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health transitions > chapter 8: pain > Flashcards

chapter 8: pain Flashcards

1
Q

NSAIDS exert their analgesic effects by blocking
__________

A

cyclooxyrgenase

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2
Q

2 kinds of primary afferent fibers

A

A-delta
C fibers

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3
Q

which type of afferent fiber conduct pain rapidly and are responsible for the initial sharp pain that accompanies tissue injury?

A

A-delta

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4
Q

which type of afferent fiber transmits painful stimuli more slowly and pain is typically aching or throbbing?

A

C fibers

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5
Q

3 segments involved in nociceptive signal transmission

A

-transmission along peripheral nerve fibers to spinal cord
-dorsal horn processing
-transmission to thalamus and cerebral cortex

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6
Q

______ ____ neuron extends the entire distance from the periphery to the dorsal horn with no synapses

A

1st order

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7
Q

_______ are areas on the skin that are inneverted primarily by a single spinal cord segment

A

dermatomes

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8
Q

neurotransmitters ______ and _________ produce activation of nearby cells

A

glutamate
substance P

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9
Q

neurotransmitters ______ and ______ inhibit the activation of nearby cells

A

GABA
seratonin

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10
Q

_____ ____ neurons project to the thalamus

A

2nd order

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11
Q

_____ ______ is the increased sensitivity and hyper flexibility of the neurons in the CNS

A

central sensitization

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12
Q

________ ______ is the increased susceptibility to nociceptor activation

A

peripheral sensitization

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13
Q

___ ____ can be caused by peripheral tissue damage or nerve injury

A

central sensitization

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14
Q

_____ is pain from a stimulus that is not typically painful

A

allodynia

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15
Q

______ is an exaggerated or increased pain response from noxious stimuli

A

hyperalgesia

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16
Q

acute, unrelieved pain leads to chronic pain through _____ ________

A

central sensitization

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17
Q

__________ are processes that allow neurons in the brain to compensate for injury and adjust their responses to new situations or changes in their environment

A

neuroplasticity

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18
Q

perception of pain assumed to occur in ____ _____

A

cerebral cortex

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19
Q

modulation of pain signals can occur at the level of the ________, _____ _____, _____ ____, and cerebral cortex

A

periphery
brain stem
spinal cord

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20
Q

descending modulatory fibers release chemicals such as: (4)

A

seratonin
norepinephrine
GABA
endogenous opioids

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21
Q

what is the treatment for nociceptive pain?

A

non-opioids and/or opioids

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22
Q

_____ pain is caused by damage to somatic or visceral tissue

A

nociceptive

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23
Q

______ pain caused by damage to peripheral nerves or structure in CNS

A

neuropathic

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24
Q

what is the treatment for neuropathic pain?

A

adjuvant analgesics

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25
Q

______ pain results from loss of or altered afferent input secondary to either peripheral nerve injury or CNS damage

A

deafferation

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26
Q

______ pain is caused by CNS lesions or dysfunction

A

central

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27
Q

______ _____ pain syndrome causes dramatic changes in color and temp if skin over affected limb or body part, accompanied by intense, burning pain, skin sensitivity, sweating and swelling

A

complex regional pain

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28
Q

complex regional pain syndrome type 1 frequently triggered by ____ injury, _____, or ______ event

A

tissue injury
surgery
vascular

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29
Q

complex regional pain syndrome type 2 has all the same features in addition to ______ ______ ______

A

peripheral nerve lesion

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30
Q

______ ______ products are used to treat breakthrough pain

A

transmucousal fentanyl

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31
Q

transmucousal fentanyl products are used to treat __________ pain

A

breakthrough

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32
Q

side effects of pain meds can be managed by:

decreasing dose by _____ to ______ %
using an administration route that _______ drug concentration

A

10-15%
decreases

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33
Q

older NDAIDS like ibuprofen inhibits both forms of _____ and are ___-____ NSAIDS

A

COX
non-selective

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34
Q

_____ _____ effect is when an NSAID is combined with opioid allowing for lower opioid dose leading to fewer adverse effects

A

opioid sparing effect

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35
Q

using ____ with an opioid produces an opioid sparing effect

A

Tylenol

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36
Q

using Tylenol with an opioid produces an ______ _____ effect

A

opioid sparing

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37
Q

______-___ is found in almost all tissues and is responsible for several protective physiological functions

A

COX-1

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38
Q

____-__ is produced mainly at sites of tissue injury

A

COX-2

39
Q

___-___ mediates inflammation

A

COX-2

40
Q

inhibition of ____-___ causes many of the adverse effects of NSAIDS

A

COX-1

41
Q

inhibition of ___-__ is associated with the therapeutic anti-inflammatory effects of NSAIDS

A

COX-2

42
Q

most commonly administered subclass of opioids is ______ ______ ______

A

pure opioid antagonists

43
Q

pure opioid antagonists bind to _____ receptors

A

MU

44
Q

pure opioid antagonists are also referred to as ____ ____ opioids

A

morphine like

45
Q

when opioids are prescribed for moderate pain, they are usually combined with a ___-______

A

non-opioid

46
Q

______ can cause _____ prolongation

A

methadone
QT

47
Q

_____ is associated with higher incidence of nausea and constipation than other mu antagonist

A

codeine

48
Q

_____ plus ______ used as sublingual preparation to treat opioid dependence for easier withdrawal when tapering from opioids

A

duprenorphine plus nalaxone

49
Q

opioid induced pruritus can be managed through low dose ____ infusions

A

naloxone

50
Q

_____ _____ _____ is a paradoxic response in which pts become more sensitive to certain painful stimuli and report increased pain with opioid use

A

opioid induced hyperalgesia

51
Q

opioid induced hyperalgesia is due to ______ changes

A

neuroplasticity

52
Q

do not give _______ at same time as NSAID

A

corticosteroid

53
Q

corticosteroids have the ability to decrease _____ and ______

A

edema
inflammation

54
Q

____ antidepressants enhance descending inhibitory system by preventing the cellular reuptake of seratonin and norepinephrine

A

tryclic

55
Q

______ _____ anatagonist can interfere with transmission of nociceptive impulses

A

GABA receptor

56
Q

GABA receptor antagonists are used to treat (2)

A

-neuropathic pain
-muscle spasms

57
Q

A2 adrenergic agonists are used to treat(2)

A

-chronic headaches
-neuropathic pain

58
Q

___% _____ patch used as first line agent for several types of neuropathic pain

A

5% lidocaine

59
Q

chronic severe neuropathic pain treated with oral therapy of ________

A

mexilefine

60
Q

larger doses needed of oral meds bc of ___ _____ effect

A

first pass

61
Q

first pass effect:

oral opioids are absorbed from ____ tract into portal of ______ and shunted to the _______

A

GI
circulation
liver

62
Q

transmucousal absorption allows the drug to enter the bloodstream and travel directly to the _____

A

CNS

63
Q

pain relief from transmucousal absorption usually occurs ___-____ mins after admin

A

5-7

64
Q

____ and ____ commonly used in PCAs

A

morphine
hydrocodone

65
Q

what are these signs of?

-diffuse back pain
-pain or paresthesia during bolus injection
-unexplained sensory or motor deficits in lower limbs

A

intraspinal infection

66
Q

____ ____ _____ most commonly used for chronic back pain secondary to nerve damage

A

spinal cord stimulation

67
Q

_____ ______ _____ stimulation delivers electrical currents through electrodes applied to the skin surface over painful region, at trigger points, or over a peripheral nerve

A

transcutaneous electrical nerve stimulation (TENS)

68
Q

typical opioid tapering schedule may involve reducing dose by ___-____% each day

A

20-50

69
Q

what is the max amount of Tylenol that can be given daily?

A

4 grams or 4000mg

70
Q

in opioids overdoses ______ always comes before respiratory depression

A

sedation

71
Q

in opioids overdoses sedation always comes before _____ ______

A

respiratory depression

72
Q

stop opioid and give nalaxone if RR is below ____or the pt is difficult to arouse

A

8/min

73
Q

example of deafferation pain

A

amputation

74
Q

______ approach used to treat neuropathic pain

A

multimodal

75
Q

______ drugs can be used to treat neuropathic pain

A

antiseizure

76
Q

____ pain decreases over time as pt recovers

A

acute

77
Q

____ _____ system activated with acute pain

A

sympathetic nervous

78
Q

acute pain manifestations include:

increased ______ ____
increased ______ ____
increased ___ _____
_______, pallor

A

hr
rr
bp
diaphoresis

79
Q

____ pain continues past normal recovery time

A

chronic

80
Q

if pt receives PO pain med, evaluate effectiveness in ___-____

A

30 mins to 1 hr

81
Q

if pt receives IV pain med, reassess after ___-___ mins

A

15-30

82
Q

acetaminophen has the potential to cause _____

A

hepatotoxicity

83
Q

acetaminophen has ______ effects

A

antipyretic

84
Q

____ don’t have an analgesic ceiling

A

opioids

85
Q

mixed agonists-antagonists bind as agonists on ______

A

kappa

86
Q

______ primarily used in the treatment of chronic pain

A

methadone

87
Q

when Tylenol doesnt provide enough pain relief and opioids would provide too much what med is used?

A

tramadol

88
Q

_______ most common side effect of opioids

A

constipation

89
Q

______-____ pts have a higher risk for respiratory depression

A

opioid naive

90
Q

____ used first when discontinuing IV opioid therapy

A

Percocet

91
Q

____ route used when pt has high fever and can’t tolerate oral Tylenol

A

rectal

92
Q

anything over level ____ on opioid induced sedation scale is unacceptable

A

2

93
Q

in level 3 of opioid induced sedation consider administering ____ or an _____ if not contraindicated

A

acetaminophen
NSAIDS

health transitions (6 decks)

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