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SF quizzes > Pain Management > Flashcards

Pain Management Flashcards

1
Q

Classify pain by duration

A

Acute or Chronic

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2
Q

Classify pain by nature

A

Nociceptive vs Non-Nociceptive

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3
Q

What are the 2 types of nociceptive pain?

A

Somatic

Visceral

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4
Q

Non-nociceptive pain, is broken down into ? (2)

A

Neuropathic

Sympathetic

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5
Q

Neuropathic pain, involves a lesion in what?

A

Neural tissue

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6
Q

Nociceptive pain is usually secondary to pain in what kind of tissue?

A

Non-neural tissue

Somatic or Visceral

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7
Q

What is somatic pain broken down into?

A

Surface tissue (skin, nose, mouth mucosa)

Deep tissue (bone, joint, muscle, connective tissue)

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8
Q

What structures are involved in visceral pain?

A

Thoracic, abdominal wall organs

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9
Q

What kind of pain is it? Diffuse, dull, achy crampy, pressure, tight, associated with nausea and vomiting

A

Nociceptive, visceral

pneumonia, liver mets, gas pains

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10
Q

What kind of pain is it? well localized, sharp, local burning or prickly sensation

A

Nociceptive - superficial somatic

incision, superficial burn

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11
Q

Well localized pain, dull achy and throbbing?

A

Nociceptive - deep somatic

fx, bone mets, muscle cramps

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12
Q

Poorly localized pain, follows nerve distribution, and is sharp/shooting/burning?

A

Neuropathic

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13
Q

What is the risk with an epidural should a patient be on anti-coagulation (beyond usual prophylaxis)

A

Epidural hematoma

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14
Q

What is acetaminophen’s mechanism of action?

A

Inhibits prostaglandin synthesis (weakly) via COX-1, COX-2 and COX-3 (likely) inhibition

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15
Q

Besides PG inhibition, what else may acetaminophen inhibit

A

Inhibit serotonin re-uptake and act at NMDA receptors

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16
Q

What is the maximum child dosage for acetaminophen?

A

75mg/kg/day

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17
Q

What is one caution with Acetaminophen?

A

May cause hepatic necrosis (esp if combined with ETOH abuse)

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18
Q

Two types of NSAIDS?

A 
Non-selective (COX-1 and COX-2)
and Selective (for COX-2)
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19
Q

What are the 5 non-selective (COX-1, COX-2) inhibitors?

A

Ketorolac, ibuprofen, naproxem, indomethacin, ASA

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20
Q

What are the risks with non-selective NSADS? (name 3)

A

Gastric Ulcer
Platelet dysfunction
Impaired renal blood flow

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21
Q

What is one COX-2 selective NSAID?

A

Celebrex

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22
Q

Advantage of a selective over a non-selective NSAID?

A

No effect on platelet function or bleeding, nor gastric mucosa

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23
Q

What are cons of a selective NSAID?

A 
Increased risk of AKI in select populations
Cardiovascular events (MI/Stroke)
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24
Q

What drugs are first line neuropathic pain?

A

Anti-convulsants (pregabalin, gabapentin)

TCAs

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25
Q

Is there a difference in the analgesic efficacy between gabapentin and pregabalin?

A

No

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26
Q

How do pregabalin and gabapentin act?

A

On pre-synaptic calcium channels

Dorsal horn and brainstem/forebrain

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27
Q

Which of the two pregabalin and gabapentin is usually dosed BID?

A

Pregabalin, although you may see TID

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28
Q

What percent of patients experience drowsiness and dizziness with anti-convulsants

A

50%

Tend to resolve with prolonged administration

29
Q

Anti-convulsants, hepatic or renally cleared?

A

Renal cleared (must adjust with impairment)

30
Q

Starting dose for gabapentin?

A

100 mg qHs, titrate up to TID

31
Q

How does tramadol act?

A

Weak opioid
Acts on opioid receptors
Inhibits re-uptake or norepinephrine and serotonin

32
Q

Which medication tends to interfere with analgesia from tramadol?

A

Ondansetron

33
Q

With what CrCl would you dose adjust Tramadol

A

Only if CrCl

34
Q

What proportion of Caucasians wont get much analgesia from Tramadol?

A

7-10% who lack CYP 2D6

35
Q

Tramadol can be useful in which 2 types of pain?

A

Neuropathic AND Nociceptive

36
Q

3 advantages of Tramadol

A

Less dependence

Less constipation or resp depression

37
Q

Two risks with Tramadol

A

Seizures

Serotonin syndrome

38
Q

Which narcotic should you no longer use? Why (two reaons)?

A

Codeine (a pro-drug turned into morphine)

1- 40-50% lack CYP 2D6 activity and experience less analgesia
2- Constipates more than any

39
Q

What are the strong opioids?

A

Morphine, hydromorphone, oxycodone

Fentanyl (sufentanil, remifentanil, alfentanil)

40
Q

What is the name for immediate release morphine?

A

Statex

41
Q

What is the name for sustained release morphine?

A

MS contin

42
Q

Time to peak for morphine PO? IV ? SC?

A

PO (IR tabs)

43
Q

What organ metabolizes morphine?

A

Liver, reduce dose in severe liver failure

Kindey clears active metabolites

44
Q

In renal failure, how should you adjust morphine dosing?

A

Lengthen dosing interval (since metabolites renally cleared)

45
Q

What is the synthetic analogue of morphine?

A

Hydromorphone

Same metabolism

46
Q

What are the 3 oral formulations of oxycodone?

A

OxyIR
OxyNEO
Percocet

47
Q

How did OxyNEO arise?

A

Tamper resistant replacement for Oxycontin (issue with abuse)

48
Q

How is oxycodone metabolized?

A

Metab by liver, excreted by kidneys

49
Q

Fentanyl’s mechanism of action?

A

Weak serotonin re-uptake inhibitor

50
Q

What metabolizes fentanyl?

A

CYP 3A4

51
Q

Which drugs can increase plasma concentration of fentanyl?

A

Clarithromycin and fluconazole

inhibit CYP 3A4

52
Q

Which opioid is safer in severe renal impairement?

A

Fenatyl, as its inactive metabolites are cleared by kidneys

53
Q

What is a typical morphine PCA bolus dose? 4 hour limit?

A 
1 mg
30 mg (4 hr limit)
54
Q

How do PCAs fair with regards to rates of resp depression?

A 
Same rate as with PRN opioid use
Negative feedback (drowsy patient wont press button as often)
55
Q

In surgical patient, indication for PCA?

A

More invasive/larger surgery
Pre-existing Hx of pain
Surgeries with regional techniques were block wanes

56
Q

Example of a non-surgical patient who can benefit from a PCA?

A

Sickle cell crisis patient

57
Q

What are 2 less common opioid side effects?

A

Pruritis

Neurotoxicity

58
Q

What are 2 rare opioid side effects?

A

Respiratory depression

Dependence

59
Q

Delirium as an opioid side effect, is common initially or with ongoing dosing?

A

Initially

60
Q

Patient on methadone awaiting surgery, continue or stop?

A

Almost always continue

61
Q

What is Suboxone?

A

Combination of buprenorphine and naloxone

62
Q

What is Buprenorphine?

A

It is an opioid agonist/antagonist

63
Q

What is the role of naloxone within the Suboxone formulation?

A
  • Deters crushing/injecting SL tabs
  • Inactive orally
  • But if injected causes WiTHDRAWAL by antagonizing opioid agonist of buprenorphine
64
Q

How long does buprenorphine bind opioid receptors?

A

A long-time: 3-5 days

this means can be difficult to achieve pain relief in patients who haven’t come off suboxone

65
Q

If someone is not opioid naive, how do you start opioids in hospital?

A

Calculate their typical daily dose
Continue their SR formulation
INCREASE breakthrough dose and make it q1h (i.e. more frequent)

66
Q

What is the opioid conversion from dilaudid?

A

Dilaudid:Morphine (1 : 5)
Dilaudid:Oxycodone (1 : 2.5)
Dilaudid:tramadol (1: 50)

67
Q

In an opioid naive patient continually having pain on oral morphine, what would you add?

A

Q1h breakthrough dose that is 50-100% of the q4h dose

68
Q

Define pain (4 key words)

A

Unpleasant SENSORY and EMOTIONAL experience

due to ACTUAL or POTENTIAL tissue damage

SF quizzes (9 decks)

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