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Neuro Path (2nd Year) > Pain Management > Flashcards

Pain Management Flashcards

Pain Management

1
Q

What are the 5 kinds of pain

A

acute, chronic, somatic, neuropathic visceral

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2
Q

Allodynia

A

pain to a stimulus that would other wise not be painful

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3
Q

Analgesia

A

decreased/ absence of pain in response to stimulus which would normally be painful

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4
Q

Dysesthesia

A

unpleasant abnormal sensation whether spontaneous or evoked

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5
Q

Hyperalgesia

A

increased pain response to a stimulus that is normally painful

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6
Q

Hyperesthesia

A

increased pain reaction to any stimulus with increased threshold

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7
Q

Paresthesia

A

abnormal sensation

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8
Q

Hypesthesia

A

decreased sensitivity to stimulation excluding special senses

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9
Q

4 steps in pain modulation

A

transuction, transmission, perception, modulation

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10
Q

Drugs used for transduction

A

LAs
capsaicin
anticonvulsants
NSAIDs
ASA
acetaminophen
nitrate

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11
Q

Drugs used for transmission

A

local anesthetic

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12
Q

Drugs used for perception

A

opioids
a2 agonists
TCAs
SSRIs
SNRIs

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13
Q

endogenous NTs important for pain modulation

A

endorphins and norepi

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14
Q

drugs used for modulation

A

TCAs
SSRIs
SNRIs

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15
Q

Excitatory NTs

A

glutamate, norepi, epi

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16
Q

schedule 2

A

cocaine
meth
methadone
hydromorphone
meperidine
oxycodon
fentanyl
dexedrine
amphetamine
methylphenidates

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17
Q

schedule 3

A

products w/

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18
Q

Schedule 4

A

BZDs

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19
Q

schedule 5

A

cough preps w/

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20
Q

Indomethacin primarily used for

A

acute gout and osteoarthritis

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21
Q

is Diclofenac selective?

A

COx-2

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22
Q

Potassium or Sodium for fast release?

A

potassium

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23
Q

diclofenac used for

A

significant pain relief

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24
Q

Indomethacin what class and subclass of pain killer

A

NSAID, acetic acid

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25
Q

Diclofenac what class and what subclass of pain killer

A

NSAID, acetic acid

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26
Q

Ketorolac class and subclass

A

NSAID, acetic acid

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27
Q

is Ketorolac selective Cox?

A

no

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28
Q

Ketorolac ACRs

A

use must be limited to less than 5 days, allergies= reaction

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29
Q

Ketorolac route

A

enteric, opthalamic, parental, nasal

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30
Q

Ketorolac analgesic effect in how long?

A

30 minutes

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31
Q

Ketorolac duration

A

4-6 hours

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32
Q

Indomethacin primarily used for

A

acute gout and osteoarthritis

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33
Q

is Diclofenac selective?

A

COx-2

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34
Q

Potassium or Sodium for fast release?

A

potassium

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35
Q

diclofenac used for

A

significant pain relief

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36
Q

Indomethacin what class and subclass of pain killer

A

NSAID, acetic acid

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37
Q

Diclofenac what class and what subclass of pain killer

A

NSAID, acetic acid

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38
Q

Ketorolac class and subclass

A

NSAID, acetic acid

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39
Q

is Ketorolac selective Cox?

A

no

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40
Q

Ketorolac ACRs

A

use must be limited to less than 5 days, allergies= reaction

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41
Q

Ketorolac route

A

enteric, opthalamic, parental, nasal

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42
Q

Ketorolac analgesic effect in how long?

A

30 minutes

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43
Q

Ketorolac duration

A

4-6 hours

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44
Q

Meloxicam class and subclass

A

NSAID enolic acid

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45
Q

is Meloxicam selective for a COX?

A

COX-2

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46
Q

Meloxicam half life

A

20 hours

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47
Q

Meloxicam good to use in which 2 situations

A

renal or hepatic insuffieicency

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48
Q

Celecoxib class and subclass

A

NSAID COX 2- inhibitors

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49
Q

Celecoxib clinical use

A

mild to moderate pain

50
Q

Celecoxib decreases efficacy of which drugs (3)

A

ACE-I, diuretics, increases lithium

51
Q

Does Celecoxib interefere w/ platelet aggregation

52
Q

Celecoxib contrainidcation

A

sulfa allergy/ sulfonamide

53
Q

acetaminophen class and subclass

A

NSAID, analine derivative

54
Q

does acetaminophen have anti-platelet activity

55
Q

does acetaminophen inhibit central or peripheral prostaglindin synthessi

A

central, so weak anti-inflammatory

56
Q

acetaminophen clinical use

A

mild to moderate pain, fever

57
Q

acetaminophen peak

A

0.5- 3 hours

58
Q

acetaminophen half life

59
Q

acetaminophen duration of action

60
Q

acetaminophen major benefit of parenteral form

A

reduces opioid consumption 35-45%

61
Q

NSAID mechanism

A

block cyclooxygenase and stop production of prostaglanding and thromboxanes

62
Q

Which prostaglandin is predominant one that mediates peripheral and central pain sensitization

63
Q

Which Cox is more responsible for pain modulation/ inflammation

64
Q

How do prostaglandins contribute to pain peripherally

A

sensitize nerve endings to mediators like histamine/bradykinin

65
Q

How do prostaglandins contribute to pain centrally

A

direct action at spinal cord: enhanced nociception at terminal sensory neurons of dorsal horn

66
Q

qualitatively how selective is ketorolac for COX2/COX1

A

very selective for COX-1, not selective for Cox 2

67
Q

NSAID side effects

A

gastritis, renal dysfunction

68
Q

what attentuates GI side effects of NSAIDs

A

misoprostol >PPI> H2 blockers

69
Q

a patient over 75’s risk of bleeding from NSAIDs is ___x more likely than a younger person

70
Q

proposed mechanism for renal impairment caused by NSAIDs

A

decrease in prostaglandin production, reduced renal blood flow, medullary ischemia

71
Q

acetaminophen dosing limit for helath adults

A

3-4g/ 24 hour

72
Q

mechanism for cardiac effects of NSAIDs

A

vasoconstriction, increased afterload and decreased contractility, decreased output

73
Q

why should NSAID be avoided in children w/ viral illnesses

A

reyes syndrome

74
Q

2 general types of allergy and hypersensitivity

A

syndrome of asthmatic attacks
syndrome of urticaria and angioedema (prostaglandin E2 inhibition destabilizes histamine in mast cells)

75
Q

acetaminophen’s threhhold for hepatic toxicity in adults and children

A

adults 10-15 g
kids 150mg/kg

76
Q

Opioid interactions

77
Q

can morphine be used in hepatic failure

A

yes , but lower doses

78
Q

Meperidine drug class

79
Q

meperidine clinical use

A

severe pain, but not recommended for routine use

80
Q

meperidine interacions

A

MAO-I cause fatal/severe reactions

81
Q

What was the 1st or 2nd most abused opioid until it came in abuse deterrent formulation ?

82
Q

How is oxycodone metabolized

A

to oxymorphone by 2D6 and noroxycodone by 3A4

83
Q

oxycodone half life

84
Q

what does liver disease do to oxycodone metabolism

A

increases oxycodone, decreases oxymorphone…oxycodone half lfie increased to 14 hours

85
Q

oxymorphone relationship to oxycodone

A

metabolic end product

86
Q

oxymorphone relationship to morphine

A

2x as strong

87
Q

Methadone works in which stage of nociception/ pain physiology

A

modulation

88
Q

methadone mechanism

A

NMDA receptor antagonist, can inhibit the reuptake of serotonin

89
Q

methadone ADRs

A

same as morphine, but can prolong QTc and cause arrhythmias

90
Q

methandone half life

A

8.5-47 hours

91
Q

methadone potency

A

depends on dosage

92
Q

Fentanyl relationship to morphine

A

80x as strong morphine

93
Q

what happens to half life of Fentanyl in liver disease

94
Q

Hydrocodone is one of the strongest analgesics t/f

95
Q

what is most widely abused drug in US

A

hydrocodone

96
Q

hydrocodone mechanism

A

modulation phase of nociception

97
Q

hydromorphone relationship to morphine

A

7.5x as potent as morphine

98
Q

when should sustained release version of hydromorphone be avoided?

A

hepatic disease

99
Q

tapentadol class

100
Q

tapentadol side effects

A

same as morphine + inhibits reuptake of norepi and serotonin

101
Q

tramadol class

102
Q

tramadol mechanism of action

A

modulation phase of nociception and norepi and serotonin reuptake inhibition

103
Q

tramadol side effects

A

methadone/ antidepressants that inhibit serotonin reuptake

104
Q

buprenorphine relationship w/ morphine

A

30x as potent as morphine

105
Q

what is safest drug to use in hepatorenal syndrome

A

buprenorphine

106
Q

Meperidine cuases mydriases/ meiosis. Other opiates caue mydriases/ meiosis

A

Meperidine= mydriasis (dilation)
Meiosis= other opioids

107
Q

methadone structue/function relationship of enantiomers

A

levo= mu agonist
dextro= NMDA receptor

108
Q

TCA Mechanism of action

A

norepi and serotonin reuptake inhibitor

109
Q

TCA clinical use

A

neuropathic pain, appetite, stimulant, sleep aide

110
Q

TCA Side Effect that is really bad for chronic pain

A

weight gain

111
Q

venlafexine class

112
Q

duloxetine class

113
Q

milnaciprin class

114
Q

SNRI side effect

A

weight gain

115
Q

TCA used in caution in which population

116
Q

Gabapentin,pregablin class

A

anticonvulsants

117
Q

Gabapentin mechanism of action

A

preventing Ca influx in dorsal horn

118
Q

Gabapentin clinical use

A

neuropathic pain

119
Q

gabapentin, pregablin side effects

A

dizziness, fatigue, weight gain, drowsiness, and peripheral edema

120
Q

gabapentin interactions

121
Q

how is volume of distribution different in the elderly

A

decreased water, increased fat, alteration in protein binding

Neuro Path (2nd Year) (6 decks)

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