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GNURS625/Pharmacology for Anesthesia > Quiz 3 Pain Manament > Flashcards

Quiz 3 Pain Manament Flashcards

1
Q

What are the two types of pain?

A

Nociceptive and Neuropathic

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2
Q

Which of the two types of pain does Opiates work best for?

A

Nociceptive pain

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3
Q

What kind of meds work best for Neuropathic pain?

A

Tricyclic Antdepressants and Neuropathic meds like Lyrica, Neurontin, Carabmazipine.

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4
Q

Describe the basic Nociception pathway

A

Stimulation - noxious stimulus releases neural chemicals that also stimulate other nociceptors

Transmission - Action potential moves from site of stimulus to the dorsal horn of the spinal cord then to the CNS

From Dorsal horn, neurotransmitters are released (Glutamate, Substance P, Calcitonin related peptide)

Perception - Concious experience of pain releayed through thalamus. Higher cortical structures transmit pain

Modulation - inhibition of impulses via the brainstem by releasing endogenous opioids, serotonin, NE, GABA

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5
Q

What are some common characteristics of Neuropathic pain?

A

Burning, Tingling, Shocks, Hyperalgesia, Allodynia (pain from stiumuli that is not normally painful)

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6
Q

What does PQRST stand for when assessing pain?

A

P - Palliative and provocative factors (agravating or alleviating)

Q - Quality

R - Radiation

S - Severity (can use pain scale)

T - Temporal relations (??)

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7
Q

Analgesia produced by neuraxial opioids is not associated with?

A
  • SNS denervation
  • Skeletal muscl weakness
  • Loss of proprioception
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8
Q

What lab test can be used to measure pain?

A

NONE. Pain is subjective. Need to evaluate for outward signs of pain like grimacing, guarding, HTN, tachycardia, ….

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9
Q

What is neuraxial opioids?

A

Placement of opioids in epidural or subarachnoid space.

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10
Q

Where are Opioid receptors located?

A

the brain, spinal cord, and GI Tract

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11
Q

What are the 4 types of Opioid pain receptors?

A

Delta, Kappa, Mu, Nociceptive

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12
Q

What are the opioids routes of uptake into the body from an epidural?

A
  • Diffusion of the drug across the dura to gain access to mu opioid receptors
  • systemic absorption
  • uptake into the epidural fat
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13
Q

What happens when the Mu1 receptor is stimulated?

A

Analgesia, Miosis (constricted pupil), Dependence

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14
Q

How long until CSF concentration of fentanyl will peak?

A

20 minutes.

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15
Q

What happens when the Mu2 receptor is stimulated?

A

Respiratory depression

Euphoria

Reduced GI motility

Dependence

**Spinal Analgesia**

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16
Q

Where do opioids work on the nerve - Pre or Postsynapse?

A

They work on both the Pre and Postsynapse.

They help to hyperpolarize the cell to decrease pain sensation

NMDA will pump in excess Ca++ into cell to hyperpolarize. Mu receptor will stimulate pump to push K+ out of cell.

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17
Q

What can happen if NMDA receptors are overstimulated by glutamate?

A

Can lead to Neuropathic pain

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18
Q

What are four classic side effect for Neuraxial opiods?

A
  • Pruritus
  • Nausea and vomiting
  • Urinary retention
  • Depression of ventilation
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19
Q

What will occur if epi is added to opioid epidural does?

A

Decrease systemic asorption of opioid but not effect diffusion across dura into the CNS.

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20
Q

What are the point for opioid use intrathecal?

A
  • Vascular absorption is limited and clinically insignificant
  • Cephalad movement of opioid in CSF depends on lipid solubility
  • Coughing or straining can affect movement in CSF
  • Positioning has no affect.
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21
Q

How does Naloxone work?

A

Nonselective antagonist at all 3 opioid receptors.

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22
Q

How is Nalooxone metabolized and what is the metabolite?

A

Hepatic microsomal enzyme and naloxone-3-glucuronide.

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23
Q

T or F - Opioids must exist in the ionized state in order to form a strong bond at the opioid receptor?

A

True

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24
Q

What is the peak effect of morphine after IV administration?

A

15-30 mins

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25
Q

What are the advantages for opioid agonist-antagonist?

A
  • Analgesia withlimited deprssion of ventilation
  • Potential for physical dependence is low
  • Drug has a ceiling effect
26
Q

Does morphine easily enter the CNS?

A

No. It has poor lipid solubility so <0.1% will enter the CNS.

27
Q

What is the active metabolite of Morphine, is it Morphine 3-glutamate (M3G) or Morphine-6-glutamate (M6G)?

A

Morphine-6-Glutamate is the ACTIVE metabolite and is 100X more potent in the CNS than Morphine

Morphine-3-Glutamate is the INACTIVE metabolite

28
Q

What receptors do opioid agonist-antagonist work on? Do they fight?

A

The partial agonist produce limited effect at mu receptor and cause partial agonist action at kappa and delta. Antagonists are competitive for the same site and yes they will fight for the same sites.

29
Q

Is Morphine-6-Glutamate hydrophyllic or Lipophyllic?

How does Morphine-6-Glutamate enter the CNS?

A

M6G is hydrophyllic

M6G will enter the CNS by mass action if the pt is chronically administer MS or in renal failure (unable to excrete)

30
Q

What receptors does meperidine(demero) work on?

A

Mu and kappa

31
Q

What are the other analogues of meperidine?

A
  • Fentanyl
  • Sufentanil
  • Alfentanil
  • Remifentanil
32
Q

What are some common cardiac side effects of Morphine?

A

Bradycardia

Reduced SNS response

Histamine release

  • itching
  • vasodilation
33
Q

How is meperidine metabolized?

A
  • extensive hepatic metabolism
  • meperidine to demethylation to normeperidine (hydrolzed) to meperidinic acid
  • metabolites are primarily excreted by the kidney
34
Q

What are some key facts about meperidine?

A
  • Elimination half time is 3-5 hours
  • clearance depends on hepatic metabolism and renal excretion
  • 60 % protein bound
35
Q

What are some common Respiratory side effects of Morphine?

A

Respiratory depression

  • decreased response to CO2)
  • Increase resting PCO2
  • Prolonged periods between breaths
  • apnea

Cough suppression

  • can put your pt at risk for aspiration
36
Q

What is normeperidine?

A

Metabolite of demerol

37
Q

What points should be remembered about normeperidine?

A
  • Half the analgesic properties of demerol
  • half time 15 hours (more with CKD)
  • CNS stimulation
  • CNS toxicity leads to myoclonus and seizures
  • Demerol induced delirium
38
Q

What are some common CNS side effects from Morphine?

A

Decreased CBF and ICP

39
Q

What cautions should you keep in mind if using Morphine on head injured patients?

A

Morphine could cause Miosis and could throw off your neuro assessment

Increases in ICP can be accompanied by decreased breathing before morpine is even given

Blood Brain Barrier integrity could be damaged with a resultant increased sensitivity to opioids

40
Q

Remifentanil is structurally unique how?

A

It has ester like linkage

41
Q

What are the cardiovascular side effect of meperidine?

A
  • interferes with the compensatory SNS reflexes
  • may cause orthostatic hypotension
  • Increase heart rate
  • Increased doses cause decrease in contractility
42
Q

What precautions with sedation should you be aware of before using Morphine?

A

Onset of sedation preceeds analgesia

Allow for full onset of clinical effect before rebolusing to prevent dose stacking (wait at least 15 min)

Sedation does not equal pain relief

43
Q

What are the respitory side effects of meperidine?

A

-dose related imparment of ventilation (effect is greater than morphine).

44
Q

What effect does morphine have on the billiary tract?

A

May cause spasm of biliary smooth muscle

During Cholecystectomy, can cause spasm of sphincter of Oddi.

45
Q

What is Meperidine and serotonin syndrome?

A

-Autonomic instability

*HTN, Hyperthermia, Hyperreflexia (most seen)

*Tachycardia, diaphoresis,confusion(Others)

SEVERE: Coma, Seizures, COagulopathy, Metabolic acidosis.

46
Q

If morphine causes a spasm of the Sphincter of Oddi, what can be given to the pt to counteract this effect?

A

Glucagon 2mg IV

47
Q

How does Morphine cause N/V?

A

through stimulation of the Chemoreceptor Trigger Zone (CTZ)

and

Heightened vestibular sensitivity

48
Q

Other than N/V, what are some other effects of Morphine on the GI Tract?

A

Constipation - through slowing of peristalsis

Biliary Colic

Delayed gastric emptying

49
Q

What are some effects of Morphine on the GU system?

A

Increased tone and peristaltic activity of the ureter

Increased vesicle sphincter tone (voiding is difficult)

Increase detrussor muscle tone (increased urgency)

summary - feel you have to pee but can’t

50
Q

What are the pharmokenetic of Remifentanil?

A
  • small Vd
  • Rapid clearance 3 L/min
  • low inter-individual variability (dosing should be done on IBW)
  • Minimal accumalation
51
Q

How is remifentanil metabolized?

A

-metobolyzed by nonspecific plasma and tissue esterases to inactive metabolites which gives the drug

*brevity of action

*precise reliability due to rapid onset and offset

*noncumulative effects

52
Q

Remifentanil side effect is?

A

post op patients appear to have high post-operative analgesic requirements.

53
Q

What is Alfentanil?

A
  • analogue of fentanyl
  • Decrease potency and duration than fentanyl
  • Rapid effect-site equilibration time of 1.4 minutes
  • Quick short elimination half-time
54
Q

The metabolism of Alfentanil is?

A
  • Hepatic microsomal enzymes

(*Piperdine N-dealkylation to noralfentanil)

(*Amide N-dealkylation to N-phenylpropionamide)

-Less the half is unchanged in the urine

55
Q

What is Sufentanil?

A

Thienyl analogue of fentanyl

-Potency is 5 - 10 times

56
Q

What are the pharmokenetics of Sufentanil?

A

-Elimination half time is intermediate

(fentanyl>sufentanil>Alfentanil)

  • Significant 60 % 1st pass pulmonary reuptake
  • Elimination is not effected by liver desease
57
Q

How is Sufentanil metabolized?

A

Hepatic microsomal enzymes

(N-dealkylation and O- demethylation

-Patient with CKD have a harder time with elimination

58
Q

How do opioid react on cardiopulmonary bypss?

A
  • Opioids decrease in plasma concentationwith iniwith initiation of cardiopulmonary.
  • Fentenyl loves to cling onto the lines during use of CABG.
59
Q

What is fentanyl?

A
  • synthetic agonist
  • phenyl-piperdine derivative
  • (75 - 125 more potent the morphine)
  • effect site equilibrium about 6 minutes
60
Q

What are the pharmokenetic of fentanyl?

A

Pulmonary system 75% of 1st pass. of people

61
Q

What should be known opioids?

A

patients on MAO inhibitors may experience exaggerated CNS depresion and hyperpyrexia after an opiod agonist.

GNURS625/Pharmacology for Anesthesia (13 decks)

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