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Advanced Pharmacology 2 > Exam 2 Castillo > Flashcards

Exam 2 Castillo Flashcards

1
Q

Define Sedative

A

A drug that induces a state of calm or sleep

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2
Q

Define Hypnotic

A

A drug that induces hypnosis or sleep

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3
Q

Define Anxiolytic

A

A drug that reduces anxiety and that has sedation as a side effect

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4
Q

Define Sedative-Hypnotics

A

A drug that reversibly depresses the activity of the CNS

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5
Q

Define General Anesthesia

A

State of drug-induced unconsciousness

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6
Q

5 Components of anesthesia

A
  1. Hypnosis 2. Analgesia 3. Muscle Relaxation 4. Sympatholysis 5. Amnesia
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7
Q

Besides sedation, what useful dose dependent effect do volatile anesthetics have?

A

Dose dependent muscle relaxation

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8
Q

What are the 4 stages of General Anesthesia?

A
  1. Analgesia 2. Delirium 3. Surgical Anesthesia 4. Medullary Paralysis (Gone too far)
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9
Q

What do you see first in Medullary Paralysis, htn/tachycardia or hypotension/bradycardia?

A

Hypertension and Tachycardia

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10
Q

Describe Anesthesia Stage 1: Analgesia

A

Begins with the initiation of an anesthetic agent and ends with the loss of consciousness

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11
Q

What are the airway protective reflexes, and which are lower airway reflexes?

A
  1. Sneezing (upper airway) 2. Swallowing (lower airway) 3. Coughing (lower airway) 4. Gagging (lower airway)
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12
Q

What sensory and mental depression signs are associated with stage 1 of anesthesia?

A
  1. Able to open eyes on command 2. Breathe normally 3. Maintain protective reflexes 4. Tolerate mild stimuli
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13
Q

Describe Anesthesia Stage 2: Delirium

A

Starts with the loss of consciousness to the onset of automatic rhythmicity of vital signs

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14
Q

What has caused stage 2 of anesthesia to go more quickly?

A

Anesthetic agent becoming more rapid and the use of short acting barbituates

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15
Q

What is stage 2 of anesthesia characterized by?

A

Excitement such as undesired CV instability, dysconjugate ocular movement, laryngospasm and emesis

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16
Q

What is the response to stimuli in stage 2 of anesthesia?

A

Exaggerated and violent

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17
Q

When would you place an IV in pedi patients?

A

AFTER stage 2 of anesthesia

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18
Q

Describe Anesthesia Stage 3: Surgical Anesthesia

A

Absence of response to surgical stimulation

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19
Q

What 5 signs of nervous system depression are associated with stage 3 of anesthesia?

A
  1. Hypnosis 2. Analgesia 3. Muscle relaxation 4. Sympatholysis 5. Amnesia
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20
Q

Describe Anesthesia Stage 4: Medullary Paralysis

A

Associated with cessation of spontaneous respiration and medullary cardiac reflexes

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21
Q

What 4 characteristics are associated with stage 4 of anesthesia?

A
  1. All reflexes absent 2. Flaccid paralysis 3. Marked hypotension with weak, irregular pulse 4. May lead to death
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22
Q

When a patient is emerging from anesthesia, how do you determine what signs of distress you should be looking for as time goes by?

A

The patient will come out of anesthesia the opposite of how the went in, meaning a patient will go from stage 3 to stage 2 to stage 1 during emergence

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23
Q

What is an example of a noninvasive maneuver to treat laryngospasm?

A

continuous positive pressure ventilation

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24
Q

What was the issue with diethyl ether?

A

It was slow, unpleasant and a more dangerous tool for induction of general anesthesia

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25
Q

Why are barbiturates not used anymore?

A

Because they were part of the lethal injection cocktail for capital punishment

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26
Q

When can we use barbiturates in OB patients?

A

As a last resort if epidural is not working to ease pain

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27
Q

What is the mechanism of action of barbiturates?

A

Potentiate GABA-a channel activity (directly mimic GABA)

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28
Q

What type of receptors do barbiturates act on?

A

Glutamate, adenosine, and neuronal nicotinic acetylcholine receptors

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29
Q

What effect if any do barbiturates have on cerebral blood flow?

A

They cause cerebral vasoconstriction, causing a decrease in CBF and decrease in cerebral metabolic requirement of oxygen by 55%

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30
Q

What is the primary target of barbiturates?

A

the brain

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31
Q

Why do we see rapid awakening when using barbiturates?

A

There is a rapid uptake and distribution of the drug to other tissues

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32
Q

What is the onset time of barbiturates?

A

30 seconds

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33
Q

What is the half-time of barbiturates?

A

5 minutes

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34
Q

What is the effect of prolonged infusions of barbiturates on its pharmacokinetics?

A

Lengthy context sensitive half-time

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35
Q

Describe the 4 compartments of drug distribution

A
  1. Compartment 1 = Blood 2. Compartment 2 - Vessel rich groups such as the brain, lungs, kidneys, heart, and liver 3. Compartment 3: Vessel poor groups such as the subcutaneous fat and ligaments 4. Compartment 4: Even more vessel poor groups such as the hair, skin and nails
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36
Q

Where are barbiturates metabolized and excreted?

A

99% hepatocyctes metabolism and excreted in kidneys

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37
Q

What pharmacokinetics do we take into account when giving pediatric patients barbiturates?

A

Elimination half time is shorter (Pediatric metabolism is very high and requires higher and more frequent dosing)

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38
Q

What do barbiturates bind to in the body?

A

70-85% bound to albumin

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39
Q

What is the initial site of redistribution for barbiturates?

A

Skeletal muscles

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40
Q

How fast does barbiturate redistribution to skeletal muscle reach equilibrium with the plasma?

A

15 minutes

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41
Q

When would redistribution of barbiturates be decreased? Mass decreased?

A

Decreased: Shock Mass decreased: Elderly

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42
Q

What is dosing of barbiturates based on and why?

A

Barbiturates dosing is based on lean body weight because larges doses show cumulative effect as fat is a reservoir for the drug

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43
Q

Describe non-ionized drugs

A

More lipid soluble and favored in acidosis

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44
Q

Describe ionized drugs

A

Less lipid soluble and favored in alkalosis

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45
Q

4 Previous uses of barbiturates

A
  1. Premedication for hangovers (not anymore) 2. Grand mal seizures (benzos have replaced) 3. Rectal admin w/ uncooperative/young patients 4. Increased ICP, cerebral protection and induction
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46
Q

What are the oxybarbiturates?

A
  1. Methohexital 2. Phenobarbital 3. Pentobarbital
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47
Q

What are the thiobarbiturates?

A
  1. Thiopental 2. Thiamylal
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48
Q

Which isomer, S or R is more potent?

A

S-isomer

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49
Q

Dose of thiopental (sodium pentothal)?

A

4mg/kg IV

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50
Q

How long after administering sodium pentothal is only 10% of the drug found in the brain?

A

30 minutes (will need to re-dose)

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51
Q

What is the dose of thiopental calculated based off of?

A

ideal body weight

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52
Q

How does methohexital (brevital) compare to pentathol?

A
  1. Has a lower lipid solubility 2. At normal pH, 76% is nonionized compared to pentothals 61% 3. Faster metabolism 4. More rapid recovery (still a change of re-sedation)
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53
Q

What is administration of methohexital associated with?

A

Excitatory phenomena such as myoclonus an hiccoughs

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54
Q

IV dose of methohexital? Rectal dose?

A

IV dose: 1.5mg/kg Rectal dose: 20-30mg/kg

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55
Q

What adverse effect do we see in patients post methohexital infusion?

A

1 out of 3 patients will have seizure activity

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56
Q

What effect does methohexital have that is useful for ECT patients?

A

Duration of seizures are 35-45% less than if etomidate was used

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57
Q

What effect does methohexital have on seizure threshold?

A

lowers seizure threshold

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58
Q

Cardiovascular effects when given 5mg/kg of thiopental and normovolemia?

A
  1. Transient 10 to 20 mmHg decrease in SBP 2. Transient 15 to 20 BPM increase in heart rate
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59
Q

What does the lack of baroreceptor response when using barbiturates cause?

A

Hypovolemia, CHF, beta blockade

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60
Q

What type of allergic response is seen with a patient who has had previous exposure to thiopental is administered it again?

A

Anaphylactoid (non-IGE mediated)

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61
Q

What effect if any do barbiturates have on ventilation?

A
  1. Dose dependent depression of ventilatory centers 2. Ventilatory centers are less sensitive to CO2
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62
Q

What area do barbiturates effect that are involved in the ventilatory centers?

A
  1. Medullary and pontine
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63
Q

What effect do barbiturates have on the return to spontaneous ventilation?

A

Slow frequency and lower tidal volumes

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64
Q

What is the immediate response if barbiturates are injected intraarterially?

A

Intense vasoconstriction and excruciating pain that radiates along the distribution of the artery

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65
Q

What is the treatment if intraarterial injection of barbiturates occurs?

A
  1. Vasodilators such as lidocaine or Papaverine 2. Sustain adequate blood flow
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66
Q

What is seen with the artery and side effect of intraarterial injection of barbiturates?

A
  1. Distal arterial pulses are obscured 2. Blanching of the extremity followed cyanosis 3. Gangrene and permanent nerve damage
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67
Q

What enzyme variability must we be aware of when utilizing barbiturates?

A
  1. Enzyme induction is approximately 2 to 7 days of infusion 2. Accelerated metabolism of anticoagulants, phenytoin, TCAs, digoxin, coritocosterioids, bile salts and vitamin K 3. May persist for 30 days
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68
Q

What effect on the kidneys do we see from barbiturates?

A

Modest, transient decrease in RBF and GFR

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69
Q

What type of monitoring should we utilize when administering barbiturates?

A

SSEP (somatosensory evoke potential)

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70
Q

What is the fat/blood partition coefficient of thiopental?

A

11

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71
Q

What is propofol an agonist of?

A

Relatively selective to GABA-a receptors

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72
Q

Dose of propofol for induction, conscious sedation and maintenance?

A

Induction: 1.5-2.5mg/kg IV Conscious sedation: 25 to 100 mcg/kg/min Maintenance: 100-300 mcg/kg/min

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73
Q

How quickly does rapid injection of propofol lead to unconsciousness?

A

30 seconds

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74
Q

What can happen to the soybean oil droplets in propofol solution?

A

They can coalesce and cause pulmonary embolism

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75
Q

What part of the egg is lecithin found?

A

The yolk

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76
Q

What are 3 components found in propofol constitutions that we should be aware of?

A
  1. Soybean oil 2. Glycerol 3. Purified egg phosphatide (lecithin)
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77
Q

Disadvantages to propofol constitutions?

A
  1. Supports bacterial growth, will turn the medication from white to green after 6 hours 2. Causes increased plasma triglyceride concentrations in prolonged infusions (6-24 hours) 3. Pain on injection (do not mix with lidocaine)
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78
Q

How long after drawing up a syringe of propofol is it required of you to discard the entire syringe?

A

1 hour

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79
Q

2 key points associated with Ampofol as compared to propofol

A
  1. Low-lipid emulsion with no preservative 2. Higher incidence of pain on injection
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80
Q

3 key points associated with Aquavan as compared to propofol

A
  1. Prodrug that obviates pain on injection 2. By-product causes dysesthia 3. Slower onset, larger Vd and higher potency
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81
Q

What is a strange side effect associated with lidocaine administration?

A

metallic taste in the mouth

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82
Q

What occurs when GABA-a receptors are activated?

A

Transmembrane chloride conductance increases causing hyper polarization of the postsynaptic cell membrane and functional inhibition of the postsynaptic neuron

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83
Q

Would you contribute the immobility from propofol anesthesia to spinal cord depression?

A

No, immobility associated with propofol is not associated with skeletal muscle relaxation

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84
Q

Describe the clearance pharmacokinetics of propofol

A
  1. Plasma (lungs) > hepatic 2. Tissue uptake > CYP450
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85
Q

How is propofol metabolized and then excreted?

A

Hepatic metabolism leads to water-soluble sulfates and glucuronic acid metabolites that are excreted by the kidneys

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86
Q

What is the elimination half time and context sensitive half time of propofol?

A
  1. Elimination half-time: 0.5-1.5 hours 2. Context-sensitive half-time: 40 minutes (8 hour infusions)
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87
Q

What is the effect of propofol on systemic blood pressure and heart rate?

A

Decrease both

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88
Q

What is the effect of etomidate on systemic blood pressure and heart rate?

A

No change or decreased systemic blood pressure, but no change at all in heart rate

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89
Q

What is the effect of ketamine on systemic blood pressure and heart rate?

A

Increases both

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90
Q

What effect does cirrhosis of the liver have on propofol?

A

Similar awakening time with alcoholic and normal patients

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91
Q

What is the effect of renal dysfunction on propofol clearance?

A

Renal dysfunction has no influence on propofol clearance

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92
Q

What concerns do we have when utilizing propofol on pregnant patients?

A

Propofol crosses the placenta but is rapidly cleared in neonatal circulation, nonetheless, you will stay have some bradycardia

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93
Q

What do we give prior to propofol administration to counteract the expected bradycardia?

A

Glycopyralate 3 minutes prior

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94
Q

What type of solution of propofol is used in the ICU to reduce the amount of lipid emulsion administered?

A

2% solution

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95
Q

What meds are not utilized when doing TIVA?

A

isoflurane, desflurane, and sevoflurane

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96
Q

Why do children require higher doses of propofol?

A

They have a larger central distribution volume and clearance rate

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97
Q

What consideration do we give to elderly patients when administering propofol for induction?

A

Utilize a 25-50% lower dosage

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98
Q

What are the plasma levels of propofol for unconsciousness on induction and awakening?

A

Unconsciousness on induction: 2 to 6 mcg/mL Awakening: 1 to 1.5 mcg/mL

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99
Q

Why do patients report “such good sleep” after being on propofol?

A

Propofol induces REM sleep very quickly

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100
Q

5 key points associated with intravenous sedation utilizing propofol?

A
  1. Minimal analgesic and amnestic effects 2. Prompt recovery without residual sedation 3. Low incidence of PONV 4. Anti-convulsant and amnestic properties 5. Midazolam and opioids used as adjuncts
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101
Q

What is the agent of choice in brief GI endoscopy procedures?

A

Propofol

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102
Q

What is the dose of propofol when administering for anti-emetic properties in the PACU? What is the sub-hypnotic infusion dose?

A

IV push: 10-20mg (1-2mL) Sub-hypnotic infusion: 10-15mcg/kg/min

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103
Q

What is the mechanism of action that allows propofol to be utilized for PONV?

A

Depression of subcortical pathways and direct depressant effects on the vomiting center

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104
Q

What dose and what procedure can we use propofol for as an anti-pruritic?

A

10mg IV post neuraxial opioids or cholestasis

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105
Q

Anti-convulsant dose of propofol?

A

1mg/kg IV

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106
Q

What are the 6 other benefits associated with propofol?

A
  1. Anti-pruritic 2. Anti-convulsant 3. Bronchodilator 4. Potent antioxidant 5. Analgesia at low doses 6. Not a trigger for MH
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107
Q

What are the 2 known triggers for malignant hyperthermia?

A
  1. Volatile agents 2. Succinylcholine
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108
Q

5 CNS side effects of propofol?

A
  1. Decreases CMRO2, CBF and ICP (auto regulation maintained) 2. Large doses may decrease CPP (may need to support MAP) 3. EEG changes similar to Thiopental (suppresses EEG) 4. No SSEP suppression unless volatiles or nitrous added 5. Excitatory movements on induction/emergency (does not product seizure)
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109
Q

What causes the decrease in SBP with propofol administration?

A

Inhibition of SNS, vascular smooth muscle relaxation and decreased SVR (See a decrease in intracellular calcium)

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110
Q

When do we see an exaggerated response to decreased SBP when administering propofol?

A

Hypovolemia, elderly patients, Left ventricular compromise

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111
Q

Why do we see bradycardia with propofol administration?

A

Decreased SNS response and possible depressed baroreceptor reflexes

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112
Q

What response with heart rate in health adult patients can we see with propofol administration?

A

Profound bradycardia and asystole

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113
Q

What are the effects of propofol on the pulmonary system?

A
  1. Dose dependent depression of ventilation to apnea 2. Synergistic with depression w/ opioids 3. Intact hypoxic pulmonary vasoconstriction response 4. Painful surgical stim`. counteracts the ventilatory depressant effects
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114
Q

What effects does propofol have on liver transaminase enzymes or creatine concentrations?

A

None, they remain normal

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115
Q

What effects does long term infusion of propofol have on the body?

A
  1. Hepatocellular injury 2. Propofol infusion syndrome 3. Green urine from phenol excretion (no alteration in renal function) 4. Cloudy urine from uric acid crystallization (no alteration in renal function)
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116
Q

What are the 3 points of propofol infusion syndrome?

A
  1. Lactic acidosis 2. Brady-dysrhythmias 3. Rhabdomyolysis
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117
Q

What decreases the amount of pain felt on injection of propofol?

A
  1. Lidocaine prior 2. Using larger veins (AC and up)
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118
Q

6 other side effects of propofol not related to pulmonary, cardiovascular or cerebral.

A
  1. Pain on injection 2. Decreased IOP 3. Inhibits platelet aggregation 4. Allergic reactions 5. Prolonged myoclonus 6. Abuse and misuse
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119
Q

What dose of propofol can lead to propofol infusion syndrome?

A

>75 mcg/kg/min for longer than 24 hours

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120
Q

How would we diagnose propofol infusion syndrome?

A

ABG and serum lactate concentrations

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121
Q

2 Unique characteristics of etomidate?

A
  1. Etomidate is the only carboxylated imidazole-containing compound 2. Etomidate is the only drug with direct systemic absorption in oral mucosa that bypasses hepatic metabolism
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122
Q

When is etomidate water soluble? Lipid soluble?

A

Water soluble: Acidic pH Lipid soluble: Physiologic pH (7.4)

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123
Q

What is the common theme with the 4 medications utilized for induction?

A

They all cause Myoclonus

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124
Q

What does the 35% propylene glycol mixture with etomidate cause?

A

Pain on injection

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125
Q

MOA of etomidate?

A

Selective modulator of GABA-a receptors

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126
Q

Onset of action of etomidate? Elimination half time?

A

Onset: 1 minute of IV admin Elimination half time: 2-5 hours

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127
Q

What is the metabolism and elimination of etomidate?

A

Metabolism: Hydrolysis by hepatic microsomal enzymes and plasma esterases Elimination: 85% in urine, 10-13% in bile

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128
Q

What is the Vd of etomidate and what does it tend to bind to in the body?

A

Vd: large Binds to: 76% bound to albumin

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129
Q

Dose of etomidate?

A

0.2 to 0.4 mg/kg IV

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130
Q

What is a benefit to using etomidate as an induction medication?

A

There is no hangover or cumulative drug effect

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131
Q

What patient populations is etomidate best used in?

A

Unstable cardiac patients who have little or no cardiac reserve (Good for low EF)

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132
Q

Heart induction meds?

A

1000mcg fentanyl and 10mg versed

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133
Q

Why does myoclonic movement occur?

A

Alteration in balance of inhibitory and excitatory influences on the thalamocortical tract

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134
Q

How would you attenuate myoclonic activity with administration of etomidate?

A

Admin opioids such as fentanyl 1-2mcg/kg IV or benzos such as versed prior to administration

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135
Q

What is the occurrence rate of myoclonic activity associated with etomidate administration?

A

50-80% (higher than thiopental, methohexital and propofol)

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136
Q

Which patient population should we be cautious when giving etomidiate?

A

Patients with a history of seizure activity, patients who have sepsis or patients who are hemorrhaging

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137
Q

What occurs if we don’t have an adequate stress response?

A

You will not be able to extubatne the patient after surgery

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138
Q

What effect does etomidate have on the adrenocortical system?

A

Dose dependent inhibition of the conversion of cholesterol to cortisol

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139
Q

How long does enzyme inhibition last post etomidate administration?

A

4 to 8 hours

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140
Q

CNS side effects of etomidate?

A
  1. Decrease CBF and CMRO2 by 35-45% 2. Similar EEG changes except more frequent excitatory spikes
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141
Q

Why does etomidate decrease CBF and CMRO2?

A

It is a potent, direct cerebral vasoconstrictor

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142
Q

What considerations should we give to the EEG readings when giving etomidate?

A
  1. May activate seiure foci 2. May augment amplitude of SSEP
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143
Q

CV side effects of etomidate? (5)

A
  1. CV stable 2. Minimal changes in HR, SV, CO, Contractility 3. Mild decrease in MAP (will have sudden hypotension in hypovolemic patients) 4. No intra-arterial damage 5. Does not release histamine
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144
Q

What induction dose of etomidate predisposes hypovolemic patients to severe, sudden hypotension?

A

0.45 mg/kg IV

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145
Q

Ventilatory side effects of etomidate?

A
  1. Ventilation depressant is less than barbiturates 2. Rapid IV injection leads to apnea 3. Transient (3-5min) tidal volume decrease offset by compensatory increases in frequency of breathing 4. Stimulates CO2 medullary centers
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146
Q

What is ketamine a derivative of?

A

Phencyclidine (PCP)

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147
Q

What type of anesthesia does ketamine cause?

A

Dissociative

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148
Q

How will the patient present after administration of ketamine?

A

Cataleptic state in which the eyes remain open with a slow nystagmic gaze

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149
Q

What does the EEG show after administration of ketamine?

A

Dissociation between the thalamocortical and limbic systems

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150
Q

What properties does ketamine have as a drug?

A

Amnestic and analgesic properties

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151
Q

Signs and symptoms of ketamine use?

A

Noncomunicative, but wakefulness is present; hypertonus and purposeful skeletal muscle movements

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152
Q

What two advantages does ketamine show over propofol and etomidate?

A
  1. Lipid emulsion vehicle is not required 2. Profound analgesia at sub anesthetic doses
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153
Q

What psychiatric issue can ketamine assist in treating?

A

PTSD, bipolar, OCD, pill-resistant depression

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154
Q

2 Disadvantages of ketamine use?

A
  1. Frequent emergence delirium 2. Potential for abuse
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155
Q

What preservative is used with ketamine that we have to consider for patient allergies?

A

Benzethonium Chloride

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156
Q

5 Properties associated with S (+) Ketamine?

A
  1. Left-handed optical isomer 2. More intense analgesia than racemic and R (-) 3. More rapid metabolism and recovery 4. Less Salivation 5. Lower incidence of emergence delirium
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157
Q

3 Properties of both S (+) and S (-) Isomer of Ketamine?

A
  1. Inhibit uptake of catecholamines back into the postganglionic sympathetic nerve endings (cocaine-like) 2. Less fatigue 3. Less cognitive impairment
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158
Q

What receptor does ketamine bind to?

A

Noncompetitively to the phencyclidine recognition site on NMDA receptors

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159
Q

What occurs when ketamine binds to NMDA receptors?

A

Inhibition of activation of NMDA receptors by glutamate and decreased presynaptic release of glutamate

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160
Q

6 other receptors that ketamine binds to

A
  1. All opioid 2. Monoamingergic 3. Muscarinic 4. Voltage-sensityive sodium channels 5. L-type calcium channels 6. Nueronal nicotinic acetylcholine (Ketamine has weak actions at GABA-a receptors)
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161
Q

Peak plasma concentration and length of duration of action of ketamine?

A

Peak plasma: 1 minute after IV and 5 mins IM Duration: Short

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162
Q

What does the large Vd of ketamine do to its elimination half time?

A

Longer elimination half time of 2 to 3 hours

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163
Q

What solubility does ketamine show?

A

High lipid solubility (5-10x thiopental)

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164
Q

How is ketamine metabolized and then excreted?

A

Metabolism: Hepatic, CYP450 Excretion: Kidneys

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165
Q

What is the metabolite of ketamine and what effect does it have on analgesia>

A

Active metabolites norketamine and it prolongs analgesia

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166
Q

Pharmacokinetic consideration when giving ketamine to burn patients?

A

Tolerance

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167
Q

Induction (IV and IM), sub anesthetic, post sedation and neuraxial doses of ketamine

A

Induction: 1-2 mg/kg IV ; 4-8mg/kg IM Subanesthetic (analgesic dose): 0.2-0.5 mg/kg IV Post Sedation and Analgesia: 1-2mg/kg/hr (pedi sx) Neuraxial Analgesia: 30mg epidural or 5-50mg in mL of saline intrathecal

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168
Q

What physical effects do we consider when giving ketamine for induction?

A
  1. Induction of salivary secretions d/t muscarinic-R stimulation 2. Maintenance of pharyngeal and laryngeal reflexes predisposes to coughing and laryngospasm
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169
Q

What antisialagogue should we use prior to ketamine admin?

A

Glycopyrrolate>Atropine/Scopolamine

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170
Q

Timing for loss of consciousness IM/IV, timing of return of consciousness, timing of return to full consciousness with ketamine administration

A

LOC: 30-60 seconds IV ; 2-4min IM ROC: 10-20 minutes Full consciousness: 60-90 minutes

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171
Q

How long would we expect amnesia post ketamine use persist after return of consciousness?

A

60-90 minutes

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172
Q

7 clinical uses of ketamine

A
  1. Acutely hypovolemic patients 2. Asthmatic and MH patients 3. Coronary artery disease cocktail 4. Pediatric induction (IM route especially) 5. Burn dressing changes, debridements and skin grafting 6. Reversal of opioid tolerance 7. Restless leg syndrome (PO)
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173
Q

Patient populations to avoid ketamine use?

A

Systemic/pulmonary hypertension and Increased ICP

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174
Q

CNS side effects of ketamine?

A
  1. Potent vasodilation 2. Excitatory activity on EEG dose not alter seizure threshold 3. Increased amplitude with SSEP reduced by N2O
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175
Q

Why do we worry about ketamine use in patients with high ICP?

A

Ketamine increases CBF by 60%

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176
Q

At what dose of ketamine do we no longer see increases in ICP?

A

0.5 to 2 mg/kg IV

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177
Q

CV side effects of ketamine?

A
  1. Resembles SNS stimulation so can give to hypovolemic and sepsis patients 2. Increases SBP, PAP, HR, CO, MRO2 3. Unexpected drops in SBP and CO when catecholamine stores are depleted
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178
Q

Why dose ketamine cause increased SBP, PAP, HR, CO, and cardiovascular MRO2?

A

It increases plasma epinephrine and norepinephrine levels (Can be blunted by pre-med with benzos or inhaled anesthetics and N2O)

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179
Q

Ventilatory and Airway side effects of ketamine? (6)

A
  1. No significant depression of ventilation 2. Ventilatory response to CO2 maintained so will continue to breathe unless given paralytics 3. PaCO2 is unlikely to increase more than 3 mmHG 4. Upper airway skeletal tone and reflex remain intact 5. Bronchodilator activity without histamine release 6. Increased salivary and tracheobronchial mucous gland secretions
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180
Q

Method of action of ketamine that predisposes patients to emergence delirium?

A

Depression of the inferior colliculus and medial geniculate nucleus

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181
Q

How do we prevent emergence delirium with ketamine use?

A

Benzos 5 min IV prior to admin of ketamine

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182
Q

Signs and symptoms associated with emergence delirium induced by ketamine

A
  1. Visual, auditory, proprioceptive and confusional illusions. 2. Morbid and vivid dreams and hallucinations up to 24 hours
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183
Q

What and why do we expect to see an altered response when administering succinylcholine to a patient who has received ketamine?

A

What we see: Prolonged apnea Why we see it: Inhibition of plasma cholinesterase’s

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184
Q

What and why do we expect to see an altered response when administering non-depolarizing NMBD’s to a patient who has received ketamine?

A

What we see: Enhancement of non-depolarizing NMBD’s Why we see it: Inhibition of cytosolic free calcium concentrations

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185
Q

Effects of ketamine on platelets?

A

Inhibition of platelet aggregation

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186
Q

What is the expected interaction when we administer ketamine with volatile anesthetics?

A

Hypotension

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187
Q

What are the two components included in the defiintion of pain?

A
  1. Sensory-discriminitive
  2. Motivational-affective
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188
Q

What is the pathway for sensory-discrimintive information?

A
  1. Ascending projectiong of spinothalamic and trigeminothalamic tracts
  2. Cerebral Cortex
  3. Sensory Processing
  4. Response
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189
Q

When we feel pain, what information is the cerebral cortex processing?

A
  1. Quality of pain: pricking, burning, itching
  2. Location of the painful stimulus
  3. Intensity of pain
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190
Q

What are the 4 responses to motivation-affective painful stimuli?

A
  1. Attention and arousal
  2. Somatic and autonomic reflexes
  3. Endocrine responses
  4. Emotional Changes
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191
Q

What type of information are most pain signals considered to be?

A

Afferent

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192
Q

Definition of pain from the international association for the study of pain?

A

Emphasizes the complex nature of pain as a physical, emotional, and psychological condition

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193
Q

What is the definition of nociception?

A

The experience of pain with a series of complex neurophysiologic processes

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194
Q

How do medications target causes of pain?

A
  1. Actions on transduction
  2. Transmission
  3. Interpretation
  4. Modulation in both PNS and CNS
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195
Q

What is the annual cost of pain?

A

40 billion

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196
Q

Describe Transduction of pain

A

Nerve endings: Noxious stimulus to electrical impulses

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197
Q

Describe Transmission of Pain

A

Conduction of impulses to the dorsal horn of the spinal cord and the thalamus

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198
Q

What are the 3 cortices that recieve pain impulses

A
  1. Cingulate
  2. Insular
  3. Somatosensory
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199
Q

Describe Modulation of Pain

A

Process of altering pain transmission; likely both inhibitory and excitatory mechanisms in the PNS and CNS

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200
Q

What is the central relay station for pain that allows us to actually percieve pain?

A

The thalamus is the central relay station for incoming pain signlas and the primary somatosensory cortex serving for discmination of specific stimulus

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201
Q

5 Locations of Nociceptors

A
  1. Skin
  2. Muscles
  3. Joints
  4. Viscera
  5. Vasculature
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202
Q

Describe afferent pain fibers

A

Unmyelinated C-fibers and Myelinated A-fibers

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203
Q

What type of pain do C-fibers percieve?

A

burning pain from heat and pressure from sustained pressure

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204
Q

What type of pain fiber percieves heat, mechanical and chemical stimulus?

A

Type 1 Myelinated A-fibers (A beta(largest) and A delta)

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205
Q

What type of pain A-fibers percieve heat?

A

Type 2

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206
Q

What chemical mediators of pain are considered peptides?

A
  1. Substance P
  2. Calcitonin
  3. CGRP
  4. Bradykinin (1st released)
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207
Q

What chemical mediators of pain are considered lipids?

A
  1. Prostaglandins
  2. Thromboxanes
  3. Leukotrines
  4. Endocannabinoids
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208
Q

7 Types of receptors and ion channels for pain (Dorsal root ganglion and peripheral terminals)

A
  1. Purinergic
  2. Metabotropic
  3. Glutametergic
  4. Tachykinin
  5. TRPV 1
  6. Neurotrophic
  7. Ion channels (Nav 1.8)
209
Q

Describe Chronic Pain

A

Pain that does not resolve even after tissue healing

210
Q

What type of shift does hyperalgesia cause on the stimulus-response function?

A

Leftward shift that relates magnintude of pain to stimulus intensity

211
Q

Describe primary hyperalgesia

A

Pain at the original site of injury from heat and mechanical injury

212
Q

4 factors included in primary hyperalgesia

A
  1. Decreased pain threshold
  2. Increased response to suprathreshold stimuli
  3. Spontaneous pain
  4. Expansion of receptive field (highly guarded)
213
Q

Describe secondary hyperaglesia

A

Uninjured skin surroudning the injury only from mechanical stimul

214
Q

What factor is included in secondary hyperalgesia?

A

Sensitization of central neuronal circuits

215
Q

What is the purpose of the spinal dorsal horn?

A

Relay center for nociceptive and other sensory activity

216
Q

Describe the ascending pathways of the spinal dorsal horn

A

Pain-related activity to brainstem and forebrain (S1 and S2) pereception ofpain location and intensity

217
Q

What type of pain is percieved by the limbic cortex and thalamus?

A

Perception of motivational-affective pain components

218
Q

Describe the Periaqueductal gray-rostral ventromedial medulla (PAG-VRM) descending system of pain?

A

Depress or facilitate the integegration of pain information in the spinal cord

219
Q

What type of fibers connect to lamina 1 in the spinal dorsal horn?

A

Afferent C fibers (dull pain)

220
Q

What type of pain fibers and receptors are in lamina 2, the substantia gelatinosa?

A

Afferent C fibers and opioid receptors where spinal anesthesia takes action

221
Q

What are the type of fibers that synpase at laminae 1, 4, 7, and the ventral horn to innervate muscles and viscera?

A

Myelinated fibers

222
Q

What receptor and chemical synapses with laminae 3 and 4?

A

NKI recpetors with substance P

223
Q

Descibe the gate control theory of pain

A

The theory that there is a neurological gate in the spinal dorsal horn for pain

224
Q

Describe what it means that a pain gate is open

A

Pain is projected to supraspinal brain regions

225
Q

Describe what it means when a pain gate is closed

A

Pain is not felt with simultaneous inhibitory impulses

226
Q

Describe the Gate Open/Gate Closed when you are rubbing your elbow because you bumped it on a shelf

A

Gate open: A delta and C fibers send signals

Gate Closed: A beta fibers, which are fast and myelinated deliver information about pressure and touch (rubbing)

227
Q

7 Neuromodulators of pain

A
  1. Substance P
  2. Glutamate
  3. CGRP
  4. NMDA
  5. AMPA
  6. BDNF
  7. Cytokines
228
Q

What nociceptors are released with tissue injury in the periphery?

A
  1. Substance P
  2. Glutamate
229
Q

What are the mediators released in the periphery by damaged cells, mast cells, and platelets?

A
  1. Bradykinin
  2. Histamine
  3. Prostaglandins
  4. Serotonin
  5. Hydrogen Ion
  6. Lactic Acid
230
Q

5 Excitatory impulses in the spinal area?

A
  1. Glutamate
  2. Calcitonin
  3. Neuropeptide Y
  4. Aspartate
  5. Substance P
231
Q

5 Inhibitory Impulses in the spinal area

A
  1. GABA
  2. Glycine
  3. Enkephalins
  4. Norepinpehrine
  5. Dopamine
232
Q

What are the 4 ascending pathways of nociceptive information?

A
  1. Spinothalamic
  2. Spinomedullary
  3. Spinobulbar
  4. Spinohypothalamic
233
Q

What laminae do pain, temperature and itch impulses synapse with and what ascending pathway does it follow?

A

Lamina 1, 7 and 8 (all afferent) and it travels through the spinothalamic tracts

234
Q

What type of information and what laminae do the fibers synapse in for Spinobulbar pain?

A

Behaviour towards pain and laminae 1, 5 and 7

235
Q

What aspects of pain and what laminae do the fibers synpase in for spinohypothalamic?

A

Autonomic, neuroendocrine and emotional aspects of pain. They synapse in lamina 1, 5, 7, and 10

236
Q

What Supraspinal Modulationof Nociception does the Forebrain S 1 and S 2 percieve?

A

Location and intensity

237
Q

6 Places of supraspinal modulation of nociception?

A
  1. Forebrian S1 and S2
  2. Anterior cingulate cortex (ACC)
  3. Insular Cortex (IC) Emotional and motivational aspects
  4. Prefrontal Cortex
  5. Thalamus
  6. Cerebellum
238
Q

What inhibitory pain tracts are associated with supraspinal modulation?

A

Descending inhibitory tracts

239
Q

Where does supraspinal modulation of pain originate in?

A

Periaqueductal gray

240
Q

3 Facts associated with Inhibitory signals that originate in the periaqueductal gray?

A
  1. Through the rostral ventromdial medulla (RVM)
  2. Dorsolateral funiculus
  3. Synapse in the dorsal horn
241
Q

Neurotransmitters associated with supra-spinal modulation of pain?

A
  1. Endorphins
  2. Enkephalins
  3. Serotonin
242
Q

What does hyperpolarizing A-delta and C fibers do?

A

Decreased release of subtance P and opening of K+ channels/inhibition of Calcium Channels

243
Q

What are the Descending Pathways of Pain modulation?

A
  1. Descending Inhibition Pathway (DI)
  2. Descending Facilitation Pathway (DF)
244
Q

Factors associated with descending pathways of pain modulation

A
  1. Other somatic stimuli
  2. Psychological factors (arousal, attention and expectation)
245
Q

PAG-RVM system factors associated with descending pathways of pain modulation?

A
  1. Opioid receptors
  2. Hypperalgesia and allodynia
246
Q

Primary objective of pain treatment?

A

Tissue healing without repeated injury

247
Q

How long does acute pain last? Chronic pain?

A

Acute: Days to weeks after injury

Chronic: >3 to 6 months, persisting beyond tissue healing

248
Q

What pathways do unpleasant emotional experiences and affective qualities use?

A

The same pathways as pain

249
Q

Describe Neuropathic pain, the increased risk factors for it and treatment

A
  1. Persisting after tissue has healed results in allodynia and hyperalgesia
  2. Risk factors: Cancer patients d/t chemo and radiation therapy
  3. Treatment: Symptomatic (opioids, gabapentin, amitryptiline, and cannabis)
250
Q

Descibe visceral pain, where it is referred to and what it is due to

A
  1. Diffuse and poorly localized
  2. Referred to somatic sites such as skin and muscle
  3. Due to: Ischemia, stretching of ligamentous attachments, spasms, distention
251
Q

Where is gallbladder pain referred to?

A

The shoulder

252
Q

Describe complex regional pain syndromes

A

A variety of painful conditions following injury in a region with impairment of sensory, motor and autonomic systems

253
Q

What are complex regional pain syndomes due to?

A

Spontaneous pain, allodynia, hyperalgesia, edema, autonomic abnormalities, active and passie movement disorders, trophic changes of skin and SQ tissues

254
Q

Describe Pain in Neonates and Infants

A
  1. Pain perception at 23 weeks of gestation
  2. Lower pain threshold and exaggerated pain responses
255
Q

Prominent cardiovascular responses to pain

A

Hypertension, tachycardia, myocardial irritability, increased SVR

256
Q

Pulmonary responses to pain

A
  1. Increased total body O2 consumption/CO2 production with increased work of breathing
  2. Splinting
  3. Decreased movement of chest wall leading to atelectasis or intrapulmonary shunting
  4. Impaired coughing
257
Q

GI/GU responses to pain

A
  1. Enhances sympathetic tone causes increased sphincter tone and decreased motility which can lead to ileus or urinary retention
  2. Hypersecretion of acid leading to stress ulceration or aspiration
  3. N/V
  4. Abdominal distention
258
Q

Endocrine response to pain?

A
  1. Increased catabolic hormones such as cortisol, glucagon and catecholamines
  2. Decreased anabolic hormones such as insulin and testosterone
259
Q

What are the effects of endocrine response to pain?

A
  1. Negative nitrogen balance
  2. Carbohydrate intolerance
  3. Increases renin, aldosterone and angiotensin
260
Q

Hematologic response to pain?

A

Platelet adhesiveness, reduced fibronlysis, hypercoagulability

261
Q

3 emotional responses to pain

A
  1. Anxiety
  2. Sleep disturbance
  3. Depression
262
Q

What are immune responses of pain related to?

A

Stress related such as leukocytosis and depressed reticuloendothelial system, which increases risk of infection

263
Q

What are the areas labeled 1-5 in the image

A
  1. Somatosensory and association cortices
  2. Limbic System
  3. Thalamic Nuclei
  4. Periaqueductal Gray
  5. Nucleus Raphe Magnus
264
Q

What are the pain pathways labeled 1 and 2?

A
  1. Descending pain-inhibitory tracts
  2. Spinothalamic tract projection neuron
265
Q

Name the areas on the pain signal reception labeled 1-3

A
  1. Cingulate Cortex
  2. Somatosensory Cortex
  3. Insular Cortex
266
Q

What are opiates a derivative of

A

Papaver somniferum

267
Q

What is different about papeverine than other opiates?

A

No analgesic effect, mainly used for smooth muscle relaxation to promote oxygenation

268
Q

What is the greek word for narcotic?

A

Stupor, has the potential for physical dependence

269
Q

What is the most common opioid antagonist?

A

Naloxone

270
Q

Examples of phenanthrenes

A

morphine, codeine and thebaine

271
Q

Examples of benzylisoquinoles

A

papaverine and noscapine

272
Q

What are the two main targets of opioid agonists?

A

Brainstem and spinal cord

273
Q

What endogenous substances also bind to opioid receptors?

A

enkephalin, endorphins and dynorphins

274
Q

What ion increases in conductance with the use of opioids?

A

Potassium, which leads to hyperpolarization

275
Q

What post-synaptic nociceptive neurons are inhibited with the use of opioids?

A

acetylcholine, dopamine, norepinephrine, and substance P

276
Q

4 sites of opioid receptors in the brain

A

periaqueductal gray (PAG), locus ceruleus, rostral ventral medulla, and hypothalamus

277
Q

What do opioids effect in the spinal cord?

A

Interneurons and primary afferent neurons in the dorsal horn

278
Q

What area in the spinal cord is specifically targeted by opioids?

A

Substantia gelatinosa of the dorsal horn

279
Q

How many hours post knee surgery do we see pain relief with intraarticular morphine administration?

A

12-24 hours

280
Q

What are the effects of agonists binding to Mu1 receptors? (7)

A
  1. Analgesia supraspinal and spinal
  2. Euphoria
  3. Miosis (pupil constriction)
  4. Bradycardia
  5. Hypothermia
  6. Urinary Retention
  7. Low abuse potential
281
Q

What are the effects of agonists binding to Mu2 receptors? (4)

A
  1. Analgesia Spinal
  2. Depression of ventilation
  3. Physical dependence
  4. Constipation
282
Q

What are the effects of agonists binding to Opioid Kappa receptors? (6)

A
  1. Anaglesia supraspinal and spinal
  2. Dysphoria
  3. Sedation
  4. Miosis
  5. Diuresis
  6. Low abuse potential
283
Q

What are the effects of agonists binding to opioi Delta receptors? (5)

A
  1. Analgesia supraspinal and spinal
  2. Depression of ventilation
  3. Physical Dependence
  4. Constipation (minimal)
  5. Urinary retention
284
Q

3 examples of Mu1 and Mu2 agonists?

A

endorphines, morpine, synthetic opioids

285
Q

Example of a opioid kappa receptor agonist

A

Dynorphines

286
Q

Example of an opioid delta agonist?

A

Enkephalines

287
Q

3 opioid receptor antagonists?

A

naloxone, naltrexone, nalmefene

288
Q

Do we see myocardial ischemia with opioids?

A

If given alone, opioids do not promote myocardial ischemia

289
Q

When does anesthetic care start?

A

Pre-op setting

290
Q

Which opioid has no direct cardiac depressant effect, but does cause bradycardia?

A

Morphine

291
Q

Cardiovascular side effects of opioids? (3)

A
  1. Orthostatic hypotension and syncope leads to SNS tone decreased and we see a reduction in venous return CO and BP
  2. Bradycardia or histamine release cause decreased BP
  3. If administered together with N2O or Benzos we see depression of the CV system
292
Q

What is the opioid effect on ventilation?

A

Decreased responsiveness of ventilation centers to CO2

293
Q

What s/s do we see in opioid overdose?

A

Apnea, miosis, hypoventilation and coma

294
Q

How does an increase in PaCO2 shift the oxy-hemoglobin dissociation curve?

A

shifts to the right

295
Q

What is the benefit of using physostigmine in the reversal of opioid respiratory depression?

A

Increased CNS levels of Ach will antagonize the ventilatory depression without reversing analgesia

296
Q

What happens with hypercapnia?

A

Overdose of CO2 can be a ventilatory suppressant (has a narcotic effect)

297
Q

Since opioids can be utilzed as cough suppressants, when would we see reflex coughing with opioid administration?

A

Large dose given on induction

298
Q

What determines the levels of CO2 that will cause a patient to breathe again?

A

Comorbidities and baseline ETCO2

299
Q

CNS side effects of opioids?

A
  1. Decreased CBF and possibly ICP; Caution with head injuries
  2. Myoclonus in large doses with negative EEG
  3. Sedation
300
Q

What is the effect of opioids on the thoracic (chest) wall and abdominal muscles?

A

Rigidity

301
Q

What would we notice if a patient is experiencing thoracic wall and abdominal muscle rigidity from the adminstration of opioids?

A

The patient would be harder to ventilate

302
Q

What are the GI effects of opioids?

A
  1. Spasm of biliary smooth muscle, specifically the sphincter of Oddi
  2. Delayed gastric emptying and constipation which can lead to nausea and vomiting
303
Q

What can we give to counteract spasming of the sphincter of Oddi due to opioid adminstration?

A

Up to 2mg of Glucagon

304
Q

List in order from greatest to least occurrence of Sphincter of Oddi spasms between morphine, meperidine and fentanyl

A

Fentanyl, Morphine, Meperidine

305
Q

What is N/V due to with opioid adminstration?

A

Direct stimulation of the CTZ, increased GI secretions and delayed emptying

(this is seen more with IM admin than IV)

306
Q

What area of the brain is the CTZ found in?

A

4th ventricle

307
Q

GU side effects of opiods?

A

urinary urgency

308
Q

Cutaneous side effects of opioids?

A

histamine release causing flushing of the face, neck and upper chest

309
Q

Placental effects of opioid admin?

A

neonate depression and dependence

310
Q

Hormonal side effects of opioid use?

A

decreased plasma cortisol levels

311
Q

Drug interactions associated with opioid administration?

A

Exaggeratted with amphetamines, phenothiazines, MAOI and TCA

312
Q

What is tolerance and when does it usually occur with opioids?

A

Tolerance is the development of the requirement for increased doses of a drug, usually occurs after 2 to 3 weeks of use

313
Q

When does Morphine show tolerance?

A

25 days

314
Q

What does tolerance of opioids upregulate?

A

cAMP system

315
Q

Why can cross tolerance develop between all opioids?

A

CYP450 metabolism

316
Q

Onset, peak intensity and duration of meperidine and fentanyl withdrawal?

A
  1. Onset: 2-6 hours
  2. Peak intensity: 6-12 hours
  3. Duration: 4-5 days
317
Q

Onset, peak intensity and duration of Morphine and Heroin withdrawal?

A
  1. Onset: 6-18 hours
  2. Peak intensity: 36-72 hours
  3. Duration: 7-10 days
318
Q

Onset, peak intensity and duration of Methadone withdrawal?

A
  1. Onset: 24-48 hours
  2. Peak intensity: 3-21 days
  3. Duration: 6-7 weeks
319
Q

Effects of Morphine? (9)

A
  1. Analgesia
  2. Euphoria
  3. Sedation
  4. Diminshed ability to concentrate
  5. Nausea
  6. Feeling of body warmth
  7. Heaviness in extremities
  8. Dryness of mouth
  9. Pruritis
320
Q

What type of pain is morphine best at treating?

A

Visceral, skeletal muscle, joints and integumental dull pain

321
Q

IM and IV Morphine onset, peak and duration

A
  1. Onset for both is 15 to 30 minutes
  2. IM peak is 45 to 90 minutes
  3. IV peak is 15 to 30 minutes
  4. Duration of both is 4 hours
322
Q

Where does morphine accumulate rapidly?

A

Kidneys, liver and skeletal muscle

323
Q

Why does morphine take longer to peak in the plasma?

A

It is highly water soluble

324
Q

PO first pass effect on morphine when it comes to hepatic metabolism? lungs?

A

25% hepatic first pass and no first pass in the lungs

325
Q

How is morphine metabolized and excreted?

A

Metabolized through glucuronidation in hepatic and extrahepatic sites. Secreted by the kidneys

326
Q

How does renal failure effect morphine excretion?

A

Prolonged depression of ventilation

327
Q

Why do we need to be aware of the active metabolite of morphine, morphine-3-glucuronide?

A

Elimination half time is longer, so caution in renal dysfunction

328
Q

What is the effect of morphine on women as compared to men?

A

Greater analgesic potency and slower speed of offset

329
Q

At what receptors is meperidine an agonist of opioid receptors?

A

Mu and K

330
Q

What opioid analogues came from Meperidine?

A
  1. Fentanyl
  2. Sufentanil
  3. Alfentanil
  4. Remifentanil
331
Q

What medications is meperidine structurally similar to?

A

Lidocaine and Atropine

332
Q

If given intrathecally, what channels does Meperidine block?

A

Na+ channels

333
Q

How do we adjust Meperidine for the elderly? Alcoholics?

A

We give less to the elderly and more to alcoholics

334
Q

What is the best route to give meperidine and why

A

IV because it has an 80% 1st pass effect

335
Q

4 effects of meperidine

A
  1. Sedation
  2. Euphoria
  3. N/V
  4. Depression of ventilation
336
Q

Potency of meperidine compared to morphine? Duration of meperidine?

A

1/10 as potent as morphine and duration is 2 to 4 hours

337
Q

How is meperidine metabolized? Excreted?

A

90% hepatic metabolism into normeperidine and excreted through the kidneys

338
Q

Alkalosis/Acidosis of the Urine can increase the speed of elimination of meperidine?

A

Acidic urine (give cranberry juice)

339
Q

Elimination half time of meperidine?

A

3 to 5 hours

340
Q

Elimination half time of meperidine with renal failure?

A

35 hours

341
Q

What do we see with meperidine toxicity?

A

Delerium (confusion, hallucinations), myoclonus and seizures

342
Q

By about what % of normal is kidney function reduced in kidney failure?

A

15%

343
Q

List the meds in order from greatest effect to least on post-op shivering

A

Clonidine ($$$)>physostigmine>meperidine

344
Q

Where is meperidine a potent agonist of that makes it good for post-op shivering?

A

alpha 2 receptors

345
Q

What are 3 example of when meperidine is not useful?

A

Diarrhea, cough suppressant, bronchoscopy

346
Q

Side effects associated with meperidine?

A
  1. Tachycardia
  2. Mydriasis w/ dry mouth
  3. Negative inotropy
  4. Serotonin Syndrome (If combined with Amitriptyline or Nardil)
  5. Impaired ventilation
  6. Crosses placenta
347
Q

Where does fentanyl tend to linger?

A

The fat

348
Q

How does fentanyl compare to morhpine so far as potency goes?

A

Fentanyl is 75 to 125 more potent than morphine

349
Q

Where is the effect site of fentanyl?

A

The Brain

350
Q

How long does it take to reach equilibration with fentanyl?

A

6.4 minutes, meaning fentanyl has a rapid onset and is very lipid soluble

351
Q

What is a large storage site of fentanyl?

A

The lungs, it has a 75% first pass effect

352
Q

How is fentanyl metabolized?

A

Hepatic CYP450 enzymes

353
Q

What is the principle metabolite of fentanyl?

A

Norfentanyl

354
Q

How do we adjust dosing of fentanyl in the elderly? Alcoholics with cirrhosis?

A

Give less to elderly and cirrhosis does not effect the metabolism

355
Q

How is fentanly excreted?

A

Through the kidneys

356
Q

What is the volume of distribution of fentanyl?

A

Large, it is distributed within less than 5 minutes

357
Q

Why is fentanyls context-sensitive half-time greater than sufanetanil?

A

Fentanyl saturates inactive tissues

358
Q

What happens to fentanyl with cardiopulmonary bypass?

A

A portion of the drug sticks to the tubing used for bypass

359
Q

Analgesic dose of fentanyl? inducton dose?

A

Analgesic: 1 to 2 mcg/kg IV

Induction: 1.5 to 3 mcg/kg IV 5 minutes prior

360
Q

What is the dose of fentanyl when used as an ajunct with inhaled anesthetics? Solo anesthesia?

A

Adjunct: 2 to 20 mcg/kg IV

Solo: 50 to 150mcg/kg IV

361
Q

What is the one-shot intrathecal dose of fentanyl?

A

25 mcg

362
Q

Transmucosal (Oral) dose of fentanyl? Dose for 2 to 8 year olds?

A

Transmucosal: 5 to 20mc/kg

2 to 8 year olds: 15 to 20 mcg/kg PO 45 minutes prior

363
Q

What does 1 mg of Fentanyl PO translate to in mg of IV morphine?

A

1 mg of PO fentanyl is equal to 5 mg IV morphine

364
Q

What is the transdermal dose of fentanyl?

A

75 to 100 mcg which gives 18 hours of stead delivery

365
Q

CV effects of fentanyl?

A

No histamine release, depressed carotid sinus baroreceptor reflex results in bradycardia and decreased BP/CO

366
Q

S/E of Fentanyl?

A
  1. Seizure like activity
  2. SSEP and EEG changes at doses >30 mcg/kg IV
  3. Modest increse in ICP (6 to 9 mmHG)
367
Q

What is the effect of fentanyl synergism with benzos? Propofol?

A

Potentiates benzos and reduces dose requirement of propofol

368
Q

What are two examples of when fentanyl is good to use with inhaled anesthetics?

A
  1. Direct laryngoscopy during intubation
  2. Sudden changes in surgical stimulation level
369
Q

How does sufentanils potency compare to fentanyl?

A

5 to 12 times more potent than fentanyl

370
Q

What protein does Sufentanil bind to?

A

Alpha1-acid glyocprotein

371
Q

What is the first pass uptake of the lungs on sufentanil?

A

60%

372
Q

How is sufentanil metabolized? Excreted?

A

Metabolized by the liver and exreted through the renal and fecal means

373
Q

Analgesic dose of sufentanil? induction dose?

A

Analgesic: 0.1 to 0.4 mc/kg IV

Induction: 18.9 mcg/kg IV

374
Q

S/E of sufentanil?

A

Bradycardia and chest wall/abdominal muscle rigidity

375
Q

What procedures do we combine sufentanil with local anesthetics?

A

OB epidurals

376
Q

How does alfentanil’s potency compare with that of fentanyl?

A

alfentanil is 1/5 less potent than fentanyl

377
Q

What disease prolongs the elimination half-time of alfentanil?

A

Cirrhosis

378
Q

What protein does alfentanil bind to?

A

Alpha1-acid glycoprotein

379
Q

What is the lipid solubility of alfentanil?

A

Alfentanil is 90% nonionized at normal pH so it shows a lower lipid solubility

380
Q

What is the potency of the opioid analogues in order from greatest to least?

A

Sufenta>fentanyl=remifentanil>alfentanil>morphine>meperidine

381
Q

What anesthetic characteristic do opioids not promote?

A

Amnesia

382
Q

What is the dose of alfentanil for induction laryngoscopy (meaning it is adjunct with something else)? Induction alone?

A

Induction laryngoscopy: 15 to 30 mcg/kg IV 90 seconds prior

Inudction alone: 150 to 300 mcg/kg IV

383
Q

What is the maintenance dose of alfentanil?

A

25 to 150 mcg/kg/hour IV with inhaled anesthetics

384
Q

What disease process do we not utilzie alfentanil in due to possibility of acute dystonia?

A

Parkinson’s Disease

385
Q

What receptor is remifentanil selective for?

A

Mu opioid agonist

386
Q

How does the potency of remifentanil compare to alfentanil?

A

Remi is 15 to 20 times more potent

387
Q

What effect does the ester structure of remifentanil have on its pharmacokinetics?

A

Remifentanil undergoes hydrolysis by nonspecific plasma and tissue esterase, meaning it can be used in liver failure

388
Q

Describe the pharmacokinetics of remifentanil (4)

A
  1. Brief action, rapid onset and offset (15 minutes)
  2. Precise and rapid tirtatable effect
  3. Lack of accumulation
  4. Rapid recovery when d/c (15 minutes max)
389
Q

How does remifentanil effect propofol?

A

Synergistic depression of ventilation

390
Q

How do we dose remifentanil?

A

IBW

391
Q

What is the peak effect site timing of remifentanil? Plasma steady state timing with inufsion?

A

Peak effect site: 1.1 minute

Plasma Steady state: 10 minutes

392
Q

Elimination half-time of remifentanil? Clearance time?

A

Elimination half-time: 6.3 minutes

Clearance: 3L/min which is 8x more rapid than alfentanil

393
Q

How is remifentanil excreted?

A

Excreted through the kidneys, but excretion is unchanged by renal or hepatic disease

394
Q

What is the induction dose or remifentanil? How much do you give every 10 minutes?

A

Induction: 1 mcg/kg IV over 60 to 90 seconds

Give 0.5 mcg to 1.0 mcg/kg IV every 10 minutes

395
Q

What is the maintenance dosing of remifentanil?

A

0.25 to 1 mcg/kg IV or 0.005 to 2 mcg/kg/min IV

396
Q

What procedures is remifentanil not recommended in?

A

Not recommended for spinal or epidural use

397
Q

Why do we want to give longer acting opioids before stopping remifentanil?

A

Because of the rapid offset, pain neurotransmitters will begin to effect nociceptors

398
Q

S/E of remifentanil? (5)

A
  1. Seizure-like activity
  2. N/V
  3. Depression of ventilation
  4. Decreased BP and HR
  5. Hyperalgesia
399
Q

What causes hyperalgesia with remifentanil?

A
  1. Previous acute exposure to large opioid doses
  2. Tolerance
  3. Anion equilibrium between microglia and neuron pathway
400
Q

How does the potency of hydromorphone compare to that of morphine? What about the hydrophillicity?

A

5x more poten than morphine and it is less hydrophillic than morphine

401
Q

What are the administration paramaeters of hydromorphone?

A

0.5 mg IV, re-dose every 4 hours up to 1 to 4mgs total

402
Q

What is a beneficial effect seen with hydromorphone when compared with morphine?

A

No histamine release

403
Q

What are the side effects of codeine when given IV?

A

Histamine induced hypotension, this is why we only give it PO or IM

404
Q

Elimination half time of codeine and metablism?

A

Elimination half-time is 3 to 3.5 hours

Metabolized by the liver

405
Q

Analgesic dose of codeine? Cough suppressant dose?

A

Analgesic: 60 mgs

Cough suppressant: 15 mgs

406
Q

How many mgs of codeine is equal to 10 mgs of morphine?

A

120 mgs of codeine is equal to 10mgs of morphine

407
Q

5 side effects of codeine

A
  1. Physical dependence
  2. Minimal Sedation
  3. N/V
  4. Constipation
  5. Dizziness
408
Q

When is methadone used?

A

Opioid withdrawal and chronic pain

409
Q

Pharmacokinetics of Tramadol?

A
  1. 5-10x less potent as morphine
  2. Mu receptor agonist with weak kappa and sigma
  3. PO: 3mg/kg
  4. Interact with coumadin
410
Q

When do we utilize opioid agonist-antagonists?

A

If the patient is unable to tolerate a pure agonist

411
Q

If an opioid-antagonist binds to Mu receptor and has no effect, what would we classify the drug as?

A

A competitive antagonist

412
Q

In addition to the usual side effects of opioid agonists, what do opioid agonist-antagonists cause?

A

Dysphoric reactions (a state of mental discomfort or suffering)

413
Q

4 advantages of opioid agonist-antagonists?

A
  1. Analgesia
  2. Limited depression of ventilation
  3. Low potential for physical dependence
  4. Ceiling effect prevents additional responses
414
Q

What agonist/antagonist effect does pentazocine show?

A

Agonist effects at sigma and kappa receptors (may hae withdrawal symptoms) with weak antagonistic activity

415
Q

What can we use to antagonize Pentazocine?

A

Naloxone

416
Q

What is the bioavailability of Pentazocine after hepatic first pass effect?

A

20% post PO admin

417
Q

What is the elimination half time of Pentazocine and how is it excreted?

A

Elimination half-time is 2 to 3 hours and it is excreted in the urine

418
Q

What is the moderate chronic pain dose of pentazocine?

A

10 to 30mg IV or 50mgs PO

419
Q

What is the IM dose of Pentazocine that causes analgesia, sedation and depression of ventilation similar to 10mgs of morphine?

A

20 to 30 mgs IM

420
Q

What can we expect in regards to the duration of action of Pentazocine for Epidurals as compared to Morphine?

A

The duration will be shorter

421
Q

S/E associated with Pentazocine? (5)

A
  1. Sedation
  2. Diaphoresis
  3. Dizziness
  4. Dysphoria with high doses
  5. Increased LVEDP, HR, BP, PA BP
422
Q

Does Pentazocine cross the placental barrier?

A

Yes and it causes fetal depression

423
Q

What is agonist and antagonist activity of Butorphanol as compared to Pentazocine?

A

Agonist activity is 20x greater and antagonistic activity is 10x to 30x more

424
Q

How many mg IM of burotphanol is equal to 10mg of morphine?

A

2 to 3 mg IM and it causes depression of ventilation due to being rapidly and completely absorbed

425
Q

Describe butorphanol’s affinity to opioid Mu, kappa and sigma receptors?

A
  1. Low affinity for Mu receptors to produce antagonism
  2. Moderate affinity for kappa receptors to produce analgesia and anti-shivering effects
  3. Minimal affinity for sigma receptors so dysphoria is low
426
Q

Elimination half-time, metabolism, and elimination route of Butorhpanol?

A
  1. Elimination half-time: 2.5 to 3.5 hours
  2. Hepatic metabolism
  3. Eliminated through the bile more than urine
427
Q

Why do we use caution with using butorphanol in combination with another opioid agonist?

A

Could potentiate the effects

428
Q

S/E associated with Butorphanol? (6)

A
  1. Sedation
  2. Nausea
  3. Diaphoresis
  4. Dysphoria
  5. Depression of ventilation
  6. Withdrawal symptoms occur
429
Q

What is the potency of Nalbuphine as compared to morphine?

A

It is a Mu receptor agonist and is equally as potent to morphine (10mg = 10mg)

430
Q

How is nalbuphine metabolized? What is its elimination half-time?

A

Metabolized by the liver and the elimination half-time is 3 to 6 hours

431
Q

S/E associated with Nalbuphine? (3)

A
  1. Sedation
  2. Dysphoria
  3. Withdrawal symptoms
432
Q

What procedure is nalbuphine good for and what do we need to consider when administering it?

A

It is good for cardiac cath patients, but it may counteract sympathomimetic drugs

433
Q

What is the Mu receptor agonist activity of Buprenorphine when compared to Morphine?

A

50x greater agonist affinity

434
Q

What dose of Buprenorphine is equal to 10mg of morphine?

A

0.3mg IM

435
Q

What is the onset of action and duration of action of Buprenorphine?

A

Onset: 30 minutes

Duration: 8 hours (will need to re-dose naloxone)

436
Q

5 uses of buprenorphine?

A
  1. Post-op
  2. Cancer
  3. Renal colic
  4. MI
  5. Epidural (5x more potent)
437
Q

2 unique side effects associated with buprenorphine?

A

Pulmonary edema and low risk of abuse

438
Q

Why is nalorphine not used clinically?

A

high incidences of dysphoria b/c no sigma activity

439
Q

4 characteristics of Dezocine

A
  1. delta and Mu activity causing analgesia and no CV side effects
  2. 0.15mg/kg IM = morphine
  3. 10-15 mg IM rapid absorption
  4. Onset is 15 minutes
440
Q

2 characteristics of Bremazocine

A
  1. kappa receptors are 2x more potent as morphine
  2. Naloxone is not effective as a reversal
441
Q

5 characteristics of meptazinol

A
  1. Mu1 receptors
  2. 100mg = 8 mg of morphine
  3. Rapid onset
  4. Druation is less than 2 hours
  5. Protein binding = 25%
442
Q

Name 3 opioid antagonists

A
  1. Naloxone
  2. Naltrexone
  3. Nalmefene
443
Q

What opioid receptor do opioid antagonists show competitive antagonism for?

A

Pure Mu opioid receptor antagonist with no agonist activity

444
Q

Describe Naloxone

A

Nonselective antagonist with all 3 opioid receptors

445
Q

6 uses of Naloxone?

A
  1. Opioid-induced depression in post-op
  2. Neonates with opioid abusing or naloxone dependent moms
  3. Opioid overdose
  4. Detect dependence
  5. Hypovolemic/Septic shock to increase contractility
  6. Antagonism of general anesthesia in high doses
446
Q

IV Dose of Naloxone and continuous infusion dose?

A

IV dose: 1 to 4 mcg/kg

Continuous Infusion: 5mcg/kg IV

447
Q

Duration of Naloxone? Elimination half-time?

A

Duration: 30 to 45 minutes

Elimination half-time: 60 to 90 minutes

448
Q

S/E associated with Naloxone? (5)

A
  1. Reversal of analgesia
  2. N/V
  3. Increased SNS
  4. Pulmonary Edema
  5. V-fib
449
Q

Metabolism and 1st pass effect of Naloxone?

A

Hepatic metabolism through glucuronidation and hepatic 1st pass effect is 1/5th PO

450
Q

3 Key facts associated with Naltrexone

A
  1. More Effective PO
  2. Duration 24 hours
  3. Used for alcoholism
451
Q

3 key facts assosciated with Nalmefene

A
  1. Equipotent to naloxone
  2. Dose is 15 to 25 mcg IV Q2-5min up to 1 mcg/kg
  3. Elimination half-time is 10.8 hours
452
Q

Pharmacokinetics of Methylnaltrexone? (3)

A
  1. Highly ionized and quarternary structure that affects the periphery
  2. Promotes gastric emptying and antagonizes N/V
  3. No alteration in centrally mediated analgesia b/c does not cross the blood brain barrier
453
Q

4 facts associated with Alvimopan

A
  1. Newer, Mu selective PO peripheral opioid antagonist
  2. Used for post-op ileus
  3. Metabolizd by gut flora
  4. Long term use can lead to cardiac events
454
Q

What is Suboxone a combination of?

A

Buprenorphine plus naloxone

455
Q

What is Embeda a combination of?

A

Extended release morphine plus naltrexone

456
Q

What is Oxynal a combination of?

A

Oxycodone plus naltrexone

457
Q

Side effects of opioids that are mistaken for allergic reactions? (3)

A
  1. Histamine release causing trunchal redness
  2. Orthostatic Hypotension
  3. Nausea and Vomiting
458
Q

When do we usually see immunosuppression with opioids?

A

Prolonged use and abrupt withdrawal

459
Q

What is fentanyl’s effect on MAC?

A

3mcg/kg IV 25 to 30 minutes before surgical incision decrease MAC of Iso or Des to 50%

460
Q

How does sufentanyl effect MAC?

A

Reduces MAC with Enflurane by 70-90%

461
Q

How does alfentanyl effect MAC?

A

Up to 70% decrease

462
Q

How does Remifentanyl effect MAC?

A

50 to 90% decrease

463
Q

How does the opioid agonist-antagonist effect MAC? Butorphanol, nalbuphine and pentazocine

A

Butorphanol: 11% decrease

Nalbuphine: 8% decrease

Pentazosine: 20% decrease

464
Q

What receptors and location is the target for Neuraxial Opioids?

A

Opioid receptors in substantia gelatinosa (Lamina 2)

465
Q

Since opioids do not cause sympathectomy, sensory block or weakness, what would we attribute those findings to?

A

The local anesthetic administered with the opioids

466
Q

How is the dose of an epidural compared to the dose of a spinal?

A

The epidural dose is 5 to 10x more because the drug will diffuse across the dura and result in systemic absorption

467
Q

What is the benefit of the high lipophillicity of fentanyl and sufentanil?

A

Absorbed quicker

468
Q

Describe morphines onset and duration of action when administered as an epidural?

A

Slower onset and longer duration

469
Q

What are the 3 different areas that a drug can be taken up by when administering an epidural?

A
  1. Epidural fat
  2. Epidural venous plexus = systemic absorption
  3. Diffusion across the dura into the CSF
470
Q

How could we prevent systemic absorption when administering opioids in the epidural space?

A

Utilize epinephrine to cause local vasocsontriction

471
Q

2 complications associated with epidurals

A
  1. Could be in spinal space
  2. Could be in vein
472
Q

Fentanyl peak neuraxial absorption? Sufentanil?

A

Fentanyl: 20 minutes

Sufentanil: 6 minutes

473
Q

What does cephalid movement of opioids depend on when adminstering meds intrathecally?

A

Lipid solubility, coughing or straining

474
Q

How does fentanyl and sufentanil’s cephalid movement compare to morphine?

A

They are less than morphine because of their high lipid solubility, wherease morphine is highly hydrophillic

475
Q

Peak CSF (epidural), Peak Plasma (epidural) and Peak CSF (Intrathecal) timing of fentanyl?

A

Peak CSF (epidural): 20 minutes

Peak Plasma (epidural): 5-10 minutes similar to IM

Intrathecal/CSF Levels: Minimal

476
Q

Peak CSF (epidural), Peak Plasma (epidural) and Peak CSF (Intrathecal) timing of Sufentanil?

A

Peak CSF (epidural): 6 minutes

Peak Plasma (epidural): <5 minutes, similar to IM

Intrathecal/CSF levels: Minimal

477
Q

Peak CSF (epidural), Peak Plasma (epidural) and Peak CSF (Intrathecal) timing Morphine?

A

Peak CSF (epidural): 1-4 hours

Peak Plasma (epidural): 10-15 minutes, similar to IM

Peak CSF/Intrathecal levels: 1-5 hours

478
Q

Dose dependent side effects of neuraxial opioids? (8)

A
  1. Pruritus
  2. N/V
  3. Urinary retention in males
  4. Depression of Ventilation
  5. Sedation
  6. CNS excitation
  7. Herpes simplex labialis viral reactivation 2 to 5 days after epidural
  8. Neonatal morbidity
479
Q

Describe pruritus when it comes to neuraxial opioids

A
  1. Most common, especially in OB
  2. Face, neck, upper thorax
  3. Cause: Cephalid migration to trigeminal nucleus
  4. Treatment: Naloxone, antihistamines, gabapentin
480
Q

Why do we see urinary retention in males with neuraxial procedures?

A

Interaction at sacral spinal cord causes PNS outflow

481
Q

Ventilation depression with neuraxial opioids facts (4)

A
  1. Early depression is classified as within 2 hours
  2. Delayed depression is classified as 6 to 12 hours
  3. Most reliable sign is depressed LOC secondary to hypercarbia
  4. Treat with naloxone 0.25 mcg/kg/hr IV
482
Q

What CNS excitation effects do we see with neuraxial anesthetics?

A

Tonic skeletal muscle rigidity like seizure activity

483
Q

What would be a key sign telling you that the tonic seizure-like activity a patient experienced post neuraxial anesthesia might be caused by the local anesthetic used?

A

Patient reported a metallic taste beforehand

484
Q

Describe non-opioid anesthesia

A

Non-opioid anesthesia refers to the anesthetic technique of using medications to provide anesthesia and post-operative pain relief in a way that does not require opioids

485
Q

5 factors in considered to be stimulations of pain

A
  1. Sensation
  2. Transduction
  3. Transmission
  4. Perception
  5. Modulation
486
Q

Pharmacokinetics of Gabapentin (6)

A
  1. Structural analogue of GABA that does not have GABA activity
  2. Binds to Ca++ channels to inhibit excitatory neurotransmitter release
  3. More lipid soluble
  4. Not protein bound
  5. No drug-drug interactions
  6. Re-dosing required due to brief elimination half-time
487
Q

3 uses of Gabapentin

A
  1. Partial seizures in adults/children
  2. Chronic pain syndromes such as diabetic neuropathy
  3. Decrease pain scores, probably through synthesis of GABA
488
Q

Dose, MOA and contraindications to Gabapentin

A
  1. Dose: 300-1200mg PO 1-2 hours prior to OR (reduce in elderly)
  2. MOA: GABA analogue
  3. Contraindications: Myasthenia Gravis, myoclonus
489
Q

7 SE associated with Gabapentin

A
  1. Somnolence
  2. Weight gain
  3. Abrupt Withdrawal in seizure pts causes seizures
  4. Constipation
  5. Fatigue
  6. Ataxia
  7. Vertigo
490
Q

Where is COX 2 expressed?

A

sites of injury

491
Q

Is COX 1 or COX 2 pathophysiologic? physiologic?

A

COX 1 is physiologic and COX 2 is pathophysiologic

492
Q

What does cyclooxygenase catalyze the synthesis of?

A

PGE

493
Q

What properties do NSAIDS have?

A

Analgesic, anti-inflammatory, antipyretic

494
Q

7 effects of NSAIDS

A
  1. Decrease activation of peripheral nociceptors
  2. No addictive potential
  3. Preemptive analgesia
  4. Abscence of ventilatory depression
  5. Less nausea and vomiting
  6. Long duration of action
  7. Absence of cognitive effects
495
Q

Compare Cox 2 inhibitors to nonsepecific inhibitors

A
  1. Comparable analgesia
  2. Lack of platelet effects
  3. May be associated with decreased GI effects
  4. Possible increase in MI and CVA
496
Q

Dose and peak time of celecoxib (celebrex) a cox2 inhibitor

A
  1. Dose: 200 to 400 mg PO QD
  2. Peak: 3 hours
497
Q

What properties does acetaminophen have?

A

No significant anti-inflammtory property, but does have analgesic and antipyretic effects

498
Q

MOA and contraindications of Acetaminophen

A
  1. MOA: Reduction in prostaglandin synthesis
  2. Contraindications: Hepatic dysfunction
499
Q

Dose, peak time and duration of Acetaminophen

A
  1. Dose: 1 gram IV
  2. Peak times: PO is 1 to 3 hours, IV is 30 minutes to 1 hour
  3. Duration: 6 to 8 hours
500
Q

MOA and Contraindications to Ketorolac (Toradol)

A

MOA: Inhibits PG synthesis by inhibiting COX 1 and 2

Contraindications: Severe renal impairment, significant risk for bleeding, CAD, CABG, pregnancy, decrease does in elderly

501
Q

Dose and peak effect of Ketorolac

A

Dose: 30mg or 60mg IM Q6 (1/2 dose in elderly)

Peak effect: 45 to 60 minutes IV

502
Q

Analgesic Property and GI/Respi/Cardiac effects of Ketorolac

A

Potent anaglesic property, but only moderate anti-inflammatory, may potentiate opioids

No effect on the biliary tract, and no depression of respiratory or cardiac function

503
Q

Ibuprofen MOA and contraindications

A

MOA: Anti-inflammatory, analgesic, and antipyretic inhibition of COX 1 and COX 2

Contraindications: Allergies to NSAIDS, CABG, bleeding ulcers

504
Q

Dose, peak effect time and excretion of Ibuprofen

A

Dose: 400 to 800 mg IV over 30 minutes Q6H PRN (4200 mg daily max)

Peak effect: 1 to 2 hours

Excretion: Urine and Bile

505
Q

Dose of Lidocaine and patient populations to monitor

A

Dose: 1-2mg/kg IV bolus over 2 to 4 minutes

1-2mg/kg/hour gtt terminated 12-72 hours

Carefully monitor cardiac, hepatic and renal dysfunction patients

506
Q

Dose dependent effects of lidocaine

1-5mcg/ml

5-10mcg/ml

10-15mcg/ml

15-25mgc/ml

>25mg/ml

A
  1. 1-5mcg/mL: analgesia
  2. 5-10mcg/mL: numbness, tinnitus, skeletal muscle twitching, systemic hypotension, myocardial depression
  3. 10-15mcg/mL: seizures and unconsciousness
  4. 15-25mcg/mL: Apnea, coma
  5. >25mcg/mL: Cardiovascular depression
507
Q

What effects and what receptors does magnesium show?

A

Anti-nociceptive effects

NMDA receptor antagonist

508
Q

What does magnesium regulate?

A
  1. Ca++ access into cell and actions within cell
  2. Neurotransmission
  3. Cell signaling
  4. Enzyme Function
509
Q

Contraindications to magnesium administration?

A

Myasthenia gravis and renal failure

510
Q

Dose of magnesium?

A

50mg/kg IV preop then 8mg/kg/hr intraoperatively

(intraop dose significantly decreases fentanyl requirement)

511
Q

What class of drug is odansetron?

A

5-HT3 antagonist approved for chemo induced nausea and vomiting

512
Q

What is the plasma half life of ondanseton? what dose do we use?

A

4 hours and we use a 4-8mg IV dose

513
Q

What do corticosteroids increase the effectiveness of?

A

5 HT3 antagonists and droperidol

514
Q

What dose of dexamethasone do we use and what is the onset?

A

Dose is 8 to 10mgs, there is a delay in onset of 2 hours

515
Q

What is the method of action of dexamethasone?

A

Anti-inflammatory, inhibition of phospholipase and cytokines and stabilization of cellular membrane

516
Q

What adverse side effect would we see from adminsitration of corticosteroids?

A

Perineal burning/itching

517
Q

TEAMHealth dosing of magnesium?

A

30 to 50mg/kg IV loading dose, can continue 8 to 10mg/kg/hour; be prepared to treat bradycardia or hypotension

518
Q

TEAMHealh dosing of lidocaine?

A

1.5mg/kg at induction then 1 to 2 mg/kg/hr for 24 to 48 hours

519
Q

TEAMHealth formula for ketamine?

A

0.25 to 0.5 mg/kg pre incision then 0.25 to 0.5mg/kg intraop; stop 1 hour prior to end then 0.12mg/kg/hr for 24 hours postop or 5mg boluses keeping doses between 0.3 to 0.5mg/kg/hr

Advanced Pharmacology 2 (5 decks)

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