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Anesthesia Pharmacology > Lecture 8 (Exam 2) - Opioid Agonists > Flashcards

Lecture 8 (Exam 2) - Opioid Agonists Flashcards

1
Q

Opioids ____ CBF and possibly also ____.

⚠️Why should you proceed with caution with opioids and head injury?

A

⬇️ CBF, ICP

Bc opioids have some of the same effects a brain injury can cause. (Mask the injury); can affect wakefulness, can have miosis, ⬆️ PaCO2 levels and cross the BBB.

slide 16

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2
Q

What is a common S/E that opioids share with our induction agents?

A

Myoclonus! (with large doses)

slide 16

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3
Q

What is a severe S/E of opioids involving the chest & abdominal walls?

How do you treat this?

A

Skeletal muscle Rigidity!!! -makes it harder to ventilate them (fighting vent)
*have you ever fast pushed fentanyl?? (it will cause this)

Treat with: Naloxone or muscle relaxer (if you’re not gonna extubate) 😎

slide 16

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4
Q

Your pt is having an ERCP. You fuck up and accidentally give an opioid to help them out. (we usually don’t)
This is why:

A common GI S/E of opioids is spasm of the Sphincter of _____.
This happens 99% with ______.
To treat the spasm, you give Nalaxone but you can also give incremental doses of _________ up to 2mg IV to not reverse the opioid effects.
If your patient had angina and was spasming, you know to give _____ bc it will help both. 😊

A

Sphincter of Oddi
Fentanyl 99%
Glucagon 2mg IV
Angina, too? NTG will help both the CP and spasm 😎

slide 17

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5
Q

Other than spasm of the Sphincter of Oddi, other GI S/E of opioids include? (💩, 🤮)

A

Delayed gastric emptying, n/v (from stim of the CTZ-chemoreceptor trigger zone), ⬆️ GI secretions, & constipation.

slide 17

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6
Q

Misc Opioid S/E

GU:
Cutaneous:
Placental:

A

urinary urgency!
flushing - histamine release. 🥵
neonatal depression, dependence 👶🏻

*basically a pregnant women’s worst nightmare - gotta pee, get really hot & flushed and now their baby is an addict.

Slide 18

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7
Q

Your patient is now requiring increased drug doses after about 25 days taking PO morphine for chronic pain. This is called ______?

Opioid receptors become desensitized & ⬇️ in number simultaneously. This is called ________?

T/F? Cross-tolerance can develop btwn all opioids?

A

Tolerance! (or physical dependence)

Downregulation

True!

Slide 19

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8
Q

In the ascending tract of pain:

How do opioids hyperpolarize neurons to make it less likely for them to fire an action potential?

How do they work on presynaptic neurons to inhibit release of NTMs?

A

-opioids promote K+ conductance on second order neurons = hyperpolarization.

-inhibit Ca++ conductance

slide 20 (video), pg. 390 Stoeltings

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9
Q

In the descending tract of pain:

What area in the brainstem has heavy Opioid receptors that can inhibit pain signaling via the medulla to the spinal cord?

A

PAG (periaqueductal gray)

Slide 20 (video)

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10
Q

In the CNS: opioids can reduce the emotional impact of pain by acting on regions such as the _______ _______ ______ to ⬆️ dopamine levels in areas like the nucleus accumbens (may lead to reinforcing qualities of the drug).

A

Anterior Cingulate Cortex

Slide 20 (video)

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11
Q

Which has a greater context-sensitive half-time, Fentanyl or Sufentanil?

A

Fentanyl
Slide 34

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12
Q

What is the analgesia dose for fentanyl?

A

1-2 mcg/kg IV
Slide 35

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13
Q

Induction dose for fentanyl?

A

1.5-3 mcg/kg IV 5 mins prior to induction
Slide 35

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14
Q

When giving fentanyl as an adjunct with inhaled anesthetics, what dose would you give?

A

2-20 mcg/kg IV
Slide 35

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15
Q

If using only Fentanyl for surgical anesthesia (Solo), what dose would be given?

A

50-150 mcg/kg IV
Slide 36

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16
Q

According to Lil Wayne, kids can also have fentanyl in the form of what?

A

A lollipop with the dose of 5 to 20 mcg/kg
Slide 36

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17
Q

A fentanyl patch dose can range from 75 to 100 mcg and has a steady delivery time of ….

A

18 hours
Slide 36

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18
Q

1 mg of PO Fentanyl is equal to how many mgs of Morphine?

A

5 mg
Slide 36

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19
Q

True or False: Fentanyl releases histamine

A

False - It does not
Slide 37

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20
Q

Fentanyl depresses which reflex, leading to bradycardia, decreased BP, and decreased cardiac output?

A

Carotid Sinus Baroreceptor
Slide 37

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21
Q

Fentanyl has synergistic effects with which two drugs discussed in lecture?

A

Benzos and propofol
Slide 38

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22
Q

How much does Fentanyl increase ICP?

A

6 to 9 mmHg
Slide 38

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23
Q

At which dose of fentanyl would you maybe get an EEG?

A

> 30 mcg/kg IV
Slide 38

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24
Q

Sufentanil is how many times more potent than fentanyl?

A

5 to 12 times
Slide 39

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25
Q

Where are the opioid receptors found in the brain?

A

Periaqueductal gray (PAG),
Locus ceruleus,
Rostral ventral medulla (RVM),
Hypothalamus

(Slide 10)

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26
Q

Sufentanil is 92.5% bound to which protein?

A

alpha-1-acid glycoprotein
Slide 39

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27
Q

Where are the opioid receptors found in the spinal cord?

A

Interneurons and primary afferent neurons in the dorsal horn (substantia gelatinosa).

(Slide 10)

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28
Q

Which has a larger Vd, Alfentanil or Sufentanil?

A

Sufentanil
Slide 39

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29
Q

Where are the opioid receptors found outside of the CNS?

A

Sensory neurons and immune cells.

(Slide 10)

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30
Q

How is Sufentanil metabolized?

A

Hepatic enzymes
Slide 39

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31
Q

What medications (discussed in class) can be used on opioid receptors that are found outside of the CNS?

A

Morphine and Ketorolac!
(Intraarticular morphine after knee surgery)
(NSAIDS like ketorolac can also be given through IV!)
(Slide 10)

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32
Q

What medications (discussed in class) can be used on opioid receptors that are found outside of the CNS?

A

Local anesthetics! They are directly applied for intense analgesia!
** With L&D some places (like florida) use sufentanil**

(Slide 10)

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33
Q

What are the effects, agonists, and antagonists of the Mu1 receptors?

A

Effects: Analgesia (supraspinal, spinal), Euphoria,
Low abuse potential, Miosis (pinpoint pupils), Bradycardia, Hypothermia, Urinary retention.

Agonists: Endorphins, Morphine, Synthetic Opioids

Antagonists: Naloxone, Naltrexone, Nalmefene

(Slide 11)

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34
Q

What are the effects, agonists, and antagonists of the Mu2 receptors?

A

Effects: Analgesia (spinal), Depression of ventilation, Constipation (marked)

Agonists: Endorphins, Morphine, Synthetic Opioids

Antagonists: Naloxone, Naltrexone, Nalmefene

(Slide 11)

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35
Q

What are the effects, agonists, and antagonists of the Kappa receptors?

A

Effects: Analgesia (supraspinal, spinal), Dysphoria, Sedation, Low abuse potential, Miosis, Diuresis,

Agonists: Dynorphins

Antagonists: Naloxone, Naltrexone, Nalmefene

(Slide 11)

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36
Q

What are the effects, agonists, and antagonists of the Delta receptors?

A

Effects: Analgesia (supraspinal, spinal), Depression of ventilation, Physical dependence, Constipation (minimal), urinary retention

Agonists: Enkephalins

Antagonists: Naloxone, Naltrexone, Nalmefene

(Slide 11)

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37
Q

Which receptor produces physical dependence?

A

Mu2 and Delta

(Slide 12)

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38
Q

What are the side effects of opioids on the cardiovascular system?

A
  1. Decreased SNS tone in peripheral veins!
    -Decrease in venous return, CO, & BP
    -Orthostatic hypotension & syncope
  2. Decreased BP
    -Due to Bradycardia or Histamine release!
    -Bradycardia is also due to direct inhibition of the SA node!
    -Morphine displaces histamine!

(Slide 13)

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39
Q

True or False!
Opioids + N20 or benzo = CV depression (CO & BP).

A

True!

(Slide 13)

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40
Q

What are the benefits we get from the the side effects on the cardiovascular system caused by opioids?

A

Cardioprotective from myocardial ischemia!

(Slide 13)

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41
Q

If your patient is being sewn up, would you give a 10 mg bolus of morphine or give it in increments?
Why?

A

Increments!
A bolus will displace a lot of histamine, especially if they are predisposed to it.
Giving the morphine in increments will allow you to have better control of BP and reduce the risk of a large histamine release causing hypotension. Also you will have a happy patient and a happy PACU nurse.

(Slide 13 and Dr Castillo’s Pearls of Wisdom)

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42
Q

You accidentally give your patient a large bolus of morphine while they are stitching him up towards the end of the case. You notice your patient is now bradycardia and hypotensive, what drugs would you want to give and in what order?

A

To counter act the bradycardia from narcotics you first give atropine,

If atropine doesn’t work then you can give them EPI! Not the whole 1 mg like in a code, a lesser amount! You can dilute the 1 mg dose in a 10 or 20 mL syringe and give it 1 cc at a time!

Vasopressin (40 units) would be up next! Same thing, dilute it with 10 mL and give it 0.5 to 1 cc at a time. Depending on how bad the hypotension is!

(Slide 13 and Dr Castillo’s Pearls of Wisdom)

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43
Q

What are the side effects of opioids with ventilation?

A

Decreased responsiveness of ventilation centers to CO2!

-Increase in resting PaCO2 (Shift to the right)! End tidal will need to be higher than 35-45 [~50] for the patient to start breathing!

-Going up to 60 PaCO2 will cause CO2 narcosis and the patient will be in a deeper sleep and be harder to wake up!

-Effects on mu2 receptors will cause a change in rhythm (decreased rate with compensatory increase in tidal volume), pauses, & periodic breathing!

(Slide 14)

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44
Q

What are signs of opioid overdose?

A

APNEA, Miosis, Hypoventilation & Coma

(Slide 14)

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45
Q

How does Physostigmine help a patient that is overdosed with opioids during a case?

A

It increases CNS levels of Acetylcholine (Ach) which antagonize ventilatory depression but not analgesia! You give it in increments.

(Slide 14)

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46
Q

If you overdose a patient with a volatile anesthetic, how can giving a narcotic be beneficial?

A

Volatile anesthetics cause fast and shallow breaths. Narcotics decrease rate with compensatory increase in tidal volume.
The increase in tidal volume can help blow out volatile anesthetics.
(Surfing the curve -Castillo)

(Slide 14 and Castillo’s Pearls of Wisdom)

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47
Q

What two drugs presented in class cause cough suppression and do not provocate the cough reflex?

A
  1. Codeine (Opioid)
  2. Dextromethorphan: no analgesia (It is a non-opioid derivate of morphine)

(Slide 14)

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48
Q

What should you be concerned with when giving a pre-induction dose of narcotics?

A

Reflex coughing!
(Make sure you have your suction! You do not have to get ready if you stay ready!)

(Slide 14)

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49
Q

What causes the elimination 1/2 time of Morphine longer?
And what organ dysfunction contributes to this?

A

Longer with morphine-3-glucuronide metabolites

Renal dysfunction

(slide 28)

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50
Q

Does Morphine exhibit a greater analgesic potency and slower speed of offset more In women or men?

A

Women

(slide 28)

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51
Q

Which 4 pt populations should we be more careful in administering Morphine due to its increased effects?

A
  • women
    -neonates
    -elderly (due to decreased kidney function and protein levels)
    -renal dysfunction pts
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52
Q

Prolonged depression of ventilation (>7 days) days has been observed in patients with renal failure after the administration of what medication?

A

Morphine

-pg. 407

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53
Q

Morphine causes hypoxic sensitivity decrease in women or men more?

A

Women
(morphine decreases the slope of the ventilatory response to carbon dioxide in women, whereas in men, there was no significant effect)

-pg. 407

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54
Q

Meperidine (AKA pethidine) is an agonist at what 2 opioid receptors?

A

agonist at µ and κ opioid receptors

(slide29)

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55
Q

What are the 4 analogues of Meperidine?

A
  • Fentanyl
  • Sufentanil
  • Alfentanil
  • Remifentanil

(all of the “nils”)
(slide 29)

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56
Q

What 2 drugs and 3 groups is Meperidine structurally similar

A
  • Lidocaine: tertiary amine, ester group, & lipophilic phenyl group
  • Atropine

(slide 29)

57
Q

Meperidine administered intrathecally blocks what electrolyte channels to a degree? AND due to this, is comparable with what medication?

A

Sodium channels
Lidocaine

(slide 29, & pg. 408)

58
Q

Structurally, Meperidine is similar to WHAT medication causing antispasmodic effect on smooth muscle.

A

Atropine

(slide 29 & pg. 408)

59
Q

Meperidine (AKA pethidine) was discovered in what year?

A

1939

(slide 29)

60
Q

Compared to Morphine, Meperidine is what fraction as potent?

A

1/10th as potent as morphine.

(making it a shorter acting opioid agonist than morphine.)

(slide 30)

61
Q

For Meperidine, what is the:
Dose:
Duration:
Uses:
Effects:
Elimination 1/2 time:

A
  • 12.5mg
  • 2-4 hrs
  • Intrathecal, IM for postop analgesia/ post-op shivering (κ receptors; potent agonist at α2 receptors)
  • Effects cause sedation, euphoria, N/V, depression of ventilation.
  • E 1/2 time: 3-5 hrs (35hrs with renal failure)

(slide 30/31)

62
Q

For Meperidine, what is the:
Hepatic 1st pass:
Metabolism:
Protein Bound %:
Elimination:

A
  • 80%
  • 90% Hepatic –> into normeperidine (metabolite)
  • 60% (elderly considerations)
  • Renal elimination (urinary excretion)
63
Q

In elimination for Meperidine, what can speed up this process?

A

acidic urine.

(elimination route is pH dependent. acidification of the urine can be considered in an attempt to speed the elimination of meperidine)

(slide 30)

64
Q

In equianalgesic doses, does Meperidine produces equivalent sedation, euphoria, nausea, vomiting, and depression of ventilation as to Morphine?

A

Yes!

(-pg. 408)

65
Q

WHAT medication is the only opioid considered adequate for surgery when administered intrathecally, owing to its ability to block WHAT type of electrolyte channels?

A

Meperidine
Sodium

(-pg. 409)

66
Q

(extra)
Evidence for the role of κ receptors in the antishivering effects of Meperidine post-op, contributes to the failure of WHAT drugs. ability to completely inhibit this effect?

A

Naloxone

(-pg. 410)

67
Q

Meperidine Toxicity can cause what effects?

A

delirium (confusion, hallucinations) myoclonus & seizures

(slide 30)

68
Q

What are the major side effects of Meperidine?

A

tachycardia & mydriasis with dry mouth, (-) inotropy, serotonin syndrome (MAOIs & TCAs), impaired ventilation, crosses placenta,
Withdrawal symptoms develop more rapidly > than Morphine
( note- Meperidine is not used in high doses because of significant (-) cardiac inotropic effects plus due to its histamine release)

(slide 31)

69
Q

What are 2 other medications that have a greater effect than Meperidine for post-op shivering?

A
  • Clonidine (also agonist at α2 receptors)
  • Butorphanol (a κ receptor agonist-antagonist)
70
Q

What is Meperidine’s active metabolite?

A

Normeperidine

(slide 31)

71
Q

Meperidine (in comparison to Morphine) is NOT useful in the treatment of what 3 conditions?

A

-diarrhea
- as a cough suppressant
- during a bronchoscopy (r/t its lack of antitussive activity)

72
Q

Per Dr. Castillo, is it better to give more or less of Meperidine?

A

LESS!

73
Q

Fentanyl is what range x more potent than morphine?

A

75-125 times more potent than morphine

(slide 32)

74
Q

In 1960’s what was Fentanyl’s trade name?

A

Sublimaze

(slide 32)

75
Q

how long is the Blood: Brain Effect-site Equilibration of Fentanyl?
What’s its distribution qualities?

A

6.4 min
Potent, rapid onset, very lipid soluble

(more lipid soluble than Morphine)

(slide 32)

76
Q

What’s Fentanyl’s Lung first- pass %?

A

75%

(slide 32)

77
Q

What’s Fentanyl:
Metabolism:
Principal metabolite:
Excretion:
Vd:

A
  • hepatic P450 enzymes (CYP3A)
  • Norfentanyl
  • Kidneys
  • Large
    IV (<5 mins 80% is gone)
    highly vascular tissues
     inactive tissue sites
    Elderly? = No change.
    Hepatic cirrhosis? = not prolonged.
78
Q

What are the Side effects of Remifentanil?

A
  1. Seizure like activity
  2. N/V
  3. Depression of ventilation
  4. Decreased BP and HR
  5. Hyperalgesia d/t previous acute exposure to large opioid doses and tolerance (due to mu1 receptors)
    Slide 46
79
Q

Morphine derivative, Hydromorphone is ___more potent and _____hydrophilic than morphine.

A

5X more potent and less hydrophilic
(less hydrophilicity leads to faster onset of analgesia)
Slide 47

80
Q

What is the dosage for Hydromorphone?

A

0.5mg IV up to 1 - 4 mgs total.
Re-dose q4hrs.
Slide 47

81
Q

What are the uses and side effects of Hydromorphone?

A

Similar to morphine but no histamine release and has active metabolite.
(It evokes more sedation and less euphoria than morphine)
Slide 47

82
Q

How is codeine given to the patient?

A

PO or IM but no IV
Slide 48

83
Q

What is elimination half time of codeine and where does the metabolism occurs?

A

3 to 3.5 hours elimination half time and metabolism occurs in liver.
Slide 48

84
Q

What is the dosage of codeine for cough suppressant and analgesia?

A

Cough suppressant: 15 mg
Analgesia: 60mg (120mg =10 mg of morphine)
Slide 48

85
Q

What are the side effects of codeine?

A

Physical dependence, minimal sedation, N/V, constipation, dizziness, and histamine induced hypotension.
Slide 48

86
Q

What are the other opioids which are listed in slide 49?

A

Oxymorphone
oxycodone
methadone
Propoxyphene
Tramadol
Heroin
(methadone is used in opioid withdrawal and chronic pain)
Slide 49

87
Q

Tramadol is ______potent than morphine and interacts with _______.

A

5-10x less potent than morphine
Coumadin
Slide 49

88
Q

what are the receptor sites and dosages of Tramadol?

A

Receptor site: mu with weak k and delta
PO: 3mg/kg
Slide 49

89
Q

Which opioid when it came out said to have no addiction?

A

Heroin
(Great potential for dependency, less N/V, more rapid onset–> we do not use in clinical practice)
slide 49

90
Q

Based on Table 7-4, which pharmacokinetic category best describes onset of action?
A. Effect site equilibration
B. Protein binding
C. Elimination half time
D. pK

A

A. Effect site equilibration
not in powerpoint
Make sure you remember slide 50

91
Q

Fentanyl has effect-site equilibrium time of 6.8 min and remifentanil has effect site equilibrium of 1.1, which one is fast onset?

A

Remifentanil is quick on and quick off.
Slide 50

92
Q

What’s considered our mainstay of modern perioperative care and pain management?

A

Opiates

(slide 5)

93
Q

What movie was the poppy plant apparently popularized?
HINT: It has flying monkeys and Castillo HATES flying monkeys

A

Wizard of Oz

Fun fact: Toto (the dog) made more money than the any of the actors who played the Munchkins

(Castillo)

94
Q

Greek definition of “Narcotic”

A

Stupor; which has the potential to produce physical dependence

(slide 6)

95
Q

Opioids are …

A

ALL Exogenous substances

(slide 6)

96
Q

Your pt admits they use heroin and their last dose of it was 6 hrs ago. Should you be concerned about withdrawal symptoms at this point?

A

Yes! The onset of withdrawal for heroin can start 6 hrs from last dose. It’s very important to know what opiates (legal and illegal) pt is on, and then know times for when withdrawal symptoms can occur. (Slide 21)

97
Q

What are the opioid agonists from Table 7-1?
HINT: there’s 16 of them. Name them all. JK. Just name 15 of them.

A

Morphine; Morphine-6-glucuronide; Merperidine; Sufentanil; Fentanyl; Alfentanil; Remifentanil; Codeine; Hydromorphone; Oxymorphone; Oxycodone; Hydrocodone; Propoxyphene; Methadone; Tramadol; Heroin

(slide 6)

98
Q

Your pt got some illegal fentanyl, and now they’re at the hospital. They state they last took a dose 2 hrs ago. Is it possible for them to start withdrawing this soon?

A

Yes! The onset of fentanyl withdrawal is 2 - 6 hrs, which is the same for meperidine. For morphine and heroin, 6 - 18hr for onset of withdrawal symptoms. (Slide 21, Table 7 - 3)

99
Q

Phenanthrenes include which meds?

A

Thebaine, Codeine, and Morphine

(My Phen’s and I love watching TCM [Turner Classic Movies])

(slide 7)

100
Q

Higher doses of intra op opioids can cause (more or less) post op pain.

A

Per an anesthesiology news article, “higher doses of intra op opioids causes greater post op pain.” (Slide 22)

101
Q

What is the gold standard of opioids?

A

Morphine. Fun fact: this is named after Morpheus, the Greek god of dreams. (Slide 25)

102
Q

Benzylisoquinolines include which meds?

A

Papaverine & Noscapine are both Benzylisoquinolines

Easy way to remember this structural name is by starting out saying “Bbbbb” and then have a seizure and you should produce a word close enough

(slide 7)

103
Q

Morphine effects?

A

Analgesia, euphoria, sedation, diminished ability to concentrate, nausea, feeling of body warmth, heaviness of extremities, dryness of mouth, pruritis (slide 25)

104
Q

Is morphine better for treating dull pain or sharp pain? What other types of pain is morphine ideal for?

A

Morphine is better for treating dull pain. Can also treat visceral, skeletal muscle, joint, integumental, and intermittent pain. (Slide 25)

105
Q

Morphine IV vs IM peak times? Dose? Onset? Duration?

A

Morphine IV and IM have the same dose, onset, and duration. For dose: 1 - 10 mg. Onset: 10 - 20 min. Duration: 4 - 5 hrs.

For IV Peak time: 15 - 30 min.
IM peak time: 45 - 90 min.
(Slide 26)

106
Q

__________ is used as a direct ________ vaso_______.

This drug is the response drug given in the event of what med accidentally injected into artery?

A

Papaverine; arterial; vasodilator

Sodium thiopental, aka pentathol

(Castillo)

107
Q

What is the bioavailability of oral morphine?

A

Bioavailability = 75%. 25% is metabolized in the liver on first pass. (Slide 26)

108
Q

How is morphine metabolized?

A

Conjugation with glucoronic acid in hepatic and extrahepatic sites. (Slide 27)

109
Q

What are the 2 metabolites of morphine? Which is active and which is inactive?

A

Morphine 3 glucuronide = inactive metabolite, majority of morphine turns into this (75-95%)

Morphine 6 glucoronide = active metabolite, can contribute to resp. depression
(Slide 27)

110
Q

What effect will occur when morphine is given to a pt in renal failure?

A

You will see prolonged respiratory depressive effects. (Slide 27)

111
Q

What 3 centers in the brain are opioid receptors located?

These brain centers are originations of what type of pathway?

A

Thalamus
Periaqueductal gray
Locus coeruleus

Descending inhibitory

(Professor Youtube video on slide 8)

112
Q

Mu receptors are responsible for including but not limited to:

A

analgesia, euphoria, sedation, respiratory depression, ⬇️ peristalsis in the gut –> constipation

(PYT vid on slide 8)

113
Q

Delta receptors in the brain may have ______________ effects and are also located in the ___ and cause ⬇️ __ secretions

A

hallucinogenic; gut; gastrointestinal

(PYT slide 8)

114
Q

Kappa receptors mediate _________ by reducing ________ release

A

dysphoria; dopamine

(PYT slide 8)

115
Q

Pain signals are transmitted from the periphery to the CNS by way of light myelinated _-_____ fibers and/or non-myelinated _ fibers which make up the _______ neuron in the __________ __________ of the spinal cord.
The _______ neuron synapses with a _________ neuron that carries the pain signal to the brain.

A

A-delta; C;
primary; substantia gelatinosa

primary; secondary

(slide 8)

116
Q

In the substantia gelatinosa, _________ and _________ _ are __________ pain associated neurotransmitters released from the primary neuron to bind to receptors on the secondary neuron causing epsp’s, otherwise known as ________________________________ in the membrane of the secondary neuron leading to an AP (action potential) sent down the secondary neuron to the brain.

A

Glutamate; Substance P

excitatory; Excitatory postsynaptic potentials

(slide 8)

117
Q

Activation of ____’s by _______ in the membrane of the axon terminal cause closure of __++ channels leading to ____ release of excitatory neurotransmitters like Substance P and Glutamate from the axon of the ________ neuron.

A

GPCR’s; opioids
Ca; less
primary

(slide 8)

118
Q

⬇️ release of excitatory NT (neurotransmitters) from the primary neuron (r/t opioids) leads to what effects?

A

reduction in release of excitatory NT’s –> less excitation of secondary neuron;
hyperpolarization and a ⬇️ in the AP frequency –> decreasing pain signals sent to the brain

(slide 8)

119
Q

opioids bind to opioid __ receptors in the membrane of the _________ (aka cell body) of secondary neurons and cause _______ of _+ channels causing hyperpolarization of the secondary neuron, which decreases pain AP frequency causing ____ pain signals to be sent to the brain.

A

Mu; dendrite
opening; K

less

(slide 8)

120
Q

What does Castillo love to shove down our throats?

A

Pictures, Graphs, and Diagrams
So here’s another one to choke on

(slide 8)

121
Q
A

The answer is C

(slide 8)

122
Q

Which of the following is NOT an opioid receptor?
A. Mu
B. Sigma
C. Delta
D. Kappa

A

B

(slide 8)

123
Q

Which of the following locations for opioid receptors is NOT in the brain?
A. Periaqueductal gray
B. Locus coeruleus
C. Substantia gelitanosa

A

C - (it’s in the spinal cord)

(slide 8)

124
Q

Which of the following is NOT a therapeutic effect or side effect of opioids?
A. analgesia
B. diarrhea (aka the skitters)
C. respiratory depression
D. pupillary constriction
E. antidiuresis

A

B

(slide 8)

125
Q

Agonists at specific opioid receptors at pre and postsynaptic sites in the CNS are also activated by …?
(HINT: there’s 3)

A

Enkephalins, Endorphins, and Dynorphines

Castillo called them our “endogenous opioids”

(slide 9)

126
Q

Opioids cause presynaptic inhibition of what?
(HINT: there’s 4)

A

acetylcholine, dopamine, norepi, and substance P

(slide 9)

127
Q

Presynaptic inhibition of ACh, dopamine, norepi, and substance P causes what?
(HINT: there’s 4)

A
  • ⬆️ K+ conductance (hyperpolarization)
  • Ca++ channel activation
  • ⬇️ neurotransmission
  • pain modulators or anti-nociceptive (?)

(slide 9)

128
Q

Why is a combo of spinal LA with opioids beneficial?

A

Spinal LA STOPS neurotransmission up to the duration of the LA, while Opioids only ⬇️ neurotransmission

(Castillo)

129
Q

What is the analgesia dose and the induction dose of Sufentanil?

A

Analgesia: 0.1 - 0.4 mcg/kg IV
Induction: 18.9 mcg/kg IV

Slide 40

130
Q

Alfentanil is _________ potent than fentanyl and the onset is _______ than Fentanyl and Sufentanil.

A

1/5th less
1.4 minutes and >

Slide 41

131
Q

Alfentanil doses for:
Induction laryngoscopy:
Induction alone:
Maintenance:

A

Induction laryngoscopy: 15 - 30mcg/kg IV
Induction alone: 150 - 300mcg/kg IV
Maintenance: 25 - 150 mcg/kg/hour IV with inhaled anesthetics

Slide 42

132
Q

What is different about Remifentanil? (think propofol, etomidate, Succ)

A

It is hydrolyzed by nonspecific plasma and tissue esterases due to its ester structure.
Rapid onset and offset
Lack of accumulation

Slide 43

133
Q

Is Remifentanil dosed with ABW or IBW?

A

IBW

Slide 44

134
Q

Remifentanil:
Peak Effect:
Clearance:
Plasma Steady State:
Elimination 1/2 time:

A

Peak Effect: 1.1 minutes
Clearance: 3L/min
Plasma Steady State: @ 10 minutes
Elimination 1/2 time: 6.3 minutes

Slide 44

135
Q

Remifentanil Clinical doses:
Induction:
Maintenance:

A

Induction: 0.5 - 1mcg/kg IV over 30-60 seconds
Maintenance: 0.25 - 1mcg/kg IV or 0.05 - 2mcg/kg/min IV

Slide 45

136
Q

What is important to remember when stopping a dose of Remifentanil?

A

Very short action so we need to give a longer acting pain medication before stopping to keep our patients pain under control.

SLide 45

137
Q

You’re pre-op evaluating a pt and prepping your care plan. Your pt admits to significant use of opioid abuse. What are some alternative pain management therapies mentioned by Castillo?

A

ERAS (Enhanced Recovery After Surgery) multimodal analgesia

effort to avoid opioids as much as possible

(slide 4)

138
Q

memorize

A

memorize

Anesthesia Pharmacology (20 decks)

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