*Opioid Agonist-Antagonists & Antagonists (Exam II) Flashcards
(75 cards)
1
Q
What is the primary indication for opioid agonist-antagonists?
A
Used if unable to tolerate full agonist
S4
2
Q
Which receptors that Opioid Agonist-Antagonists binds to and their effects?
A
µ receptors: partial effect (agonist) or no effect (competitive antagonist)
Κ and δ receptors: partial effect (agonist)
S6
3
Q
Name the four advantages of Opioid Agonist-Antagonists.
A
- Analgesia
- Less respiratory depression
- Low dependence potential
- Ceiling effect (prevents ODing)
S6
4
Q
How potent is Pentazocine?
A
1/5 as potent as Morphine
S7
5
Q
What receptors does pentazocine bind to?
What type of activity does it exhibit?
A
- κ & δ receptor
-Agonist effects with weak antagonist activity
S7
6
Q
What is Pentazocine antagonized by?
A
Naloxone
S7
7
Q
What is the elimination 1/2 time of Pentazocine?
A
2 - 3 hours
S7
8
Q
How is Pentazocine excreted?
A
Glucuronide conjugates in the urine.
S7
9
Q
What is the chronic pain dose of Pentazocine?
What dose and route would be equivalent to Morphine 10mg?
A
- 10 - 30mg IV or 50 mg PO
- 20-30mg IM= 10mg Morphine
S8
10
Q
What is the epidural analgesia duration of Pentazocine?
A
Shorter duration < Morphine
S8
11
Q
What are the side effects of Pentazocine?
A
- sedation
- diaphoresis
- dizziness
- dysphoria (high doses)
- increased HR, BP, PA bp, LVEDP
S8
12
Q
Which opioid agonist-antagonist crosses the placental barrier causing fetal depression?
A
Pentazocine
S8
13
Q
What type of drug is Butorphanol?
A
Agonist 20x and antagonist 10x to 30x > Pentazocine
S9
14
Q
What receptors does Butorphanol bind to?
A
- κ = analgesia & anti-shivering
- μ (low)
- σ (low)
S9
15
Q
Sigma (σ) receptors are associated with what side effect?
A
Dysphoria
S9
16
Q
2 to 3 mg of butorphanol is equivalent to _____ mg of morphine.
A
10
s9
17
Q
By what route is butorphanol rapidly and completely absorbed?
A
Intramuscular
S9
18
Q
Where is Butorphanol excreted?
A
Bile > urine
S10
19
Q
What are the side effects of Butorphanol?
A
- sedation
- nausea
- diaphoresis
- dysphoria
- depression of ventilation
- withdrawal symptoms occur
- increased BP, PA BP, & C0
S10
20
Q
What is the caution with Butorphanol?
A
difficult to use with another opioid agonist
S10
21
Q
What receptors does Nalbuphine bind to?
How potent is it?
A
μ receptor agonist that is equipotent to Morphine.
S12
22
Q
Where is Nalbuphine metabolized?
A
Liver
S12
23
Q
What is the elimination 1/2 time of Nalbuphine?
A
3 to 6 hours
S12
24
Q
What are the side effects of Nalbuphine?
A
- sedation
- dysphoria
- withdrawal symptoms
S12
25
What drug is an excellent choice for cardiac catheterization patients?
Why?
- **Nalbuphine**
- No increase in BP, pBP, HR or atrial filling.
## Footnote
S12*
26
Which agonist-antagonist has 50 times greater μ receptor affinity than morphine?
Buprenorphine
## Footnote
S13
27
Analgesic potency of ____ mg IM of Buprenorphone = 10 mg Morphine?
0.3 mg IM
## Footnote
S13
28
What is Buprenorphine's onset?
Duration?
- 30min onset
- 8 hour duration
## Footnote
S13
29
What is Buprenorphine's used for?
* Post op
* cancer
* renal colic
* MI
* epidural
## Footnote
S13
30
Which two drugs have resistance to Naloxone?
- Buprenorphine and Bremazocine.
## Footnote
S13 and S14
31
# Opioid Agonist-Antagonist
What are drug facts of Nalorphine?
* equally potent with Morphine
* Not used clinically: high incidence of dysphoria (σ receptors)
## Footnote
S14
32
# Opioid Agonist-Antagonist
What are drug facts of Bremazocine?
* **κ receptors 2x potent > Morphine**
* Naloxone = not effective as reversal (could be other receptors)
## Footnote
S14
33
# Opioid Agonist-Antagonist
What are drug facts of Decozine?
* *δ & µ:* analgesia, no CV
* **0.15 mg/kg IM**= Morphine
* *10 to 15 mg IM rapid* absorption
* Onset: **15 mins.**
## Footnote
S14
34
What are drug facts of Meptazinol?
* mu1 receptors
* **100 mg** = 8 mg Morphine
** Rapid onset
* Duration: **< 2 hrs**
* Protein binding: 25%
## Footnote
S14
35
Which drugs are pure μ-opioid receptor antagonists?
- Naloxone
- Naltrexone
- Nalmefene
| Competitive antagonist --> High affinity to opioid receptors
## Footnote
S18
36
What receptors is Naloxone effective on?
- μ, κ, δ (non-selective)
## Footnote
S19
37
What are the uses of Naloxone?
* opioid-induced depression in post op
* neonate* (from mom)
* opioid overdose
* detect dependence
## Footnote
S19
38
What **non-opioid** uses does Naloxone have?
- ↑ contractility for shock
- Antagonism of general anesthesia (at high doses)
39
What is the naloxone IV push dose?
Continuous infusion?
1-4 mcg/kg IVP
## Footnote
S20
40
What is the continuous infusion of Naloxone?
5 mcg/kg IV infusion
## Footnote
S20
41
What dose of naloxone is use for shock?
> 1mg/kg IV
42
What dose will cause epidural side effect of Naloxone?
0.25 µg/kg/hour IV
## Footnote
S20
43
How long does Naloxone last?
- 30 - 45 minutes
*Often needs redosing for overdoses*.
## Footnote
S20
44
What are the possible side-effects of naloxone?
- **Analgesia reversal**
- **N/V**
- ↑ SNS ( ↑ HR, BP, dysrhythmias, etc.)
## Footnote
S20
45
Where is Naloxone metabolized and the first pass effect?
metabolized in Liver (glucorinic acid)
1/5th PO Hepatic first pass
## Footnote
S20
46
What is the elimination 1/2 time of Naloxone?
60 to 90 mins
## Footnote
S20
47
What use does Naltrexone have?
How long does it last and how is it adminstered?
- EtOH
- Given PO (more effective) lasts for 24 hours.
## Footnote
S21
48
How does Nalmefene's potency compare to naloxone?
What is it's dose and max?
- Nalmefene = naloxone
- **15 - 25 mcg IV (max of 1 mcg/kg)**
## Footnote
S21
49
What is the elimination 1/2 time of Nalmefene?
10.8 hours
## Footnote
S21
50
What is Methylnaltrexone's use?
- Anti-emetic (antagonizes N/V from opioids)
- promotes gastric emptying
## Footnote
S22
51
What is Alvimopan and what is it used for?
Why can't it be used long term?
- μ-selective PO peripheral opioid antagonist for **post-op ileus**.
- CV problems long term
## Footnote
S22
52
Where is Alvimpan metabolized?
gut flora
## Footnote
S22
53
What are the abuse-resistant opioid formulations?
- **Suboxone** (buprenorphine + naloxone)
- **Embeda** (long-release morphine + naltrexone)
- **OxyNal** (oxycodone + naltrexone)
## Footnote
S23
54
What causes immunosuppression with Opioid use?
* Prolonged exposure to opioids
* abrupt withdrawal
| Less in short term opioid use
## Footnote
S24
55
What Opioids-Agonists have a significant effect on volatile anesthetics?
What do they do?
- Fentanyl & it's derivatives
- decrease the MAC of volatiles by 50% or greater.
## Footnote
S25*
56
Fentanyl 3 μg/kg IV 25-30 min prior to incision will have what effect on which volatile gasses?
50% MAC reduction for Isoflurane and Desflurane.
## Footnote
S25*
57
Which Opioid Agonist-Antagonists have an effect on MAC?
- Pentazocine (20%)
- Butorphanol (11% decrease)
- Nalbuphine (8% decrease)
## Footnote
S25
58
Where are receptors targeted with opioid neuraxial anesthesia?
Opioid receptors of the substantia gelatinosa.
## Footnote
S28*
59
Neuraxial Opioids can be used on what sites?
1. Epidural
2. Subarachnoid/Spinal/Intrathecal
## Footnote
S29*
60
What is general rule of dosing for epidural opioids?
- Dose = 5 - 10 x normal
## Footnote
S29*
61
Which Neuraxial Opioid drug has slower onset but longer duration?
Morphine
## Footnote
S29
62
Diffusion of opioids across the _____ ______ results in systemic absorption.
dura mater
## Footnote
S30*
63
Where can opioids be injected during an epidural that results in systemic absorption?
What should be done if this occurs?
- Epidural venous plexus
- Add epi to the infusion.
## Footnote
S30*
64
What is Cephalad movement (in regards to epidurals)?
Cephalad Movement = the movement of drug/injectate up the spinal cord towards the brain.
## Footnote
S31*
65
What drug attribute decreases cephalad movement?
Lipid solubility
## Footnote
S31
66
This drug exhibits much more cephalad movement than __________.
Why is this?
**Morphine > Fentanyl & Sufentanil**
- Fentanyl and it's derivatives are much more lipid soluble and thus exhibit less cephalad movement.
-More in spinal cord < remains in CSF and migrate cephalad
## Footnote
S31
67
What can cause cephalad movement? (besides characteristics of drugs themselves)
Coughing and/or straining
## Footnote
S31
68
When would *epidural admin/ CSF levels peak* for the following drugs:
- Fentanyl
- Sufentanil
- Morphine
- Fentanyl - **20min**
- Sufentanil - **6min**
- **Morphine - 1-4 hours**
## Footnote
S32*
69
When would *epidural admin/ plasma levels peak* for the following drugs:
- Fentanyl
- Sufentanil
- Morphine
- Fentanyl - **5-10 min**
- Sufentanil - **5 min or less**
- **Morphine - 10 - 15 min**
## Footnote
S32*
70
When would *intrathecal/cervical/CSF levels* peak for the following drugs:
- Fentanyl
- Sufentanil
- Morphine
- Fentanyl - N/A
- Sufentanil - N/A
- Morphine - 1 - 5 hours (due to cephalad movement)
## Footnote
S32
71
What is the most common side effect from neuraxial opioid administration?
Why does this occur?
- Pruritis
- Cephalad migration to trigeminal nucleus
| most common in OB
## Footnote
S33
72
What are the treatments for pruritis induced by neuraxial opioids?
- 10mg **Propofol**
- Naloxone
- Antihistamines
- Gabapentin
## Footnote
S33
73
Name the list (its a lot) of side effects that can occur with neuraxial opioid administration.
- Pruritis
- N/V
- Urinary retention
- Respiratory depression
- Sedation
- Skeletal muscle rigidity
- Herpes virus reactivation
- Neonatal effects.
## Footnote
S33 to S35
74
What sign would indicate respiratory depression from neuraxial opioid administration?
What is the treatment?
- ↓LOC from ↑CO₂
- **Naloxone 0.25 μg/kg/hr IV**
## Footnote
S34
75
If neuraxial opioids induced a reemergence of a herpes virus, how long would this occur after opioid administration?
- 2 - 5 days
## Footnote
S35
