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Analgesic Agents (Week2) Flashcards

1
Q

A-δ Fibers

A

(alpha delta)

Free (naked) nerve endings.

Myelinated

Diameter = 1–4 μm.

Transmit “first pain” or “fast pain”

Well-localized discriminative sensation (sharp, stinging, pricking).

Duration of pain coincides with duration of painful stimulus.

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2
Q

C Fibers

A

Free (naked) nerve endings.

Unmyelinated

Diameter = 0.4–1.2 μm.

Transmit “second pain” or “slow pain”

Diffuse and persistent burning, aching, throbbing sensation.

Duration of pain exceeds duration of stimulus.

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3
Q

The “fast” and “slow” pain pathways are activated in the periphery when _______

A

the free nerve endings of the A-δ and C fibers are stimulated (damaged)

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4
Q

_______ stimulate the same receptors that are stimulated by the body’s endorphins and enkephalins.

A

Opioids

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5
Q

Classes of Opioids

A
  • naturally occurring (ex: morphine, codeine)
  • semisynthetic (ex: buprenorphine)
  • synthetic (ex: fentanyl, sufentantil)
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6
Q

Clinical Uses of Opioids & Routes of Admin

A

Component of most anesthesia techniques

  • Reduce pain and anxiety
  • Decreased somatic and autonomic responses (e.g., airway manipulation)
  • Improved hemodynamic stability
  • Less inhaled or infused anesthetic agent required
  • Postop analgesia

Routes

Intermittent: varying plasma concentrations and effect

Continuous: titratable, reduced total dose, less need for reversal

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7
Q

Mechanism of Action of Opioids

A

Opioids bind to Mu1, Mu2, Kappa, and delta receptors to decrease neurotransmitter release by increasing potassium efflux and MARK cascade and decreasing adenyl cyclase production and calcium influx of ascending and descending pain pathways.

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8
Q

Where is the activation site of supraspinal opiate receptors?

A

Medulla, midbrain to inhibit neurons in the pain pathway

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9
Q

Mechanism of spinal opiate receptor(s) activation

A

decreases calcium influx and decreases release of neurotransmitters related to nociception

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10
Q

Where is the activation site of peripheral opiate receptors?

A

Gastrointestinal (GI), vasculature, lung, heart, immune systems

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11
Q

Mu (μ) opiate receptor

Tell me what you know about its effects on the body when stimulated

A

IUPHAR name for it: MOP

EFFECTS

  • analgesia: spinal, supraspinal
  • CV: Bradcardia
  • Resp: Depression
  • CNS: Euphoria, sedation, prolactin release, mild hypothermia, catalepsy, indifference to environmental stimulus
  • Miosis (shrinking pupils)
  • GI: Inhibition of peristalsis, N/V
  • URINARY RETENTION

*Pruritis & physical dependence

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12
Q

Kappa (μ) opiate receptor

Tell me what you know about its effect on the body

A

IUPHAR name for it: KOP

EFFECTS analgesia: spinal, supraspinal

Resp: Possible depression

CNS: Sedation, dysphoria, psychomimetric reactions (hallucinations/delirium)

Miosis (shrinking pupils) GI: Inhibition of peristalsis, N/V

GU: Diuresis (inhibition of vasopressin release)

*low abuse potential and ?used for antishivering

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13
Q

Delta (δ) opiate receptor

Tell me what you know about its effects on the body when stimulated

A

IUPHAR name for it: DOP

EFFECTS

analgesia: supraspinal, spinal, modulates mu-receptor activity

Resp: depression

GU: Urinary retention

*Pruritis and physical dependence

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14
Q

Name drugs which are agonists to all three opiate receptors?

A

Morphine

Meperidine

Fentanyl

Sufentanil

Alfentanil

Remifentanil

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15
Q

Name drugs which are:

Antagonist of Mu receptor

Partial agonist of Kappa receptor

Agonist of Delta receptor

A

Butorphanol

Nalbuphine

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16
Q

Name drugs which are antagonists of all three opiate receptors?

A

Naloxone

Naltrexone

Nalmefene

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17
Q

Effect of Opioid on the Respiratory System

A
  • Cough suppressant (however a rapid bolus can cause a cough)
  • Depress upper and lower respiratory track reflexes
  • Decrease ventilatory response to hypercapnia and hypoxia
  • Onset of apnea occurs before unconsciousness
  • Potential for skeletal muscle rigidity
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18
Q

Effects of Opioids on the Cardiovascular System

A
  • Relatively hemodynamically stable
  • Bradycardia resulting from medullary vagal stimulation with little effect on BP in healthy patients •Dose dependent vasodilation

If the drug releases histamine, can induce hypotension

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19
Q

Effects of Opioids on the Gastrointestinal System

A
  • Decrease gastric and intestinal motility
  • constipation, ileus
  • Prolong gastric emptying time
  • Reduce GI track secretory activity
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20
Q

Effects of Opioids on the Endocrine System

A
  • Reduced stress response (immunosuppressive)
  • Inhibition of hormones (ex corticotropin) from the pituitary gland (HPA axis)
  • Decreased BMR (basal metabolic rate) and temperature by resetting hypothalamus temperature regulation
  • Inhibition of vasopressin release
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21
Q

Describe what happens after an opioid such as morphine is injected into the intrathecal or epidural space

A

it diffuses into the substantia gelatinosa (Rexed’s lamina II) and unites with opioid receptors on the nerve terminal of the primary pain afferent.

The release of substance P is reduced, and, hence, the transmission of impulses through the substantia gelatinosa is inhibited.

THIS IS KNOWN AS SPINAL ANESTHESIA

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22
Q

Mu-1, mu-2, kappa, and delta receptors mediate ______ analgesia.

A

spinal

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23
Q

Spinal opioid analgesia is mediated primarily by

A

mu-2 receptors

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24
Q

How does spinal anesthesia side effects differ from systemic opioid administration?

A

Same side effects as systemic opioids with increased frequency of pruritus and urinary retention

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25
Antagonism of Pruritis
* **Nalbuphine** most effective as a mu/kappa opioid partial agonist * Retains analgesia and treats pruritis * **Droperidol, antihistamines, odansetron** * May reverse analgesia: **naloxone, naltrexone (be thoughtful administering this one)**
26
Pruritis, what does it occur with? Mechanism of action?
•Rash, itching, warmth in blush are of face, upper chest, arms, nausea & vomiting **Occurs with**: * Histamine (morphine) and nonhistamine-releasing (fentanyl) opiates * Prominent with neuraxial route (morphine) **Mechanism**: Central mu receptors, not local histamine release
27
Fentanyl Absorption & Dosing
Absorption •Routes: Transmucosal, IM, IV, epidural, intrathecal, transdermal Dosing * **Induction dose as adjunct: 1 – 3 mcg/kg** * Infusion: 0.01 – 0.05 mcg/kg/min * Small dose boluses: **25 – 50 mcg**
28
Distribution & Redistribution of Fentanyl
Distribution (intravenous) * Onset: **2** – 5 **minutes** * Peak effect: **20** – 30 **minutes** * DOA: **0.5** – 1 hours Redistribution •Extensive uptake in lungs and red blood cells
29
Metabolism & Excretion of Fentanyl
Metabolism •Hepatic metabolism to inactive metabolite norfentanyl Excretion •Eliminated in feces and urine
30
Pulmonary first pass of Fentanyl can cause \_\_\_
coughing
31
Special considerations for a Fentanyl patch
* Once applied, it takes 11 hours for peak effect * Once removed, it takes 18 hours for plasma concentration to decrease by half
32
Meperidine Absorption & Dosing
Absorption •Routes: PO, IV, IM Dosing •Intravenous small dose boluses: **12.5 – 25 mg**
33
Distribution of Meperidine
Distribution (intravenous) * Onset: **5 minutes** * Peak effect: 30 - 60 minutes * DOA: 2 - 4 hours
34
Metabolism, Excretion & clinical effect of Meperidine
Metabolism * Hepatic metabolism via **CYP450 system to its active metabolite = normeperidine** (½ the analgesic & ½ life significantly longer than meperidine) * **Lowers seizure threshold**, induces CNS excitability * Accumulation causes CNS excitation * Tremors, muscle twitches, seizures * **Risk with renal failure**, high dose chronic use Excretion •Eliminated by the kidneys
35
Meperidine is structurally similar to ____ and may cause \_\_\_\_\_
atropine, tachycardia
36
Meperidine has significant drug interactions with \_\_\_
MAO inhibitors
37
Meperidine demonstrates similarities to local anesthetics when administered \_\_\_\_\_\_\_\_\_
intrathecally
38
Meperidine (and morphine) can cause \_\_\_\_\_\_
histamine related bronchospasm
39
Meperidine is effective in decrease postoperative shivering because of \_\_\_\_\_\_\_\_\_
its effects at the Kappa receptor
40
Absorption & Dosing of Morphine
Absorption •Routes: PO, IV, IM, Epidural Dosing •Intravenous **small dose boluses**: **1-5 mg**
41
Distribution of Morphine (IV)
* Onset: 20 minutes * Peak effect: **30 - 60 minutes** * DOA: **4** - 5 **hours**
42
Metabolism & Excretion of Morphine
Metabolism * **Hepatic and renal metabolism to metabolites**: 90% morphine-3-glucuronide (inactive) and 10% morphine-6-glucuronide (active) * morphine 6-glucuronide is a more potent and longer-lasting opioid agonist than morphine * **Caution in patients with renal failure** because **ACTIVE METABOLITE** and portion excreted unchanged can result in narcosis and ventilatory depression Excretion •**Eliminated by the kidneys** (5-10% is excreted unchanged)
43
Special considerations of morphine
Morphine is the **least lipophilic opioid** Morphine is the **least nonionized at physiologic pH** Morphine has the **longest DOA when administered intrathecally** Morphine (and meperidine) **can cause histamine related bronchospasm**
44
Absorption & Dosing of Hydromorphone
**Absorption**: Routes: PO, IV, epidural, intrathecal **Dosing**: Intravenous small dose boluses: **0.2 mg**
45
Disribution of IV Hydromorphone
* Onset: **15** - 30 minutes * Peak effect: **30** - 90 minutes * DOA: **4** - 5 hours
46
Metabolism & Excretion of Hydromorphone
**Metabolism**: Hepatic metabolism via CYP system to hydromorphine-3-glucuronide (inactive) **Excretion**: Eliminated by the kidneys
47
Absorption & Dosing of Methadone
Absorption •Routes: PO, IV Dosing * Intravenous dose: 0.5 mg/kg * Dosing is influenced on patient’s chronic opioid regimen
48
Disribution of IV Methadone
Distribution (intravenous) * Onset: **5** -10 minutes * Peak effect: **15** – 20 minutes * DOA: **4** - 6 hours * Half-life: **15** – 30 hours * **Highly protein bound (90%)**
49
Metabolism & Excretion of Methadone
Metabolism •Hepatic metabolism via CYP system Excretion •Eliminated by the kidneys
50
What is unique about methadone?
* Methadone is used primarily for **chronic pain** and treatment of opioid abstinence syndromes * Methadone has **NMDA receptor antagonism** properties * Compared to other opioids, methadone **produces less euphoria**, has a long half-life, extensive protein binding and slow release
51
Absorption & Dosing of Remifentanil
Absorption •Routes: IV Dosing •Intravenous **induction dose**: **2** - 5 **mcg/kg** **•r/f opioid induced muscle rigidity** •Intravenous **infusion**: **0.05** – 0.25 mcg/kg/min
52
Distribution of IV Remifentanil
* Onset: 1 minutes * Peak effect: 1 minute * **DOA**: **5** – 10 minutes
53
Metabolism & Excretion of Remifentanil
Metabolism: **Ester hydrolysis via blood and tissue esterases** Excretion •Eliminated by the kidneys
54
Induction doses of reminfentanil may cause \_\_\_\_\_
•profound bradycardia and are often administered with ephedrine
55
Why is Remifentanil beneficial in patients with renal or hepatic failure?
Remifentanil’s metabolism by plasma esterases (not pseudocholinesterases)
56
Why is Remifentanil beneficial in the OR?
rapid onset, short DOA and titratability
57
What special consideration does the CRNA need to think about with Remifentanil?
•may contribute to **post-operative hyperalgesia**, therefore the CRNA should create a plan for postoperative analgesia
58
Absorption & Dosing of Sufentanil
Absorption •Routes: IV Dosing * Intravenous **induction dose**: **0.1 – 0.3 mcg/kg** * Intravenous infusion: **0.0015** – 0.01 **mcg/kg/min**
59
Distribution of Sufentanil
Distribution (intravenous) * Onset: **1 – 3 minutes** * DOA: Dose dependent
60
Metabolism & Excretion of Sufentanil
Metabolism •Metabolized by the liver Excretion •Eliminated by the kidneys
61
Context sensitive half-time
how long does it take for the plasma concentration to decrease by half once an infusion of a medication has been turned off
62
Special considerations for Sufentanil
* Sufentanil is one of the most potent * In general, an infusion of sufentanil has a longer context sensitive half-time than remifentanil infusion being administered for a similar duration
63
Medication class of Buprenorphine
mu **partial agonist**
64
Mechanism of Action of Buprenorphine
strongly binds to mu receptors •Strongly binding to a receptor is not synonymous with strong clinical effects as this partial agonist **has a ceiling effect**
65
Use, Peak, and considerations of Buprenorphine
Use: Moderate analgesia with **limited respiratory depression** Peak effect: **3 hours** | **DOA: 10 hours** Special Considerations Ceiling effect, **difficult to supplement with other opioids**, active metabolites
66
Naloxone Medication Class & Use
**Class**: nonselective opioid antagonist **Use**: Reverses opioid induced respiratory depression, analgesia, sedation, nausea, puritis and constipation
67
Absorption & Dosing of Naloxone
Absorption: IV, intranasal, SQ Dose: **40 mcg boluses** (titrate slowly)
68
Onset and Side Effects of Naloxone
Onset: **1 minute** | DOA: **30 minutes** (shorter than most opioids) Side effects: pulmonary edema, tachycardia, hypertension
69
Naltrexone
* Similar antagonist and receptor binding properties with naloxone * Extended-release formulation is used for alcohol withdrawal programs * Used with opioid addiction to block euphoric effects of opioids
70
What medication class is Ketorolac?
•nonselective COX 1 and 2 inhibitor
71
Absorption & Dosing of Ketorolac
Absorption: Oral, IV, IM **Dosing** (intravenous): **15 - 30 mg** * Dose decreased in elderly and CKD * Administered during emergence
72
Distribution of Ketorolac
Distribution: •Onset: 30 min | **DOA**: **4** – 6 hours
73
Metabolism & Excretion of Ketorolac
Metabolism: Hepatic Excretion: Renal (60% unchanged)
74
Advantages of Ketorolac
Advantages * Decrease post-operative opioid requirements * Low incidence of nausea and vomiting * Lack of respiratory depression
75
Things to consider w/ use of Ketorolac
Considerations * Communicate with surgical colleagues prior to administration * Bone healing delays by NSAIDs, **not used in ortho surgery**, OK with stable and healing fracture * **Bleeding risk in intercranial surgery** * **Caution in patients with asthma r/t bronchoconstriction** d/t decrease leukotriene productions * **Caution in patients with renal disease** r/t renal vasoconstriction d/t decrease prostaglandin production
76
Class & Absorption of Acetaminophen
Class: Analgesic and antipyretic Absorption: Oral, PR, and IV
77
Dosing of Acetaminophen (Offirmev)
Dose (intravenous): * Pediatric: 15 mg/kg * Adult: **1G over 10 minutes** * PO dose administered preoperatively, or IV dose administered during emergence * **Max dose: 4 g/day** * Dosing decreased in patients with liver dysfunction
78
Distribution of Acetaminophen
Distribution: •Onset: **10 min** | DOA: **4** – 6 hours
79
Metabolism & Excretion of Acetaminophen
Metabolism: **Hepatic**: increased doses yields large concentrations of N-acetyl-p-benzoquinone imine to produce hepatic failure Excretion: Renal
80
What are the advantages of Acetaminophen?
Advantages * Decrease post-operative opioid requirements * Low incidence of nausea and vomiting * Lack of respiratory depression
81
What are the disadvantages of Acetaminophen?
* Black box warning: Hepatoxicity * Be aware of liver enzymes (if appropriate) * Be are of patient’s cumulative dose * Reversal agent is N-acetylcysteine
82
Medication Class of Gabapentin (Pregablin)
Antileptic
83
Mechanism of Action of Gabapentin
Although these agents have been shown to bind to voltage-gated calcium channels and N-methyl-D-aspartate (NMDA) receptors, their exact mechanism of action remains speculative
84
Special Considerations for Gabapentin
* Can be administered preoperatively (orally) to decrease post-operative opioid requirements * Can contribute to post-operative sedation
85
Opioids that release histamine = \_\_\_\_
morphine & meperidine
86
Opioids that do not release histamine = \_\_\_\_\_
fentanyl, sufentanil, alfentanil, remifentanil
87
What can you give together to block CV vasodilation, tachycardia and hypotension
•H1 and H2 antagonists

Anesthesia-phar (18 decks)

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