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Fall'20 Pharmacology III > Med Exam Prep from Prodigy > Flashcards

Med Exam Prep from Prodigy Flashcards

1
Q

what is the chemical composition of propofol?

A

Propofol is a 2,6-diisopropyl phenol prepared in an emulsion of 10% soybean oil, 2.25% glycerol, and 1.2% purified egg lecithin.

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2
Q

How does propofol affect respiratory function?

A

Dose-dependent respiratory depression occurs, with decreases in tidal volume more prominent than decreases in the respiratory rate. Apnea often occurs following initial induction doses.

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3
Q

What accounts for the rapid reawakening of patients following sedative and anesthetic doses of propofol?

A

Rapid redistribution from the central compartment to the peripheral compartment

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4
Q

When should an open vial or prepared syringe of propofol be discarded? Why?

A

Opened vials and syringes should be thrown away if they are not used within 12 hours or within 6 hours if the drug was transferred from the original vial. The chemical composition of propofol makes it favorable to bacterial contamination.

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5
Q

Describe how propofol affects CMRO2, ICP, cerebral blood flow, and CPP.

A

CMRO2, ICP, cerebral blood flow, and CPP are all decreased following administration of propofol.

This is a result of a decrease in MAP and cerebral vasoconstriction.

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6
Q

Describe how the pain on injection of propofol can be attenuated.

A

Concominant mixture or pretreatment with lidocaine or pretreatment with an opioid is useful in minimizing the pain on injection seen with propofol.

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7
Q

Does age affect propofol’s kinetics?

A

Yes. Elderly patients require less of the drug, while children require higher doses due to their increased volume of distribution.

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8
Q

How does total body clearance of propofol exceed hepatic blood flow?

A

Extrahepatic mechanisms exist in addition to metabolism by the liver.

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9
Q

Describe the cardiovascular effects of propofol.

A

Direct myocardial depression occurs, hypotension, decreased CO and SVR, and peripheral vasodilation. Peripheral vasodilation and direct myocardial depression are concentration and dose-dependent. There is arterial vasodilation and venodilation caused by reduction in sympathetic activiity and by a direct effect on vascular smooth muscle.

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10
Q

What is the maintenance infusion dose for propofol?

A

100-200 mcg/kg/min (or more like 300mcg/kg/min??)

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11
Q

What is the standard induction dose of propofol in a healthy adult?

A

1 to 2.5 mg/kg

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12
Q

Does propofol trigger malignant hyperthermia?

A

No. Propofol is safe to use on patients susceptible to MH

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13
Q

In what patients would there be an exaggerated cardiac depressive response to propofol?

A

Standard induction doses of propofol are associated with significant cardiac depression, however patients greater than 50, ASA 3-4, MAP <70, and concomitant administration of large doses of fentanyl will see an increased myocardial depression greater than normal.

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14
Q

On what receptors does propofol exert its effects?

A

GABA is the primary inhibitory neurotransmitter of the CNS. Although propofol has been linked to other receptors such as alpha and NMDA receptors, it primarily functions by enhancing GABA inhibitory pathways.

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15
Q

Pretreatment with what drug is recommended in use with ketamine to reduce adverse effects?

A

Benzodiazepines such as midazolam and diazepam reduce the incidence of sensory and perceptual illusions, nightmares, and postoperative disorientation associated with the use of ketamine. Midazolam appears to be more effective than diazepam in this respect.

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16
Q

Ketamine causes what type of state upon its administration? What are its effects?

A

A dissociative state. Patient’s feel separated from the environment, catatonic, have amnesia, analgesia, with or without a loss of consciousness.

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17
Q

How does ketamine affect BP, CO, HR, and CVP?

A

They are all increased. Ketamine is the only IV induction agent that is a circulatory stimulant. This is caused by stimulation to the central sympathetic nervous system, and by the inhibition of the reuptake of norepinephrine at sympathetic nerve terminals.

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18
Q

What is the primary route of metabolism for ketamine?

A

Ketamine is metabolized by microsomal cytochrome P450 enzmes

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19
Q

Does ketamine cross the placental border?

A

Yes. Ketamine is very lipid soluble and quickly crosses from the placenta to the fetus. Induction doses of 0.5-1 mg/kg, however, does not compromise neonatal status at delivery. Uterine blood flow is maintained as well as uterine tone. Induction doses of 2-2.5 mg/kg result in a depressed neonate upon delivery.

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20
Q

Describe the CNS effects of ketamine.

A

The patient is in a dissociated state, is cataleptic, often with the eyes being open. Horizontal nystagmus is present. The pupils are reactive to light. There is an increase in salivary gland secretions, lacrimation and eye blinking remain, there is an increase in skeletal muscle tone, and airway reflexes are intact. This cataleptic state is the result of electrophysiologic inhibition of thalamocortical pathways and by the stimulation of the limbic system.

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21
Q

Following a single induction dose of ketamine, what is the duration of anesthesia?

A

Ketamine-induced anesthesia lasts about 15 minutes.

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22
Q

On what receptor does ketamine exert its effects?

A

The NMDA receptor.

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23
Q

How does ketamine affect CBF, CMRO2, and ICP.

A

They are all increased.

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24
Q

How does ketamine affect myocardial oxygen consumption and cardiac work?

A

They are both increased. Since there is an increase in cardiac work and myocardial oxygen consumption, there is a negative balance between myocardial oxygen supply and demand. Due to this, ketamine should be avoided in patients with severe coronary artery disease

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25
Q

Should ketamine be used in adult patients with poor right ventricular reserve?

A

No. Ketamine is contraindicated in patients with poor right ventricular reserve due to the increase in pulmonary artery pressure. This increase is not as prominent in the pediatric patient.

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26
Q

Why would ketamine be the IV induction agent of choice in the patient with active bronchospasm?

A

Ketamine decreases pulmonary resistance and increases pulmonary compliance.

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27
Q

Are airway reflexes intact following ketamine administration?

A

Yes. Protective airway reflexes are preserved. Muscle tone of the jaw and tongue are maintained as well. Swallowing, gagging, and coughing occur in response to stimulation of the airway.

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28
Q

How does ketamine affect salivary gland, bronchial, and tracheal secretions?

A

They are all increased. Treatment with an antisialagogue is used to attenuate these effects.

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29
Q

Does ketamine cause respiratory depression?

A

Yes. This respiratory depression is minimal, however in clinically relevant doses. The decrease in tidal volume is more significant over the decrease in the respiratory rate.

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30
Q

Describe the ocular effects of ketamine.

A

Ketamine causes increased muscle tone, nystagmus, muscle spasms, and increased IOP.

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31
Q

Ketamine administration should be used cautiously in what patients?

A

Ketamine should be used cautiously in patients with increased ICP, angina, CHF, high blood pressure, increased IOP, and pyschiatric disease.

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32
Q

What is the induction dose of ketamine?

A

1-2 (hammon)

2-4 mg/kg

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33
Q

Ketamine is chemically related to what drug?

A

Phencyclidine (PCP)

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34
Q

What is the IM induction dose for ketamine

A

4-6 mg/kg

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35
Q

What is the recommended dose of ketamine used for preemptive analgesia?

A

10-20 mg IV

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36
Q

What are the side effects of etomidate?

A

Adrenocortical suppression, myoclonia, pain on injection, thrombophlebitis, and postoperative nausea and vomiting,

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37
Q

In what patient populations would induction with etomidate be advantageous?

A

Etomidate causes minimal cardiovascular depression, therefore, making it useful in patients with limited cardiovascular reserve.

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38
Q

Does etomidate possess any analgesic properties?

A

No. Etomidate does not have any intrinsic analgesic properties.

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39
Q

Describe the cardiovascular effects of etomidate.

A

Etomidate administration causes minimal changes in hemodynamic status. It is considered the induction drug of choice in patients with cardiovascular disease, as well as any other patients in whom maintenance of a normal BP is imperative. Slight decreases in BP following administration of etomidate are due to a minor decrease in SVR.

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40
Q

How does etomidate affect cerebral blood flow, CMRO2, and ICP?

A

They are all decreased. Adequate CPP is maintained due to etomidate’s hemodynamic stability.

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41
Q

What is the standard induction dose for etomidate?

A

0.2-0.4 mg/kg

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42
Q

What are the respiratory effects of etomidate?

A

Respiratory rate increases but minute volume decreases in a dose-dependent fashion. Brief periods of apnea may be seen followed by hyperventilation, and the ventilatory response to CO2 is decreased.

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43
Q

What accounts for the myoclonic movements often seen with induction doses of etomidate?

A

Subcortical disinhibition that is unrelated to cortical seizure activity. Single muscles or many muscle groups can be affected. Propofol and etomidate can actually both produce myoclonic-like activity . This differs from what is seen with methohexital administration, which is true epileptogenic activity.

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44
Q

How is etomidate metabolized?

A

Etomidate is metabolized in the liver via hepatic microsomal enzymes and plasma esterases. The primary mode of metabolism in the plasma and liver is ester hydrolysis.

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45
Q

Which IV sedative-hypnotic agent has the highest degree of protein binding?

A

From greatest to least, the degree of protein-binding is as follows:

Propofol > Midazolam > Etomidate > Ketamine

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46
Q

Which intravenous anesthetic has the fastest elimination half-life?

A

Propofol has the fastest elimination half-life of the common agents at 1-5 hours.

Etomidate and midazolam are about the same duration of 2-4 hours.

The elimination half-life of ketamine is about 2-3 hours.

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47
Q

Will propofol terminate a seizure?

A

Yes, propofol has been used successfully in the treatment of status epilepticus.

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48
Q

When administered as a premedication, the sympatholytic properties of dexmedetomidine may increase the incidence of _________.

A

When given as a premedication, the sympatholytic properties of dexmedetomidine may increase the incidence of intraoperative bradycardia and hypotension.

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49
Q

What are the treatment options for an inadvertent intra-arterial injection of thiobarbiturates?

A

Inadvertent intra-arterial injections of thiobarbiturates should be treated immediately with intra-arterial papaverine. Heparinization as well as a sympathectomy induced by a regional anesthetic block should also be employed.

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50
Q

What is the intravenous anesthetic of choice for ECT?

A

Methohexital is the IV anesthetic of choice for ECT because is causes less depression of EEG activity when compared to propofol and thiopental.

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51
Q

What intravenous anesthetic has the chemical name 2,6-disopropylphenol and is insoluble in aqueous solution?

A

Propofol (2,6-disopropylphenol) is an alkylphenol compound and is insoluble in aqueous solution.

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52
Q

How is etomidate structurally similar to midazolam?

A

Midazolam and etomidate are both imidazole ring derivatives.

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53
Q

Which intravenous anesthetic produces minimal effects on cardiac parameters?

A

Etomidate produces little if any effect on mean arterial pressure, pulmonary artery pressures, CVP, stroke volume, SVR, or PVR.

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54
Q

During the initial recovery period, which intravenous anesthetic has been associated with a high incidence of altered short-term memory and cognition, hallucinations, and nightmares?

A

During the initial recovery period, ketamine has been associated with a high incidence of psychomimetic reactions. These include altered short-term memory and cognition, hallucinations, and nightmares.

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55
Q

NMDA receptors conduct which three ions?

A

NMDA receptors are glutamate-activated ion channels that conduct sodium, potassium, and calcium.

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56
Q

Besides ketamine, what other anesthetic agents have been shown to have an effect on the NMDA receptor?

A

Nitrous oxide and xenon have been shown to be potent inhibitors of NMDA-activated currents. Studies also have shown that halothan and enflurane reduced calcium movement by NMDA channels by as much as 50%.

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57
Q

How does ketamine affect BIS levels?

A

When used alone, ketamine does not decrease BIS levels. When added to a propofol, fentanyl, or sevoflurane anesthetic, ketamine can actually increase BIS levels.

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58
Q

Between midazolam, diazepam, and lorazepam, which agent would be least affected by hepatic disease?

A

Because lorazepam is less reliant on hepatic cytochrome enzymes for metabolism (it primarily undergoes phase 2 conjugation), it is less affected by liver disease.

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59
Q

From what cells does morphine stimulate histamine release? What other opioids stimulate histamine release?

A

Morphine stimulates the release of histamine from tissue mast cells. At high doses, codeine and meperidine also release histamine.

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60
Q

How does morphine-6-glucuronide reach the CNS?

A

M6G is not lipid soluble. Despite its CNS potency, only small amounts cross the blood-brain barrier. After chronic administration, however, it can accumulate and begin to cross the blood-brain barrier by mass action.

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61
Q

How do the potency of the metabolites of morphine compare to that of the parent drug?

A

Morphine-6-glucuronide appears to exert a CNS effect that is more potent than morphine. Morphine-3-glucuronide is inactive.

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62
Q

Why does morphine often cause prolonged sedation in patients with renal impairment?

A

Morphine’s metabolite, morphine-6-glucuronide is a powerful CNS depressant. It is eliminated by the kidneys and will accumulate in high enough levels in patients with kidney disease that it begins to cross the blood-brain barrier despite its low lipid solubility.

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63
Q

What non-opioid drug is meperidine structurally most similar to? What similar actions does meperidine exhibit that are similar to this drug?

A

Like its structurally similar counterpart, atropine, meperidine can produce dry mouth and blurred vision.

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64
Q

What is the active metabolite of meperidine and what are its effects?

A

Normeperidine is the active metabolite of meperidine. It has an elimination half-life that is much longer than that of meperidine and most significantly, reduces the seizure threshold. As normeperidine accumulates, it can cause symptoms of CNS excitation such as tremors, muscle twitching, and seizures.

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65
Q

Is meperidine’s ability to reduce shivering mediated by mu receptors?

A

No. It is thought to be mediated by kappa receptors.

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66
Q

What are the onset and peak effect times for intravenous fentanyl? What is the significance of this relationship?

A

The onset of fentanyl is typically listed at about two minutes, but laboratory studies have demonstrated onset times as short as ten seconds. The peak effect occurs at about 20 minutes. The significance is that without closely monitoring the time between doses, the desire to relieve an awake patient’s pain rapidly can result in overadministration of fentanyl with resultant respiratory depression.

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67
Q

What is the duration of action of fentanyl?

A

Between 20 and 40 minutes.

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68
Q

What is the primary determinant of the clearance of fentanyl?

A

hepatic blood flow

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69
Q

Does fentanyl have active metabolites?

A

No, fentanyl is dealkylated and hydroxylated to inactive metabolites. These metabolites are excreted in the urine and bile.

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70
Q

Why is the oral route of administration for fentanyl not as effective as other routes?

A

Fentanyl undergoes extensive first-pass metabolism, so the oral route is typically insufficient for administration.

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71
Q

How does fentanyl affect MAC? Specifically, what dose of fentanyl affects MAC by what amount?

A

Fentanyl decreases MAC in a dose-dependent fashion. Studies demonstrate that 3 mcg/kg of intravenous fentanyl decrease the MAC of isoflurane and desflurane by 50%.

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72
Q

How much drug do fentanyl patches deliver?

A

Fentanyl patches typically deliver 75-100 mcg/hour.

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73
Q

How long after placement of a fentanyl patch does the drug’s peak effect occur?

A

A fentanyl patch won’t produce a peak effect until 18 hours after placement of the patch. A consistent dose of fentanyl won’t be delivered to the bloodstream until the subcutaneous tissue is saturated with the drug.

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74
Q

How does the potency of sufentanil compare to that of fentanyl?

A

Sufentanil has a potency about 5-10 times that of fentanyl.

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75
Q

What is the context sensitive half-life of remifentanil?

A

Remifentanil has a context-sensitive half-life of 2 minutes. Its plasma concentration can decrease by nearly half in as little as 40 seconds.

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76
Q

How is remifentanil metabolized?

A

Remifentanil contains a methyl ester side chain and is rapidly metabolized by blood and tissue esterases.

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77
Q

Does remifentanil exhibit the potential for prolonged effects due to the accumulation of the drug?

A

No, it is metabolized so rapidly by esterases that it doesn’t accumulate and exhibits little potential for exaggerated effects due to repeat dosing or infusion.

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78
Q

Is the metabolism of remifentanil affected by succinylcholine administration?

A

No, remifentanil is hydrolyzed by nonspecific esterases, not plasma cholinesterases like succinylcholine.

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79
Q

Why is remifentanil not recommended for use in monitored anesthesia care or the postoperative setting?

A

It has a high potential for respiratory depression and muscle rigidity that makes it unsuitable for use in these settings.

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80
Q

How does the onset, duration, and lipid solubility of alfentanil compare to fentanyl?

A

Despite the fact that alfentanil has a lower lipid solubility than fentanyl, its onset is faster and its duration is shorter.

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81
Q

What antibiotic prolongs the metabolism of alfentanil?

A

Erythromycin prolongs the metabolism of alfentanil and results in prolonged respiratory depression and sedation.

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82
Q

Which opioid is currently recommended only for shivering?

A

Because of the risk of seizures from the metabolite normeperidine, meperidine is now only recommended for the treatment of shivering.

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83
Q

Which organs are primarily responsible for excreting opioids and their metabolites?

A

Opioids and their metabolites are primarily excreted by the kidneys.

84
Q

The major metabolite of fentanyl is

A

The major metabolite of fentanyl is the inactive compound norfentanyl.

85
Q

How does the potency of fentanyl compare to that of morphine?

A

Fentanyl is approximately 100 times more potent that morphine. It has a highly lipophilic structure which allows it to quickly cross the blood-brain barrier.

86
Q

What is the duration of action of naloxone?

A

The duration is dose-dependent, but 0.2 mg intravenously last about 30 minutes.

87
Q

What opioid receptor(s) is responsible for producing miosis?

A

Mu and kappa

88
Q

What is the suggested dose of naloxone for ventilatory depression.

A

In the face of postoperative ventilatory depression or apnea, naloxone should be administered in a dose of 1-4 mcg/kg.

89
Q

What is the usual dose for a naloxone infusion?

A

Respiratory depression can be prevented by administering an initial loading dose of naloxone followed by an infusion of 5 mcg/kg/hour.

90
Q

When would a naloxone infusion be appropriate?

A

Because naloxone is short-acting, it is possible that the antagonist effects of the naloxone could wear off before the effects of the opioid administered did. As the naloxone’s action terminated, the patient could become sedated again and ventilatory depression could ensue once more. An initial loading dose of naloxone followed by an infusion can prevent this from occurring.

91
Q

What are the potential hazardous effects of naloxone administration?

A

The sudden reversal of opioid analgesic effects can produce severe pain that can result in tachycardia, hypertension, ventricular arrhythmias, and severe and possibly fatal pulmonary edema.

92
Q

List the most frequent uses of sodium nitroprusside.

A

Hypertensive emergencies, acute cardiac disorders, and controlled hypotension to decrease surgical blood loss.

93
Q

What is the advantage of using nitroprusside for the rapid control of blood pressure?

A

It has a rapid onset and a short duration of action.

94
Q

How does nitroprusside affect arterioles, veins, and cardiac filling pressures?

A

Nitroprusside causes dilation in both veins and arteries. The result is a reduction of both preload and afterload which causes a reduction of cardiac filling pressures.

95
Q

How does nitroprusside affect systemic vascular resistance (SVR)?

A

It causes a significant decrease in SVR

96
Q

What are the pulmonary effects of nitroprusside?

A

There is dilation of the pulmonary vasculature and a reduction of pulmonary vascular resistance (PVR).

Nitroprusside causes direct inhibition of hypoxic pulmonary vasoconstriction (HPV).

97
Q

Can nitroprusside produce coronary steal?

A

Yes. Nitroprusside can cause blood to be shunted away from areas of myocardial ischemia.

98
Q

List perioperative uses of IV nitroglycerin.

A

Nitroglyercerin can be used perioperatively in the treatment of CHF, myocardial ischemia, systemic and pulmonary hypertension, acute volume overload, coronary artery spasm, and controlled hypotension.

99
Q

How does nitroglycerin affect the coronary arteries?

A

It is a direct dilator of the coronary arteries. Because of this property, nitroglycerin is extremely useful in the treatment of angina due to coronary vasospasm.

100
Q

By what routes may nitroglycerin be administered clinically?

A

IV, transdermal, oral, and sublingual.

101
Q

Can patients develop a tolerance to nitroglycerin?

A

Yes, it is both dose and duration-dependent and usually occurs within 24 hours of continuous treatment. When it occurs, a drug-free interval of 12-24 hours will help reverse the tolerance to the drug.

102
Q

Can nitroglycerin be used in the treatment of narcotic induced biliary spasm?

A

Yes. Nitroglycerin causes relaxation of biliary tract smooth muscle.

103
Q

Why is a nitroprusside infusion bottle covered in a protective wrap?

A

Nitroprusside decomposes when exposed to light.

104
Q

What are the hemodynamic effects of nitroglycerin?

A

Nitroglycerin produces venodilation and an increase in venous capacitance. The result is:

  • a reduction in preload.
  • There are decreases in left ventricular end-diastolic volume, pulmonary vascular resistance, pulmonary artery pressure, and right ventricular end-diastolic pressure.
  • Myocardial wall tension is decreased which results ultimately in a reduction in myocardial oxygen requirements.
105
Q

What are the presenting signs of cyanide toxicity associated with sodium nitroprusside?

A

Signs of cyanide toxicity include: increased mixed venous 02, increased nitroprusside dosage requirements (tachyphylaxis), and metabolic acidosis.

106
Q

What are the treatments for cyanide toxicity?

A

Treatment of cyanide toxicity should consist of:

  • discontinuing the nitroprusside infusion,
  • administering 100 percent oxygen, and
  • administration of amyl nitrate, IV sodium nitrite or IV thiosulfate.
107
Q

All of the available neuromuscular blocking agents bear a chemical resemblance to what chemical?

A

Acetylcholine. Succinylcholine is composed of two acetylcholine molecules linked by acetate methyl groups.

108
Q

Besides their chemical similarity to acetylcholine, what chemical structure is common to all neuromuscular blocking agents? What is the significance of this feature?

A

They all are quaternary ammonium compounds which makes them water-soluble and prevents their entry into the central nervous system.

109
Q

How do volatile anesthetics affect the action of neuromuscular blocking drugs?

A

Volatile anesthetics potentiate the effects of neuromuscular blocking drugs. Most studies demonstrate that desflurane, sevoflurane, and isoflurane are roughly equal in the degree to which they potentiate NDMRs. Nitrous oxide does not demonstrate a significant potentiation.

110
Q

How does hypothermia affect neuromuscular blockade?

A

Hypothermia can augment a block by decreasing metabolism or delaying excretion of the drug.

111
Q

What nondepolarizing neuromuscular agents will have a prolonged duration of action in patients with hepatic disease?

A

The steroidal derivatives, rocuronium, vecuronium, and pancuronium will be prolonged in the presence of hepatic disease.

112
Q

Which of the steroidal muscle relaxants is most affected by renal disease?

A

Pancuronium is about 85% dependent upon renal elimination and is the most affected.

All three steroidal relaxants (rocuronium, vecuronium, and pancuronium) are affected by renal disease.

113
Q

What are the two major classifications of nondepolarizing neuromuscular blockers? What commonly used agents fall into each class?

A
  1. Benzylisoquinoliniums, which includes atracurium and cisatracurium and
  2. steroid derivatives which includes pancuronium, rocuronium, and vecuronium.
114
Q

What is the intubating dose of rocuronium?

A

0.6-1.2 mg/kg

115
Q

What method is used clinically to speed the onset of rocuronium?

A

Priming, which is the administration of 10% of the intubating dose about 1-3 minutes prior to anesthetizing the patient and administering the remaining dose.

116
Q

How is rocuronium eliminated?

A

Rocuronium is primarily eliminated in unchanged form via biliary excretion.

117
Q

What is the duration of action of rocuronium?

A

Rocuronium is an intermediate-acting muscle relaxant. The duration of action is dose-dependent. An intubating dose of 0.6 mg/kg to 1.2 mg/kg usually provides a duration of action between 30 and 90 minutes.

118
Q

How does the elimination half-life of rocuronium differ between pediatric patients, adults, and the elderly?

A

The elimination half-life of rocuronium in children is about 38 minutes, in adults it is 56 minutes, and in the elderly it is 137 minutes.

119
Q

What cardiovascular changes may be seen with the administration of rocuronium or vecuronium?

A

No cardiovascular changes are seen with the administration of rocuronium or vecuronium, and no increases in histamine levels are seen with doses up to 1.2 mg/kg of rocuronium.

120
Q

About what should you be cautious when using vecuronium in conjunction with thiopental?

A

If administered shortly after thiopental, vecuronium can react with thiopental to produce barbituric acid, a precipitate that can obstruct the IV.

121
Q

What is the intubating dose of vecuronium?

A

0.1 mg/kg

122
Q

How is vecuronium eliminated?

A

Vecuronium undergoes hepatic and renal elimination. The majority of is eliminated in the bile.

123
Q

What may be responsible for the prolonged duration of action of vecuronium when used in intensive care unit patients?

A

One of vecuronium’s metabolites, 3-OH vecuronium, accounts for about 60% of the activity of vecuronium and is excreted by the kidneys. The reduced clearance of this metabolite in the presence of altered renal status can result in a prolongation in the action of vecuronium.

124
Q

What is the intubating dose of pancuronium?

A

0.06mg/kg

125
Q

What difficulty does the use of pancuronium present in noncardiac surgery?

A

It is associated with a higher incidence of postoperative muscle weakness and is more difficult to reverse than intermediate-acting agents. A mild pancuronium block can be reversed with sugammadex, however.

126
Q

What cardiac effect of pancuronium has increased its usefulness in the cardiac surgery setting?

A

Pancuronium can cause an increase in heart rate, blood pressure, and cardiac output via a vagolytic effect at the postganglionic nerve terminal, an increase in catecholamine release, and an antimuscarinic effect. This offsets the bradycardia associated with large doses of fentanyl used in cardiac surgery.

127
Q

What is the intubating dose of atracurium?

A

0.5 mg/kg

128
Q

What are the most common side effects of atracurium administration?

A

Atracurium can cause significant histamine release which can result in hypotension, tachycardia, flushing, and bronchospasm.

129
Q

What are the metabolic byproducts of the metabolism of atracurium and what side effects can result from them?

A

Laudanosine and acrylate are metabolic byproducts of the degradation of atracurium. They can produce CNS excitement and even seizures if they accumulate in enough quantity.

130
Q

What is the structural difference between atracurium and cisatracurium? What are the clinical effects of this difference?

A

Cisatracurium is a potent isomer of atracurium that, unlike atracurium, is devoid of any histamine release. Cisatracurium has a higher potency and requires less of the drug to be administered to reach the same clinical endpoint. As a result, less laudanosine and acrylate byproducts are produced and the toxic effects of these agents is essentially nonexistent.

131
Q

What are the two metabolic pathways for atracurium and cisatracurium?

A

The first means of metabolism of atracurium and cisatracurium is via Hofmann elimination, which is a nonenzymatic degradation of the drug.

The second is via degradation by the same tissue esterases that degrade remifentanil and esmolol. About 1/3 of atracurium undergoes Hofmann elimination and the remainder undergoes degradation by tissues esterases.

132
Q

What is the intubating dose of cisatracurium?

A

0.1mg/kg

133
Q

What are the muscle relaxants of choice for the patient with renal disease?

A

Atracurium and cisatracurium are the preferred muscle relaxants in patients with renal disease. The onset and duration are not affected by renal impairment.

134
Q

How does succinylcholine affect serum potassium levels?

A

Succinylcholine increases the serum potassium level by about 0.5 mEq/L in most patients.

A defasciculating dose of a nondepolarizing muscle relaxant does not have any effect on the increase in potassium, but large doses of nondepolarizing muscle relaxants will abolish it. The increase in potassium is much more dramatic and can be life-threatening in patients with denervation injuries in which there is an upregulation in extrajunctional receptors. This includes patients with spinal cord transection, stroke, extensive burns, trauma, muscular dystrophies, and prolonged immobility due to disease.

135
Q

What is fasciculation and with what drug does it occur?

A

Fasciculation is disorganized muscle activity that occurs after the administration of succinylcholine but before muscle paralysis occurs.

136
Q

What are the contraindications to the use of succinylcholine?

A

Hyperkalemia, severe muscle trauma, severe burns, denervation injuries, renal failure with hyperkalemia, malignant hyperthermia, Duchenne muscular dystrophy, rhabdomyolysis, Guillain-Barre syndrome, and severe sepsis. It is recommended for use in children under the age of 8 only in emergency situations.

137
Q

What is a sigificant side effect of succinylcholine re-administration, particular in children?

A

Bradycardia and potentially asystole.

138
Q

Why does succinylcholine have such a short duration of action compared to the nondepolarizing agents?

A

Succinylcholine is rapidly hydrolyzed by plasma cholinesterase (butyrylcholinesterase) and to a lesser extent, butyrylcholinesterase in the liver.

139
Q

What is the intubating dose of succinylcholine and how long does it typically last until full neuromuscular recovery?

A

The intubating dose is 1-1.5 mg/kg. It takes 12-15 minutes on average before full neuromuscular recovery occurs.

In emergency situations where no intravenous access is present, the intramuscular dose of succinylcholine is 4 mg/kg.

140
Q

How does the intubating dose of succinylcholine in children compare with that of adults?

A

Children require a higher dose of succinylcholine than adults, typically requiring 1.5-2 mg/kg. Infants require an even higher dose of 2-3 mg/kg to facilitate intubation. Defasciculating doses of nondepolarizing neuromuscular blockers are rarely given because fasciculations are uncommon in children.

141
Q

How does succinylcholine affect intracranial pressure?

A

Succinylcholine may increase intracranial pressure, but this effect is blocked by the administration of a defasciculating dose of a nondepolarizing muscle relaxant.

142
Q

How does succinylcholine affect intragastric pressure?

A

Succinylcholine increases intragastric pressure, but it also increases the lower esophageal sphincter (LES) tone.

This results in no net change in the pressure gradient between the stomach and esophagus and no increased risk of aspiration.

143
Q

How does succinylcholine affect intraocular pressure?

A

The administration of succinylcholine can raise intraocular pressure up to 15 mmHg.

The administration of a defasciculant has little to no affect on this increase. Although there is no documented cases where the administration of succinylcholine has led to blindness or the extrusion of ocular contents, the use of succinylcholine in open-eye injuries is widely avoided.

144
Q

What is succinylcholine-induced myalgia, and how can it be prevented?

A

Myalgia can occur 24-48 hours after the administration of succinylcholine in a large percentage of patients. It primarily affects young, ambulatory patients (particularly females). Although the degree of fasciculations seen do not have a correlation with the degree of myalgia, administering a defasciculating dose of a nondepolarizing muscle relaxant prior to the succinylcholine has been shown to prevent myalgia.

145
Q

What is the difference between a phase I block and a phase II block with succinylcholine?

A

A phase I block is a depolarizing block that is antagonized, not reversed by cholinesterase inhibitors. Succinylcholine is the only drug available in the US that can produce a phase I block.

A phase II block is also known as a desensitizing block. This can occur with prolonged exposure to succinylcholine (from large or repeated doses) in which the initial end plate depolarization decreases and the membrane repolarizes again. A phase II block becomes clinically indistinguishable from the block produced by nondepolarizing muscle relaxants and can, in some cases, be reversed by cholinesterase inhibitors. It rarely occurs now because the large doses required are rarely given

146
Q

What is the significance of a dibucaine number?

A

Dibucaine is used to diagnose the different genetic forms of plasma cholinesterase deficiency. A patient with a dibucaine number of 70-80 is normal and the duration of action of succinylcholine will be normal.

A patient with a dibucaine number of 50-60 is considered to have heterozygous atypical plasma cholinesterase and the duration of action of succinylcholine will be prolonged by 8-20 minutes.

A patient with a dibucaine number of 20-30 is considered to have homozygous atypical plasma cholinesterase and the duration of succinylcholine will be markedly prolonged.

147
Q

What are some non-genetic causes of a decrease in plasma cholinesterase activity?

A 
pregnancy
newborns
pts with acute infections
muscular dystropy
myocardial infarction
148
Q

Are the cholinesterase inhibitors edrophonium, neostigmine, and pyridostigmine lipid-soluble? Why or why not?

A

quaternary ammoniums that are not lipid-soluble

149
Q

What anticholinesterase drug is able to cross the blood-brain barrier?

A

Physostigmine crosses the blood-brain barrier and, for this reason, is not used as a reversal agent for neuromuscular blockade.

150
Q

What is the maximum recommended dose of neostigmine?

A

The maximum dose is 0.07 mg/kg in adults.

5mg

151
Q

What symptoms can cholinesterase inhibitors produce?

A

Cholinesterase inhibitors produce increased salivary secretion, bronchoconstriction, and increased intestinal motility.

152
Q

What dose of glycopyrrolate is typically administered to counteract the muscarinic side effects of neostigmine? What are the advantages of glycopyrrolate over atropine for this purpose?

A

Glycopyrrolate 0.2 mg per 1 mg of neostigmine is administered to counteract the muscarinic effects of neostigmine. Glycopyrrolate has an onset of action that closely matches neostigmine and results in less tachycardia than atropine.

153
Q

Besides using a defasculating dose of a non-depolarizing neuromuscular blocking agent, what is the most effective way to prevent myalgias from succinylcholine administration?

A

Besides using a defasculating dose of a non-depolarizing neuromuscular blocking agent, pretreatment with a nonsteroidal anti-inflammatory agent is the most effective way to prevent myalgias from succinylcholine administration.

154
Q

Name two anticonvulsants that may shorten neuromuscular blockade in patients using them to treat seizures.

A

Duration of rocuronium blockade is significantly shorter in patients receiving chronic therapy of anticonvulsants including

*phenytoin and carbamazepine.

155
Q

What are the ED95 values for rocuronium, vecuronium, atracurium, cisatracurium, and pancuronium?

A

Rocuronium = 0.3 mg/kg.
vecuronium is 0.05 mg/kg.
pancuronium is 0.07 mg/kg.

atracurium is 0.25 mg/kg.
cisatracurium is 0.05 mg/kg.

156
Q

What is the half-life of rocuronium? Vecuronium? Pancuronium?

A

Rocuronium is 0.7 hours.
Vecuronium is 0.9 hours.
Pancuronium is 1.7 hours.

157
Q

The nondepolarizing neuromuscular blocker competes with acetylcholine receptor for the active binding sites that are post synaptic. This type of competitive interaction at the nicotinic receptor is called ______.

A

Competitive antagonism. there is a competition at the receptor binding site. An antagonist sits at the receptor and does NOT activate the receptor.

158
Q

The depolarizing agent succinylcholine activates the ion channel by donating two acetylcholine molecule to cause an agonist action at the receptor. The type of activation causes what type of change to the receptor? Does this activate or deactivate the receptor?

A

It produces a conformation change in the channel and it activates or opens the channel.

159
Q

Depolarizing agents work at the end plate and desensitize the channel to which they bind. At what type of receptor does this occur? On what type of voltage-gated channel does this take place?

A

The correct response is nicotinic, voltage-gated SODIUM channel. The key in this question is knowing that neuromuscular drugs work at the nicotinic receptor. The activation of the sodium channel allows potassium to permeate the surrounding membrane.

160
Q

The two enzymes that are vital to hydrolyze choline are _______ and _________.

A

Acetylcholinesterase and butyrylcholinesterase are the two enzymes are vital and work at the neuromuscular junction and work by causing rapid hydrolyze action of choline.

This rapid breakdown takes acetylcholine and reduces it to acetic acid and choline.

161
Q

A patient presents with elevated liver enzymes, yellow eyes, and diagnosed liver failure. He is scheduled for an ERCP procedure that requires general anesthesia. The liver is critical in creating what enzyme that could be low in this patient? Which paralytic has a relative contraindication as a result of this deficiency?

A

The correct response is butyrylcholinesterase and succinylcholine. Butyrylcholinesterase is created in the liver. This patient has liver failure and will have a low level of the important enzyme that is required to break down succinylcholine. If the patient lacks this enzyme or is on another drug that inhibits this enzyme there is a relative contraindication in using succinylcholine. Be aware it is a relative contraindication, if you choose to use the succinylcholine know there will be a prolonged action of the effects of using the agent.

162
Q

What is the elimination half-life of succinylcholine?

A

Succinylcholine has a very short half-life (47 seconds).

163
Q

The elimination of succinylcholine follows what type elimination kinetics?

A

The metabolism of succinylcholine follows first order kinetics.

164
Q

What is the typical intubating dose of succinylcholine and how long before there is complete suppression of response of the neuromuscular response?

A

1mg/kg is the typical intubating dose. Complete suppression of the neuromuscular response typically occurs in 60 seconds.

165
Q

You see a patient in the anesthesia preop clinic and they tell you that they were slow to wake up last time and needed a breathing tube for a period of time after surgery. They cannot provide any additional information. You suspect an of pseudocholinesterase deficiency. Your hospital does not have the ability to test for a dibucaine number. What test could you order?

A

The correct response is fluoride-resistant test. If the patient has pseudocholinesterase deficiency the fluoride number of 60 indicates normal function, 36 indicates homozygous atypical genotype.

166
Q

What are the metabolites of succinylcholine?

A

Succinylcholine is rapidly degraded into succinylmonocholine which is then degraded into choline and succinic acid.

167
Q

What medications or electrolyte abnormalities are known to potentiate muscle relaxants?

A

Many antibiotics, furosemide, phenytoin, propranolol, hypocalcemia, and hypermagnesemia are all known to potentiate muscle relaxants.

168
Q

Plain 2% lidocaine has a specific gravity between 1.0004 and 1.0066. In relation to cerebrospinal fluid, would this solution be hypobaric, isobaric, or hyperbaric?

A

CSF has a specific gravity of 1.004 to 1.009.

2% plain lidocaine is hypobaric in relation to CSF.

169
Q

What is the usual concentration of epinephrine added to local anesthetics to prolong epidural blockade?

A

The usual concentration is 1:200,000 or 5 mcg/mL. Neosynephrine may also be added to a local anesthetic to prolong the duration of action.

170
Q

All local anesthetics cause relaxation of vascular smooth muscle except for three. Name them.

A

all LAs cause venodilation except:
cocaine
lidocaine
ropivacaine

171
Q

What local anesthetic preparation has been implicated in the development of cauda equina syndrome when used as part of a continuous spinal catheter infusion?

A

The use of 5% lidocaine via infusion through small-bore continuous spinal catheters has been implicated in the development of a type of neurotoxicity known as cauda equina syndrome.

172
Q

Name two local anesthetics that can result in methemoglobinemia. What is the treatment for methemoglobinemia?

A

Prilocaine and benzocaine are both capable of converting hemoglobin to methemoglobin. Methemoglobinemia is treated with 1-2 mg/kg of a 1% solution of methylene blue administered over a period of five minutes.

173
Q

To what degree is lidocaine protein-bound in the adult? How does it compare to the other amides?

A

Lidocaine is approximately 60 percent protein-bound in the adult.

Mepivacaine is about 75 percent protein-bound.

Ropivacaine, bupivacaine, and levobupivacaine are all 95 percent protein-bound.

174
Q

What are the two most common causes of local anesthetic systemic toxicity?

A

Local anesthetic systemic toxicity (LAST) is most commonly the result of the absorption of large quantities of a drug or accidental vascular injection.

175
Q

What is the initial IV bolus of a 20 percent lipid emulsion for the treatment of local anesthetic cardiovascular toxicity?

A

The initial IV bolus of 20 percent lipid emulsion is 1.5 mL/kg followed by infusion of 0.25 mL/kg/min for at least 10 minutes after cardiac stability is maintained.

176
Q

What is considered the first-line drug for peripartum hypertension?

A

Labetolol is considered the first-line drug for peripartum hypertension.

177
Q

What are methods that can be employed to reduce the exaggerated blood pressure response to laryngoscopy seen in many hypertensive patients?

A

Continuing their regularly scheduled antihypertensive medication, achieving a deeper level of anesthesia than typical for non-hypertensive patients prior to laryngoscopy, pre-treating with lidocaine or fentanyl intravenously, and reducing the duration of laryngoscopy to less than 15 seconds.

178
Q

Name three selective beta-1 adrenergic blockers.

A

Metoprolol, atenolol, and esmolol are selective beta-1 adrenergic blockers.

179
Q

Which beta-blocker is metabolized rapidly in the blood by an esterase located in the red blood cell cytoplasm?

A

Esmolol is metabolized quickly in the blood by an esterase found in the RBC cytoplasm and has a half-life of 9.5 minutes.

180
Q

How do benzodiazepines affect CMRO2 and cerebral blood flow?

A

They decrease CMRO2 and cerebral blood flow

181
Q

Where in the brain do benzodiazepines exert their action?

A

Benzodiazepines don’t bind to GABA-A receptors directly, but act to increase the affinity of the receptor to GABA molecules, particularly in the hippocampus and amygdala.

182
Q

How do benzodiazepines exert their action on GABA receptors?

A

Specific benzodiazepine receptor sites exist on a protein complex that contains binding sites for benzodiazepines, GABA, ethanol, barbiturates, and a chloride channel. When these receptor sites are occupied by one of the drugs listed above, the GABA receptor increases the frequency of chloride channel opening which results in hyperpolarization of the postsynaptic membrane and inhibition of neuronal transmission.

183
Q

How are benzodiazepines metabolized?

A

Benzodiazepines are metabolized via hepatic oxidation and glucuronide conjugation.

184
Q

How do diazepam, lorazepam, and midazolam compare with respect to duration of action?

A

Diazepam is long-lasting with an elimination half-life of 36-50 hours,

lorazepam is of intermediate duration with an elimination half-life of 10-22 hours, and

midazolam is short-acting with an elimination half-life of about 2 hours.

185
Q

How do the formulations of midazolam, lorazepam, and diazepam differ?

A

Lorazepam and diazepam are not water soluble. They are formulated in propylene glycol which can cause pain on injection.

186
Q

What is the typical IV or IM premedication dose of midazolam? What is the typical PO premedication dose of midazolam?

A

The dose for IV or IM midazolam is 0.02-0.04 mg/kg compared to 0.4 to 0.8 mg/kg for the PO dose.

187
Q

Can midazolam be used to prevent seizures?

A

Yes. Midazolam, lorazepam, and diazepam all increase the seizure threshold.

188
Q

What is the only benzodiazepine antagonist available in the United States?

A

Flumazenil

189
Q

How does flumazenil reverse the effects of benzodiazepines?

A

Flumazenil is inert, but is able to bind with the benzodiazepine receptor. It acts as a competitive antagonist. By doing so, it simply takes the place of benzodiazepine on the receptor.

190
Q

What is the elimination half-life of flumazenil and what is the significance of this?

A

It has a half-life of about 1 hour, so it is possible that re-sedation can occur with benzodiazepines that half a longer half-life than this.

191
Q

What are the cardiovascular effects of flumazenil?

A

Flumazenil is not associated with any significant cardiovascular changes or stress response.

192
Q

What are the dose-dependent CNS depressant effects of benzodiazepines?

A

Benzodiazepines produces sedation, amnesia, hypnosis, anxiolysis, and anticonvulsant activity in a dose-dependent fashion.

193
Q

With what receptors do anticholinergic drugs combine?

A

They combine reversibly with the muscarinic cholinergic receptors and prevent acetylcholine from binding to the receptor.

194
Q

What are the three anticholinergic drugs in current use for anesthesia?

A

Atropine, scopolamine, and glycopyrrolate

195
Q

How do inhaled anticholinergics affect airway resistance?

A

They act on muscarinic receptors in the airway to produce bronchodilation. Because of their poor absorption, systemic side effects are rare.

196
Q

Will the administration of atropine or glycopyrrolate to a parturient increase the heart rate of the fetus?

A

Although atropine can cross the placenta (glycopyrrolate cannot), there is no significant change in fetal heart rate after intravenous administration to the mother.

197
Q

Which anticholinergic is considered the safest for use in patients with glaucoma? Which is the least safe?

A

Scopolamine exhibits the greatest mydriatic effect and requires the greatest amount of caution in patients with glaucoma.
Atropine 0.4 mg to 1 mg IV is considered safe when administered with an anticholinesterase drug because little to no increase in pupil size is noted.
Glycopyrrolate has little to no mydriatic effect.

198
Q

Which of the three anticholinergics has the greatest sedative effect?

A

Scopolamine has the greatest sedative effect.
Atropine causes slight sedation and
glycopyrrolate has no sedative effect at all.

199
Q

How do the anticholinergic drugs compare with respect to their antisialagogue effect?

A

Scopolamine has the greatest antisialagogue effect, followed closely by glycopyrrolate, then atropine.

200
Q

How do the anticholinergics compare with respect to their tendency to increase heart rate?

A

Atropine causes the greatest increase in heart rate, followed by glycopyrrolate, then scopolamine.

201
Q

How do anticholinergics affect gastric function?

A

Administration of anticholinergics in general results in a decrease in gastric secretions, decreased peristalsis and intestinal motility, prolonged gastric emptying time, and reduced lower esophageal sphincter tone.

202
Q

What is the treatment for central anticholinergic syndrome?

A

The anticholinesterase physostigmine administered at a dose of 1-2 mg IV will treat the symptoms of central anticholinergic syndrome and postoperative delirium. Physostigmine is a lipid-soluble tertiary amine that is able to cross the blood-brain barrier. Edrophonium, neostigmine, and pyridostigmine are quaternary ammoniums that do not cross the blood-brain barrier easily and are not appropriate treatments for this syndrome.

203
Q

What is central anticholinergic syndrome?

A

Scopolamine and atropine both cross the blood-brain barrier and block muscarinic cholinergic receptors in the CNS, producing restlessness, hallucinations, somnolence, and potentially, unconsciousness.

204
Q

What are the two primary indications for the use of acetaminophen?

A

Analgesia and antipyrexia

205
Q

What drug is administered in the treatment of acetaminophen toxicity?

A

Acetylcysteine. It is most effective if administered within the first 8 hours of overdose.

206
Q

How effective is intravenous acetaminophen in treating postoperative pain?

A

Intravenous acetaminophen has been shown to provide approximately 4 hours of analgesia in 37 percent of patients with postoperative pain.

Fall'20 Pharmacology III (14 decks)

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