therapy (ECT).

Answer 96

Propofol might play an important role in multimodal neuroprotection, including the preservation of cerebral perfusion, temperature control, prevention of infections, and tight glycemic control. However, its role as a clinical neuroprotectant is not definitively established, as studies in both animals and humans have been inconsistent.

Answer 97

Propofol is known to reduce the duration of seizures induced during electroconvulsive therapy (ECT) compared to barbiturates. This reduction in seizure duration does not appear to decrease the efficacy of ECT.

Answer 98

Propofol may induce myoclonia, spontaneous excitatory movements due to selective disinhibition of subcortical centers. Adequate dosing may prevent these movements. It also decreases intraocular pressure.

Answer 99

Propofol easily crosses the placental barrier due to its high lipid solubility. It can cause sedative effects in the neonate when used for cesarean delivery, and lower Apgar scores have been noted. Its antiemetic effects may be advantageous in obstetric patients.

Answer 100

Propofol should not be used in patients with known hypersensitivity to propofol or its components, or in those with disorders of lipid metabolism. New generic formulations containing sodium metabisulfite should not be used in sulfite-sensitive patients.

Answer 101

This is a serious condition associated with the use of propofol, especially in higher doses or prolonged infusions. Symptoms include metabolic acidosis, hyperkalemia, lipidemia disorders, hepatomegaly, and elevated liver transaminases.

Answer 102

Propofol is the most commonly used intravenous anesthetic as an induction drug and for sedation. Respiratory effects include transient respiratory depression or apnea, depending on dose. Although not a bronchodilator, safe use in asthmatics has been well established. Propofol is unique among induction agents in that it exhibits mild anti-emetic properties. It has a rapid onset and emergence after bolus or continuous infusions of the drug. Patients emerge with a mild euphoria followed by rapid dissipation of the sedative effects. Propofol reduces cerebral blood flow, CMRO2, and ICP. It decreases blood pressure, cardiac output, and systemic vascular resistance to a greater extent than etomidate at equipotent doses. The induction dose is 1-2 mg/kg followed by a maintenance infusion of 100-200 mcg/kg/min. Conscious sedation doses are 25-75 mcg/kg/min.

Answer 103

Midazolam produces dose-dependent CNS depressant effects, ranging from anxiolysis to sedation, sleep, and anesthesia at high doses. It also has anticonvulsant effects, amnesia, and muscle-relaxing properties.

Answer 104

Midazolam increases the threshold to local anesthetic-induced seizure activity and produces anterograde amnesia.

Answer 105

Midazolam exhibits a higher clearance rate compared to other benzodiazepines, making it shorter-acting. Its pharmacokinetic profile is influenced by factors such as age, gender, obesity, race, and hepatic and renal status.

Answer 106

The pharmacologic effects of midazolam are primarily terminated by redistribution out of the CNS.

Answer 107

Midazolam is commonly used for preoperative medication due to its rapid onset, short duration, and half-life. It is ideal as a preoperative anxiolytic, sedative, and amnestic.

Answer 108

Midazolam produces dose-dependent CNS depressant effects, including anxiolysis, sedation, sleep, and anesthesia at high doses. It also has anticonvulsant effects and produces anterograde amnesia.

Answer 109

In clinical doses, midazolam has minimal cardiovascular effects. A decrease in blood pressure may be seen when combined with opioids, especially in patients with heart disease or the elderly.

Answer 110

Midazolam produces dose-dependent respiratory depression and is the most respiratory depressing among benzodiazepines. Increased respiratory depression and apnea are possible when combined with other CNS depressants.

Answer 111

The most common adverse effects of midazolam are unexpected respiratory depression and oversedation.

Answer 112

Midazolam should be avoided in patients with acute porphyrias.

Answer 113

Flumazenil is the sole benzodiazepine antagonist available in the United States.

Answer 114

Flumazenil is a competitive antagonist with a high affinity for the receptor site, producing prompt and effective reversal of benzodiazepine effects.

Answer 115

Flumazenil's onset is 1 to 2 minutes, and its duration of action is 45 to 90 minutes.

Answer 116

Midazolam produces synergistic CNS, cardiovascular, and respiratory effects when combined with fentanyl.

Answer 117

Midazolam has minimal cardiovascular effects in clinical doses but may cause a decrease in blood pressure when given with opioids, particularly in patients with heart disease or the elderly.

Answer 118

Midazolam is the most respiratory depressing among benzodiazepines, and increased respiratory depression and apnea are possible when combined with other CNS depressants.

Answer 119

0.2-0.3 mg/kg

Answer 120

1 mcg/kg infused over 10 min followed by 0.2-0.7 mcg/kg/hr

Answer 121

0.1-0.2 mg/kg

Answer 122

Opioids inhibit the ascending transmission of nociception information from the spinal cord dorsal horn and activate pain control pathways descending from the midbrain. They have minimal effects on electroencephalographic and evoked-potential activity, allowing for neurophysiologic monitoring during opioid anesthetic techniques.

Answer 123

Opioids produce dose-dependent respiratory depression by affecting mu and delta receptors in the brainstem's respiratory centers. They reduce responsiveness to carbon dioxide and oxygen levels, leading to a shift in the CO2 response curve for respiration.

Answer 124

Opioids cause miosis (pinpoint pupils), especially under general anesthesia due to high doses of potent opiates. This effect is produced by opiate depression of inhibitory GABA interneurons, leading to stimulation of the Edinger-Westphal nucleus.

Answer 125

Opioids suppress cough via a depressant effect on the cough center in the medulla.

Answer 126

Opioids elicit nausea and vomiting by stimulating the chemoreceptor trigger zone in the medulla's area postrema. Serotonin type 3 (5-HT3) and dopamine type 2 (D2) receptors are involved in this process.

Answer 127

Opioids typically result in bradycardia with little effect on blood pressure in healthy patients, due to medullary vagal stimulation. They induce dose-dependent peripheral vasodilation.

Answer 128

Opioids can cause skeletal muscle rigidity.

Answer 129

Generalized itching is common with neuraxial morphine and can be treated with antihistamines or opiate receptor partial agonists or antagonists.

Answer 130

Opioids affect the gastrointestinal system, including constipation and urinary retention.

Answer 131

Opioids have hormonal effects, including the release of vasopressin and inhibition of stress-induced release of corticotropin and gonadotropins.

Answer 132

Opioids can be administered intrathecally or epidurally for pain control. Side effects with spinal administration are similar to systemic administration, but pruritus and urinary retention occur more frequently. Respiratory depression is a serious complication associated with neuraxial opioids.

Answer 133

Morphine is a naturally occurring opioid and the prototype for opioid agonists, primarily used for moderate to severe pain relief.

Answer 134

Morphine is more effective in relieving continuous dull pain than sharp intermittent pain.

Answer 135

Morphine can be administered intramuscularly, intravenously, subcutaneously, orally, intrathecally, and epidurally.

Answer 136

Sedation occurs first, followed by analgesia. Sedation should not be considered an indicator of appropriate analgesia.

Answer 137

Morphine is among the least lipophilic opioids, resulting in slow penetration of biologic membranes and a slower onset.

Answer 138

Morphine undergoes phase 2 glucuronide conjugation at the 3 and 6 positions.

Answer 139

The active metabolite is morphine-6-glucuronide (M6G), which can prolong therapeutic effects and may lead to excessive sedation in renal failure patients.

Answer 140

M6G is more potent than the parent drug within the CNS, while morphine-3-glucuronide (M3G) is inactive.

Answer 141

IV dose is 0.05 to 0.15 mg/kg, with an onset of 20 minutes, peak effect at 30-60 minutes, and duration of 4 to 5 hours.

Answer 142

The active metabolite is morphine-6-glucuronide (M6G), which can prolong therapeutic effects and may lead to excessive sedation in renal failure patients.

Answer 143

Fentanyl is the most widely used opioid analgesic in anesthesia, known for its profound dose-dependent analgesia, ventilatory depression, and sedation.

Answer 144

The duration of action for a single administered dose of Fentanyl is approximately 20-40 minutes.

Answer 145

The action of a single dose is terminated by redistribution.

Answer 146

Fentanyl's high lipid solubility allows for rapid tissue uptake.

Answer 147

Fentanyl is metabolized by N-dealkylation and hydroxylation to inactive metabolites that are eliminated in urine and bile.

Answer 148

Fentanyl elimination is prolonged in the elderly and neonates.

Answer 149

Fentanyl is the prototypic opioid for transdermal application.

Answer 150

Transdermal administration does not require cooperation from the patient, avoids first-phase hepatic metabolism, and does not produce discomfort.

Answer 151

Current formulations permit delivery of 25 to 100 mcg/hour for 24 to 72 hours.

Answer 152

The transdermal Fentanyl patch provides a relatively constant plasma concentration for 72 hours.

Answer 153

Fentanyl has many other uses, including intrathecal, epidural, and postoperative PCA intravenous use.

Answer 154

Fentanyl transdermal patches deliver 75 to 100 mcg/hour, resulting in peak plasma concentrations in approximately 18 hours.

Answer 155

Alfentanil is an opioid analgesic with a more rapid onset of action and shorter duration than Fentanyl, despite being less lipid-soluble.

Answer 156

The high nonionized fraction (90%) of Alfentanil at physiological pH and its small volume of distribution increase the amount of drug available for binding in the brain.

Answer 157

Alfentanil is metabolized in the liver by oxidative N-dealkylation and O-demethylation in the cytochrome P-450 system. The inactive metabolites are excreted in the urine.

Answer 158

Alfentanil is effective epidurally, but its duration of analgesia is short, which has limited its popularity. There is significant patient-to-patient variability in response to Alfentanil.

Answer 159

Erythromycin has been shown to prolong the metabolism of Alfentanil and interact with it to produce clinical symptoms of prolonged respiratory depression and sedation.

Answer 160

Hydromorphone is a semisynthetic opioid derived from morphine, known for its high potency and used in pain management.

Answer 161

The onset of action is 15 to 30 minutes.

Answer 162

The peak effect occurs between 30 to 90 minutes.

Answer 163

The duration of action is 4 to 5 hours.

Answer 164

The half-life is approximately 1 to 3 hours.

Answer 165

The recommended dose is 0.01 to 0.02 mg/kg.

Answer 166

It is recommended due to the lack of any known active metabolites, making it a safer option compared to other opioids.

Answer 167

Studies demonstrate similar analgesia and side effect profiles between parenteral Hydromorphone and Morphine.

Answer 168

Meperidine is a synthetic mu receptor agonist, structurally similar to atropine, and possesses an antispasmodic effect similar to atropine. It is used for its analgesic properties.

Answer 169

After demethylation in the liver, Meperidine is partially metabolized to normeperidine, which is half as analgesic as Meperidine but lowers the seizure threshold and induces CNS excitability.

Answer 170

The elimination half-life of normeperidine is significantly longer than that of Meperidine.

Answer 171

Accumulation of normeperidine can lead to CNS excitation characterized by tremors, muscle twitches, and seizures. Limitations on Meperidine use should be considered in patients with renal failure, the elderly, and for chronic use in cancer patients who may require high doses.

Answer 172

Significant drug interactions can occur between Meperidine and first-generation monoamine oxidase (MAO)-inhibiting drugs, leading to hyperthermia, seizures, and death.

Answer 173

Meperidine is effective in reducing shivering from diverse causes, including general and epidural anesthesia. This effect appears to result from kappa receptor stimulation, reducing visible shivering and the accompanying increase in oxygen consumption.

Answer 174

Remifentanil is an opioid used in anesthesia known for its rapid onset, ultrashort duration, titratability, and simple metabolism.

Answer 175

Remifentanil is a moderately lipophilic, piperidine-derived opioid with an ester link that allows for rapid metabolism by blood and tissue esterases.

Answer 176

Remifentanil has a small volume of distribution (Vd) and an elimination half-life of 8 to 20 minutes. It is metabolized by hydrolysis to a less active compound.

Answer 177

Remifentanil has a short duration of action, precise and rapid titratable effect, and noncumulative effects, leading to rapid recovery after discontinuation.

Answer 178

Bolus dosing in the preoperative or postoperative care unit is not recommended due to potential respiratory depression and muscle rigidity.

Answer 179

Approximately 10-25 times more potent than morphine.

Answer 180

About 50-100 times more potent than morphine.

Answer 181

Roughly 5-7 times stronger than morphine.

Answer 182

Generally considered less potent than morphine, with a ratio of about 1:10 (meperidine to morphine).

Answer 183

Extremely potent, with estimates ranging from 100-200 times more potent than morphine.

Answer 184

Around 500-1000 times more potent than morphine.

Answer 185

Approximately 1/5 to 1/10 as potent as fentanyl.

Answer 186

Around 1/10 to 1/20 as potent as fentanyl.

Answer 187

Significantly less potent than fentanyl, approximately 1/75 to 1/100 as potent.

Answer 188

Generally considered to be about 1/50 to 1/100 as potent as fentanyl.

Answer 189

Roughly equivalent to fentanyl in potency, though it has a much shorter duration of action.

Answer 190

About 5 to 10 times more potent than fentanyl.

Answer 191

A potent partial agonist opioid that binds mainly to the mu receptors.

Answer 192

Approximately 8 hours, due to its slow dissociation from the receptor.

Answer 193

Exhibits a ceiling effect where an increase in dose does not increase respiratory depression.

Answer 194

Minimal effect on GI motility and smooth muscle sphincter tone.

Answer 195

Commonly used in opioid use disorder treatment plans and for moderate to severe cancer pain through a transdermal system.

Answer 196

A highly lipophilic opioid, acting as an agonist at kappa receptors and a weak antagonist at mu receptors.

Answer 197

Can produce more analgesia than morphine but has a ceiling effect for respiratory depression below that of mu-agonists.

Answer 198

Used for the treatment of migraine headaches and postoperative pain, and has been studied for epidural use.

Answer 199

Acts as both an agonist and an antagonist at opioid receptors, with analgesic response equal to that of morphine.

Answer 200

Provides an agonist effect at kappa receptors and an antagonist effect at mu receptors.

Answer 201

Demonstrates a ceiling effect for respiratory depression and difficulty with reversal using naloxone.

Answer 202

Used to antagonize pruritus induced by epidural and intrathecal morphine and effectively antagonizes fentanyl-induced respiratory depression without producing adverse circulatory changes.

Answer 203

Buprenorphine and Nalbuphine exhibit a ceiling effect for respiratory depression. ## Footnote Butorphanol's ceiling effect is below that of n-agonists.

Answer 204

Buprenorphine has a high affinity for mu receptors. ## Footnote Butorphanol acts as an agonist at kappa receptors and a weak antagonist at mu receptors, while Nalbuphine provides an agonist effect at kappa receptors and an antagonist effect at mu receptors.

Answer 205

Buprenorphine is used in opioid use disorder treatment and for cancer pain. ## Footnote Butorphanol is used for migraine and postoperative pain, and Nalbuphine is used for antagonizing pruritus and respiratory depression induced by other opioids.

Answer 206

An oxymorphone derivative, Naloxone is a pure opioid antagonist.

Answer 207

It blocks opioid receptor sites, reversing respiratory depression and opioid analgesia through competitive antagonism at mu, kappa, and delta receptors.

Answer 208

The duration of action of Naloxone is less than that of most opioid agonists, which can allow the return of respiratory depression in some patients treated with Naloxone.

Answer 209

Naloxone may antagonize intrinsic analgesic systems and can reverse the side effects of epidural opioids while preserving some analgesic effects.

Answer 210

Naltrexone has antagonist and receptor-binding properties similar to those of Naloxone but with higher oral efficacy and longer duration of action.

Answer 211

It produces an active metabolite with a half-life even longer than that of Naltrexone.

Answer 212

Approximately 24 hours.

Answer 213

Routinely used in alcohol use disorder programs and administered to patients addicted to opioids to prevent the euphoric effects of opioids.

Answer 214

Structurally similar to Naloxone, Nalmefene is a long-acting parenteral opioid antagonist.

Answer 215

It has an elimination half-life of approximately 10 hours and a duration of action of 8 hours when given in usual doses.

Answer 216

Primarily used in alcohol use disorder programs. In acute opioid overdose, it is recommended that 0.5 to 1.6 mg be given intravenously.

Answer 217

An oxymorphone derivative, Naloxone is a pure opioid antagonist.

Answer 218

It blocks opioid receptor sites, reversing respiratory depression and opioid analgesia through competitive antagonism at mu, kappa, and delta receptors.

Answer 219

The duration of action of Naloxone is less than that of most opioid agonists, which can allow the return of respiratory depression in some patients treated with Naloxone.

Answer 220

Naloxone may antagonize intrinsic analgesic systems and can reverse the side effects of epidural opioids while preserving some analgesic effects.

Answer 221

Naltrexone has antagonist and receptor-binding properties similar to those of Naloxone but with higher oral efficacy and longer duration of action.

Answer 222

It produces an active metabolite with a half-life even longer than that of Naltrexone.

Answer 223

Approximately 24 hours.

Answer 224

Routinely used in alcohol use disorder programs and administered to patients addicted to opioids to prevent the euphoric effects of opioids.

Answer 225

Structurally similar to Naloxone, Nalmefene is a long-acting parenteral opioid antagonist.

Answer 226

It has an elimination half-life of approximately 10 hours and a duration of action of 8 hours when given in usual doses.

Answer 227

Primarily used in alcohol use disorder programs. In acute opioid overdose, it is recommended that 0.5 to 1.6 mg be given intravenously.

Answer 228

Naloxone has the shortest duration of action, while Naltrexone and Nalmefene have longer durations.

Answer 229

Naloxone is primarily used for the emergency treatment of opioid overdose.

Answer 230

Naltrexone and Nalmefene are used in alcohol use disorder programs.

Answer 231

Naltrexone produces an active metabolite contributing to its longer duration of action.

Answer 232

Nalmefene's longer action is due to its inherent pharmacokinetic properties.

Answer 233

An intravenous nonsteroidal anti-inflammatory drug (NSAID) used for mild to moderate pain.

Answer 234

Can be administered via both intramuscular and intravenous routes.

Answer 235

Primary advantages include a lack of significant GI and cardiovascular side effects.

Answer 236

Atopic or asthmatic patients, the elderly, patients with renal or GI dysfunction, or bleeding disorders.

Answer 237

An intravenous formulation of Ibuprofen (Caldolor) available as an analgesic and antipyretic.

Answer 238

Similar to Ketorolac.

Answer 239

400 to 800 mg intravenously over 30 minutes, with an onset of 30 minutes and a duration of 4 to 6 hours.

Answer 240

An intravenous analgesic and antipyretic drug for use in both adults and children over 2 years old.

Answer 241

Significant opiate-sparing effect.

Answer 242

1000 mg infused over 15 minutes.

Answer 243

Rare, but hepatotoxicity is a concern with doses less than 4000 mg/day.

Answer 244

Both Ketorolac and Ibuprofen are NSAIDs and work by inhibiting cyclooxygenase enzymes.

Answer 245

Acetaminophen's mechanism is less clear but is believed to involve central inhibition of prostaglandin synthesis.

Answer 246

Ketorolac and Ibuprofen are effective for mild to moderate pain.

Answer 247

Acetaminophen is used for mild pain and fever.

Answer 248

Ketorolac and Ibuprofen can have gastrointestinal and cardiovascular side effects.

Answer 249

Acetaminophen is generally safer but can cause hepatotoxicity at high doses.

Answer 250

1. Fresh Gas Flow Rate: A higher fresh gas flow rate leads to a closer match between the inspired gas concentration and the fresh gas concentration. 2. Breathing System Volume: A smaller breathing system volume helps in achieving a concentration closer to the set value on the vaporizer. 3. Circuit Absorption: Lower absorption by the machine or breathing circuit also helps in maintaining the inspired gas concentration closer to the fresh gas concentration.

Answer 251

1. Uptake: Anesthetic agents are taken up by the pulmonary circulation during induction, causing alveolar concentrations to lag behind inspired concentrations. 2. Solubility in Blood: Insoluble agents like nitrous oxide are taken up less avidly by the blood compared to more soluble agents like sevoflurane, affecting the rate at which alveolar concentration rises and achieves a steady state. 3. Alveolar Blood Flow/Cardiac Output: An increase in cardiac output increases anesthetic uptake, slowing the rise in alveolar partial pressure and delaying induction. 4. Partial Pressure Difference: The gradient between alveolar gas and venous blood, which depends on tissue uptake, also affects the uptake of anesthetic by the pulmonary circulation.

Answer 252

It refers to the discrepancy between alveolar and arterial anesthetic partial pressures, often due to venous admixture, alveolar dead space, and nonuniform alveolar gas distribution.

Answer 253

It increases the alveolar-arterial difference, leading to an increase in alveolar partial pressure and a decrease in arterial partial pressure.

Answer 254

Increasing the inspired concentration raises both the alveolar concentration and its rate of rise, particularly significant with nitrous oxide.

Answer 255

The primary route is through the alveolar membrane, especially significant for nitrous oxide.

Answer 256

Administer 100% oxygen for 5 to 10 minutes to prevent diffusion hypoxia.

Answer 257

It generally accounts for a minimal increase in the rate of decline of alveolar partial pressure but has a greater impact on soluble anesthetics like methoxyflurane.

Answer 258

Halothane undergoes greater biotransformation compared to isoflurane, despite its higher solubility.

Answer 259

Factors include elimination of rebreathing, high fresh gas flows, low anesthetic-circuit volume, low absorption by the anesthetic circuit, decreased solubility, high cerebral blood flow, and increased ventilation.

Answer 260

It refers to the discrepancy between alveolar and arterial anesthetic partial pressures, often due to venous admixture, alveolar dead space, and nonuniform alveolar gas distribution.

Answer 261

It increases the alveolar-arterial difference, leading to an increase in alveolar partial pressure and a decrease in arterial partial pressure.

Answer 262

Increasing the inspired concentration raises both the alveolar concentration and its rate of rise, particularly significant with nitrous oxide.

Answer 263

The primary route is through the alveolar membrane, especially significant for nitrous oxide.

Answer 264

Administer 100% oxygen for 5 to 10 minutes to prevent diffusion hypoxia.

Answer 265

It generally accounts for a minimal increase in the rate of decline of alveolar partial pressure but has a greater impact on soluble anesthetics like methoxyflurane.

Answer 266

Halothane undergoes greater biotransformation compared to isoflurane, despite its higher solubility.

Answer 267

Factors include elimination of rebreathing, high fresh gas flows, low anesthetic-circuit volume, low absorption by the anesthetic circuit, decreased solubility, high cerebral blood flow, and increased ventilation.

Answer 268

Diffusion hypoxia is a condition that can occur due to the rapid elimination of nitrous oxide from the body.

Answer 269

Nitrous oxide is eliminated quickly from the body through the alveolar membrane.

Answer 270

The rapid elimination of nitrous oxide speeds up recovery from anesthesia.

Answer 271

There is a dilution of oxygen (O2) and carbon dioxide (CO2) concentrations in the alveolar gas.

Answer 272

The dilution can lead to a relative state of hypoxia.

Answer 273

To prevent diffusion hypoxia, it is recommended to administer 100% oxygen for 5 to 10 minutes after discontinuing nitrous oxide.

Answer 274

Administering 100% oxygen helps to maintain adequate oxygen levels in the alveoli and bloodstream.

Answer 275

It counteracts the dilution effect caused by the rapid exit of nitrous oxide.

Answer 276

Nitrous oxide is a gas at room temperature and ambient pressure, and can be kept as a liquid under pressure. It is relatively inexpensive but raises safety concerns.

Answer 277

Nitrous oxide has raised safety concerns, leading to interest in alternatives like xenon. It is an NMDA receptor antagonist and has environmental impacts, including ozone depletion and greenhouse effects.

Answer 278

Nitrous oxide stimulates the sympathetic nervous system, masking its direct myocardial depressant effects. In patients with coronary artery disease or severe hypovolemia, myocardial depression may be unmasked.

Answer 279

Nitrous oxide increases respiratory rate and decreases tidal volume due to CNS stimulation, with minimal change in minute ventilation and resting arterial pCO2. It significantly depresses the hypoxic drive.

Answer 280

Nitrous oxide increases cerebral blood flow (CBF) and cerebral blood volume, mildly elevating intracranial pressure and increasing cerebral oxygen consumption. It provides analgesia at concentrations below MAC for various procedures.

Answer 281

Nitrous oxide does not provide significant muscle relaxation and can cause skeletal muscle rigidity at high concentrations. It decreases kidney blood flow and glomerular filtration rate, and may reduce hepatic blood flow.

Answer 282

Nitrous oxide is primarily eliminated by exhalation, with less than 0.01% undergoing reductive metabolism in the gastrointestinal tract. It can irreversibly oxidize the cobalt atom in vitamin B12, inhibiting vitamin B12 dependent enzymes.

Answer 283

Nitrous oxide is often used in combination with more potent volatile agents, reducing their required concentrations.

Answer 284

Nitrous oxide is contraindicated in conditions where rapid diffusion into air-containing cavities can be hazardous, such as pneumothorax, bowel distention, or intracranial air.

Answer 285

MAC is defined as the alveolar concentration of an inhaled anesthetic that prevents movement in 50% of patients in response to a standardized stimulus, such as a surgical incision.

Answer 286

MAC reflects the partial pressure of the anesthetic in the brain, allows for comparisons of potency between different anesthetic agents, and serves as a standard for experimental evaluations.

Answer 287

MAC is a median value and has limited utility in managing individual patients, especially during periods of rapidly changing alveolar concentrations, such as during induction and emergence from anesthesia.

Answer 288

The MAC values for combinations of anesthetic agents are roughly additive.

Answer 289

A mixture of 0.5 MAC of nitrous oxide and 0.5 MAC of isoflurane produces a similar effect in suppressing movement in response to surgical incision as 1.0 MAC of isoflurane alone.

Answer 290

No, the degree of myocardial depression may not be equivalent at the same MAC for different agents.

Answer 291

0.5 MAC of halothane causes more myocardial depression than 0.5 MAC of nitrous oxide.

Answer 292

MAC multiples are clinically useful if the concentration-response curves of the compared anesthetics are parallel, nearly linear, and continuous.

Answer 293

Approximately 1.3 MAC of any volatile anesthetic prevents movement in about 95% of patients, approximating the EC95.

Answer 294

A concentration of 0.3 to 0.4 MAC is associated with awakening from anesthesia when the inhaled drug is the sole anesthetic agent.

Answer 295

MAC can be altered by various physiological and pharmacological variables.

Answer 296

There is a 6% decrease in MAC per decade of age, regardless of the volatile anesthetic.

Answer 297

MAC is relatively unaffected by species, sex, or duration of anesthesia.

Answer 298

No, MAC is not altered after spinal cord transection in rats, suggesting that the site of anesthetic inhibition of motor responses may be in the spinal cord.

Answer 299

1.17 (per table)

Answer 300

Dilates coronary arteries, with potential myocardial depression unmasked in certain patients.

Answer 301

Causes respiratory depression with less pronounced tachypnea and is a good bronchodilator.

Answer 302

Increases cerebral blood flow (CBF) and intracranial pressure at concentrations >1 MAC.

Answer 303

Provides muscle relaxation.

Answer 304

Decreases renal blood flow and may reduce total hepatic blood flow, but maintains hepatic oxygen supply.

Answer 305

Metabolized to trifluoroacetic acid; limited oxidative metabolism minimizes hepatic dysfunction risk.

Answer 306

No unique contraindications; potentiates nondepolarizing neuromuscular blocking agents (NMBAs).

Answer 307

Similar to isoflurane, with a decline in systemic vascular resistance and arterial blood pressure.

Answer 308

Airway irritant.

Answer 309

Increases CBF and intracranial pressure; cerebral vasculature remains responsive to Paco2 changes.

Answer 310

Associated with a dose-dependent decrease in response to peripheral nerve stimulation.

Answer 311

Does not cause significant nephrotoxic effects; hepatic function tests generally unaffected.

Answer 312

Undergoes minimal metabolism; degraded by desiccated CO2 absorbent into carbon monoxide.

Answer 313

Shares contraindications with other volatile anesthetics; potentiates NMBAs.

Answer 314

Mildly depresses myocardial contractility; causes a slight decline in systemic vascular resistance and arterial blood pressure.

Answer 315

Depresses respiration and reverses bronchospasm similarly to isoflurane.

Answer 316

Causes slight increases in CBF and intracranial pressure; high concentrations may impair CBF autoregulation.

Answer 317

Produces adequate muscle relaxation for intubation.

Answer 318

Slightly decreases renal blood flow; maintains total hepatic blood flow and oxygen delivery.

Answer 319

Metabolized at a rate lower than halothane but higher than isoflurane or desflurane; can be degraded into nephrotoxic compound A and hydrogen fluoride.

Answer 320

Similar contraindications to other volatile anesthetics; potentiates NMBAs without sensitizing the heart to catecholamine-induced arrhythmias.

Answer 321

All three anesthetics have similar effects on the cardiovascular system, primarily causing a decrease in systemic vascular resistance and arterial blood pressure.

Answer 322

Isoflurane and sevoflurane both depress respiration and act as bronchodilators. Desflurane is an airway irritant.

Answer 323

All increase CBF and intracranial pressure, with sevoflurane and desflurane having similar effects on CBF autoregulation.

Answer 324

Isoflurane and sevoflurane provide muscle relaxation, while desflurane decreases response to peripheral nerve stimulation.

Answer 325

Isoflurane and sevoflurane have similar effects on renal and hepatic systems, while desflurane is noted for minimal nephrotoxic effects.

Answer 326

Isoflurane has limited oxidative metabolism, desflurane undergoes minimal metabolism, and sevoflurane has a higher rate of metabolism with potential nephrotoxic byproducts.

Answer 327

All three anesthetics share similar contraindications and potentiate NMBAs.

Answer 328

Involves a single supramaximal electrical stimulus ranging from 0.1-1.0 Hz. It requires a baseline before drug administration and is generally used as a qualitative assessment.

Answer 329

Consists of four twitches at 2 Hz every 0.5 sec for 2 sec. It reflects blockade from 70-100% and is useful during onset, maintenance, and emergence of neuromuscular blockade.

Answer 330

Involves two short bursts of 50-Hz tetanus separated by 0.75 sec. It's similar to TOF and may be easier to detect fade than with TOF.

Answer 331

Generally consists of rapid delivery of a 30-, 50-, or 100-Hz stimulus for 5 sec. It should be used sparingly for deep block assessment as it can be painful.

Answer 332

Involves 50-Hz tetanus for 5 sec, a 3-sec pause, then single twitches of 1 Hz.

Answer 333

Ulnar Nerve: Preferred for determining the level of neuromuscular blockade (NMB). It's usually accessible and convenient. The response at the ulnar nerve is best for measuring recovery.

Answer 334

Facial Nerves: Used when access to the arm is not practical. The facial nerve monitoring generally involves the orbicularis oculi muscle around the eye or the corrugator supercilii that moves the eyebrow.

Answer 335

At least 5mL/kg is necessary but insensitive as an indicator of neuromuscular function.

Answer 336

Should be qualitatively as strong as baseline, indicating 75-80% receptor occupancy.

Answer 337

No palpable fade suggests 70-75% receptor occupancy. It's uncomfortable but more sensitive as an indicator of recovery than single twitch.

Answer 338

TOF involves delivering four separate stimuli at a frequency of 2 Hz every 0.5 seconds for a total duration of 2 seconds. It is used to approximate the degree or percent of paralysis present, being most sensitive between 70% and 100% paralysis.

Answer 339

The size of the fourth twitch (T4) is compared to the first twitch (T1), referred to as the TOFR.

Answer 340

The disappearance of T4 represents a block of 75% to 80%.

Answer 341

The absence of T4 and T3 indicates an 80% to 85% block.

Answer 342

When T4, T3, and T2 are absent, it suggests a 90% to 95% neuromuscular blockade (NMB).

Answer 343

100% paralysis is achieved when no responses can be elicited.

Answer 344

TOF is useful during the onset, maintenance, and emergence from neuromuscular blockade.

Answer 345

The TOFR is crucial for guiding the reversal of neuromuscular blockade. A TOFR of 0.9 should be the standard attained, as even small degrees of residual block can increase the incidence of adverse respiratory events.

Answer 346

When there is only one response to TOF stimulation, successful reversal may take as long as 30 minutes.

Answer 347

With a TOF count of two or three responses, recovery usually takes 4 to 15 minutes after intermediate-acting drugs.

Answer 348

Adequate recovery can be achieved within 5 minutes of reversal with neostigmine or 2 to 3 minutes after using edrophonium.

Answer 349

TOF monitoring is significant in avoiding residual paralysis and ensuring patient safety, particularly in higher-risk or elderly patients.

Answer 350

Even small degrees of residual block can lead to complications like hypoxia, hypercarbia, atelectasis, and airway obstruction in the PACU.

Answer 351

Succinylcholine is formed by the joining of two acetylcholine (ACh) molecules. Its chemical formula is C14H30N204.

Answer 352

Succinylcholine contains a quaternary ammonium structure, making it water-soluble in the body.

Answer 353

No, succinylcholine does not pass the blood-brain barrier and has no direct central nervous system (CNS) effects.

Answer 354

Succinylcholine mimics the action of ACh by depolarizing the motor endplate.

Answer 355

No, succinylcholine does not act on ganglionic nicotinic receptors but may cause bradycardia by acting on cardiac cholinergic muscarinic receptors.

Answer 356

It leads to initial stimulation of cholinergic receptors, followed by desensitization, resulting in less drug needed at the receptor site to produce neuromuscular block.

Answer 357

Succinylcholine has an extremely rapid onset, with effects usually within 3 minutes after administration.

Answer 358

The plasma half-life is 2 to 4 minutes, with a clinical duration of 5 to 10 minutes.

Answer 359

It is hydrolyzed by plasma cholinesterases into succinylmonocholine and choline, and further into succinic acid and choline.

Answer 360

A bolus of 0.5 to 1.5 mg/kg is recommended for adequate adult paralysis and relaxation for intubation.

Answer 361

The ED95 is approximately 0.30 mg/kg.

Answer 362

It does not pass the blood-brain barrier and has no direct CNS effects, but may indirectly increase intracranial pressure (ICP).

Answer 363

It can cause slight tachycardia or bradycardia, especially in children or with repeat dosing in adults.

Answer 364

It is metabolized by plasma cholinesterase produced in the liver.

Answer 365

Yes, it can be used if preoperative potassium levels are normal, but it is contraindicated in patients with elevated preoperative potassium levels.

Answer 366

Onset may be slightly prolonged due to slower circulation time, and reduced plasma cholinesterase levels may allow for reduced dosage.

Answer 367

The recommended dose is 1.0 mg/kg based on total body weight.

Answer 368

It should be used only in emergency situations for children under 8 years old, not for routine intubation.

Answer 369

There is a risk of cardiac arrest from hyperkalemic rhabdomyolysis.

Answer 370

Myalgias and fasciculations, particularly in the face, trunk, neck, and shoulders, are common after administration. Small doses of nondepolarizing muscle relaxants or pretreatment with sodium channel blockers or NSAIDs may prevent myalgia.

Answer 371

Hyperkalemia, which results in a transient increase in serum potassium levels, can be profound in patients with burn injuries or underlying muscle disorders.

Answer 372

Malignant Hyperthermia (MH), a pharmacogenetic skeletal muscle disorder, is a contraindication for succinylcholine.

Answer 373

Pseudocholinesterase variants can result in a prolonged response and apnea. Notable variants include fluoride-resistant (F), silent (S), and K variants.

Answer 374

Succinylcholine may cause bradycardia, especially in children or with repeat dosing in adults.

Answer 375

It indirectly increases intracranial pressure (ICP), raising concerns for its use in neurosurgical procedures or patients with brain pathology.

Answer 376

A Phase II block, also known as a desensitization block, is a specific type of neuromuscular block that occurs with large doses of depolarizing neuromuscular blocking agents (NMBAs), such as succinylcholine.

Answer 377

In Phase I, depolarizing NMBAs mimic acetylcholine (ACh) at the neuromuscular junction, leading to depolarization of the muscle membrane and muscle paralysis.

Answer 378

With prolonged exposure to high doses of depolarizing agents, the muscle membrane starts to repolarize but becomes less responsive to acetylcholine, characterizing the Phase II block.

Answer 379

Phase II block shows a fade in response to tetanic or train-of-four (TOF) stimulation, unlike Phase I block which shows no fade.

Answer 380

Yes, Phase II blocks can often be reversed with anticholinesterase drugs, which is not the case with Phase I blocks.

Answer 381

It is important for anesthesia providers to recognize a Phase II block because its management differs from a Phase I block, with the presence of fade in response to TOF stimulation being a key indicator.

Answer 382

If a Phase II block is identified, it can often be treated with anticholinesterase drugs, similar to the treatment of a block induced by nondepolarizing NMBAs.

Answer 383

To prevent the development of a Phase II block, careful dosing of depolarizing agents is crucial, avoiding excessive or repeated doses of drugs like succinylcholine.

Answer 384

Rocuronium bromide is a monoquaternary aminosteroid neuromuscular blocker.

Answer 385

1-(17B-(acetyloxy)-3a-hydroxy-2B-(4-morpholinyl)-5a-androstan-16ß-yll-1-(2-propenyl) pyrrolidinium bromide.

Answer 386

Formulated with a pH adjusted to 4.0 and contains no preservative.

Answer 387

It is stable at room temperature for up to 30 days.

Answer 388

It competes with acetylcholine for binding to nicotinic receptors at the motor endplate, leading to muscle relaxation.

Answer 389

In usual ED95 doses, it lasts 30 to 60 minutes.

Answer 390

The onset time is dose-dependent.

Answer 391

Biliary elimination of unchanged drug is the primary method.

Answer 392

Renal excretion accounts for 33% of elimination.

Answer 393

The elimination half-life is 60 to 120 minutes.

Answer 394

Primarily used as a nondepolarizing neuromuscular blocker in anesthesia.

Answer 395

Doses ranging from 0.6 to 1.2 mg/kg provide good to excellent intubating conditions within 45 to 90 seconds.

Answer 396

It has no significant cardiac effects at clinical doses and does not result in histamine release.

Answer 397

Its duration of action is prolonged in patients with hepatic disease.

Answer 398

A small portion of the drug is excreted unchanged in the urine, leading to a prolonged elimination half-life in patients with renal disease.

Answer 399

The onset times of rocuronium are generally delayed in elderly patients due to slower circulation times and other kinetic changes associated with aging. The dosing interval and duration of action are prolonged due to decreased hepatic and renal clearance and an increased volume of distribution.

Answer 400

The use of rocuronium in obese patients requires special clinical considerations due to their higher risk for gastroesophageal reflux disease and pulmonary aspiration. The duration of action is prolonged likely due to a decrease in elimination.

Answer 401

Rocuronium undergoes deacetylation via the liver. Its plasma levels follow a three-compartment open model, resulting in extensive redistribution after intravenous injection.

Answer 402

The elimination half-life of rocuronium is 60 to 120 minutes, with variations in children (38.3 minutes), normal adults (56 minutes), and elderly persons (137 minutes).

Answer 403

The priming technique involves giving 10% of the calculated intubating dose prior to inducing anesthesia, followed by the remaining dose after 1 to 3 minutes. This speeds the onset by valuable seconds.

Answer 404

Rocuronium is approximately 46% bound to human plasma proteins, which is somewhat less than other neuromuscular blockers. This decreased binding may lead to a slightly more rapid onset.

Answer 405

Vecuronium bromide is a monoquaternary aminosteroid neuromuscular blocker developed from pancuronium.

Answer 406

It was developed by altering the steroid nucleus from a bisquaternary to a monoquaternary compound.

Answer 407

Vecuronium is more lipophilic than pancuronium but remains predominantly hydrophilic.

Answer 408

Vecuronium is chemically designated as piperidinium.

Answer 409

Vecuronium acts by competing with acetylcholine for binding to nicotinic receptors at the motor endplate, leading to muscle relaxation.

Answer 410

Vecuronium is 1.5 times more potent than pancuronium.

Answer 411

The induction dose of vecuronium is 0.1 mg/kg, producing maximum suppression of muscle twitch within 3 minutes.

Answer 412

The onset varies with the concurrent anesthetic administered and is inversely proportional to the dose.

Answer 413

The duration of action varies with the type of anesthetic and the dose administered.

Answer 414

Vecuronium is administered intravenously.

Answer 415

Vecuronium has no significant cardiac effects at clinical doses and does not cause histamine release.

Answer 416

Vecuronium is eliminated via hepatic and renal mechanisms.

Answer 417

Only 20% to 30% of the administered dose is recovered unchanged in the urine within 24 hours.

Answer 418

Onset times are generally delayed in the elderly due to slower circulation and other kinetic changes.

Answer 419

In patients with hepatic disease, the elimination half-life of vecuronium is prolonged, resulting in a longer duration of action.

Answer 420

Vecuronium undergoes elimination via a three-compartment model and is more lipophilic than other agents in its class. A major portion of the dose (40%-80%) is taken up by the liver and excreted in bile.

Answer 421

The elimination half-life of Vecuronium ranges from 51 to 90 minutes in healthy adults. Total clearance has been reported from 3 to 5.6 mL/kg/min.

Answer 422

The duration of Vecuronium is 36.2 ± 6.4 minutes after a dose of 0.1 mg/kg in patients undergoing intravenous anesthesia. The time from 25% twitch recovery to 75% twitch recovery at this dose was 11 to 12 minutes, and the overall duration was 30 to 45 minutes.

Answer 423

Vecuronium is metabolized in the liver and has been administered to patients with hepatic disease. In patients with cirrhosis, the elimination half-life was prolonged approximately 60%, resulting in a longer duration of action.

Answer 424

Cisatracurium besylate (Nimbex) is a nondepolarizing muscle relaxant, three times more potent than atracurium with a slower onset of action.

Answer 425

It is the most notable of the 10 stereoisomers of atracurium.

Answer 426

Cisatracurium is available as a sterile, nonpyrogenic aqueous solution in various vial sizes with a pH of 3.25 to 3.65 and a concentration of 2 mg/mL (10 mg/mL in the 20-mL vial for convenience).

Answer 427

Cisatracurium acts as a nondepolarizing muscle relaxant by competing with acetylcholine for binding to nicotinic receptors at the motor endplate.

Answer 428

Cisatracurium undergoes ester hydrolysis catalyzed by nonspecific esterases into a quaternary alcohol and a quaternary acid, which are excreted primarily in bile and urine.

Answer 429

Cisatracurium's elimination is nonorgan-dependent, making it a suitable choice for patients with renal or hepatic impairment.

Answer 430

It is used in anesthesia for muscle relaxation, particularly advantageous in settings where cardiovascular stability is essential and in patients with ARDS.

Answer 431

The typical intubating dose of Cisatracurium is 0.1 mg/kg.

Answer 432

Cisatracurium maintains cardiovascular stability and does not cause histamine release, avoiding hypotension and tachycardia associated with other muscle relaxants.

Answer 433

The kinetics of cisatracurium are not significantly changed in elderly patients, making it a reliable agent in this population.

Answer 434

Cisatracurium is preferred in obese patients due to its lack of histamine release and reliable kinetics, with dosing recommended at ideal body weight.

Answer 435

Cisatracurium undergoes Hofmann elimination, which is pH and temperature-dependent, accounting for 77% of total body clearance.

Answer 436

Nonspecific esterases are responsible for 23% of total body clearance.

Answer 437

16% of organ-dependent clearance occurs through renal pathways.

Answer 438

The half-life of cisatracurium is approximately 26 to 36 minutes.

Answer 439

Several differences exist among neonates, infants, and children in relation to their response to neuromuscular blocking agents (NMBAs). ## Footnote The neuromuscular junction is incomplete at delivery and continues to mature throughout infancy.

Answer 440

The sensitivity to any relaxant may change from birth through childhood.

Answer 441

It is classified as a benzylisoquinoline.

Answer 442

Atracurium loses potency at the rate of 6% per year when refrigerated at 5°C and approximately 5% per month at room temperature. Its recommended unrefrigerated shelf life is 14 days.

Answer 443

Atracurium is a competitive bisquaternary neuromuscular blocker, highly selective in action, and degradable without renal or hepatic intervention.

Answer 444

The ED95 of Atracurium is 0.10 to 0.25 mg/kg.

Answer 445

Atracurium has an onset time that is inversely proportional to dosage, ranging from 1.2 to 2.8 minutes.

Answer 446

On average, as an intermediate relaxant, the duration of action is 30 to 60 minutes.

Answer 447

Atracurium undergoes Hofmann elimination, a temperature- and pH-dependent breakdown, and ester hydrolysis catalyzed by nonspecific esterases.

Answer 448

These metabolites are excreted primarily in bile and urine.

Answer 449

It is used as a competitive bisquaternary neuromuscular blocker in anesthesia, suitable for patients with liver and kidney diseases.

Answer 450

The dosage is adjusted based on the patient's condition and the desired level of muscle relaxation.

Answer 451

Atracurium can cause histamine release, which may produce hypotension and tachycardia.

Answer 452

The pharmacokinetics of Atracurium in these patients show no differences in plasma elimination half-lives compared to nonimpaired subjects.

Answer 453

The duration of Atracurium is not affected by aging, making it predictable in the elderly population.

Answer 454

The use of Atracurium in obese patients does not demonstrate a difference in recovery indices or times compared with normal weight patients.

Answer 455

The pharmacokinetics of atracurium in patients with hepatic and renal disease show no differences in plasma elimination half-lives compared to nonimpaired control subjects. This indicates that atracurium is suitable for use in patients with liver and kidney diseases.

Answer 456

Atracurium can cause histamine release, leading to hypotension and tachycardia. This release is associated with decreases in blood pressure and increases in heart rate at usual clinical doses.

Answer 457

There are differences in the response to neuromuscular blocking agents (NMBAs) among neonates, infants, and children compared to adults. The neuromuscular junction in neonates is incomplete at delivery and matures throughout infancy, affecting sensitivity to relaxants from birth through childhood.

Answer 458

Prophylaxis against histamine release requires the administration of both H1 (antihistamines)and H2 (Pepcid/ -dine)receptor blockers to mitigate all receptor responses elicited by endogenous histamine release.

Answer 459

Complete and effective reversal of muscle relaxants is crucial. Incomplete reversal can lead to significant challenges, including postoperative residual paralysis.

Answer 460

Neostigmine is the most commonly used anticholinesterase agent for reversal.

Answer 461

Edrophonium may be used for faster onset or if there are shortages of neostigmine, but its efficacy is less than neostigmine.

Answer 462

Pyridostigmine is largely historical and rarely used.

Answer 463

The degree of spontaneous recovery from neuromuscular block at the time of edrophonium administration should be at least a TOF count of 4.

Answer 464

Neostigmine does not reverse deep NMB and should be used cautiously to avoid incomplete reversal or false belief in safe return of muscular function.

Answer 465

Sugammadex is known for its high efficacy and emphasizes the need for quantitative monitoring of residual blockade at the end of a procedure.

Answer 466

Assessment of TOF, and if no response, the PTC (Post-Tetanic Count), guide dose selection for sugammadex reversal.

Answer 467

Several factors influence the incidence of postoperative residual NMB, including the type of anesthesia used, type and dose of NMBD administered, type and dose of anticholinesterase reversal drug, duration of anesthesia, use of neuromuscular monitoring, and patient factors.

Answer 468

Cholinesterase Inhibitors primarily act due to their structural relationship and interaction with acetylcholinesterase (AChE), a protein that hydrolyzes acetylcholine (ACh) molecules.

Answer 469

Edrophonium and neostigmine contain an ionized center that combines at the active center or a site removed from the active center of AChE.

Answer 470

Edrophonium is a reversible inhibitor of cholinesterase that electrostatically attaches to the anionic site of AChE and is stabilized by hydrogen bonding at the esteratic site.

Answer 471

Edrophonium has a shorter duration of action than compounds that form a bond.

Answer 472

Neostigmine is a carbamic acid ester of alcohol that forms a carbamyl-ester complex at the esteratic site of cholinesterase.

Answer 473

The drug-enzyme complex of Neostigmine degrades similarly to the ACh-cholinesterase complex, leaving AChE unable to hydrolyze ACh.

Answer 474

Edrophonium binds reversibly to the negatively charged enzyme site, while Neostigmine forms a more stable carbamylated enzyme, leading to differing pharmacokinetic profiles.

Answer 475

Both are quaternary ammonium compounds with poor lipid solubility, limiting their penetration through lipid barriers.

Answer 476

Cholinesterase inhibitors are used to reverse neuromuscular blockade by increasing the concentration of endogenous ACh around cholinoreceptors.

Answer 477

They increase the likelihood that ACh will reoccupy the receptor site once occupied by the neuromuscular blocker and prolong the time ACh remains in the cleft.

Answer 478

Neostigmine is a carbamic acid ester of alcohol that contains a quaternary or tertiary ammonium group.

Answer 479

Neostigmine forms a carbamyl-ester complex at the esteratic site of cholinesterase, preventing the hydrolysis of acetylcholine.

Answer 480

Approximately 50% is eliminated by glomerular filtration, while the other 50% is hydrolyzed by plasma esterases and hepatic metabolism.

Answer 481

The metabolites are 3-hydroxyphenyltrimethyl ammonium (3-OH PPM) and conjugated 3-OH PPM, which have about one-tenth the activity of the parent compound.

Answer 482

The elimination half-life is 70 to 80 minutes, increasing to 181 to 183 minutes in anephric patients.

Answer 483

Neostigmine is used to reverse neuromuscular blockade by increasing the concentration of endogenous acetylcholine around cholinoreceptors.

Answer 484

It may increase the incidence of postoperative nausea and vomiting.

Answer 485

The dose range is 25-75 mcg/kg.

Answer 486

Onset is 5-15 minutes, and duration is 45-90 minutes.

Answer 487

Neostigmine should not be administered to patients with deep neuromuscular blockade to avoid incomplete reversal.

Answer 488

Sugammadex is biologically inactive and shows a linear dose relationship up to 8.0 mg/kg.

Answer 489

The clearance of Sugammadex is approximately 120 L/min.

Answer 490

The volume of distribution of Sugammadex is 18 L.

Answer 491

The elimination half-life of Sugammadex is 2.3 hours.

Answer 492

Up to 80% of an administered dose of Sugammadex is eliminated in the urine within 24 hours.

Answer 493

Sugammadex does not bind to plasma proteins or erythrocytes.

Answer 494

Sugammadex should be avoided in patients with significant renal disease.

Answer 495

The dosage of Sugammadex varies from 2 to 16 mg/kg depending on the depth of blockade at the time of reversal.

Answer 496

A dose of 2 mg/kg is recommended.

Answer 497

A dose of 4 mg/kg is recommended if spontaneous recovery of the twitch response has reached 1 to 2 PTC.

Answer 498

A dose of 16 mg/kg is recommended if there is a clinical need to reverse NMB soon after administration of a single dose of 1.2 mg/kg of rocuronium.

Answer 499

Common adverse effects include nausea, vomiting, allergy, hypertension, and headache.

Answer 500

Anaphylaxis has been reported, which initially delayed FDA approval.

Answer 501

Hypersensitivity to Sugammadex appears to be relatively low, with only 15 cases reported in a recent review.

Answer 502

Most anaphylactic reactions were evident within the first 4 minutes after administration.

Answer 503

Cardiovascular collapse was treated successfully with fluid resuscitation and epinephrine therapy.

Answer 504

Sugammadex binds oral contraceptives, and women of childbearing age should use alternative contraceptive methods for 1 week after exposure.