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Anesthesia Pharm > Opiods and Nonopioids > Flashcards

Opiods and Nonopioids Flashcards

1
Q

What are the four opioid receptors?

A

Mu (MOR)

Kappa (KOR)

Delta (DOR)

Nociceptive (NOR)

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2
Q

_____ fibers cause dull burning pain

_____ fibers cause sharp pain

A

Unmyelinated C cause dull

A delta cause sharp, pricking pain

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3
Q

Afferent fibers enter the spinal cord at the ______

A

dorsal horn, terminating in lamina I-II

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4
Q

There are three examples of analgesia driven by endogenous opioid systems:

A
  1. Stress-induced Analgesia (delayed onset of pain in stressful situation)
  2. Placebo-induced analgesia
  3. Conditioned Pain Modulation (CPM) (Pain arising from noxious stimuli in one part of the body is reduced if a second application of noxious stimuli is introduced)
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5
Q

What causes the pain associated with diabetic polyneuropathy?

A

Damage to the descending pain inhibition pathway

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6
Q

How does the inflammatory cascade balance the pain caused by its mediators?

A

Leukocytes release opioid peptides

The inflammatory process stimulates opioid receptor upregulation, increasing the action of those peptides

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7
Q

A patient who is taking carbamazepine may have (Increased/decreased) clinical effects from opioids

A

decreased

carbamazepine is a CYP3A inducer, meaning metabolism of morphine will be increased

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8
Q

Which morphine metabolite is a full MOR agonist?

A

M6G

M3G (which accounts for 60% of metabolites) has no analgesic or anesthetic action

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9
Q

If morphine is metabolized in the liver, why does severe renal failure sometimes prolong the action of opioids?

A

Because of M6G. It’s already been metabolized, but the substrate isn’t being excreted and it’s active on the MOR

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10
Q

List the piperidines

A

Fentanyl

Alfentanil

Sufentanil

Remifentanil

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11
Q

Morphine is metabolized by a Phase ____ reaction

Fentanyl is metabolized by a Phase _____ reaction

A

Phase 2 (UGT2B7, not CYP450 dependent)

Phase 1 (CYP450 system)

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12
Q

Why doesn’t oral naloxone effect the pain control of patients?

A

It has a 95% first pass effect, so it really only reaches the intestinal cells

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13
Q

During surgery opioids are titrated to ______

Postoperatively, opioids are titrated to ______

A

during surgery, they’re titrated to dampen and prevent hemodynamic response to painful surgical stimuli

Postoperatively they’re given for perceived pain

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14
Q

Fentanyl is _____ times more potent that morphine

A

100

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15
Q

How potent is sufentanil?

A

10x more potent than FENTANYL

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16
Q

Why do opioids cause reduced RR and Vt?

A

RR: activate MORs on respiratory neurons

Vt: opioid-induced decreased afferent input into the brainstem from peripheral chemosensors

17
Q

Why does speed of administration impact the respiratory effects of opioids?

A

When it’s given slowly, the increased CO2 from depression of the respiratory neurons has a chance to stimulate peripheral and chemoreceptors before they’re blunted by the opioid

If given slowly the arterial CO2 will still be higher, but the patient will continue to breathe

18
Q

How do opioids impact sleep apnea?

A

Most patients who receive opioids will develop sleep apnea while taking them

opioids suppress the neurons in the brainstem that are involved in maintaining upper airway muscle tone, causing collapse

19
Q

Besides decreased RR and Vt, what is another effect of opioids on respiratory sufficiency?

A

Strong, high dose opioids given rapidly cause skeletal muscle rigidity in thoracic, abdominal, and pharyngeal muscles

Bad news

20
Q

A patient who is dependent on opioids and smoke 2 ppd suddenly stops smoking. What may happen?

A

They may be exposed to high opioid concentrations in the blood

tobacco smoke induces the CYP system

21
Q

Why does morphine cause the most cardiovascular effects?

A

it mediates histamine release

22
Q

What are the central cardiovascular effects of opioids?

A

activation of vagal nuclei

depression of vasomotor centers in the brainstem

23
Q

What are the peripheral cardiovascular effects of opioids?

A

Direct myocardial depression

Arterial and venous dilation

24
Q

Describe the cellular signaling pathway of opioids

A

G protein-coupled receptor activation causes cAMP and Adenyl cyclase production

OR

direct interaction with ion channels on presynaptic neurons

25
Q

Stimulation of the mu receptor produces:

A

supraspinal analgesia, euphoria, decreased ventilation

26
Q

Kappa receptor stimulation causes

A

spinal analgesia, sedation, and miosis

27
Q

Delta receptor stimulation causes

A

spinal analgesia and modulation of mu receptors

28
Q

Which opioids are associated with histamine release?

A

Morphine, codeine, and meperidine

29
Q

What causes facial flushing from opioids?

A

Interestingly, not histamine release, but mu receptor activation

Also, most common with neuraxial administration

30
Q

What can be done to relieve pruritis in the patient receiving neuraxial opioids?

A

Nalbuphine, droperidol, antihistamines, ondansetron

31
Q

Which opiate is least likely to cause sphincter of Oddi spasms?

A

Meperidine

32
Q

Tolerance develops to all of the side effects of opioids EXCEPT

A

miosis and constipation

33
Q

Which opioid has anticholinergic effects?

A

Meperidine

It is structurally related to Atropine

34
Q

Which A2 adrenergic Agonist is most selective for Alpha 2 receptors?

A

Precedex

35
Q

What happens when Neostigmine is administered intrathecally?

A

Stimulates muscarinic cholinergic receptors, resulting in anti-nociceptive activity

Decreases the amount of drug needed and prolongs duration

36
Q

What is the biggest downside to using spinal neostigmine?

A

VERY high instance of PONV

but this is NOT true with epidural administration

37
Q

How do COX inhibitors prevent prostaglandin synthesis?

A

They prevent arachidonic acid from binding with the COX enzyme

38
Q

What is the most COX-1 selective NSAID?

A

Ketoralac

39
Q

Why do COX-2 inhibitors cause so many CV issues?

A

Prostaglandins formed from Arachidonic acid include both Prostaglandin I2 (made from COX-2) which is a potent vasodilator, AND Thromboxanes (made from COX1) which are vasoconstrictive

Ordinarily this ensures balance: anytime constrictive thromboxanes are developed, so are vasodilatory prostaglandins

BUT when you just inhibit COX 2, you knock out the vasodilatory prostaglandin synthesis and leave the vasoconstrictive synthesis intact, leading to cardiovascular distress

Anesthesia Pharm (12 decks)

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