opioids pt 2 Flashcards
(137 cards)
1
Q
____________ = pain producing
A
algogenic
2
Q
___________ = normally nonharmful stimulus that is perceived as painful
A
allodynia
3
Q
______________ = absence of pain in the presence of a normally painful stimulus
A
analgesia
4
Q
_________________ = unpleasant painful abnormal sensation whether evoked or spontaneous
A
dysesthesia
5
Q
_______________ = heightened response to normally painful stimulus
A
hyperalgesia
6
Q
_______________ = pain in the distribution of peripheral nerves
A
neuralgia
7
Q
________________ = abnormal distrubance in the fx of a nerve
A
neuropathy
8
Q
______________ = abnormal sensation whether spontaneous or evoked
A
paresthesia
9
Q
T/F: poorly controlled acute pain may lead to chronic pain states
A
TRUE
10
Q
acute pain is _____________, and lasts ____________
A
self-limited; 1-14 days
11
Q
_______________ & ______________ are types of nociceptive pain
A
somatic and visceral
12
Q
somatic pain comes from tissue damage –> activation of _____________ fibers
A
a delta; C fibers
13
Q
_________________ pain is described as well localized and sharp
A
somatic (nociceptive)
14
Q
_________________ pain is described as dull, cramping, squeezing, vague, and poorly localized
A
visceral (nociceptive)
15
Q
what type of pain is often accompanied by ANS reflexes like N/V/D, HR, BP increase
A
visceral (nociceptive)
16
Q
____________ pain is caused by damage to CNS or PNS nerves and is due to dysfunction of the CNS (spontaneous excition) –> abnormal processing of painful stimuli
A
neuropathic
17
Q
what pain is described as burning, tingling, shocklike
A
neuropathic
18
Q
what are the non-nociceptive pains
A
neuropathic
19
Q
T/F: chronic pain often exhibits more than 1 type of pain classification
A
TRUE
20
Q
T/F: opioids normally manage neuropathic pain really well
A
false; normally does not work on neuropathic pain
21
Q
what are the four processes of somatic nociceptive pain
A
- transduction
22
Q
_______________ = transformation of a noxious stimuli into an action potential
A
transduction
23
Q
______________ = process by which an action potential is conducted from the periphery to the CNS
A
transmission
24
Q
________________ = the recognition of pain signal from various areas of the brain
A
perception
25
________________ = brains response to action potential, alteration of neural afferent activity along the pain pathway (suppresses/enhances pain signals)
modulation
26
what is the primary treatment for pain
reducing transduction through inhibiting neurochemical mediators
27
what areas of the brain are responsible for perception of pain
1. amygdala
2. somatosensory area of cortex
3. hypothalamus
4. anterior cingulate cortex
28
describe the process of transduction
1. noxious stimuli detected by primary afferent nociceptors (a-delta and C fibers)
2. release of chemical mediators and neurotransmitters
3. stimulate periperpheral nociceptors: depol = Na influx; K efflux = repol
4. AP travels up to dorsal root of spinal cord & pain impulse generated
29
what are your excitatory neurotransmitters with pain
1. substance P
2. glutamate
30
what are your inhibitory neurotransmitters with pain
1. glycine
2. GABA
3. enkephalin
4. serotonin
5. norepi
31
inhibitory neurotransmitters are released via the ________________ pain pathway
descending
32
what receptors does substance P work on
neurokinin 1 and 2
33
what receptors does glutamate work on
NMDA, AMPA, kainite, mGluR
34
_________________ pain is acute pain on top of chronic pain
breakthrough pain
35
______________ pain is < 3-6 months; ____________ pain is > 3-6 months
acute; chronic
36
what are some mechanisms at which acute pain transitions to chronic
1. initiated by either periperhal or central mechanisms (peripheral or central sensitization)
2. hyperexcitable nerve endings (change from direct nerve injury, or sprouting of new nerve endings)
3. neuroma formation
4. damaged nerves have lower pain threshold so respond to non-noxious stimuli
37
_______________________ hyperalgesia occurs at the original site of injury, enhanced pain from heat and mechanical stimuli
primary
38
_______________ hyperalgesia occurs in uninjured tissues surrounding the injury, enhanced pain response to mechanical stimuli
secondary
39
aggressive pain management is essential to preventing _________________
post-op cardiac complications
40
CV physiologic effects of acute pain
1. increased catecholamines
2. increased cortisol --> increased HR, increased vascular resistance, increased myocardial activity, and increased ABP
3. increased myocardial O2 demand & consumption
41
respiratory physiologic effects of acute pain
1. decreased TV due to decreased movement
2. muscle spasms = decreased/limited respiratory movement (lose breath)
3. poor cough --> atelectasis and PNA
4. decreased VC & TLC
42
GI physiologic effects of acute pain
1. decreased gastric emptying
2. decreased intestinal mobility
3. increased smooth muscle sphincter tone
43
what are the coagulation effects of acute pain
1. increasd plt aggregation
2. venostasis
44
with acute pain immunologic function is ______________
decreasedc
45
GU effects of acute pain
increased urinary sphicter tone --> oliguria and urinary retention
46
psychological effects of acute pain
1. fear
2. anxiety
3. depression
4. helplessness
5. anger
47
what medications act on transduction of pain signals
1. NSAIDs
2. LA
3. steroids
4. antihistamines
5. opioids
48
what medications act on transmission of pain signals
LA
49
what mediations act on modulation of pain signals
1. neuraxial opioids
50
what medications act on perception of pain signals
1. GA
51
MOA of NSAIDs
blocks COX-1 and 2 --> decreased prostaglandin synthesis --> decreased nociception and tissue damage/inflammation
52
what type of pain responds to NSAIDs the best
nociceptive
53
NSAIDs are mostly metabolized in the _______________ with excretion into __________________
liver; urine/bile
54
responsibilities of COX- 1
1. plt aggregation (via thromboxane A2)
55
inhibition of COX-1 -->
1. gastric irritation
56
COX_____ is widespread throughout the body, necessary for homeostasis and is working all the time
1
57
______________ is an inducible enzyme that releases prostaglandins in the presence of inflammation, comes into play when theres injury
COX-2
58
COX _________ mediates pain, fever, and carcinogenesis
2
59
inhibition of COX2 -->
analgesia
60
adverse reactions of NSAIDs
1. GI dyspepsia
61
MOA of how NSAIDs --> GI toxicity
decreased prostaglandin synthesis --> decreases in GI blood flow and secretion of mucus
62
risk factors for GI toxicity with NSAIDs
1. high dose
63
conventional NSAIDs and COX-1 have what effect of platelets
impairs the ability of the plts to aggregate (i.e. activity)
64
T/F: COX-2 has no effect on plt aggregation
TRUE
65
factors that increase risk of NSAID induced nephrotoxicity
1. advanced age
66
all _________________ have potential for adverse renal effects but are usually reversible, except in case of high dose administraiton
NSAIDs
67
prostaglandins play what role in the kidney
autoregulation of RBF and GFR
68
what is the NSAID of choice in those at risk for CV complicatios
naproxen
69
effects of NSAIDs on the liver
1. increase in plasma concentrations of liver transaminases
70
which NSAID has the ability to induce asthma exacerbation
ASA
71
ASA induced asthma exacerbation is related to the _______________ inhibitory effects on prostaglandin synthesis
COX-1
72
T/F: COX-2 selective NSAIDs have been shown to be safe in patients with asprin induced asthma
TRUE
73
Sx of NSAID OD
1. N/V
74
what drugs will increase the plasma levels/effects of acetaminophen and asprin
1. warfarin
75
acetaminophen and asa cause decreased levels/effects of what drugs
1. ACE -I
76
what drugs will increase the levels/effects of ibuprofen and ketorlac
1. aminoglycosides
77
what drugs will decrease the levels/effects of ibuprofen and ketorolac
1. ACE - I
78
_____________________ catalyzes the synthesis of prostaglandins from arachodonic acid
COX
79
_______________ block the action of the COX enzyme which DECREASES prostaglandin production
NSAIDs
80
advantages of COX-2 selective inhibitors
1. reversible inhibition
81
disadvantages of COX-2 selective inhibitors
1. increased CV risk
82
what is the ONLY COX-2 selective inhibitor currently available
celecoxib
83
metabolism of celecoxib
hepatically via CYP2C9
84
excretion of celecoxib
urine and feces
85
dose of celecoxib should be reduce in wht situations
hepatic impairment/renal dz
86
celecoxib inhibits CYP_________ --> increased levels of _____________ & __________ meds
2D6; beta blockers; psychiatric meds
87
celecoxib should be cautioned in those with _____________ allergy
sulfa
88
NSAIDS are thought to reduce pain by suppressing the COX mediated production of prostaglandin __________
E2
89
effects of non-selective COX inhibitors
1. analgesia
90
which meds are non-selective COX inhibitors
1. ASA
91
MOA of asa
1. salicyclate that acetylates and irreversibly inhibits COX enzyme
92
metabolism of ASA
rapidly hydrolyzed to salicyclic acid then salicyluric acid in the liver
93
ASA is excreted in the _______________
urine
94
what would delay absorption of ASA
1. presence of food and higher pH
95
clinical uses of ASA
1. low intensity pain
96
s/e of ASA
1. GI irritation/ulceration
97
what is the first sign of ASA OD
tinnitus
98
T/F: chronic use of ASA increases the incidence of ESRD
false; other NSAIDs can lead to ESRD, but ASA has not proven that
99
pts with ASA allergy have a cross sensitivity to ________________
all inhibitors of PG synthesis
100
ketorolac has potent analgesic effects, but only moderate anti-inflammatory effects when administered ____________
IV or IM
101
dose of ketorolac IM (> 50kg)
30 mg
102
30 mg dose of ketorolac (toradol) = _____________ mg of morphine
10-12
103
IM onset of ketorolac (toradol)
30 - 60 minutes
104
elimination half life of ketorolac (toradol)
5 hours
105
ketorolac (toradol) is ________% protein bound
99
106
why does ortho avoid ketorolac (toradol)
decreases osteoblast activity
107
what decreases clearance of ketorolac (thus may consider decreased dose)
1. if administered with opioids
108
what NSAIDs are proprionic acid derivatives
1. ibuprofen
109
which NSAID class if very useful for treating arthritis
proprionic acid derivatives
110
_________________ = a proprionic acid derivative NSAID that has a longer elimination half-life which allows for BID dosing
naproxen
111
effects of proprionic acid derivative NSAIDS
1. less GI irritation
112
which proprionic acid derivative NSAID will exacerbate pre-exisiting renal dz the most
fenoprofen
113
T/F: Acetaminophen is an NSAID
false; due to minimal (if any) peripheral inflammatory effects
114
acetaminiophen is aka
paracetamol
115
chronic use of acetaminophen < _______g/day is NOT typically associated with hepatic dysfunction
2
116
_______________ = leading cause of liver failure in the US
acetaminophen
117
________________ is an antipyretic and non-narcotic analgesic
acetaminophen
118
T/F: acetaminophen has NO GI or plt dysfunction
TRUE
119
clinical manifestations of hepatic damage 2/2 acetaminophen use may present after ____________ days
2-6
120
how do you tx acetaminophen OD
N-acteylcysteine
121
what is the toxic metabolite of acetaminophen that depletes glutathione and accumulates in renal cells --> renal necrosis and ESRD
N-acetyl-P-benzoquinone imine (NAPQI)
122
MOA of acetaminophne
1. unknown, likely central inhibition of prostaglandin synthesis an blocking generation of pain impluse
123
acetaminophen is ____________ % protein bound
20-50
124
acetaminophen is metabolized in the ____________ and eliminated in the ______________
liver; urine
125
acetaminophen provides _______ hours of effective analgesia for 37% of pts with acute postoperative pain
4
126
adverse reactions of acetaminophen
1. liver dysfunction
127
what is the maximum daily dose of acetaminophen
4 gm
128
what should be avoided with acetaminophen to prevent increased risk of toxicity
1. long-term/excesssive etoh intake
129
combination of acetaminophen with ______________ may offer superior analgesia compared to either drug alone
NSAIDS
130
monitor toxicity s/sx of acetaminophen if used concomitantly with what drugs?
1. phenytoin
131
what can you administer with ketamine to avoid hallucinations/catatonic state
benzos
132
ketamine causes dissocation btwn the ________________ & ______________ systems causing dissociative analgesia
thalamocortical; limbic
133
dissociative anesthesia with ketamine resembles a ______________ state
catatonic
134
s/sx of dissociative anesthesia with ketamine
resembles catatonic state: eyes open, slow nystagmic gaze, varying degrees of hypertonus/muscle movement
135
effects of ketamine
1. dissociative anesthesia
136
_____________ isomer of ketamine produces more intense analgesia, more rapid metabolism, less salivation, and lower incidence of emergence reactions; however, only the ______________ form is used in the US
S(+); racemic
137
MOA of ketamine
NMDA antagonist of glutamate
