Pain Management Flashcards
Pain Management (121 cards)
1
Q
What are the 5 kinds of pain
A
acute, chronic, somatic, neuropathic visceral
2
Q
Allodynia
A
pain to a stimulus that would other wise not be painful
3
Q
Analgesia
A
decreased/ absence of pain in response to stimulus which would normally be painful
4
Q
Dysesthesia
A
unpleasant abnormal sensation whether spontaneous or evoked
5
Q
Hyperalgesia
A
increased pain response to a stimulus that is normally painful
6
Q
Hyperesthesia
A
increased pain reaction to any stimulus with increased threshold
7
Q
Paresthesia
A
abnormal sensation
8
Q
Hypesthesia
A
decreased sensitivity to stimulation excluding special senses
9
Q
4 steps in pain modulation
A
transuction, transmission, perception, modulation
10
Q
Drugs used for transduction
A
LAs
capsaicin
anticonvulsants
NSAIDs
ASA
acetaminophen
nitrate
11
Q
Drugs used for transmission
A
local anesthetic
12
Q
Drugs used for perception
A
opioids
a2 agonists
TCAs
SSRIs
SNRIs
13
Q
endogenous NTs important for pain modulation
A
endorphins and norepi
14
Q
drugs used for modulation
A
TCAs
SSRIs
SNRIs
15
Q
Excitatory NTs
A
glutamate, norepi, epi
16
Q
schedule 2
A
cocaine
meth
methadone
hydromorphone
meperidine
oxycodon
fentanyl
dexedrine
amphetamine
methylphenidates
17
Q
schedule 3
A
products w/
18
Q
Schedule 4
A
BZDs
19
Q
schedule 5
A
cough preps w/
20
Q
Indomethacin primarily used for
A
acute gout and osteoarthritis
21
Q
is Diclofenac selective?
A
COx-2
22
Q
Potassium or Sodium for fast release?
A
potassium
23
Q
diclofenac used for
A
significant pain relief
24
Q
Indomethacin what class and subclass of pain killer
A
NSAID, acetic acid
25
Diclofenac what class and what subclass of pain killer
NSAID, acetic acid
26
Ketorolac class and subclass
NSAID, acetic acid
27
is Ketorolac selective Cox?
no
28
Ketorolac ACRs
use must be limited to less than 5 days, allergies= reaction
29
Ketorolac route
enteric, opthalamic, parental, nasal
30
Ketorolac analgesic effect in how long?
30 minutes
31
Ketorolac duration
4-6 hours
32
Indomethacin primarily used for
acute gout and osteoarthritis
33
is Diclofenac selective?
COx-2
34
Potassium or Sodium for fast release?
potassium
35
diclofenac used for
significant pain relief
36
Indomethacin what class and subclass of pain killer
NSAID, acetic acid
37
Diclofenac what class and what subclass of pain killer
NSAID, acetic acid
38
Ketorolac class and subclass
NSAID, acetic acid
39
is Ketorolac selective Cox?
no
40
Ketorolac ACRs
use must be limited to less than 5 days, allergies= reaction
41
Ketorolac route
enteric, opthalamic, parental, nasal
42
Ketorolac analgesic effect in how long?
30 minutes
43
Ketorolac duration
4-6 hours
44
Meloxicam class and subclass
NSAID enolic acid
45
is Meloxicam selective for a COX?
COX-2
46
Meloxicam half life
20 hours
47
Meloxicam good to use in which 2 situations
renal or hepatic insuffieicency
48
Celecoxib class and subclass
NSAID COX 2- inhibitors
49
Celecoxib clinical use
mild to moderate pain
50
Celecoxib decreases efficacy of which drugs (3)
ACE-I, diuretics, increases lithium
51
Does Celecoxib interefere w/ platelet aggregation
no
52
Celecoxib contrainidcation
sulfa allergy/ sulfonamide
53
acetaminophen class and subclass
NSAID, analine derivative
54
does acetaminophen have anti-platelet activity
no
55
does acetaminophen inhibit central or peripheral prostaglindin synthessi
central, so weak anti-inflammatory
56
acetaminophen clinical use
mild to moderate pain, fever
57
acetaminophen peak
0.5- 3 hours
58
acetaminophen half life
2-3 hours
59
acetaminophen duration of action
4-6 hours
60
acetaminophen major benefit of parenteral form
reduces opioid consumption 35-45%
61
NSAID mechanism
block cyclooxygenase and stop production of prostaglanding and thromboxanes
62
Which prostaglandin is predominant one that mediates peripheral and central pain sensitization
PGE2
63
Which Cox is more responsible for pain modulation/ inflammation
COX-2
64
How do prostaglandins contribute to pain peripherally
sensitize nerve endings to mediators like histamine/bradykinin
65
How do prostaglandins contribute to pain centrally
direct action at spinal cord: enhanced nociception at terminal sensory neurons of dorsal horn
66
qualitatively how selective is ketorolac for COX2/COX1
very selective for COX-1, not selective for Cox 2
67
NSAID side effects
gastritis, renal dysfunction
68
what attentuates GI side effects of NSAIDs
misoprostol >PPI> H2 blockers
69
a patient over 75's risk of bleeding from NSAIDs is ___x more likely than a younger person
20
70
proposed mechanism for renal impairment caused by NSAIDs
decrease in prostaglandin production, reduced renal blood flow, medullary ischemia
71
acetaminophen dosing limit for helath adults
3-4g/ 24 hour
72
mechanism for cardiac effects of NSAIDs
vasoconstriction, increased afterload and decreased contractility, decreased output
73
why should NSAID be avoided in children w/ viral illnesses
reyes syndrome
74
2 general types of allergy and hypersensitivity
syndrome of asthmatic attacks
syndrome of urticaria and angioedema (prostaglandin E2 inhibition destabilizes histamine in mast cells)
75
acetaminophen's threhhold for hepatic toxicity in adults and children
adults 10-15 g
kids 150mg/kg
76
Opioid interactions
MAO-Is
77
can morphine be used in hepatic failure
yes , but lower doses
78
Meperidine drug class
opiate
79
meperidine clinical use
severe pain, but not recommended for routine use
80
meperidine interacions
MAO-I cause fatal/severe reactions
81
What was the 1st or 2nd most abused opioid until it came in abuse deterrent formulation ?
Oxycodone
82
How is oxycodone metabolized
to oxymorphone by 2D6 and noroxycodone by 3A4
83
oxycodone half life
2-3 hours
84
what does liver disease do to oxycodone metabolism
increases oxycodone, decreases oxymorphone...oxycodone half lfie increased to 14 hours
85
oxymorphone relationship to oxycodone
metabolic end product
86
oxymorphone relationship to morphine
2x as strong
87
Methadone works in which stage of nociception/ pain physiology
modulation
88
methadone mechanism
NMDA receptor antagonist, can inhibit the reuptake of serotonin
89
methadone ADRs
same as morphine, but can prolong QTc and cause arrhythmias
90
methandone half life
8.5-47 hours
91
methadone potency
depends on dosage
92
Fentanyl relationship to morphine
80x as strong morphine
93
what happens to half life of Fentanyl in liver disease
prolonged
94
Hydrocodone is one of the strongest analgesics t/f
false
95
what is most widely abused drug in US
hydrocodone
96
hydrocodone mechanism
modulation phase of nociception
97
hydromorphone relationship to morphine
7.5x as potent as morphine
98
when should sustained release version of hydromorphone be avoided?
hepatic disease
99
tapentadol class
opioid
100
tapentadol side effects
same as morphine + inhibits reuptake of norepi and serotonin
101
tramadol class
opioid
102
tramadol mechanism of action
modulation phase of nociception and norepi and serotonin reuptake inhibition
103
tramadol side effects
methadone/ antidepressants that inhibit serotonin reuptake
104
buprenorphine relationship w/ morphine
30x as potent as morphine
105
what is safest drug to use in hepatorenal syndrome
buprenorphine
106
Meperidine cuases mydriases/ meiosis. Other opiates caue mydriases/ meiosis
Meperidine= mydriasis (dilation)
Meiosis= other opioids
107
methadone structue/function relationship of enantiomers
levo= mu agonist
dextro= NMDA receptor
108
TCA Mechanism of action
norepi and serotonin reuptake inhibitor
109
TCA clinical use
neuropathic pain, appetite, stimulant, sleep aide
110
TCA Side Effect that is really bad for chronic pain
weight gain
111
venlafexine class
SNRI
112
duloxetine class
SNRI
113
milnaciprin class
SNRI
114
SNRI side effect
weight gain
115
TCA used in caution in which population
elderly
116
Gabapentin,pregablin class
anticonvulsants
117
Gabapentin mechanism of action
preventing Ca influx in dorsal horn
118
Gabapentin clinical use
neuropathic pain
119
gabapentin, pregablin side effects
dizziness, fatigue, weight gain, drowsiness, and peripheral edema
120
gabapentin interactions
none
121
how is volume of distribution different in the elderly
decreased water, increased fat, alteration in protein binding
