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*Pharmacology > Apex- Opioid & Non-opioid analgesics > Flashcards

Apex- Opioid & Non-opioid analgesics Flashcards

1
Q

What are pain receptors called

A

Nociceptors

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2
Q

What is it called when a nociceptor converts a noxious stimulus to an action potential?

A

Transduction

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3
Q

How is facial pain transmitted?

A

via cranial nerve V (trigeminal)

*bypasses the spinal cord and conducts pain stimuli directly to the brain

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4
Q

What is pain transduction blocked by? (5)

A

(converting the stimulus into an action potential)

-Nsaids, opioids, local anesthetic CREAMS, steroids, antihistamines.

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5
Q

What is pain TRANSMISSION blocked by?

A

(pain transmitted from the periphery to the CNS)

Local anesthetics for peripheral or neuraxial nerve blocks

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6
Q

When doing a peripheral or neuraxial nerve block, do you block pain transmission or transduction?

A

transmission

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7
Q

Pain is transmitted via what types of fibers?

A

A delta & C

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8
Q

What are the 2 important excitatory NTs in the dorsal horn?

A

Glutamate and substance P

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9
Q

Discuss the transmission of pain and where the 1st, 2nd, and 3rd order neurons synapse

A
  1. 1st order neuron transmits signal from site of injury

> dorsal horn: can synapse with a 2nd order neuron at the level it enters or travel along the tract of Lissauer before synapsing at a higher or lower level

> after synapsing with the 2nd order neuron it CROSSES to the contralateral side of the spinal cord and ASCENDS to the brain via the SPINOTHALMIC tract

> the 2nd and 3rd order neurons synapse in the thalamus

> 3rd order neuron projects to other brain regions (cortex, limbic system, etc)

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10
Q

Order of steps of the pain process

(modulation, transduction, perception, transmission)

A
  1. Transduction
  2. Transmission
  3. Modulation
  4. Perception
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11
Q

allodynia

A

Pain resulting from a non-painful stimulus (pain from ALL the things)

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12
Q

Drugs that target pain transduction (5) vs transmission (1) vs modulation (6) vs perception (3)

A

transduction (5)
> NSAIDS
> LA creams
> Steroids
> Antihistamines
> Opioids

transmission (1)
> local anesthetics via peripheral nerve or neuraxial blocks

modulation (6)
>neuraxial opioids
>NMDA antagonist
>alpha-2 agonists
>AchE inhibitors
>SSRIs
>SNRIs

perception (3)
>general anesthetics
>opioids
>alpha-2 agnoists

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13
Q

Re: Modulation: what 2 things is pain augmented (enhanced) by?

A

Central sensitization & Wind-up

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14
Q

Re: Modulation: what 2 things is pain inhibited by?

A
  1. spinal neurons releasing GABA & Glycine
  2. Descending pathway releases NE, serotonin, and endorphins
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15
Q

Opioid receptor stimulation results increased/decreased:

cAMP
adenylate cyclase activity
calcium conductance
potassium conductance

A

cAMP - decreased

adenylate cyclase activity - decreased

calcium conductance- decreased (reduces NT release)

potassium conductance- increased (hyperpolarizes nerve so it’s less responsive to stimulation)

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16
Q

Where does pain modulation typically take place?

A

in the dorsal horn of the spinal cord

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17
Q

MOP receptor is what

A

Mu

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18
Q

DOP receptor is what

A

Delta

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19
Q

KOP receptor is what

A

Kappa

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20
Q

NOP receptor is what

A

ORL1 ?

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21
Q

6 key physiologic effects of Mu receptor stimulation

A
  1. analgesia
  2. euphoria
  3. Physical dependence
  4. resp depression
  5. bradycardia
  6. constipation

(Try to answer in systems, from top to bottom)

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22
Q

Endogenous ligands for the Mu, delta, kappa, and NOP receptors

A

Mu- endorphins
Delta- Enkephalins
Kappa - dynorphins (thinks dysphoria)
NOP - nociceptins

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23
Q

What does pre-synaptic mu receptor stimulation result in?

A

reduced calcium conductance via N-type calcium channels
>decreased NT release

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24
Q

What does stimulation of mu receptors on the post-synaptic neuron result in?

A

increase of K+ conductance
>hyperpolarizes neuron
>decreased RMP
>makes it more resistant to stimulation

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25
Q

Where are mu receptors found?

A
  1. Peripheral NS
    >A-delta & C fibers
  2. CNS
    >dorsal horn
    >RAS
    >thalmus
    >somatosensory cortex
  3. Descending inhibitor pathway
    >periadquaductal gray
    >nucleus raphe magnus
  4. Immune cells
    >leukocytes
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26
Q

What does stimulation of mu receptors in the descending spinal pathway?

A

stimulates the release of endorphins, serotonin, and NE in the dorsal horn of the spinal cord

(via mu receptors in the periaqueductal gray and nucleus raphe Magnus)

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27
Q

What happens when opioids bind to an opioid receptor (chemical processes)

A
  1. opioid binds
  2. G-protein is activated
  3. Adenylate cyclase is turned off
  4. Less cAMP is produced
  5. CA+ conductance is decreased (presynaptic)
  6. K+ conductance is increased (post-synaptic)
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28
Q

T/F all opioid receptor stimulation result in bradycardia

A

False- just Mu

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29
Q

Which opioid receptor does not produce miosis

A

Delta

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30
Q

Which opioid receptor produces diuresis?

A

Kappa

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31
Q

T/F- all opioid receptors result in N/V, increased biliary pressure and decreased peristalsis

A

false- just mu

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32
Q

Stimulation of which opioid receptor does NOT result in pruritis

A

kappa

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33
Q

What’s associated with Mu-3 stimulation

A

Immune suppression

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34
Q

Which mu-subtype targets spinal analgesia only (not supraspinal)

A

Mu-2

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35
Q

Which Mu-subtype is associated with resp depression

A

Mu-2

-resp depression, phsycial deprendence > constipation

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36
Q

Which mu-subtype is associated with bradycardia

A

Mu-1

37
Q

Which mu-subtype is associated with supraspinal and spinal analgesia?

A

Mu-1

38
Q

T/F: delirium and hallucinations are caused by mu receptor stimulation

A

False- kappa

(kappa/dynorphan/dysphoria)

39
Q

Opioids produce bradycardia through Mu receptor stimulation. What is the exception to this and why?

A

Meperidine - it can increase HR due to an atropine-like ring in its structure

40
Q

Where are opioid receptors located in the:

Brain (3), Spinal Cord (2), & Periphery (2)

A

Brain:
>periaquaductal gray
> locus coeruleus
>rostral ventral medulla

Spinal Cord:
> primary AFFERENT neurons in the DORSAL HORN
>interneurons

Periphery:
>sensory neurons (A delta & C)
>immune cells

41
Q

The mechanisms by which opioids contribute to urinary retention (2)

A

Detrusor relaxation (contraction needed to pass urine into the urethra)

& urinary sphincter contraction

42
Q

How do opioids affect RR & TV?

A

decrease RR
increase TV

(just think, when your relaxed, you take a slow deep breath) - so they should be taking slow deep breaths if comfortable

43
Q

Is gastric emptying time increased or decreased by opioids?

A

increased (prolonged, takes more time to empty)

44
Q

Relative potency to Morphine:

Meperidine:
Hydrocodone:
Alfentanil:
Remifentanil:
Fentanyl:
Sufentanil:

A

Meperidine: 0.1 x
Hydrocodone: 7 x
Alfentanil: 10 x
Remifentanil: 100 x
Fentanyl: 100 x
Sufentanil: 1000x

45
Q

T/F: dependence occurs when a patient requires higher doses of a drug to achieve a given effect

A

False- tolerance

Dependence occurs when a person taking the drug will go through withdrawal upon d/c’ing the drug

46
Q

Early (3) and Late (2) S/S of opioid withdrawal

A

Early: diaphoresis, insomnia, restlessness

Late: abdominal cramping & N/V

47
Q

What are the:
phenanthrene derivatives(2):
Morphine derivatives(4):
Thebaine derivatives(2):
Piperidines(1):
Phenylpiperidines(4):
Diphenylpropylamines(1):

(Natural (N), Semi-synthetic (SS), or synthetic (S)

A

phenanthrene derivatives: (N)
>Morphine & Codeine

Morphine derivatives: (SS)
>Hydromorphone (Dilaudid)
>Heroine
>Naloxone (IV narcan)
>Naltrexone (PO narcan)

Thebaine derivatives: (SS):
Oxycodone (Percocet)
Hydrocodone (Vicodin)
___________________
Piperidines: (S)
>Meperidine

Phenylpiperidines: (S)
> Al, Remi, Fent, Su

Diphenylpropylamines:(S)
>Methadone

48
Q

10mg of morphine is equivilant to:

Meperidine:
Hydromorphone:
Alfentanil:
Remi:
Fentanyl:
Sufentanil:

A

Meperidine: 100mg
(10mg*/0.1x)
(standard mso4/relative potency)

Hydromorphone: 1.4mg
(10/7)

Alfentanil: 1,000mcg
(10/10 = 1mg)

Remi: 100mcg
(10/100 = 0.1mg)
(1 zero left, always lead)

Fentanyl: 100mcg
(10/100 = 0.1mg)

Sufentanil: 10mcg
(10/1000 = 0.01mg)

49
Q

When will you start having withdrawal s/s, when will they peak, and how long will they last?

Fentanyl & Meperidine:
Morphine & Heroin:
Methadone:

A

Fentanyl & Meperidine:
>2-6 hours
>6-12 hours
> 4-5 days
(think most potent, fastest symptoms, peaks, and in and out the fastest)

Morphine & Heroin:
>6-18 hours
>36-72 hours (days 1.5-3)
> 7 - 10 days ( 1-2 weeks)

Methadone:
>Onset 24-48 hours
>Peak: 3-21 days
>Duration: 6- 7 weeks

50
Q

Active metabolite of Morphine

A

M6G

51
Q

Morphine is broken down how?

A

in’s conjugated to morphine-3 & morphine-6 glucuronide.

*M6G = active metabolite that accumulates with renal failure and chronic morphine administration

52
Q

How is meperidine broken down?

A

It’s demethylated in the liver into normeperidine (active)

> accumulates in renal failure and elderly and increases risk of seizures

53
Q

If M6G is water-soluble and doesn’t cross the blood-brain barrier, why does it matter if it accumulates in patients on dialysis?

What law?

A

Bc it will accumulate and the larger concentration gradient between the blood and the brain helps M6G enter the CNS.

Law of Mass Action

54
Q

if someone has a pseudocholinesterase deficiency, will it prolong the effects of remifentanil?

A

No- Remi is not metabolized by pseudocholinesterases (Sux is)

Remi is metabolized by nonspecific plasma esterases

55
Q

What is Remifentanyl dosed on and why?

A

Lean body weight

bc although lipophilic, it behaves like a drug with a low Vd becasue it is rapidly metabolized in the plasma

56
Q

Which opioid causes mydriasis and why?

A

Meperidine because it’s constructed from an atropine-like ring (increase HR too)

57
Q

What receptors does meperidine stimulate?

A

Mu & Kappa (antishivering effect)

58
Q

What’s the risk of administering meperidine to a patient on isocarboxazid?

A

Serotonin syndrome

59
Q

4 S/S of serotonin syndrome

A
  1. Hyperthermia
  2. Hyperreflexia
  3. MS changes
  4. Seizures
60
Q

What pharmacologic characteristic accounts for the rapid onset of action of alfentanil?

A. Low protein binding
B. Low degree of ionization
C. High potency
D. High lipid solubility

A

B. Low degree of ionization
(remember PKA determines the onset of action)

-only 10% is ionized, and it’s the UN-ionized (the other 90%) that crosses the BBB to exert its effect

-it’s highly protein bound (alpha-1-acid glycoprotein)

-high potency and high lipid solubility go together so eliminate that

61
Q

PKA of alfentanil
-weak acid or weak base?
_____% Non-ionized

A

6.5 (less than physiologic pH)
-weak base
90% non-ionized (available to cross the BBB quickly)

62
Q

Alfentanil has a (high/low) volume of distribution and a (high/low) degree of plasma protein binding

A

low Vd
high protein binding

(alpha-1-acid glycoprotein)
(remember it’s a weak base so it’s going to bind to the acid protein)

63
Q

Which opioid has the highest and lowest Vd?

A

Highest: Fentanyl (4L/kg)
Lowest: Remi (0.4L/kg)

64
Q

Which opioids are the highest and lowest protein bound?

A

Most: Remi & Su (93%) (Al = 92%)
Least = Morphine (35%)

Fent - 84%
Meperidine = 70% (and only 7% non-ionized/active)

65
Q

Which opioid is the most and least NON- ionized?

A

most = alfentanil - 90%
least = meperidine- 7%

66
Q

PKA’s of the opioids minus dilaudid ranked from lowest to highest

A

Alfentanil- 6.5 *
Remi- 7.2 (AR)
MSO4 - 7.9
Sufent - 8.0
Fent - 8.4
Meperidine- 8.5 *

67
Q

Because Alfentanil has a comparatively (lower/higher) hepatic extraction ratio, its metabolism is more susceptible to alterations in which CYP enzyme function?

A

lower hepatic ER
CYP 3A4

(think alfent - CYP A)

68
Q

Which drug, co-administered with alfentanil can inhibit its metabolism and result in prolonged resp depression?

A

Erythromycin

(enzyme inhibitor) (the enzymes needed to metabolize Alfent are inhibited by erythromycin and will prolong metabolism leading to prolonged effects of the drug)

69
Q

2 main differences in the kinetics of alfentanil compared to the other opioids?

A

lowest PKA (6.5)
- highest non-ionized fraction (90%)

*Fast onset

70
Q

What opioid has the lowest non-ionized fraction at physiologic pH?

A

Meperidine

(only 7% is non-ionized)

71
Q

Attenuate vs Augment

A

Attenuate = lessen
Augment = enhance

72
Q

Which 2 agents can be used to attenuate opioid-induced hyperalgesia?

-Ketamine
-Clonidine
-Morphine
-Mag Sulfate

A

-Ketamine & Mag sulfate

*remember at RMP, the NMDA receptor is plugged by MAG- so making the plug thicker, by giving mag sulfate will make it harder for glutamate to displace the mag core to depolarize the cell.

73
Q

Context-sensitive half-time of Remifentanil

A

4 minutes (REMI) - 4 letters, half time 4 minutes

74
Q

Maintenance infusing dosing of Remi

A

0.1-1 mcg/kg/min

75
Q

Methadone provides analgesia by all of the following ways EXCEPT:

-mu receptor agonism
-NMDA receptor antagonism
-monoamine reuptake inhibition
-cholinergic receptor antagonistm

A

-cholinergic receptor antagonism

76
Q

3 indications for methadone

A

-chronic tx of opioid abuse
-chronic pain syndromes
-cancer pain

77
Q

3 mechanisms by which methadone decreases pain

A
  1. mu agonist
  2. NMDA antagonist
  3. inhibits reuptake of monoamines in the synaptic cleft
78
Q

T/F: methadone can prolong the QT interval

A

True

79
Q

What is Oliceridine?

2 contraindications

A

an IV opioid selctive for the mu-receptor.

-for patients with acute pain when other agents fail to provide adequate relief

Contraindicated in GI obstruction or paralytic ileus

80
Q

List the following as full agonists, partial agonists, or antagonists

Nalmefene
Buprenorphine
Morphine
Butorphanol
Naloxone
Fentanyl
Nalbuphine

A

Nalmefene (ant)
Buprenorphine (p)
Morphine (f)
Butorphanol (p)
Naloxone (ant)
Fentanyl (f)
Nalbuphine (p)

Partials:
Buprenorphine, Butorphanol, Nalbuphine

81
Q

Dose and Duration of Naloxone

A

1-4mcg - q2-3 mins max 10-15mg (max 2mg/dose)
30-45 minutes

82
Q

Which opioid antagonist does NOT reverse opioid-induced respiratory depression?

A

METHylnaltrexone

(METHs also good for making you poop)

83
Q

The primary mechanism by which naloxone can cause pulmonary edema

A

SNS stimulation

(neurogenic pulm edema)

84
Q

What is the most important site for pain modulation?

A

Dorsal horn of the spinal cord

-Rexed’s laminae 2 & 3

85
Q

A patient receiving a fentanyl PCA appears sedated and is only arousable to tactile stimulation. Clinical findings in this patient MOST likely include: (2):

-decreased blood pH
-decreased tidal volume
-increased ICP
-increased A-a gradient

A

-decreased blood pH (resp acidosis)
-increased ICP

-increased PaCO2 increases ICP if ventilation is not controlled

86
Q

Which opioid inhibits nerve conduction:

Morphine
Hydromorphone
Meperidine
Sufentanil

A

Meperidine

*similar structure as local anesthetics and atropine

*inhibits sodium channels in the axon

87
Q

The endogenous pain modulation pathway terminates in the:
-Rostroventral medulla
-ventral root ganglion
-periaqueductal grey
-substantia gelatinosa

A

substantia gelantinosa

*Periaquaeductal gray > rostroventral medulla > substantia gelatinosa

(the endogenous pain pathway = the descending inhibitory pain pathway)

88
Q

Which agent is associated with the GREATEST amount of rostral spread when injected into the intrathecal space?

-Morphine
-Fentanyl
-Meperidine
-Hydromorphone

A

Morphine (most water soluble, going to stay in the intrathecal space most)

*Pharmacology (25 decks)

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