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Review > Chapter 16 Membrane Stabilizers > Flashcards

Chapter 16 Membrane Stabilizers Flashcards

1. In neuropathic pain, there is altered processing and changes in central modulation. These include pathologic activity in injured nerves (resulting in hyperexcitability, spontaneous and evoked pain), loss of C-fibers, sprouting of the large fibers in the outer laminas of the dorsal horn where the nociceptive-specific neurons are located (resulting in allodynia), and increased activity in the sympathetic nervous system. 2. Some of the molecular changes in neuropathic pain include the accumulat

1
Q

conditions resulting in chronic neuropathic pain include

A

diabetic polyneuropathy, postherpetic neuralgia,
central neuropathic pain, traumatic/surgical nerve
injury, incomplete spinal cord injury, trigeminal neuralgia, multiple sclerosis, radiculopathy, complex regional pain
syndrome (CRPS), and HIV-associated peripheral neuropathy

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2
Q

neuropathic pain

A

Defined as pain initiated or caused by a primary
lesion or dysfunction in the nervous system, neuropathic pain is often described as burning, lancinating, or tingling
in nature

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3
Q

The source of neuropathic

pain may be related to

A

damage of a peripheral nerve, with or without associated autonomic changes or CNS dysfunction. Examples of these changes include prolonged central sensitization, damage to neuronal inhibitory functions, and alteration of the effects of pain on the sympathetic nervous system.

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4
Q

Following tissue injury, the threshold of A-d and

C-fiber activation

A

decreases, and an augmented response

to a given stimulus occurs

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5
Q

What channels has alterations in ion at the site of injury?

A

Sodium and calcium channels play a fundamental role in the
propagation of hyperexcitability in central and peripheral
neurons.

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6
Q

After nerve injury, the number of ion channels

accumulates in excess, and leads to

A

ectopic, spontaneous firing of sensory nerves and dorsal root ganglion cell bodies. The result of neuronal membrane hyperexcitability is the chronic perception of pain

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7
Q

membrane stabilizer

classification

A

sodium-channel blocking
agents (antiepileptics, anticonvulsants, local anesthetics, tricyclic antidepressants, and antiarrhythmics) and calcium channel blocking agents

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8
Q

When evaluating the effectiveness of medications for neuropathic pain, outcome measures most commonly include

A 
changes in the average daily pain score by a 10-cm (100-mm) visual analog scale (VAS) and on an 11-point Likert scale (0, no pain; 10, worst possible pain) numeric
rating scale (NRS); patient-reported pain relief of 30% or greater (moderate benefit); patient-reported pain relief of 50% or greater (substantial benefit).
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9
Q

“Numbers needed to

treat” (NNT)

A

The NNT is the number of patients treated with a particular drug in order to obtain one patient with a defined degree of relief.

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10
Q

The “numbers needed to harm” (NNH)

A

is the number needed to treat with a certain drug before a patient can experience a significant side effect

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11
Q

NNT/NNH ratio

A

The drugs with a low NNT/NNH ratio are superior to the drugs with high NNT/NNH ratio

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12
Q

SODIUM-CHANNEL BLOCKERS

A

These agents include the antiepileptic/ anticonvulsants, local anesthetics, tricyclic antidepressants, and antiarrhythmics. As a group, they inhibit the development and propagation of ectopic discharges

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13
Q

The primary agents used

for neuropathic pain that are sodium channel blockers

A

antiepileptics/ anticonvulsants and local anesthetic

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14
Q

The primary agents used

for neuropathic pain that are calcium channel blockers

A

Gabapentin and pregabalin,

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15
Q

Sodium-channel blockers are used for primary therapy or adjunctive treatment for processes such as

A

trigeminal neuralgia, CRPS, diabetic neuropathy, radicular extremity pain, chemotherapy-induced peripheral neuropathy, and postherpetic neuralgia

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16
Q

The initial dosage of phenytoin

A

100 mg BID to TID

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17
Q

phenytoin is primarily used for the treatment of

A

diabetic neuropathy

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18
Q

Phenytoin provides pain

relief by

A

blocking sodium channels, thereby preventing the release of excitatory glutamate and inhibiting ectopic discharges

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19
Q

Phenytoin Side Effects

A

Sedation, motor disturbances, slowing of mentation and somnolence, with
nystagmus and ataxia seen in some patients. development of facial alterations, including gum hyperplasia and a coarsening of facial feature

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20
Q

Fosphenytoin

A

an intravenously
administered pro-drug that converts to phenytoin, is used
by some to avoid a long dosing interval or initial burning at the injection site

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21
Q

Phenytoin effect on cytochrome P450 enzyme

A

Phenytoin activates the cytochrome P450 enzyme system in the liver, and, hence, careful assessment of co-therapy is warranted. For example, phenytoin decreases the efficacy of
methadone, fentanyl, tramadol, mexiletine, lamotrigine, and
carbamazepine

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22
Q

Co-administration with

antidepressants and valproic acid could lead to

A

increased blood concentration of phenytoin, lowering the subsequent
doses required for effect in patient

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23
Q

CARBAMAZEPINE (TEGRETOL) mechanism of action

A

Na channel blockade

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24
Q

Dosage of Carbamazepine

A

initial dosage of carbamazepine is 100 to 200 mg BID, titrated to effect, with typical dose ranges of 300 to 1200 mg/day, administered in two divided doses. Common maintenance doses are 600 to 800 mg

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25
Q

The chemical structure

of this Carbamazepine is similar to that of the

A

tricyclic antidepressants

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26
Q

Carbamazepine is thought to inhibit pain via

A

peripheral and central mechanisms. Carbamazepine
selectively blocks active fibers, having no effect
on normally functioning A-d and C-fiber nociceptors

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27
Q

Major uses of Carbamazepine include

A

primary therapy for trigeminal neuralgia (tic doloreux), thalamic-mediated post-stroke pain, postherpetic neuralgia, and diabetic neuropathy.

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28
Q

Side Effects of Carbamazepine

A

Drowsiness, dizziness, and nausea and vomiting

are common side effects

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29
Q

Carbamazepine is associated with very deleterious side effects, including

A

pancytopenia (necessitating a complete blood count and monitoring while on this
therapy), Stevens Johnson syndrome, and toxic epidermal necrolysis

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30
Q

Trigeminal Neuralgia

A

a sharp severe facial pain in one or more of the distributions supplied by the trigeminal nerve. It is caused by compression of the trigeminal nerve at the pontine origin of the nerve by an aberrant loop
of an artery or vein

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31
Q

Patients on carbamazepine therapy should have blood

tests done every 2 to 4 months because

A

there is an increased risk of developing agranulocytosis and aplastic anemia with
this agent

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32
Q

OXCARBAZEPINE (TRILEPTAL)

A

the keto-analog of carbamazepine, was
developed to preserve carbamazepine’s membrane-stabilizing
effects while minimizing minor adverse effects, such as sedation and serious, life-threatening reactions

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33
Q

Major Advantage of Oxcarbazepine

A

monitoring of drug

plasma levels and hematologic profiles is generally not necessary

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34
Q

Oxcarbazepine Mechanism of Action

A

oxcarbazepine blocks

sodium channels; it does not affect gamma-aminobutyric acid (GABA) receptors

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35
Q

Oxcarbazepine Side Effect

A

Hyponatremia (Na < 125 mmol/L) somnolence, dizziness, nausea and vomiting

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36
Q

Oxcarbazepine Dosages

A

Initial Dosage: 600 mg twice daily
Titration: Increase by 300 mg daily
Max dose: 1200–1800 mg every 3 days

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37
Q

Institution of oxcarbazepine therapy requires

A

Monitoring of sodium levels should be performed

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38
Q

VALPROIC ACID (DEPAKOTE)

A

Na channel blockade;

acts at the GABA-A receptor–> increase GABA

39
Q

VALPROIC ACID indications

A

agent was effective in migraine therapy at dosages of 800 mg/day for a period of 8 week

40
Q

VALPROIC ACID Side Effects

A

Side effects include

gastrointestinal upset, somnolence, and dizziness

41
Q

VALPROIC ACID Dosage

A

Initial Dosage: 250 mg twice daily
Titration: Increase by 250 mg weekly
Maximum Dosage: 500 mg twice daily

42
Q

LAMOTRIGINE (LAMICTAL) mechanism of action

A

Stabilize slow Na channel; suppress release of glutamate from presynaptic neurons

43
Q

LAMOTRIGINE (LAMICTAL) Dosage

A

initial dosage is 25 to 50 mg at bedtime, and can be increased to 50 mg twice daily after 2 weeks. Subsequently, it may be increased by 50 mg increments every 1 to 2 weeks as tolerated, to a dose of 300 to 500 mg/day in two divided
doses

44
Q

How should LAMOTRIGINE be discontinued?

A

Upon discontinuation, drug administration should be slowly tapered over a 2-week time period

45
Q

Lamotrigine Side Effects

A

Rash (especially when lamotrigine is combined with valproic acid), dizziness, somnolence, Stevens-Johnson syndrome

46
Q

Lamotrigine Indication

A

A major use for carbamazepine-resistant neuralgia. carbamazepine is the first-line therapy. diabetic neuropathy

47
Q

Prescribing physicians should also be aware that when lamotrigine is combined with the CYP450 inhibitor

A

valproate, the initial dose should be reduced to

12.5 mg daily, and titration should be done cautiously

48
Q

TOPIRAMATE (TOPAMAX)

mechanism of action

A

Na channel blockade; potentiate GABA inhibition and inhibits the AMPA- type glutamate (excitatory) receptor

49
Q

Topiramate Dosage

A

Initial Dosage: 50 mg daily at bedtime increasing to an
upper limit of 200 mg
BID
Maximum Dosage: 1500 mg twice daily

50
Q

Topiramate Side Effects

A

Sedation (primary side effect), kidney stones, glaucoma (as topiramate is an inhibitor of the enzyme, carbonic anhydrase)

51
Q

Topiramate Indications

A

diabetic neuropathy, postherpetic neuralgia,

intercostal neuralgia, and CRPS

52
Q

LEVETIRACETAM (KEPPRA) dosage

A

A starting dose for levetiracetam is 500 mg
twice daily, and may be increased to a recommended
3000 mg/day in divided doses. Dosages up to 5000 mg/ day have been assessed in the treatment of neuropathic pain

53
Q

Why does Levetiracetam not have significant drug interactions?

A

Levetiracetam is

not metabolized by the cytochrome P450 system

54
Q

Levetiracetam was found to be ineffective in the treatment of neuropathic pain secondary to

A

a spinal cord injury and postmastectomy pain

55
Q

Levetiracetam Adverse effects

A

include asthenia, dizziness, somnolence, and headache

56
Q

Local anesthetics are used in neuropathic pain states to block

A

the aberrant firing of abnormal nerves, although they also block normally conducting (non-nociceptive) nerves

57
Q

Local anesthetics Indications

A

they are effective in the treatment of postherpetic neuralgia, trigeminal neuralgia, radiculopathies,
and peripheral neuropathies

58
Q

LIDOCAINE typical dose

A

is 1 to 5 mg/kg IV

59
Q

Lidocaine Side effects

A

dizziness, blurred vision, and seizure, typically presenting at a plasma level of 10 mg/ml

60
Q

Potential Cardiac Risks of Lidocaine

A

Given that lidocaine is an
antiarrhythmic, bradycardia and cardiac depression (present at 20 to 25 mg/ml plasma concentration) are potential risks of this agent; therefore, obtaining ECG Indicated for long-term or high-dosage use of lidocaine

61
Q

A formulation of 5% lidocaine is available in

A

transdermal application

62
Q

Lidocaine patch(Lidoderm) benefit in patients with various types of neuropathic pain, including

A

postherpetic neuralgia, post-thoracotomy pain, intercostal neuralgia, and meralgia parasthetica

63
Q

Eutectic Mixture of Local Anesthetics (EMLA)—

A

comprised of prilocaine and lidocaine

64
Q

Prilocaine is readily metabolized to

A

o-toluidine, which can lead to methemoglobinemia.However, if dosages of prilocaine are kept below 600 mg, clinical methemoglobinemia is less likely to develop

65
Q

MEXILETINE

A

This agent is an antiarrhythmic,
and, for pain relief, can be considered an oral analog
of lidocaine

66
Q

MEXILETINE dosage

A

The standard starting dose is 75 to 150 mg/day, with a

target of 300 to 450 mg/day.

67
Q

Mexiletine Indications

A

diabetic neuropathy, thalamic stroke pain, spasticity, and myotonia, although its effects are minimal.

68
Q

Mexiletine Side Effect

A

somnolence, irritability, blurred vision, and nausea and vomiting,
severely limit the utility of this medication

69
Q

Patients taking Mexiletine are at risk for developing

A

blood dyscrasias, and should have blood tests on a regular basis

70
Q

Six different types of Calcium Channel Blockers found in nervous tissue

A

L, N, P, Q, R, and T.

71
Q

Calcium-channel blockers used for treatment of neuropathic pain mechanism of action

A

They bind to the alpha2-delta subunit of L-type voltage-gated calcium channels, and result in decreased release of glutamate, norepinephrine, and substance P

72
Q

Calcium-channel blockers relation to GABA

A

While structurally derived from the inhibitory neurotransmitter, GABA, neither gabapentin nor pregabalin bind to or have activity at the GABA receptor. They also have no effect on uptake or metabolism of GABA

73
Q

GABAPENTIN (NEURONTIN) mechanism of action

A

Binds to alpha-2-delta subunit of voltage-gated

Ca channel

74
Q

GABAPENTIN (NEURONTIN)

Dosage

A

initial dose is 100 to 300 mg at bedtime; with a gradual increase to a maximum of 3600 mg/day in TID divided doses. After 2 to 5 days, the dose is increased to 300 mg twice daily, and after another 2 to 5 days to 300 mg 3 times daily thereafter. Subsequently,
the dose can be increased by 300 to 600 mg every other week as tolerated until an effective dosage is obtained or the maximum daily dose is reached.

75
Q

GABAPENTIN (NEURONTIN) Side Effect

A

The main dose limiting

side effects are fatigue, somnolence, and dizziness, which are often attenuated by gradual dose titration

76
Q

Gabapentin dosage reduction is necessary in patients with

A

renal insufficiency

77
Q

GABAPENTIN (NEURONTIN) Indications

A

postherpetic neuralgia,

CRPS, painful diabetic neuropathy, adjunctive therapy for symptomatic spinal stenosis.

78
Q

PREGABALIN (LYRICA)

Dosage

A

Initial pregabalin dosing is 150 mg/day, given in two or three divided doses, or 75 mg given at bedtime in elderly
patients. Upward dose titration can be completed after
3 to 7 days to 300 mg/day, and subsequently increased
to a maximum dose of 600 mg/day within 2 weeks of
initiatio

79
Q

PREGABALIN (LYRICA) mechanism of action

A

Pregabalin is an alpha2-delta ligand structurally related
to gabapentin. It similarly binds to calcium channels and
modulates calcium influx into hyperexcited neurons, leading
to its antinociceptive and antiseizure effects.

80
Q

Pregabalin advantages over gabapentin include

A

a more rapid onset of pain relief, linear pharmacokinetics with low intersubject variability, fewer dose-related side
effects allowing for faster dosage upward titrations, and
twice daily versus 3 times daily dosing. Additionally,maximum benefit often occurs after 2 weeks of treatment at target doses of 300 to 600 mg/day compared with up to 2 months in gabapentin-treated patient

81
Q

Pregabalin relation to GABA

A

While it
is structurally derived from the inhibitory neurotransmitter
GABA, it does not bind to GABA or benzodiazepine receptors

82
Q

PREGABALIN (LYRICA) indications

A

Pregabalin is approved for the treatment of peripheral and central neuropathic pain, including postherpetic
neuralgia and painful diabetic neuropathy

83
Q

PREGABALIN (LYRICA) side effects

A

Most common adverse effects

include somnolence and dizziness,

84
Q

How should Pregabalin be discontinued?

A

When discontinuing pregabalin,
it should be gradually tapered down over at least 1 week to minimize symptoms, including insomnia, nausea, headache, and diarrhea

85
Q

ZONISAMIDE (ZONEGRAN)

mechanism of action

A

This agent acts by blocking T-type calcium channels and sodium channels; its action also increases GABA release

86
Q

ZONISAMIDE (ZONEGRAN) dosage

A

The initial dose is 100 mg QD for 2 weeks, increasing by

200 mg/week, for a target of 600 mg/day

87
Q

ZONISAMIDE (ZONEGRAN) indications

A

It has uses in various

types of neuropathic pain.

88
Q

ZONISAMIDE (ZONEGRAN) side effects

A

Side effects include ataxia,
decreased appetite, rash, and renal calculi (due to the
carbonic anhydrase inhibitor effect). In children, there is
an increased risk of oligohydrosis and susceptibility to hyperthermia

89
Q

ZICONOTIDE (PRIALT)

A 
Ziconotide is a v-conopeptide (previously known as SNX-111) that is administered intrathecally due to its
peptidic structure. It is derived from the venom of a
marine snail (genus Conus)
90
Q

ZICONOTIDE (PRIALT) mechanism of action

A

Ziconotide blocks calcium
influx into N-type calcium channels that are present in
the dorsal horn lamina of the spinal cord, thus preventing
the afferent conduction of nerve signals

91
Q

ZICONOTIDE (PRIALT) dosage and form of administration

A

Administration occurred via an intrathecal infusion pump, and dosing should be started low, at a recommended dose of
2.4 mg/day (0.1 mg/hr). Due to a lag time, it should be
titrated up slowly, at intervals of no more than two to
three times per week, to a recommended maximum of
19.2 mg/day

92
Q

ZICONOTIDE (PRIALT) Adverse Effects

A

Ziconotide does not cause tolerance, dependence,
or respiratory depression, and adverse effects
primarily involve the CNS, including dizziness, ataxia,
confusion, and headache

93
Q

ZICONOTIDE (PRIALT) indications

A

ziconotide is approved
for the management of severe chronic pain in patients for
whom intrathecal therapy is warranted, and who are intolerant of or refractory to other treatments, including intrathecal opiates

94
Q

MAGNESIUM

A

antagonists of the N-methyl-d-aspartate (NMDA) receptor,

membrane-stabilizing effect

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