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Cuccurullo Board Pearls > Pain Medicine > Flashcards

Pain Medicine Flashcards

1
Q

Where do A-β fibers terminate in the spinal cord?

A

Dorsal horn laminae III-V

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2
Q

Where do C fibers terminate in the spinal cord?

A

dorsal horn laminae I and II

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3
Q

Where do A-δ terminate in the spinal cord?

A

dorsal horn laminae I, III-V

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4
Q

What are the second-order neurons in the pain signaling pathway?

A

Wide dynamic range (WDR) neurons: located mostly in laminae III-V, receive input from low threshold A-β, nociceptive A-δ, and C fibers. Responses from WDR are graded - reflecting the type of stimulus fiber

Nociceptive-specific (NS) neurons; I and II only respond to noxious stimuli

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5
Q

What is gate control theory (Melzack and Wall, 1965)?

A

Input along low-threshold A-β fibers inhibit responses of nociceptive input to WDR (wide dynamic range) neurons

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6
Q

What is the size, velocity, myelination status, function of A-β fibers?

A

A-β: myelinated, 12-14 microns, 30-60m/s velocity

Function: touch, pressure, vibration, proprioception

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7
Q

What is the size, velocity, myelination status, function of A-δ fibers?

A

A-δ fibers: myelinated, 6-8 microns, 10-15 m/s velocity

Function: sharp pain, light touch, temperature

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8
Q

What is the size, velocity, myelination status, and function of C-fibers?

A

C fibers: unmyelinated, < 1 microns, < 1.5 m/s velocity

Function: dull, achy, burning pain, temperature

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9
Q

Opioid receptor types and function?

A
  • *Mu1**: analgesia
  • *Mu2**: respiratory depression, sedation, vomiting, euphoria, anorexia, physical dependence, pruritus

Delta: analgesia, spinal analgesia

Kappa: analgesia, sedation, psychotomimetic effects, dyspnea, respiratory depression, euphoria, dysphoria

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10
Q

What is pKa in relation to opioid pharmacology?

A

pH at which 50% of the drug is ionized. The non-ionized form crosses lipid membranes easily → The lower the pKa, the faster the onset of the drug

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11
Q

What does the octanol/water partition coefficient indicate?

A

Indicates lipid solubility (the higher the number, the more lipophilic the drug) - lipid-soluble drugs, such as fentanyl, exert most of their effect at the localized area where they are administered (less spreading of medication)

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12
Q

Oxycodone pKa, Octanol/H2O partition coefficient, mechanism of action?

A

Oxycodone

  • pKa: 8.5 (lower pKa signifies faster onset of drug effect)
  • Octanol/H2O partition coefficient: 0.7 (higher the number = more lipophilic)
  • Mechanism: Mu agnoist (metabolites = oxymorphone, noroxycodone)
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13
Q

Oxymorphone pKa, Octanol/H2O partition coefficient, mechanism of action?

A

Oxymorphone

  • pKa 9.3 (lower = faster onset)
  • Octanol/H2O partition coefficient: 0.98 (higher = more lipophilic)
  • Mechanism: opioid agonist (metabolites = 6-hydroxy-oxymorphone)
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14
Q

Hydromorphone pKa, Octanol/H2O partition coefficient, mechanism of action?

A

Hydromorphone (Dilaudid)

  • pKa = 8.1 (lower = faster onset)
  • Octanol/H2O partition coefficient: 1.28 (higher = more lipophilic)
  • mechanism: Mu agonsit
  • Metabolites = hydromorphone-3-glucuronide
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15
Q

Tramadol pKa, Octanol/H2O partition coefficient, mechanism of action?

A

Tramadol

  • pKa: 9.4
  • Octanol/H20 coefficient: 1.35
  • Mechanism: weak mu agonist, weak NE/5HT re-uptake inhibitor
  • Metabolite: O-desmethyltramadol
  • **Contraindicated with MAOi or SSRI (increased risk of seratonin syndrome)
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16
Q

Morphine pKa, Octanol/H2O partition coefficient, mechanism of action?

A

Morphine

  • pKa = 8.0 (lower = faster onset)
  • Octanol/H2O partition coefficient = 1.4 (higher = more lipophilic)
  • Mechanism: Mu agonist
  • Metabolites: morphine-3-glucuronide, morphine-6-glucuronide, hydromorphone
  • Do not use in renal failure
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17
Q

Talpentadol pKa, Octanol/H2O partition coefficient, mechanism of action?

A

Talpentadol

  • pKa = 9.34-10.45 (lower = faster onset)
  • Octanol/H2O partition coefficient: 2.87 (higher = more lipophilic)
  • Mechanism: Mu agonist and NE reuptake inhibitor
  • Metabolites: tapentadol-O-glucouronide
  • **Do not use in severe hepatic dysfunction
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18
Q

Meperidine pKa, Octanol/H2O partition coefficient, mechanism of action?

A

Meperidine

  • pKa: 8.5 (lower = faster onset)
  • Octanol/H2O partition coefficient: 39 (higher = lipophilic)
  • Mechanism: weak mu agonist
  • Metabolite: normeperidine
  • **contraindicated with MAOi
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19
Q

Codeine pKa, Octanol/H2O partition coefficient, mechanism of action?

A

Codeine

  • pKa: 8.2 (lower = faster onset)
  • Octanol/H2O partition coefficient: N/A
  • Mechanism: weak mu and delta agonist
  • Metabolites: morphine, hydrocdone, codeine-6-glucuronide
  • **Antitussive, anti-diarrhea, metabolized to morphine for analgesia
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20
Q

Hydrocodone pKa, Octanol/H2O partition coefficient, mechanism of action?

A

Hydrocodone

  • pKa: 8.9 (lower = faster onset)
  • Octanol/H2O partition coefficient: N/A
  • Mechanism: Mu and kappa agonist
  • Metabolites: Dihydrocodeine, hydromorphone
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21
Q

Methadone pKa, Octanol/H2O partition coefficient, mechanism of action?

A

Methadone

  • pKa: 9.3 (lower = faster onset)
  • Octanol/H2O partition coefficient: 116 (higher = more lipophilic)
  • Mechanism: Mu and delta agonist, NE and 5HT re-uptake inhibitor, NMDA antagonist
  • Metabolites: EDDP (inactive)
  • **May cause QT prolongation
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22
Q

Fentanyl pKa, Octanol/H2O partition coefficient, mechanism of action?

A

Fentanyl

  • pKa: 8.4 (lower = faster onset)
  • Octanol/H2O partition coefficient: 860 (higher = more lipophilic)
  • Mechanism: Mu agonist
  • Metabolite: norfentanyl
23
Q

Buprenorphine mechanism of action?

A

partial mu and kappa agonist, delta antagonist

suboxone contains buprenorphine + naloxone [receptor antagonist]

24
Q

Mechanism of action of pentazocine (talwin); butorphanol (stadol); nalbuphine (nubain)?

A

kappa agonist, mu antagonist

25
Q

Side effects of opioids?

A
  • Respiratory suppression (act on brainstem to reduce sensitivity of respiratory center to PCO2)
  • Suppresses cough reflex (effect on brainstem nuclei in cough reflex pathway) - common use for codeine
  • Constipation (maintained contraction of smooth muscles in the gut)
  • Sexual Dysfunction (erectile dysfunction, decreased libido); correlated to hypogonadism and low testosterone levels
26
Q

NSAID mechanism of action?

A

inhibit COX-1 and COX-2 enzymes, which produce prostaglandins involved in promoting inflammatory responses after tissue injury

27
Q

NSAIDs with more COX-2 selectivity?

A

Meloxicam > Celecoxib >> diclofenac > sulindac (*most common to cause liver failure)

28
Q

NSAIDs w/ less COX-2 selectivity?

A

Ibuprofen, naproxen, salicylate >> indomethacin, ketorolac

29
Q

Concerning side effect of SSRIs/SNRIs?

A

serotonin syndrome (especially when used in conjunction with TCAs, monoamine oxidase inhibitors (MAOIs), triptans, tramadol, or some antiemetics may result in serotonin syndrome

30
Q

Gabapentin mechanism of action?

A

not entirely known, interacts with alpha-2-delta subunits of L-type calcium channels in CNS

Used to treat pain from diabetic neuropathy, postherpetic neuralgia, HIV-associated neuropathy, GBS, phantom limb pain, spinal cord injury pain, cancer-associated neuropathic pain

31
Q

Main side effects of gabapentin?

A

somnolence, dizziness, edema

32
Q

main pregabalin side effects?

A

somnolence, dizziness, dry mouth, edema

33
Q

Mechanism of action of carisoprodol?

A

blocks interneuronal activity in descending reticular formation and dorsal horn of spinal cord to depress polysynaptic reflexes

Uses: acute MSK pain

Side Effects: drowsiness, dizziness, HA, hepatotoxicity, ataxia, N/V

**Use w/ caution - increasingly abused due to metabolite meprobamate (controlled substance)

34
Q

Nociceptive/Somatic Pain is mediated by what part of the nervous system?

A

Somatic nervous system

Description:

  • deep somatic pain: dull/aching
  • superficial somatic pain: sharp, pricking
  • burning, localized, reproducible

Caused by noxious perception from tissue damage can originate from the skin, muscle, bone, or fascia

35
Q

Visceral pain is mediated by which part of the nervous system?

A

Autonomic nervous system

Description: crampy, dull, vague in location

Caused by internal structures of solid/hollow organs

36
Q

Neuropathic Pain/Central pain caused by?

A

primary lesion or dysfunction of the pain-sensing nervous system (CNS or PNS)

Description: burning, tingling, shooting, stabbing, electric-like; may be associated with numbness/tingling

37
Q

Treatment options for Myofascial Pain?

A
  • Physical therapeutics
  • Modalities (heat/ice, ultrasound, transcutaneous electrical nerve stimulation [TENS])
  • Cooling analgesic spray
  • Stretch, massage, postural alignment, acupressure
  • Trigger point injection w/ or w/o injectants (dry needling)
  • Botulinum toxin has been used in significant refractory cases (postprocedural stretching is important)
38
Q

Migraine headache presentation

A

unilateral > bilateral, pulsing/throbbing, stabbing, frontal, or temporal pain

Can occur with or without aura

Can be associated w/ N/V, photophobia, phonophobia, vertigo, diarrhea, diaphoresis

Typically lasts for 30 min to 1 day, can be intractable and last up to 1 week (status migrainosus)

39
Q

Two main migraine subtypes

A
  1. Migraine without aura (common)
  2. Migraine with aura (classic): focal neurological symptoms preceding or accompanying headache
    1. visual disturbances (bright spots, dark spots, tunnel vision), tremor, pallor, vertigo, unilateral numbness or weakness, transient aphasia, or thick speech
    2. Premonitory and resolution symptoms: hyperactivity, hypoactivity, depression, craving for particular foods, repetitive yawning, other less typical symptoms
40
Q

Migraine cortical spreading depression (CSD) theory

A

wave of neuronal depolarization in cortical grey matter followed by neuronal activity suppression, resulting in blood flow changes (hyperemia, then oligemia)

41
Q

Migraine neurovascular theory?

A

Trigeminovascular system: plexus of unmyelinated fibers from trigemical ganglion innervating cerebral and pial arteries, venous sinuses, and dura mater -→ stimulation by cortical spreading depression causes antidromic activation of trigeminovascular system, resulting in release of peptide neurotransmitters (substance P, neurokinin A, and calcitonin gene-related peptide)

42
Q

Effect of peptide neurotransmitters on vasculature in setting of migraine?

A

Peptide neurotransmitters (substance P, neurokinin A, calcitonin gene-related peptide - CGRP) vasodilate nearby blood vessels, which causes extravasation of plasma or “sterile neurogenic inflammation” -→ stimulates the trigeminal nerve endings, causing nociceptive orthodromic activation to the trigeminal ganglion, resulting in pain

43
Q

Migraine HA vascular theory?

A

Intracranial vasoconstriction results in ischemia, which then causes the aura that precedes migraines. Subsequent rebound vasodilation and activation of perivascular nociceptors results in the migraine HA

44
Q

Stratified care approach to migraine headaches?

A

Migraine Disability Assessment (MIDAS) scores to choose treatment based on severity and degree of disability

45
Q

Abortive Migraine medications

A
  1. Acetaminophen
  2. NSAIDs (ASA, ibuprofen, naproxen, ketorolac)
  3. Opioids (butalbital, meperidine)
  4. Adjunctive medications (prochlorperazine and metoclopramide)
  5. Ergotamines (FDA pregnancy category X)
  6. Triptans (5-HT 1B and 1D agonists)
46
Q

Migraine HA preventative medications?

A
  1. Beta-blockers (propranolol, timolol)
  2. NSAIDs
  3. TCAs (e.g. amitryptyline)
  4. SSRIs (e.g. fluoxetine)
  5. Anti-epileptics (valproic acid, carbamazepine, gabapentin)
  6. Magnesium
  7. Botulinum toxin injections
47
Q

Most common HA type?

A

Tension headaches (bilateral, usually lasts 30min to several days or weeks), responds to OTC analgesics (NSAIDs, acetaminophen)

48
Q

Postmastectomy pain syndrome typically affects which thoracic levels?

A

Intercostobrachial neuralgia (T1-T2) - chronic neuropathic pain that develops shortly after, or several months postsurgery. Prevalence is higher after lumpectomy than mastectomy and especially when axillary lymph node dissection has been performed. Pain is localized to the axilla, shoulder, arm, and/or chest wall.

49
Q

Hypertrophic pulmonary osteoarthropathy is associated with what malignancy?

A

Lung cancer - clubbing and periosteal proliferation of the tubular bones → causing symmetricla painful arthropathy affecting the ankles, knees, wrists, and elbows. Pain improves if tumor is resected. In advanced lung cancer, NSAIDs/bisphosphonates are treatment mainstays

50
Q

World Health Organization Analgesic Ladder for Cancer Pain relief?

A
  1. Mild to moderate pain: nonopioid analgesics +/- adjuvant
  2. Moderate pain: short-acting opioids +/- nonopioid analgesics +/- adjuvant
  3. Moderate to severe pain: short- and long-acting opioids +/- nonopioid analgesics +/- adjuvant
51
Q

When is a dorsal root entry zone (DREZ) lesioning indicated?

A

Selective destruction of neurons in the posterolateral spinal cord used to treat medically refractory chronic pain syndromes associated w/ neurons that develop paroxysmal hyperactivity following deafferention (e.g. brachial plexus avulsion)

52
Q

When is a cordotomy indicated?

A

surgical procedure that ablates the spinothalamic tract, providing selective loss of pain and temperature perception several segments below and contralateral to where the lesion is placed.

  • Used for severe pain secondary to cancer (especially for pleural and peritoneal mesothelioma) where treatment to level 3 of the WHO pain ladder is ineffective
  • B/l cordotomies may be required for visceral or bilateral pain (effect usually temporary)
53
Q

Etiology of Complex Regional Pain Syndrome

A

thought to be caused by dysfunction of the central and peripheral nervous systems, resulting in allodynia, edema, changes in skin blood flow, and/or abbnormal sudomotor activity

54
Q

What is the distinction b/t CRPS type I and type II?

A

CRPS 1: diagnosed if previous symptoms

Cuccurullo Board Pearls (5 decks)

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