Chapter 37: Medications for Management of Chronic, Non-Odontogenic Pain

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1

What are the three gnereal categories of orofacial pain?

  1. musculoskeletal disorders (e.g. TMDs)
  2. neuropathic disorders (e.g. trigeminal neuralgia)
  3. neurovascular disorders (e.g. headaches)
2

Nerve fibers in the trigeminal nerve innervate blood vessels in the (...) where vasoactive and inflammatory actions occur.

card image

dura and pia mater

3

The (...) effect generated by muscle relaxants may provide the most benefit for pain control.

sedative effect

4

(...) released from the tuberomamillary nucleus in the hypothalamus acts as a neurotransmitter that modulates wakefulness.

histamine

5

NSAIDs are often used long-term for temporomandibular joint (...), but have adverse effects.

arthritides

6

(...) is an injectable NSAID that offers rapid and effective medication in acute pain.

ketorolac

7

Ketorolac should not be used in patients whose serum creatinine is greater than (...) mg/dL.

5 mg/dL

8

Overuse of the ketorolac can cause acute renal failure and should be limited to (...) days of therapy.

5 days

9

Ketorolac is available as a nasal spray, 15.75 mg per puff in each nostril, with the recommendation of a maximum of (...) sprays per day in each nostril, which would give a total maximum daily dose of (...) mg.

  1. four
  2. 126 mg
10

(...) is particularly useful as a topical NSAID for painful TMJ capsulitis and myalgia associated with TMD.

diclofenac

11

Diclofenac potassium is available as a 50-mg tablet. It can be dosed (...) with a maximum daily dose of (...) mg.

  1. tid to qid
  2. 200 200
12

(...) is one of the preferred NSAIDs for treatment of TMJ.

naproxen sodium

13

Naproxen sodium is usually dosed at (...) mg bid due to its longer half-life.

500 mg

14

(...) are useful in the treatment of acute inflammatory pain, headache, and some neuropathic pain.

adrenocorticosteroids

15

Injectable and oral steroid therapy is effective in management of temporomandibular joint (...).

inflammation

16

Intraarticular corticosteroids reduce pain and swelling associated with (...) of both muscles and joints.

inflammatory disease

17

Cortisone and hydrocortisone injected into the joint. Up to (...) injections may be given, but there should be an interval of (...) weeks between injections.

  1. three
  2. 4 weeks
18

(...) is the most common neuropathy seen in the orofacial region.

trigeminal neuralgia

19

For trigeminal and glossopharyngeal neuralgias, (...) drugs are considered the gold standard for treatment because of their superior clinical efficacy.

antiseizure

20

(...) is considered the gold standard for the management of trigeminal neuralgia, but it is also used to treat other neuropathic pain conditions.

carbamazepine

21

The primary mode of action of carbamazepine is thought to be its action as a (...), inhibiting repetitive neuronal discharge.

Na+-channel blocker

22

Before taking carbamazepine, the patient should have baseline laboratory values. What tests should be done?

  1. liver function (LFT)
  2. complete blood count (CBC)
23

Why might the dose of carbamazepine have to be increased after 1 to 2 weeks in order to maintain pain control?

It induces CYP3A4 and other cytochrome P450 enzymes, increasing its own metabolism.

24

(...) is structurally similar to carbamazepine, but it does not induce liver microsomal enzymes.

oxcarbazepine

25

Although oxcarbazepine, does not require liver function tests or complete blood count monitoring, chemistries should be monitored, as it can induce (...).

hyponatremia

26

What is the advantage of oxcarbazepine over carbamazepine for patients in an acute phase of trigeminal neuralgia?

It can be titrated more rapidly than carbamazepine.

27

(...) is a structural analogue of GABA and was developed as a GABA agonist.

gabapentin

28

It has been hypothesized that gabapentin selectively interacts with the (...) subunit of (...) channels, which maintain mechanical hypersensitivity in neuropathic pain

  1. α2ȍ
  2. voltage-dependent Ca2+
29

(...) was the first antiepilepsy medication approved for migraine, and is also used as a mood stabilizer in manic-depressive disorders.

valproic acid

30

The mechanism of action of valproic acid is related to inhibition of (...) channels, inhibition of (...) channels, and facilitation of GABAergic neurotransmission by inhibiting (...) and activating (...).

  1. Na+
  2. T-type Ca2+
  3. GABA aminotransferase
  4. glutamic acid decarboxylase
31

(...) is a novel anticonvulsant drug that is useful for trigeminal neuralgia through its action as a Na+-channel blocker.

lamotrigine

32

(...) is a monosaccharide-derivatived antiseizure drug that modulates voltage-dependent Na+ conductance, potentiates GABA-evoked currents, and blocks certain subtypes of the glutamate receptor.

topiramate

33

What drugs can interact with topiramate, decreasing its levels by increasing its clearance? (3)

  1. carbamazepine
  2. phenytoin
  3. valproate
34

What drugs does topiramate interact with, decreasing their levels by increasing their clearance? (3)

  1. phenytoin
  2. valproate
  3. oral contraceptives
35

(...) was the first antiseizure medication used to treat neuropathic pain. Its mode of action is similar to carbamazepine (blocking Na+ channels).

phenytoin

36

(...) is similar to gabapentin, and is used treatment for painful diabetic neuropathy and post-herpetic neuralgia.

pregabalin

37

Pregabalin has been shown to improve (...) sleep and may be useful in sleep disorders.

slow-wave delta

38

Pregabalin has been designated as a Schedule (...) controlled substance because of its potential for abuse and dependence.

V

39

Patients with neuropathy are started at (...) mg of pregabalin (...) times daily and may be titrated up to (...) mg daily within 1 week based on efficacy and tolerability.

  1. 50 mg
  2. three
  3. 300mg
40

(...) is a potent and selective GABA reuptake inhibitor used in combination with another antiseizure medication when better control of pain is needed.

tiagabine

41

The antinociceptive effect of tiagabine is related to inhibition of (...) and resultant increased extracellular (...).

  1. GABA reuptake
  2. GABA
42

(...) could be a useful medication for trigeminal neuralgia, but its potential psychiatric side effects limit its use.

levetiracetam

43

(...) is a sulfonamide antiseizure medication useful for both neuropathic pain and migraine prophylaxis.

zonisamide

44

Tricyclic antidepressants inhibit the reuptake of (...) and (...), both of which appear important in neuropathic pain and pain control.

norepinephrine and serotonin

45

In the process of nerve repair, the proximal terminal forms a mass of neuronal sprouts known as a (...), which generates spontaneous pain centrally.

neuroma

46

It has been shown that 90% of (...) nerve fibers release both glutamate and substance P from their peripheral terminals when the stimulus is sufficiently long lasting

C fibers

47

Glutamate is an agonist at the (...) and (...) receptors

  1. NMDA
  2. AMPA
48

Glutamate cannot activate the NMDA receptor without the presence of the co-agonist (...).

glycine

49

Ketamine and dextromethorphan are both (...) blockers and are effective in reducin responses in the dorsal horn nociceptive system.

NMDA channel

50

(...), an α-adrenergic receptor antagonist, acts on injured nociceptors to reduce sympathetically mediated pain.

phentolamine

51

Phentolamine increases sympathetic release of (...), which stimulates the (...) receptors.

  1. norepinephrine
  2. α1-adrenergic
52

Tizanidine, like clonidine, is an (...) receptor agonist that decreases sympathetic release of (...).

  1. α2-adrenergic
  2. norepinephrine
53

Which orofacial neuropathic pain diagnosis is consistent with the following symptoms?

  1. Continuous, variable aching pain
  2. No history of trauma or dental treatment in area
  3. No obvious local cause
  4. Pain aggravated by local stimuli
  5. Normal radiograph
  6. Positive response to somatic block
  7. Response to thermography not defined
  8. Sympathetic block does not define this disorder

spontaneous chronic peripheral trigeminal neuropathy

54

Which orofacial neuropathic pain diagnosis is consistent with the following symptoms?

  1. Continuous, variable, aching pain
  2. May be punctuated by sharp jolts of pain
  3. History of trauma to area
  4. No obvious local cause
  5. Pain aggravated by local stimuli
  6. Equivocal somatic block
  7. Normal radiograph
  8. Possible response to thermography
  9. Response to sympathetic block is equivocal

chronic traumatic trigeminal neuropathy

55

Which orofacial neuropathic pain diagnosis is consistent with the following symptoms?

  1. Trigenimal nerve involvement
  2. Episodic sharp electric-like pain
  3. Periods of remission
  4. No obvious local cause
  5. Pain is triggered with minor stimulation
  6. Normal radiograph
  7. Normal thermogram
  8. Positive block

trigeminal neuralgia I (classical trigeminal neuralgia)

56

Which orofacial neuropathic pain diagnosis is consistent with the following symptoms?

  1. Continuous, variable, diurnal aching pain
  2. Responsive to sympathetic block

sympathetically mediated pain

57

Which orofacial neuropathic pain diagnosis is consistent with the following symptoms?

  1. Pain present longer than 4 months
  2. Pain aggravated by local stimuli
  3. No obvious local cause
  4. Normal radiograph
  5. Equivocal response to somatic block
  6. Positive response to sympathetic block (60%)

complex regional pain syndrome

58

Which orofacial neuropathic pain diagnosis is consistent with the following symptoms?

  1. Continuous, variable, diurnal pain
  2. History of trauma to area
  3. Pain present longer than 4 months
  4. Pain aggravated by local stimuli
  5. No obvious local cause
  6. Normal radiograph
  7. Negative response to somatic block
  8. Negative response to sympathetic block

sympathetically independent pain

59

(...) usually characterized as an intense headache.

migraine

60

The sequence of events leading to a migraine often begins with a (...) phase in pia and dura blood vessels.

vasoconstriction

61

The vasoconstrictor phase of a migrane triggers a release of (...), and glutamate transmission increases.

card image

serotonin

62

Release of serotonin during a migrane is followed by (...) of meningeal vessels and inflammation in the area.

vasodilation

63

Migraines affect serotonin pathways projecting from the (...) of the midbrain to the cortex and limbic system.

card image

raphe nuclei

64

There are two types of drugs used to treat migraine; (...) drugs are given after the attack has begun.

card image

abortive

65

There are two types of drugs used to treat migraine; (...) drugs are given before the attack occurs.

card image

prophylactic

66

(...) are the mainstay of therapy for moderate to severe migraine.

triptans

67

(...) is a 5-HT3 receptor blocker used to treat nausea occurring with migraine.

ondansetron

68

(...) are a rare form of episodic headaches.

cluster headaches

69

Compounding pharmacists are able to combine medications in bases such as (...) for application to the external skin surface or (...) for intraoral application.

card image
  1. pleuronic lecithin organogel (PLO)
  2. orabase
70

Activation of (...) receptors causes nociceptors to release substance P.

capsaicin-responsive vanilloid receptors (TRPV1)

71

Long-term topical application of capsaicin depletes (...) stores and temporarily inhibits the neuron’s ability to synthesize more.

substance P

72

Topical (...) with is useful in applications over muscles and joints, producing a local antiinflammatory effect without gastric irritation.

ketoprofen

73

Patients using ketoprofen should be cautioned regarding potential for developing (...) because of the sensitizing properties of its benzophenone moiety.

photosensitivity

74

Ultraviolet light exposure of skin covered with ketoprofen cream promotes the photolysis of (...).

erythrocytes