Test 3 Flashcards

0
Q

transition from acute to chronic pain can be initiated or maintained by peripheral and/or central mechanisms

A

dorsal root ganglion
cord
supratentorial

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1
Q

chronic pain definition

A

pain that has no biological benefit and lasts longer than 3 months (or the normal healing time)

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2
Q

what is the clinical manifestation of peripheral sensitization?

A

hyperalgesia

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3
Q

what is peripheral sensitization?

A

enhanced excitability of nerves
reduced nociceptive thresholds
renders high-threshold nerve endings responsive to normally non-noxious stimuli

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4
Q

some effects of nerve injury

A
  1. sprouting of new hyperexcitable nerve endings
  2. neuroma
  3. reduced thresholds
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5
Q

pain caused by CHANGES in peripheral or CNS is defined as

A

neuropathic pain (which leads to hyperalgesia and allodynia)

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6
Q

central sensitization involves __ neurons, which is responsive to __

A

second order wide dynamic range
responsive to GLUTAMATE (NMDA receptor)

(usually in the dorsal horn)

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7
Q

what’s the difference between acute and chronic pain?

A

constant dumping of quanta of glutamate and opening of the magnesium plug

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8
Q

how do anticonvulsants help?

A

inhibit neuron excitation and stabilize membrane

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9
Q

what are the first generation anticonvulsants?

A

carbamazepine and phenytoin

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10
Q

what are the second gen anticonvulsants?

A

gabapentin and neurontin

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11
Q

what do anticonvulsants treat?

A

postherpetic neuralgia, diabetic neuropathy, trigeminal neuralgia, others

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12
Q

what is the mech of action of anticonvulsants?

A

block alpha 2 delta subunit of PREsynaptic voltage gated calcium channels in CNS

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13
Q

how do antidepressants work?

A
  1. block reuptake of serotonin and norepi, which are inhibitory neurotransmitters in the descending inhibitory pathway
  2. block sodium and ca++ channels
  3. decrease prostaglandin and TNF
  4. block NMDA receptors
  5. enhance opioid receptors
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14
Q

How long does it take for antidepressants to enhance opioid receptors?

A

4-10 days

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15
Q

what are the three classes of antidepressants?

A

tricyclics, selective norepi reuptake inhibitors, and selective serotonin reuptake inhibitors

16
Q

name 2 selective norepi reuptake inhibitors

A

effexor (venlafaxine) and cymbalta (duloxetine)

Cymbals effect norepi

17
Q

name 2 selective serotonin reuptake inhibitors

A

prozac (fluoxetine) and celexa (citalopram)

Prozac is the flux that holds Alexis’ pram together

18
Q

what are the side effects of tricyclics?

A

muscarinic (think glyco), histaminergic (think benadryl), and adrenergic (think alpha blocker)

caution: recent MI, prolong QT interval

19
Q

what might happen if you combine a selective norepi reuptake inhibitor with a selective serotonin reuptake inhibitor or a triptan?

A

serotonin syndrome (anxiety, agitation, delirium, seizures, hyperthermia, diaphoresis, tachycardia, htn or hypotension, hyperreflexia, myoclonus, muscle rigidity)

20
Q

how would you treat serotonin syndrome due to concomitant use of SNRI and SSRI

A

lipid emulsion

21
Q

how do corticosteroids work?

A

prevent release of arachidonic acid by inhibiting phospholipase A2 on cell membranes (precursor of prostaglandins)

22
Q

what nerve fibers are blocked by corticosteroids?

A

C fibers

23
Q

the effects of corticosteroids are dependent on the degree of HPA axis suppression

A

hypothalamic - pituitary - adrenal axis

24
Q

how long can an epidural steroid injection cause HPA suppression?

A

4-5 days after injection up to 5 weeks

in the event of major surgery during that time, you should give them a dose of exogenous steroid

25
Q

how does methadone work?

A

the S isomer antagonizeS NMDA receptorS and inhibits reuptake of Serotonin and norepi

the R isomer binds to opioid Receptors

26
Q

side effects of methadone

A

resp depression, excessive sedation, QT interval