Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Basic Science II > Management of Acute Post-Op Pain (Grass) > Flashcards

Management of Acute Post-Op Pain (Grass) Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

What are eventual and adverse effects of untreated pain?

A

CV stress

Autonomic hyperactivity

Tissue breakdown

Pulmonary dysfunction

Hypercoagulability

Water retention

Immune dysfunction

Constipation

Chronic pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the neural gateway for all our pain sensations that gets afferent and efferent input?

A

Thalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are two chemicals released by our cells in response to injury that are precursors to eventual pain signal transduction?

A

Bradykinin precursors

Arachidonic acid (after modification by phospholipase A2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

In the spinal cord, where do pain signal transduction occur?

A

They run through the dorsal root ganglia which eventually congregate at the dorsal horns (carries signals up to the sensory cortex)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the axonal tracts of neurons involved in pain signal transmission in the spinal cord.

A

Nociceptive-specific and WDR (wide dynamic-range) neurons send their axons up the dorsal horn and ant-lat spinothalamic tract.

These tracts synapse on 3rd order neurons in the contralateral thalamus (opposite side).

3rd order neurons project to the somatosensory Cx.

Note: 1st order neuron = initial pain signal, 2nd order neuron = the nociceptive-specific and WDR neurons aforementioned

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

3 classes of NT cmds integral to pain transmission

List and give examples.

A

Excitatory amino acids (glutamate, aspartate)

Excitatory neuropeptides (substance P, neurokinin A)

Inhibitory amino acids (glycine,GABA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Are NMDA receptors involved in pain transmission?

A

Yes. This is why ketamine has analgesic properties.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are traits of dynamic pain?

A

Pt can move

Relief provides improved outcome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the characteristics that describe pain (general)?

A

Location

Pattern

Quality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

List 3 non-opioid systemic analgesics.

A
  • Salicylates
  • Acetaminophen
  • NSAIDs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the analgesia ceiling effect?

A

Dose at which analgesia is maximized.

Beyond that, side effects increase (greater toxicity) without any additional benefits to the patient.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the does for adults and childre for acetaminophen?

A

Adults: 1 g QID

Children: 10-15 mg/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Studies of COX inhibitors have demonstrated improved post-op analgesia with up to X percent reduction in opioid analgesia requirements. What number(s) = X?

A

30-40%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are anesthetic benefits of NSAID as shown by research?

A

Reduced pain with movement

Reduced bladder spasm pain

Opioid sparing (up to 40%)

Earlier recovery of GI function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the dosing of Ketorolac.

A

>50 kg: 30 mg IV q6

<50 kg: 15 mg IV q6

Children: 0.5 mg/kg q6

Limit dosing to < 5 consecutive days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are complications of NSAIDs? Is there a special age group we need to worry about?

A

GI bleeding

Operative site bleeding (bigger issue for cranial and ENT procedures)

Acute renal failure

Hypersensitivity reactions

**These risks are shown to be much more significant in pts > 75 y/o

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe the mechanism of current NSAIDs.

A

They inhibit COX activation of prostaglandins.

COX = cyclo-oxygenase (comes from arachidonic acid)

Prostaglandins support renal and platelet functions, protect gastric mucosa, and lead to inflammation + pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Why were COX 2 inhibitors developed?

A

COX 1 (constitutive) was known to mediate effects on GI, renal, and plt systems.

COX 2 (inducible) was known to mediate effects on inflammatory sites.

Therefore, inhibition of COX 2 would theoretically avoid all the negative effects of non-selective COX inhibitors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe what research has found out about our current COX 2 selective inhibitors.

A
  • Similar analgesic effects to non-selective COX inhibitors
  • Improved GI safety
  • No plt effects
  • Renal side effects still present
  • Possible adverse CV and neuro effects with long-term use
20
Q

What is a commonly seen COX-2 inhibitor? Describe dosing.

A

Celecoxib (Celebrex)

100-200 mg PO q12

No need to withold. Dose pre-op or immediately post-op

21
Q

Does tolerance, physiologic dependence, and withdrawal from opioids indicate addiction?

A

Nope.

22
Q

Characteristics of opioid agonists include…

A

Full mu-receptor binding

No analgesic ceiling

Equianalgesic doses = equivalant efficacy

Similar side effects profiles

Different metabolites and elimination profiles

Effects on pain are highly patient variable!

23
Q

Traits of opioid agonist-antagonist combinations include…

A
  • Kappa agonism + partial/full mu antagonism
  • Respiratory depression ceiling (although this ceiling is pretty high [~20 mg morphine], so still a concern)
  • Analgesic ceiling
  • Acute withdrawal with mu-agonists
  • Psychomimetic side effects
24
Q

Approximate differences between peak-plasma levels and time-to-peak levels between IV and IM opioids are.. (give me a multiple)

A

Compared to IV opioids, IM opioids:

Peak plasma levels: 2-5 x lower

Time to peak: 3-7 fold higher

*Peaks and troughs in plasma levels rather than a steady plasma peak as in IV opioids

Note: HIGHLY patient variable

25
Q

Are IM opioids safe?

A

Not really. Erratic absorption means severe respiratory depression can occur spontaneously.

No advantage over oral route* (more erratic)

26
Q

Describe the elimination of Morphine. (Active metabolites, excretion)

A

Active metabolite = M6G

90% renal excreted

27
Q

Any contraindications to morphine that we commonly see? What’s a good long-acting alternative opioid we commonly give?

A

Yes: renal dysfunction due to active metabolite and predominantly renal excretion

Hydromorphone: 6x as potent as morphine; good alternative

28
Q

What is the best opioid agent to use in pts with renal dysfunction?

Describe this drugs relative potency, onset, and duration to morphine.

A

Fentanyl.

80-100x more potent than morphine

Quicker onset

Shorter duration

29
Q

Compare meperidine with morphine.

When is this opioid usually used?

A

Its 1/10th as potent as morphine

Has active metabolites (normeperidine) that provide no analgesic properties like M6G.

Contraindicated in renal dysfxn, siezures, MAOIs

Its pretty much used only if pt is intolerant to all other opioid agonists.

30
Q

Give me the equianalgesic doses with 10 mg morphine for Dilaudid and fentanyl.

A

10 mg morphine = 1.5 mg hydromorphone = 100 mcg fentanyl

31
Q

Is opioid consumption for pain correlated better with weight or age?

A

Age.

Very little correlation with weight (shallow slope)

32
Q

Whhat very negative adverse effects can acute reversal of opioids cause?

A

Due to acute reversal of analgesia, reversing opioids too rapidly with Naloxone can cause acute MI, seizures, or pulmonary edema!

33
Q

How should Naloxine be dosed?

A

Titrate 40 mcg q2-3 min to RR > 12/min

Infusion (due to spinals or IM overdose): hourly rate = load/3

For full respiratory arrest: 0.2 mg increments

Note: at MHTMC and most other places, comes in 0.4 mg bottles (titrate into a 10 cc syringe)

34
Q

Risk factors for respiratory depression with PCA include..

A

Advanced age

Advanced pulmonary disease

Concurrent administration of sedatives/hypnotics (avoid benzos)

OSA

Background infusions

35
Q

When should you use PCA with a basal/background infusion of more opioids?

If used, what limit should be placed on the rate of basal infusions?

A

Opioid tolerant patients

Children 5-12 y/o

Extreme extreme pain

Keep BI < 50% of total consumption possible that hour (titrate)

36
Q

What is the dose of morphine for intrathecal/spinal and epidural analgesia?

A

Intrathecal = 0.1-0.5 mg

Epidural = 2-5 mg

37
Q

Compare the use of bupi with ropi in epidurals (general pain mngmt)

A

Bupi causes differential sensory blockade

Ropi causes less motor blockade (lumbar)

38
Q

When we give epidural opioids, where’s the site of action we hope they get to exert their effects most?

A

Dorsal horn of the spinal cord to block pain signals presynaptically

39
Q

What are hydrophilic opioids? Lipophilic opioids?

What difference does it make in spinals?

A

Hydrophilic = morphine, Dilaudid

Lipophilic = fentanyl, sufentanil, etc.

Hydrophilic = slow onset, long duration, extensive CSF spread, more side effects, delayed respiratory depression

Lipophilic = fast onset, short duration, minimal CSF spread, lower side effects profile

40
Q

What are advantages of epidurals/spinals?

A

Synergistic analgesia

Superior pain relief

Decreased DVT and graft occlusions

Earlier return of bowel function

Less pulmonary complications

41
Q

Unlike lipophilic opioids, the administration of hydrophilic opioids can cause two (rather than one) phases of respiratory depression.

Why do these two phases occur?

A

FIrst phase is an acute phase due to systemic absorption (equivalent to same dose given IM)

Second dose is due to cephalad CSF spread (lipophilics don’t spread as much or last as long)

This second phase peaks in 8-10 hours and plateaus for >18 hours. Occurs in 0.1-0.6% pts.

Treat with naloxone load + infusion.

42
Q

What are some common analgesic adjuncts?

A

Ketamines

Benzodiazepines

Hydroxyzine (first gen anti-histamine with multiple antagonistic effects, not well studied)

Clonidine (or other alpha 2 agonists)

TCA

Gabapentin (Neurontin)

43
Q

What is Gabapentin used for?

A

Used as an antisiezure drug.

Effective in treating neuropathic pain, comeplx regional pain syndrom

Can block development of hyperalgesia

Due to ability to effect nociceptive processes involving central sensitization

44
Q

What kind of surgeries have been implicated to be the most likely predictor of chronic pain outcome?

A

Limb amputations

(Followed by thoracotomies and breast surgeries)

45
Q

What are some predictive factors for chronic pain?

A

Pre-op: repeat surgery, psychologic vulnerability, worker’s comp (lol)

Intraop: nerve damage risk in surgery

Post-op: radiation Rx, chemo Rx, depression, psychologic vulnerability, anxiety, neuroticism

46
Q
A

Basic Science II (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions