Pain management Flashcards

1
Q

What is the physiology of processing pain

A
  • Pain sensation STARTS w/ stimulation of nociceptors
  • Receptors are in somatic and visceral structures, and help discriminate noxious from innocuous stimuli
  • Nociceptors are activated by mechanical, thermal, or chemical stimuli
  • Noxious stimuli may activate cytokines or chemokines that activate/sensitize nociceptors
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2
Q

What are the steps in processing pain

A
  • Transduction: stimulation of nociceptors by mechanical, thermal, or physical stimuli
  • Conduction: receptor activation causes AP along afferent fibers (large myelinated or small unmyelinated) to spinal cord.
  • Transmission: Nociceptive fibers synapse in dorsal horn and release excitatory NT, while spinothalamic tract brings signal to higher brain structures
  • Perception: you experience pain when signals reach higher cortical structures
  • Modulation: Glutamate, substance P, endogenous opioids, GABA, NE, and serotonin can modulate pain
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3
Q

What is maladaptive pain

A

Pathophysiologic pain resulting from damage or abn fxn of nerves in CNS or PNS. Pain circuits rewire themselves anatomically and biochemically= chronic pain, hyperalgesia, or allodynia

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4
Q

Examples of maladaptive pain are

A
postherpetic neuralgia 
diabetic neuropathy 
fibromyalgia 
IBS
chronic headaches
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5
Q

Explain Somatic pain

A

arise from skin, bone, joint, muscle, or connective tissue

Pain presents as throbbing and well localized

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6
Q

Explain visceral pain

A

arise from internal organs (colon, pancreas, etc.)

Manifests as pain coming from other structures (referred pain) or as a more localized phenomenon

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7
Q

During stimulation of nociceptors, noxious stimuli may lead to release of

A
Bradykinins
H+ and K+ ions 
Prostaglandins 
Histamine
Interleukins
TNF-a
Serotonin
Substance P
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8
Q

What kind of pain do different size fibers transmit

A

Large, myelinated A fibers: sharp, localized pain

Small, unmyelinated C fibers: dull, aching, poorly localized pain

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9
Q

What is the endogenous opiate system

A

consists of NT like enkephalins, dynorphins, and endorphins

Receptors mu, delta, kappa found throughout the CNS

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10
Q

Where are NMDA receptors found

A

in the dorsal horn

They can increase the receptors responsiveness to opiates

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11
Q

What is the descending system for control of pain transmission in the CNS

A

a system that originates in the brain and can inhibit synaptic pain transmission at dorsal horn
NT include endogenous opioids, serotonin, NE, and GABA

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12
Q

What cognitive and behavioral functions can decrease pain

A

Relaxation
Distraction
meditation
guided mental imagery

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13
Q

What can worsen pain

A

depression and anxiety

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14
Q

What is inflammatory pain

A

Body shifting from preventing tissue damage to promoting healing
Pain threshold is reduced and the injured area becomes more sensitive

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15
Q

What does adaptive inflammation do

A

decreases our contact with and movement of injured area, promoting healing
Increased excitability or responsiveness of neurons in CNS (central sensitization)

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16
Q

Central sensitization is a major cause of

A

hypersensitivity to pain after injury

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17
Q

What is neuropathic vs functional pain

A

Neuropathic: result of nerve damage (post-herpetic neuralgia, diabetic neuropathy
Functional: abnormal operation of nervous system (fibromyalgia, IBS, HA)
-both are types of maladaptive pain!

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18
Q

How do patients describe neuropathic and functional pain

A

burning, tingling, shock like, or shooting
hyperalgesia (exaggerated pain response to normal noxious stimuli)
allodynia (pain response to normally non-noxious stimuli)
-Explains why this type of pain manifests long after actual nerve related injury is identified

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19
Q

What are some etiologies of cancer pain

A

The disease itself: tumor invasion, organ obstruction
Treatment: chemo, radiation, surgical incisions
Dx procedures: biopsy

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20
Q

Non-pharm therapies for acute and chronic pain are

A

physical manipulation
heat or cold application
massage
exercise
Transcutaneous electrical nerve stimulation (surgical, traumatic, neuropathy, and MSK pain)
Cognitive, behavioral, and social aspects of pain Tx

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21
Q

Pain is…

A

subjective

best diagnosed based on patient description, H&P

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22
Q

How can you obtain a baseline pain description

A

PPQRSTl
Palliative (what makes it better)
Provocative factors (what makes it worse)
Quality (describe the pain)
Radiation (and location)
Severity (how does it compare to other pain you’ve felt)
Temporal (intensity change with time)

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23
Q

Describe acute pain

A
  • Not usually dependent or tolerant to medication
  • No psych component, depression, or insomnia (usually)
  • Tx goal is pain reduction
  • Usually has identifiable cause
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24
Q

Describe chronic pain

A
  • Usually dependent or tolerant to meds
  • Psych often a major problem (depression common)
  • Significant family issues
  • Usually no identifiable cause
  • Tx goal is functionality
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25
Q

How do infants present with acute pain

A

change in feeding habits
increased agitation
calling out

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26
Q

Sx of acute distress are

A

sharp, dull, shock like, tingling, shooting, radiating, fluctuating intensity, varying location
Occur in a timely relationship with obvious noxious stimuli

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27
Q

Signs of acute pain are

A
HTN 
tachycardia
diaphoresis 
mydriasis
pallor 
(signs are NOT diagnostic; sometimes there aren't even obvious physical signs of pain)
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28
Q

What must you pay attention to in chronic pain

A

mental and emotional factors that alter pain threshold; people can appear to have no noticeable suffering

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29
Q

Symptoms of chronic pain are

A

sharp, dull, shock-like, tingling, shooting, radiating, fluctuating in intensity, and varying in location
occur withOUT a temporal relationship with a noxious stimuli
Over time, pain stimulus may cause Sx to change (sharp to dull, obvious to vague)

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30
Q

Signs of chronic pain are

A

Most cases, no obvious signs
But they DO have comorbid conditions!
Outcome of Tx is not predictable (where as it IS predictable in acute pain)

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31
Q

What non-opioid analgesics can be used to alleviate pain

A

ASA: stop 7-10 days before surgery
Choline and mag trisalicylate: no anti-platelet function bc no acetyl group (750 q8hr for old)
Diflusinal: no acetyl group
APAP: 2g max for old, 3g max for gen pop. <50kg, 750mg max single dose

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32
Q

More nonopioid analgesics (used less) are

A
Anthranilic acid (Mefenamic acid): max 7 days 
Indolacetic acid (Etodolac)
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33
Q

Non-opioid analgesics approved for adults are

A
  • Phenylacetic acids: Diclofenac potassium, D. epolamine (patch over intact skin), D. sodium (voltaren gel)
  • Propionic acid: Ibuprofen (max 3.2g inflamm, 1.2g analgesia/fever), Ketoprofen, Naproxen (OA), Naproxen sodium (acute pain)
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34
Q

What are pyrrolacetic acids

A

Ketorolac! Max 5 days
parenteral
oral: only use if continuation of parenteral
nasal: old or <50kg, one spray in one nostril q6-8 hrs

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35
Q

What is the selective cox-2 inhibitor

A

Celecoxib
if cardiac concern, max 200mg x day
(use ASA before Celecoxib)

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36
Q

What do you need to monitor when taking NSAIDs

A

upper GI bleed: CBC, stool guaiac

acute renal failure: SrCr

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37
Q

What do you need to monitor when taking APAP

A

Hepatotoxicity: ALT/AST, PT/INR, albumin, APAP serum concentration

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38
Q

NSAIDS, APAP, and ASA are used in

A

mild to moderate pain
Can be used with opioid agents
NO alcohol with APAP
avoid OD when combining with products that low key include them already

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39
Q

What underlying factors expose someone taking NSAIDs to nephrotoxicity

A

Renal impairment
hypovolemia
CHF

40
Q

Describe the pain scale

A

Mild: 0-3/4
Moderate: 4-7
Severe: 8-10

41
Q

What are the Phenanthrenes

A

Morphine: naturally occurring, high histamine release
Dilaudid (hydromorphone): semi synthetic, low histamine release
Oxymorphone: semi-synthetic, low histamine release
Levorphanol
Codeine: natural, high histamine release
Hydrocodone: semi-synthetic, no histamine release
Oxycodone: semi-synthetic, low histamine release

42
Q

What is morphine used for

A

drug of choice in severe pain

can use immediate release product with controlled release product to control breakthrough pain in cancer

43
Q

What is hydromorphone used for

A

severe pain

more potent than morphine, no other benefits

44
Q

What is oxymorphone used for

A

severe pain
ER formula to deter misuse
can use immediate release with controlled release to control breakthrough cancer pain

45
Q

What is Levorphanol used for

A

severe pain
extended half life, good for cancer patients
if w/ chronic pain, wait 3 days for dose adjustment

46
Q

What is codeine used for

A

mild-moderate pain and cough suppression
Depends on CYP450 2D6 to metabolize it to morphine
weak analgesic, so use with NSAIDs, ASA, or APAP
NO in kids!!

47
Q

What is hydrocodone used for

A

mod-severe pain
best if used with NSAID, ASA, or APAP
only available as a combo product w/ other analgesics

48
Q

What is oxycodone used for

A

mod-severe pain
most effective with NSAID, ASA, or APAP
can use immediate release for breakthrough cancer pain
Reformulated to deter misuse

49
Q

What are the phenylpiperidines

A

Meperidine (demerol): synthetic, high histamine release

Fentanyl: synthetic, low histamine release

50
Q

What is Meperidine used for

A

severe pain (oral route NOT recommended)
do NOT use in renal failure
Can cause tremors, myoclonus, and seizures
Produces Mydriasis (dilation)
Can cause hyperpyrexia or Sz if used w/ MAOI

51
Q

What is Fentanyl used for

A
severe pain (no transdermal for acute pain) 
Transmucosal, intranasal, and sublingual: start low, despite daily opioid use. can Tx breakthrough cancer pain in pt already receiving or tolerant to opioids 
*Must do REMS program to Rx transmucosal, intranasal, or sublingual forms
52
Q

What are the Diphenylheptanes

A

Methadone: synthetic, low histamine release
Methadone treats severe chronic pain, but watch for sedation
Chronic pain can dose q12 hours
Do not titrate sooner than q2 weeks

53
Q

What is a large reason for lower use of methadone

A

QT prolongaiton!

can lead to torsades

54
Q

What are the agonist-antagonist, or partial agonists (all synthetic)

A

Pentazocine
Butorphanol
Nalbuohine
Buprenorphine (suboxone)

55
Q

What is pentazocine used for

A

third line for mod-severe pain
can cause withdrawal in opioid dependent patients
Parenteral dose NOT recommended

56
Q

What is Butorphanol used for

A

second line for mod-severe pain

can cause withdrawal in opioid dependent patients

57
Q

What is Nalbuphine used for

A

second line for mod-severe pain

can induce withdrawal in opioid dependent patients

58
Q

What is Buprenorphine* used for

A

second line for moderate to severe pain
can cause withdrawal in opioid dependent patient
Naloxone may NOT reverse respiratory depression in these patients
Need training to Rx this drug!

59
Q

What are the central analgesics (synthetics)

A

Tramadol

Tapentadol

60
Q

How do you dose tramadol

A

Max for non-extended release: 400mg/24hr

Decrease dose if >75 or CrCl<30 (max is 300)

61
Q

How do you dose Tapentadol

A

First day: can give another dose 1 hr after first dose. Max 700mg
After first day:max dose 600 mg
Need REMS

62
Q

If taking opioids, you must monitor for

A

Respiratory depression (RR or end tidal capnography)- higher risk if w/ OSA or COPD
constipation: BM frequency and consistency
Sedation
N/V
Tolerance
Dependence
Addiction/Abuse
Histamine release (urticaria, pruritis, bronchospasm)
Increased sphincter tone (urine retention, biliary spasm)
Hypogonadism (fatigue, depression, amenorrhea)

63
Q

Opioids to avoid and exercise caution in bc of what they do

A

Codeine: don’t use in kids or pregnancy
Meperidine: not recommended bc it doesn’t last long , can cause seizures and renal insufficiency and serotonin syndrome
Agonist/Antagonist: can cause opioid withdrawal
Tramadol: caution in old or renal dysfunction. risk of seizure, serotonin syndrome, and hypoglycemia

64
Q

What is Naloxone

A

a synthetic opioid antagonist
Duration of action of some opioids can outlast duration of naloxone, so you may need repeat doses
When you give narcan, call 911 ASAP!

65
Q

What are Tx options for neuropathic pain

A
anticonvulsants 
TCA
SNRI 
Opioids 
topical analgesics 
(she recommends methadone and tramadol)
66
Q

What is Gabapentin

A

anti-convulsant that decreases excitatory NT and nociception through voltage gated calcium channels (esp. w/ a-2 d-1 subunit)

67
Q

ADE of gabapentin are

A
peripheral edema 
weight gain
tremor
dizziness 
ataxia
fatigue
HA
abnormality in thinking, amnesia
68
Q

What is pregabalin (lyrica)

A

binds a-2d receptor of voltage gated calcium channels in CNS= inhibits excitatory NT
structurally related to GABA, but does NOT bind GABA or benzo receptors
Anti-nociceptive and anti-convulsant activity
decreases Sx of painful peripheral neuropathies
can affect descending noradrenergic and serotonergiv pain transmission from brain to SC

69
Q

ADE of pregabalin are

A
peripheral edema 
weight gain
tremor
dizziness 
ataxia
70
Q

What are adjunct therapies to use for chronic pain

A

TCA and SNRI: block reuptake of serotonin and NE in order to enhance pain inhibition

71
Q

What are topically local analgesics/anesthetics that decrease nerve stimulation

A

Lidocaine patch
NSAID patch: flector, voltaren
OTC salonpas, Tigerbalm

72
Q

How does tiger balm work

A

increases blood flow to the area and decreases pain

73
Q

What is Duloxetine (cymbalta)

A

potent SNRI
weak dopamine reuptake inhibitor
Does not significantly act on muscarinic chlinergic, H1, a-2 adrenergic receptors, or MAOI

74
Q

ADE of Suloxetine (cymbalta) are

A
HA
drowsiness 
fatigue 
nausea
xerostomia
insomnia
agitation
75
Q

What is regional analgesia

A

local anesthetics that can also provide relief of chronic and acute pain by blocking nerve impulses
injections (in joints, epidural/intrathecal space, along nerve roots, or in a nerve plexus) or topicals

76
Q

What is proven effective in treating focal neuropathic pain

A

Lidocaine patches

77
Q

ADE of regional analgesics are

A

CNS depression and excitation (dizzy, tinnitus, drowsy, disoriented, muscle twitching, seizures, respiratory arrest)
Myocardial depression, hypotension, decreased CO, heart block, bradycardia, arrhythmia, cardiac arrest

78
Q

Disadvantages of regional analgesics are

A

need for skillful technical application
need for frequent administration
highly specialized follow up procedures

79
Q

What are some local anesthetics

A

Esters: Procaine, Chloroprocaine, Tetracaine
Amides: Mepivacaine, Bupivacaine, Lidocaine, Prilocaine, Ropivacaine

80
Q

What are some intraspinal epidural opioids

A

Morphine (can also use subarachnoid)
Hydromorphone (can also use subarachnoid)
Fentanyl
Sufentanil

81
Q

What is Ziconotide (intrathecal)

A

Selectively binds N-type calcium channels on nociceptive afferent nerves of dorsal horn
blocks excitatory NT release
reduces sensitivity to painful stimuli
NO action on Mu receptor (endogenous opioid system does have effect on these!)

82
Q

ADE of Ziconotide are

A

Serious: confusion, dizziness, hallucinations, urinary retention
Eh: sedation, somnolence, nausea, HA

83
Q

Ziconotide is FDA approved for

A

first line in localized neuropathic and nociceptive pain with morphine
with morphine in diffuse neuropathic and nociceptive pain

84
Q

New guidelines say acute, subacute, and chronic back pain should be treated

A

first w/ non-pharm (heat, massage, acupuncture, CBT, mindfulness based stress reduction, PT)
Limit meds to chronic back pain or inadequate response to non-pharm Tx
Acute: NSAIDs, skeletal muscle relaxers
Chronic: NSAID (1st line). Duloxetine and tramadol (2nd line)
-There are no long term studies on back pain pts Tx with pain meds

85
Q

What Tx is or is NOT recommended in fibromyalgia

A

Use: APAP! also Tramadol, SNRI (duloxetine), AED (pregabalin)
do NOT use: opioids

86
Q

What Tx is recommended in neuropathic pain (non-cancer)

A

1st: AED, SNRI, TCA, 5% lidocaine patch
2nd: opioids
Rarely effective: APAP, NSAIDs

87
Q

How can you Tx cancer pain

A

mild: NSAIDs, APAP
mod: APAP or NSAID + opioid. TCA. AED. Radiopharmaceutical (bone pain)
severe: opioid, NSAID. TCA, AED

88
Q

What is heroin derived from

A

Poppy
Diacetylmorphine (acetyl group helps it cross the BBB) that is metabolized to morphine
UDS will show + for morphine and codeine

89
Q

Heroin can be contaminated with

A

quinine, scopolamine, strychnine

90
Q

a true opioid allergy (rare) is due to

A

IgE mediated or T cell mediated
will present with bronchospasm!
angioedema may be true allergy, but can also be pseudoallergy

91
Q

what is a pseudoallergy

A

common type of reaction to opioids; Sx can resemble a true allergy
Caused by histamine release from cutaneous, mast cells, and non-immunologic effect
Sx: itching, flushing, and sweating
hives, tachycardia, and low BP can be seen in a true or pseudo allergy

92
Q

Pseudoallergy depends on

A

concentration of the opioid at the mast cell

93
Q

If you have flushing, itching, hives, sweating, mild hypotension; or itching, flushing, and hives at injection site…

A

This may be a pseudoallergy as a result of histamine release! Options include:
non-opioid analgesic
Avoid codeine, morphine, meperidine
Use more potent opioid, less likely to release histamine. In order: Fentanyl, Levorphanol, Hydromorphone, Oxycodone, Hydrocodone
Can also admin an antihistamine, or reduce dose if tolerated

94
Q

The opioids MC associated with pseudoallergy are

A

Morphine
Codeine
Meperidine
(these all have “high histamine release”)

95
Q

If you have severe hypotension, skin rxn (not itch flush hive), difficulty breathing swallowing or talking, or swelling of face lips mouth tongue or pharynx…

A
This is a true allergy! 
Use a non-opioid analgesic 
use an opioid chemical class different than the one you gave (Phenylpiperidine, Diphenylheptanes, or Morphine group)
96
Q

Meperidine has an active metabolite that can cause

A

hallucinations and erratic behavior

Normeperidine

97
Q

What will you NEVER grow tolerant to when taking pain medication

A

Miosis (pupil constriction)
Constipation
-you will eventually grow tolerant to the other ADE!