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PHAR 255 > Pain > Flashcards

Pain Flashcards

1
Q

Pain definition?

A

unpleasant sensory and emotional experience associated w/ or resembling that associated w/, actual or potential tissue damage

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2
Q

Is pain a symptom or diagnosis?

A

Both
Ex: flank pain –> UTI
Idopathic pain

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3
Q

Ratio of ppl w/ chronic pain in Canada?

A

1 in 5
1 in 3 over 65yrs old

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4
Q

who has highest prevalence of chronic pain?

A

women over 65

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5
Q

Race in Canada w/ highest prevalence of chronic pain?

A

indigenous

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6
Q

Model of pain used today?

A

biopsychoscocial;
biological, sociological, psychological

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7
Q

Acute pain characteristics?

A

< 3 months
organic cause common
pain reduction is goal
usually not med dependant
psych usually not present
environmental factors not usual
depression uncommon
insomnia not usually

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8
Q

Chronic pain characteristics?

A

3-6 months +
organic cause may not be present
functionality is goal
med tolerance common
psych often a major concern
significant environmental
depression common
insomnia common component

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9
Q

Nociceptive pain?

A

arise from damage to body tissue
sharp, aching, or throbbing pain
Ex: burn

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10
Q

Neuropathic pain?

A

direct damage to nervous system, usually peripheral
burning, shooting/radiating, tingling, numbness
Ex: shingles pain

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11
Q

Nociplastic pain?

A

change in way sensory neurons function rather than direct nervous system damage; neurons become more responsive
similar to neuropathic pain
Ex: fibromyalgia

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12
Q

Somatic pain?

A

arises from: skin, bone, muscle, or connective tissue
Sharp, hot, stinging, or throbbing pain
Locallized w/ surrounding tenderness
Ex: burn, laceration, arthritis

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13
Q

Visceral pain?

A

arises from internal organs
dull, ramping, colicky, gnawing, aching, squeezing, pulsing pain
poorly localized
Ex: pancreatitis, peptic ulcers

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14
Q

Nociceptive pain pathopysiology?

A

Transduction: stimulation of noxious stimuli, cytokine and chemokine activate nociceptors
Conduction: chem signals converted to electrical signals and AP produced along alpha-delta and C nerves to spinal cord
Transmission: movement of impulses along spine including more chemical signals w/ glutamate and substance P
Perception: signals recieved by thalamus, make pain conscious
Modulation: signals can be made stronger w/ glutamate/ Sub P or inhibited by endogenous opiods like GABA, NE, and 5HT

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15
Q

Which is the fast channel in conduction?

A

alpha-delta

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16
Q

WHich is the slow channel in conduction?

A

C

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17
Q

Pain produced by alpha-delta stimulation?

A

sharp, localized

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18
Q

Pain produced by C-nerve?

A

achy, poorly localized

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19
Q

Receptor activation involves which channels?

A

voltage-gated Na channels

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20
Q

Channels used in transmission to regulate excitatory NTs?

A

N-type voltage-gated Ca channels

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21
Q

What acts as the relay station in the brain?

A

thalamus

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22
Q

where does perception occur?

A

higher cortical structures

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23
Q

Modulation drugs that strengthen pain signals?

A

Glutamate
Substance P

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24
Q

Modulation drugs that decrease pain signals/inhibt

A

endogenous opiods
GABA
NE
serotonin

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25
Q

Is there noxious stimuli in neuropathic pain?

A

No

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26
Q

Peripheral pain characteristics?

A

PNS
sharp, shooting/radiating, tingling, freezing, burning, itching pain
generally localized with nerve fibre

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27
Q

Central pain characteristics?

A

CNS
shooting/radiating, tingling, freezing, burning, itching pain
poorly localized

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28
Q

Acute pain treatment approach?

A

Assess pt
Select treatment: most effective analgesic with fewest AE’s, lowest dose for shortest duration, scheduled for first few days then prn
Identify non-pharm strategies
Educate pt
Communicate and document plans for transition

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29
Q

Non-pharm therapies for acute pain?

A

education
distraction and relaxation
positioning
cold <48hrs post injury
acupuncture
exercise
RICE
heat >48hrs psot injury
massage
TENS

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30
Q

Acet dosing?

A

325-500-650-1000mg q4-6h, max of 4g/d
Chronic max is 3.2g/d

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31
Q

NSAIDs MOA and dosing?

A

inhibtion of COX1 and COX2, decreasing formation of PG precursors
Ibu: 400mg po q4h
Naproxen: 250-375-500mg po BID

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32
Q

Opiods dosing and MOA?

A

bind opiod receptors, suppress neuronal firing
less than50-90 MEQ/d

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33
Q

Child acet dosing

A

10-15mg/kg/dose q4-6h
max 75mg/kg/d or 4000mg which ever is lower

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34
Q

CI’s of NSAIDs?

A

CKD
CrCl under 40mL/min
hyperkalemia
cirrhosis/ liver impairment
GI ulcers
IBD
uncntrolled HF
MI
thrombocytopenia
transplant

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35
Q

ASA dosing?

A

<300mg/d to reduce platelet aggregation
300-2400mg/dantipyretic and analgesic (325-600mg po q4h prn)
2400-4000mg anti-inflam
4000mg max/d

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36
Q

Diclo dosing?

A

50mg po BID
75-100mg SR po OD
max 100mg/d

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37
Q

ketorolac dosing?

A

10mg po QID prn
max 40mg/d, 5 days use limit b/c increase GI bleed

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38
Q

Naproxen sodium vs naproxen base max difference?

A

NS: 1500mg/d
NB: 1000mg/d

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39
Q

Which COX enzyme inhibtion is cardioprotective?

A

COX-1 inhibition (low dose ASA)

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40
Q

NSAID/COXIB that show increased CV risk?

A

Diclo >=150mg/d
Meloxicam
Celecoxib >200mg/d
Rofecoxib
Valdecoxib

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41
Q

Mechanism of how NSAIDs increase BP/ Cardiac risk?

A

Vasoconstrict, decrease renal blood flow, increase Na proxismal reabsorption

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42
Q

How are NSAIDs a GI risk?

A

COX-1 inhibtion leads to:
decreased PGs
decreased gastroduodenal mucosal protection
increased GI ulcer risk

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43
Q

NSAID GI risk factors?

A

age>60
comorbid conditions
history of GI bleeds or presence of H. pylori
multiple NSAIDs
high dose NSAIDs
SSRI, anticoag, antipaltelet therapies
HF

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44
Q

How to manage NSAID GI risk?

A

add misoprostol or PPI
–> arthrotec 75
–> Vimovo

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45
Q

Why do NSAIDs pose a renal risk?

A

COX1/COX2 inhibition leading to vasoconstriction of afferent arteriole

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46
Q

Advantage of Celecoxib?

A

COX-2 selective; reduces GI risk, minimal platelet effect

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47
Q

Celecoxib must be reduced in poor CYP_____ metabolizers

A

2C9

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48
Q

Celecoxib dosing?

A

400mg po for first day single dose
200mg po once daily for up to 7 days, max dose of 400mg/d for up to 7days

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49
Q

NSAID/COXIB DI’s?

A

anti-HTN effect (HTN drugs)
lithium, methotrexate, steroids, tenofovir, warfarin (increase= toxicity)
Heparin, warfarin, corticosteroids, SSRI (increase GI risk)
ACEI and ARB, diuretics increase nephrotoxicity
Decrease ASA efficacy if co-adminsitered

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50
Q

WHO ladder?

A

Nonopiod(acet, ASA, NSAIDs)
Weak opioid (Codeine)
Strong opioid and nonopiod (morphine, hydromorphone, fentanyl)

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51
Q

Drug used in pregnancy for pain?

A

Acet is safest, others not recommended

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52
Q

Chronic secondary pain?

A

diagnosed when pain orginates as a symptom of another underlying health condition

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53
Q

4Ps of pain treatment?

A

Prevention
Psychological
Physical
Pharmaceutical

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54
Q

WHat population is acet thr first choice for in chronic use?

A

Dementia b/c effective and safe in this population

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55
Q

What medication has been newly added to low back pain treatment?

A

Duloxetine (SNRI)

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56
Q

stepwise approach to neuropathic pain treatment?

A

Gabapentinoids (TCAs, SNRIs)
Tramadol or opioids
Cannabinoids
Forht line agents?

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57
Q

Amitriptyline dosing?

A

25-100mg/d HS

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58
Q

Duloxetine dosing?

A

40-60mg/d

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59
Q

Venalfaxine dosing?

A

75-225mg/d

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60
Q

Desvenlafaxine dosing?

A

200-400mg/d

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61
Q

pregabalin dosing?

A

300-450mg/d divided BID or TID

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62
Q

Gabapentin dosing?

A

1800mg/d (900-3600mg divided TID or QID)

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63
Q

Gabapentinoid MOA?

A

block release of excitatory NTs by binding to specific Ca channels in CNS

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64
Q

AEs of gabapentinoids?

A

dizziness
drowsiness
N/V
mood changes
tremors
nystagmus
ataxia
peripheral edema
wt gain

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65
Q

DIs of gabapentinoids?

A

CNS depresants
anticholinergics
Serotonergic agents and pontentiators

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66
Q

How are gabapentinoids eliminated? bioavailability?

A

100% renal
F is inversley proportional to dose; F goes down as dose goes up

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67
Q

How must gabapentinoids, TCAs and SNRIs be d/ced?

A

Tapers to avoid withdrawal

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68
Q

TCA MOA?

A

inhibits reuptake of serotonin and NE, blocks sodium channels, blocks N-methyl-d-aspartate (NMDA) agonist induced hyperalgesia

69
Q

AEs of TCAs?

A

anticholinergic;
dry mouth
dry eyes
constipation
urnie retention
sedation
confusion
QT prolongation
postural hypotension

70
Q

CIs of TCAs?

A

If MAOI used in past 7 days
severe liver impairment

71
Q

TCA DI’s?

A

CYP2D6 substrates
CNS depressants
anticholenergic
serotonergic
antipaltelet
NSIADs
bupropion
carbamazepine
cyclobenzaparine

72
Q

Are TCA dosing for pain and depression te same?

A

no, pain usually 1/3 to 1/5 the dose of depression dosing

73
Q

MOA of SNRIs?

A

inhibit reuptake of serotonin and NE at neuronal junctions, Duloxetine has weak inhibiton of dopamine reuptake

74
Q

AEs of SNRIs?

A

drowsiness
sedation
cosntipation
hypotension
increased HR/BP
hyponatremia

75
Q

CI of SNRIs?

A

MAOI use in past 7 days

76
Q

DI’s of SNRIs?

A

Duloxetine: CYP2D6 inhibtors
Venlafaxine: CYP 2D6 inhibtors
Serotonergic agents
antiplatelets and NSAIDs
smoking

77
Q

at what dose does venlafaxine inhbit NE reuptake?

A

> 225mg

78
Q

Timetable for full analgesic effect in neuropathic pain?

A

up to 6 weeks once titrated to target dose

79
Q

Best treatment for Nociplastic pain?

A

exercise

80
Q

Is an opiate and opioid?

A

Yes, opiates are naturally derived (opium, morphine, heroin, codeine) where as opioids are synthetic or semi-synthetic (ex fentanyl)

81
Q

Which opioid receptor is responsible for over dosed stopping breathing?

A

mu

82
Q

mu receptor characteristics?

A

analgesia**
euphoria, physical dependence, respiratory depression, reduced GI motility, sedation

83
Q

delta receptor characteristics?

A

analgesia, euphoria, physical dependance

84
Q

kappa receptor characteristics?

A

analgesia sedation, mood?, Not physically depedant.

85
Q

Which receptor is NOT physically dependant?

A

Kappa

86
Q

What occurs in the presynaptic neuron when binding of the opioid receptors?

A

decreases Ca influx
decreases transmiter release

87
Q

What occurs in the postsynaptic neuron when the mu receptor is bound?

A

increase in K conductance

88
Q

opioid MOA pharmacsit perspective?

A

opioid molecule bind to opioid receptors in CNS and PNS supressing neuronal firing from the presynaptic neuron and also inhibit postsynaptic nerves in some areas, altering transmission and perception of pain

89
Q

opioid MOA patient explanation?

A

opiods work in the brain and nerves to quiet and slow down pain signals, making it feel like there is less pain

90
Q

Opioid indications?

A

severe acute pain associated w/ surgery or medical conditions
treatment o chronic/terminal cancer pain
management of dyspnea in chronic lung diseases

91
Q

Advantages of opioid use in chronic non-cancer pts?

A

potent analgesic effect
fast onset
relatively low risk of major organ toxicity

92
Q

Disadvantages of opioid use in chronic non-cancer?

A

AEs:
- CNS depression
- falls/fractures
- constipation
- apnea
- hypogonadism
- hyperalgesia
- dependence
Risk of diversion
Tolerance
long term benefit evidence is lacking

93
Q

Strong reccomendation?

A

indicates that almost all fully informed pts would choose the recommended course of action

94
Q

Weak recommendation?

A

indicates that the majority of informed pts would choose suggested course of action but, an appreciatable minority would not.

95
Q

duration of IR products?

A

4-6hrs

96
Q

Q12hr products?

A

oxycodone
hydromorphone
morphine

97
Q

Q24h products?

A

Morphine
Tramadol

98
Q

Which buccal/sublingual tablets have a very short duration?

A

fentanyl (fentora)

99
Q

Bucall or sublingual option that is long duration?

A

buprenorphine w/ naloxone (Suboxone)

100
Q

duration of therapy of suppository? Drug?

A

4hrs
oxycodone (supeudol)

101
Q

Which transderma option is Q72hrs?

A

fentanyl patch

102
Q

WHich trandermal option is Q7d

A

buprenorphine patch

103
Q

Which opioid is a subQ monthly injection?

A

buprenorphine

104
Q

Injectable opioids?

A

morphine
hydromorphone
codeine
fentanyl
buprenorphine

105
Q

Which morphine metabolite is active analgesic?

A

morphine-6-glucuronide

106
Q

WHich morphine metabolite is not active analgesic?

A

morphine-3glucuronide

107
Q

At what CrCl should morphine be monitored closely/ avoided?

A

20-30mL/min

108
Q

Morphine MEQ?

A

1
hehehehehe

109
Q

Codeine MEQ?

A

0.15

110
Q

what would 200mg of oral codeine equate to of oral morphine?

A

30mg (200mg x 0.15)

111
Q

WHich enzyme converts codeine to morphine?

A

CYP2D6

112
Q

Factors that can cause codiene toxicity?

A

ultrarapid CYP2D6 metabolism
CYP3A4 inhibition
renal failure

113
Q

Contraindications of codeine?

A

12 or under
18 or under post tonsilectomy and or adenoidectomy

114
Q

What dose is codeine antitussive?

A

> =15mg q4-6h

115
Q

Codeine CR dosing?

A

intial: 50mg q12h
2 day minimum increase interval
50mg/d suggested dose increase
max dose: 300mg q12h

116
Q

Codeine IR dosing?

A

Intial: 15-30mg q4h prn
minimum 7 day increase interval
suggested dose: 15-30mg/d
Maximum dose: 600mg/d or acet max 4g/d

117
Q

MEQ of oxycodone?

A

1.5

118
Q

20mg oxycodone morpine equivalent?

A

30mg

119
Q

Metabolizer of oxycodone?

A

CYP3A4 major
CYP2D6 minore to active metabolite

120
Q

Characteristics of oxyneo?

A

forms gel when wet
difficult to break tablets

121
Q

Percocet ingredients?

A

5mg oxycodone
325mg acet

122
Q

Percodan ingredients?

A

oxycodone 5mg
ASA 325mg

123
Q

Targin ingredients?

A

oxycodone
naloxone

124
Q

Oxycodone CR dosing?

A

Intial: 10mg q12h
minimum 2 days increase interval
suggested: 10mg/d

125
Q

Oxycodone IR dosing?

A

5-10mg q6h prn max 30mg/d
minumum increase interval 7d
suggested: 5mg/d
Max: acet 4g/d (combo product)

126
Q

Hydromorphone MEQ?

A

5

127
Q

what does 1 mg of hydromorphone correlate to morphine?

A

5mg

128
Q

Whenis hydromorphone a good option?

A

in renal impairment

129
Q

Hydromorphone CR/PR dosing?

A

CR: 3mg q12h max of 9mg/d suggested 3mg/d
PR: 4mg q24h maximum 8mg/d suggested 4mg/dH

130
Q

Hydromorphone IR dosing?

A

1-2mg q4-6h prn
max 8mg/d
suggested 1-2mg/d

131
Q

Interval increase time of hydromorphone CR/PR?

A

CR: 2d
PR 4d but 14d recommended

132
Q

Interval increase time of hydromorphone IR?

A

7d

133
Q

Tramadol MOA?

A

Mu receptor agonist
inhibits serotonin and NE reuptake

134
Q

Binding affinity of tramadol for mu receptor in recpect to morphine?

A

~600x less potent than morphine

135
Q

Metabolizer of tramadol?

A

CYP2D6 to active

136
Q

Active metabolite of tramadol?

A

O-desmethyl tramadol

137
Q

Risks of tramadol?

A

seizures
serotonin syndrome
hypoglycemia
QT prolongation

138
Q

which tramadol CR is not maxed at 300mg? what is its maximum?

A

zytram XL
400mg

139
Q

Tramadol CR suggested dose?

A

75-100mg q24h

140
Q

Tramadol IR dosing?

A

max 400mg/d
sugested 25mg/d –> 1-2tab q4-6h

141
Q

Which non-formulary drug is similar to tramadol?

A

tapentadol

142
Q

Fentanyl MEQ?

A

~100

143
Q

what would be the morphine equivalent of 25mcg/h fentanyl patch?

A

100mg morphine (in a day not per hour)

144
Q

Controverse of switching with fentanyl patch?

A

converting TO patch is safe
but
Converting FROM patch is aggressive

145
Q

Counselling points for fentanyl patches?

A

remove old patch before applying new patch
apply to clean, dry, non-hairy area
DO NOT shave hair if neede clip hair close to skin
do not use external heat on patch

146
Q

How long to hold patch firmly on skin when applying

A

atleast 30 seconds

147
Q

which fentanyl patch do you use when titrating or tappering?

A

12mcg/h

148
Q

what kind of membrane are fentanyl patches?

A

matrix membrane

149
Q

Methadone MOA for pain?

A

mu receptor agonist
NMDA receptor antagonist

150
Q

Risks of t\methadone?

A

QTc prolongation
serotonin syndrome when combined with serotonergic drugs

151
Q

Role of buprenorphine?

A

rotation from other opiods;
switching when at low doses.

151
Q

What is the main difference in regards to the mu receptor with buprenorphine?

A

partial agonist; therfore cannot OD alone on buprenorphine

151
Q

What is the maximum starting methadone dose?

A

30mg/d

152
Q

Buprenorphine metabolized by?

A

CYP3A4

153
Q

Does constipation and miosis (pinpoint pupils) get better over time with opioid use?

A

NO

154
Q

General AEs with opioids used acutely?

A

sedation
respiratory depression
constipation
Nausea
Mioisis
itching/rash

155
Q

How is itching/rash a pseudoallergy with opioids?

A

histamine release from cutaneous mast cells, not a true allegy or immunoresponse

156
Q

When is toelrance to sedation of opioids generally seen?

A

3-4d,can take 10d but can also never go away

157
Q

General AEs of opiods used long term?

A

hypogonadism
sleep apnea
opioid induced hyperalgesia
tolerance
dependence
toxicity

158
Q

How do opioids cause hypogonadism?

A

influence HPA axis and HPG axis, morphine cuases a strong prgoressive decrease of cortisol plasma levels
modulate hormone release

159
Q

Management of opioid induced hyperalgesia?

A

taper down, opioid rotation, switch to buprenorphine or methadone

160
Q

SIgns of opioid OD?

A

difficulty walking, talking, staying awake
blue lips/nails
small pupils
cold/clammy skin
dizziness
confusion
drowsiness
chocking/gurgling or snoring sounds
not breathing
inability to wake up

161
Q

What do you give for an opioid OD?

A

Naloxone

162
Q

Naloxone MOA?

A

binds same receptors as opioids in the brain but, more tightly and dispalces opioids from the receptors.
No biological response from naloxone binding

163
Q

Why might we need to give multiple doses of naloxone for an opioid OD?

A

wears off in 30-90 minutes so overdose may return

164
Q

How much more potent is IV morphine over oral morphine? (all opioids)

A

2x

165
Q

Physical withdrawl of opioid treatment?

A

clonidine

166
Q

Sweating from opioid withdrawl treatment?

A

oxybutynin

167
Q
A

PHAR 255 (14 decks)

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