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pharm II: opioids, drugs of abuse, genomics > opioids pt 2 > Flashcards

opioids pt 2 Flashcards

1
Q

____________ = pain producing

A

algogenic

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2
Q

___________ = normally nonharmful stimulus that is perceived as painful

A

allodynia

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3
Q

______________ = absence of pain in the presence of a normally painful stimulus

A

analgesia

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4
Q

_________________ = unpleasant painful abnormal sensation whether evoked or spontaneous

A

dysesthesia

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5
Q

_______________ = heightened response to normally painful stimulus

A

hyperalgesia

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6
Q

_______________ = pain in the distribution of peripheral nerves

A

neuralgia

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7
Q

________________ = abnormal distrubance in the fx of a nerve

A

neuropathy

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8
Q

______________ = abnormal sensation whether spontaneous or evoked

A

paresthesia

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9
Q

T/F: poorly controlled acute pain may lead to chronic pain states

A

TRUE

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10
Q

acute pain is _____________, and lasts ____________

A

self-limited; 1-14 days

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11
Q

_______________ & ______________ are types of nociceptive pain

A

somatic and visceral

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12
Q

somatic pain comes from tissue damage –> activation of _____________ fibers

A

a delta; C fibers

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13
Q

_________________ pain is described as well localized and sharp

A

somatic (nociceptive)

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14
Q

_________________ pain is described as dull, cramping, squeezing, vague, and poorly localized

A

visceral (nociceptive)

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15
Q

what type of pain is often accompanied by ANS reflexes like N/V/D, HR, BP increase

A

visceral (nociceptive)

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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

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17
Q

what pain is described as burning, tingling, shocklike

A

neuropathic

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18
Q

what are the non-nociceptive pains

A

neuropathic

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19
Q

T/F: chronic pain often exhibits more than 1 type of pain classification

A

TRUE

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20
Q

T/F: opioids normally manage neuropathic pain really well

A

false; normally does not work on neuropathic pain

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21
Q

what are the four processes of somatic nociceptive pain

A
  1. transduction
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22
Q

_______________ = transformation of a noxious stimuli into an action potential

A

transduction

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23
Q

______________ = process by which an action potential is conducted from the periphery to the CNS

A

transmission

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24
Q

________________ = the recognition of pain signal from various areas of the brain

A

perception

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25
Q

________________ = brains response to action potential, alteration of neural afferent activity along the pain pathway (suppresses/enhances pain signals)

A

modulation

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26
Q

what is the primary treatment for pain

A

reducing transduction through inhibiting neurochemical mediators

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27
Q

what areas of the brain are responsible for perception of pain

A
  1. amygdala
  2. somatosensory area of cortex
  3. hypothalamus
  4. anterior cingulate cortex
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28
Q

describe the process of transduction

A
  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
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29
Q

what are your excitatory neurotransmitters with pain

A
  1. substance P
  2. glutamate
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30
Q

what are your inhibitory neurotransmitters with pain

A
  1. glycine
  2. GABA
  3. enkephalin
  4. serotonin
  5. norepi
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31
Q

inhibitory neurotransmitters are released via the ________________ pain pathway

A

descending

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32
Q

what receptors does substance P work on

A

neurokinin 1 and 2

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33
Q

what receptors does glutamate work on

A

NMDA, AMPA, kainite, mGluR

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34
Q

_________________ pain is acute pain on top of chronic pain

A

breakthrough pain

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35
Q

______________ pain is < 3-6 months; ____________ pain is > 3-6 months

A

acute; chronic

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36
Q

what are some mechanisms at which acute pain transitions to chronic

A
  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
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37
Q

_______________________ hyperalgesia occurs at the original site of injury, enhanced pain from heat and mechanical stimuli

A

primary

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38
Q

_______________ hyperalgesia occurs in uninjured tissues surrounding the injury, enhanced pain response to mechanical stimuli

A

secondary

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39
Q

aggressive pain management is essential to preventing _________________

A

post-op cardiac complications

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40
Q

CV physiologic effects of acute pain

A
  1. increased catecholamines
  2. increased cortisol –> increased HR, increased vascular resistance, increased myocardial activity, and increased ABP
  3. increased myocardial O2 demand & consumption
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41
Q

respiratory physiologic effects of acute pain

A
  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
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42
Q

GI physiologic effects of acute pain

A
  1. decreased gastric emptying
  2. decreased intestinal mobility
  3. increased smooth muscle sphincter tone
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43
Q

what are the coagulation effects of acute pain

A
  1. increasd plt aggregation
  2. venostasis
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44
Q

with acute pain immunologic function is ______________

A

decreasedc

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45
Q

GU effects of acute pain

A

increased urinary sphicter tone –> oliguria and urinary retention

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46
Q

psychological effects of acute pain

A
  1. fear
  2. anxiety
  3. depression
  4. helplessness
  5. anger
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47
Q

what medications act on transduction of pain signals

A
  1. NSAIDs
  2. LA
  3. steroids
  4. antihistamines
  5. opioids
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48
Q

what medications act on transmission of pain signals

A

LA

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49
Q

what mediations act on modulation of pain signals

A
  1. neuraxial opioids
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50
Q

what medications act on perception of pain signals

A
  1. GA
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51
Q

MOA of NSAIDs

A

blocks COX-1 and 2 –> decreased prostaglandin synthesis –> decreased nociception and tissue damage/inflammation

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52
Q

what type of pain responds to NSAIDs the best

A

nociceptive

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53
Q

NSAIDs are mostly metabolized in the _______________ with excretion into __________________

A

liver; urine/bile

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54
Q

responsibilities of COX- 1

A
  1. plt aggregation (via thromboxane A2)
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55
Q

inhibition of COX-1 –>

A
  1. gastric irritation
56
Q

COX_____ is widespread throughout the body, necessary for homeostasis and is working all the time

A

1

57
Q

______________ is an inducible enzyme that releases prostaglandins in the presence of inflammation, comes into play when theres injury

A

COX-2

58
Q

COX _________ mediates pain, fever, and carcinogenesis

A

2

59
Q

inhibition of COX2 –>

A

analgesia

60
Q

adverse reactions of NSAIDs

A
  1. GI dyspepsia
61
Q

MOA of how NSAIDs –> GI toxicity

A

decreased prostaglandin synthesis –> decreases in GI blood flow and secretion of mucus

62
Q

risk factors for GI toxicity with NSAIDs

A
  1. high dose
63
Q

conventional NSAIDs and COX-1 have what effect of platelets

A

impairs the ability of the plts to aggregate (i.e. activity)

64
Q

T/F: COX-2 has no effect on plt aggregation

A

TRUE

65
Q

factors that increase risk of NSAID induced nephrotoxicity

A
  1. advanced age
66
Q

all _________________ have potential for adverse renal effects but are usually reversible, except in case of high dose administraiton

A

NSAIDs

67
Q

prostaglandins play what role in the kidney

A

autoregulation of RBF and GFR

68
Q

what is the NSAID of choice in those at risk for CV complicatios

A

naproxen

69
Q

effects of NSAIDs on the liver

A
  1. increase in plasma concentrations of liver transaminases
70
Q

which NSAID has the ability to induce asthma exacerbation

A

ASA

71
Q

ASA induced asthma exacerbation is related to the _______________ inhibitory effects on prostaglandin synthesis

A

COX-1

72
Q

T/F: COX-2 selective NSAIDs have been shown to be safe in patients with asprin induced asthma

A

TRUE

73
Q

Sx of NSAID OD

A
  1. N/V
74
Q

what drugs will increase the plasma levels/effects of acetaminophen and asprin

A
  1. warfarin
75
Q

acetaminophen and asa cause decreased levels/effects of what drugs

A
  1. ACE -I
76
Q

what drugs will increase the levels/effects of ibuprofen and ketorlac

A
  1. aminoglycosides
77
Q

what drugs will decrease the levels/effects of ibuprofen and ketorolac

A
  1. ACE - I
78
Q

_____________________ catalyzes the synthesis of prostaglandins from arachodonic acid

A

COX

79
Q

_______________ block the action of the COX enzyme which DECREASES prostaglandin production

A

NSAIDs

80
Q

advantages of COX-2 selective inhibitors

A
  1. reversible inhibition
81
Q

disadvantages of COX-2 selective inhibitors

A
  1. increased CV risk
82
Q

what is the ONLY COX-2 selective inhibitor currently available

A

celecoxib

83
Q

metabolism of celecoxib

A

hepatically via CYP2C9

84
Q

excretion of celecoxib

A

urine and feces

85
Q

dose of celecoxib should be reduce in wht situations

A

hepatic impairment/renal dz

86
Q

celecoxib inhibits CYP_________ –> increased levels of _____________ & __________ meds

A

2D6; beta blockers; psychiatric meds

87
Q

celecoxib should be cautioned in those with _____________ allergy

A

sulfa

88
Q

NSAIDS are thought to reduce pain by suppressing the COX mediated production of prostaglandin __________

A

E2

89
Q

effects of non-selective COX inhibitors

A
  1. analgesia
90
Q

which meds are non-selective COX inhibitors

A
  1. ASA
91
Q

MOA of asa

A
  1. salicyclate that acetylates and irreversibly inhibits COX enzyme
92
Q

metabolism of ASA

A

rapidly hydrolyzed to salicyclic acid then salicyluric acid in the liver

93
Q

ASA is excreted in the _______________

A

urine

94
Q

what would delay absorption of ASA

A
  1. presence of food and higher pH
95
Q

clinical uses of ASA

A
  1. low intensity pain
96
Q

s/e of ASA

A
  1. GI irritation/ulceration
97
Q

what is the first sign of ASA OD

A

tinnitus

98
Q

T/F: chronic use of ASA increases the incidence of ESRD

A

false; other NSAIDs can lead to ESRD, but ASA has not proven that

99
Q

pts with ASA allergy have a cross sensitivity to ________________

A

all inhibitors of PG synthesis

100
Q

ketorolac has potent analgesic effects, but only moderate anti-inflammatory effects when administered ____________

A

IV or IM

101
Q

dose of ketorolac IM (> 50kg)

A

30 mg

102
Q

30 mg dose of ketorolac (toradol) = _____________ mg of morphine

A

10-12

103
Q

IM onset of ketorolac (toradol)

A

30 - 60 minutes

104
Q

elimination half life of ketorolac (toradol)

A

5 hours

105
Q

ketorolac (toradol) is ________% protein bound

A

99

106
Q

why does ortho avoid ketorolac (toradol)

A

decreases osteoblast activity

107
Q

what decreases clearance of ketorolac (thus may consider decreased dose)

A
  1. if administered with opioids
108
Q

what NSAIDs are proprionic acid derivatives

A
  1. ibuprofen
109
Q

which NSAID class if very useful for treating arthritis

A

proprionic acid derivatives

110
Q

_________________ = a proprionic acid derivative NSAID that has a longer elimination half-life which allows for BID dosing

A

naproxen

111
Q

effects of proprionic acid derivative NSAIDS

A
  1. less GI irritation
112
Q

which proprionic acid derivative NSAID will exacerbate pre-exisiting renal dz the most

A

fenoprofen

113
Q

T/F: Acetaminophen is an NSAID

A

false; due to minimal (if any) peripheral inflammatory effects

114
Q

acetaminiophen is aka

A

paracetamol

115
Q

chronic use of acetaminophen < _______g/day is NOT typically associated with hepatic dysfunction

A

2

116
Q

_______________ = leading cause of liver failure in the US

A

acetaminophen

117
Q

________________ is an antipyretic and non-narcotic analgesic

A

acetaminophen

118
Q

T/F: acetaminophen has NO GI or plt dysfunction

A

TRUE

119
Q

clinical manifestations of hepatic damage 2/2 acetaminophen use may present after ____________ days

A

2-6

120
Q

how do you tx acetaminophen OD

A

N-acteylcysteine

121
Q

what is the toxic metabolite of acetaminophen that depletes glutathione and accumulates in renal cells –> renal necrosis and ESRD

A

N-acetyl-P-benzoquinone imine (NAPQI)

122
Q

MOA of acetaminophne

A
  1. unknown, likely central inhibition of prostaglandin synthesis an blocking generation of pain impluse
123
Q

acetaminophen is ____________ % protein bound

A

20-50

124
Q

acetaminophen is metabolized in the ____________ and eliminated in the ______________

A

liver; urine

125
Q

acetaminophen provides _______ hours of effective analgesia for 37% of pts with acute postoperative pain

A

4

126
Q

adverse reactions of acetaminophen

A
  1. liver dysfunction
127
Q

what is the maximum daily dose of acetaminophen

A

4 gm

128
Q

what should be avoided with acetaminophen to prevent increased risk of toxicity

A
  1. long-term/excesssive etoh intake
129
Q

combination of acetaminophen with ______________ may offer superior analgesia compared to either drug alone

A

NSAIDS

130
Q

monitor toxicity s/sx of acetaminophen if used concomitantly with what drugs?

A
  1. phenytoin
131
Q

what can you administer with ketamine to avoid hallucinations/catatonic state

A

benzos

132
Q

ketamine causes dissocation btwn the ________________ & ______________ systems causing dissociative analgesia

A

thalamocortical; limbic

133
Q

dissociative anesthesia with ketamine resembles a ______________ state

A

catatonic

134
Q

s/sx of dissociative anesthesia with ketamine

A

resembles catatonic state: eyes open, slow nystagmic gaze, varying degrees of hypertonus/muscle movement

135
Q

effects of ketamine

A
  1. dissociative anesthesia
136
Q

_____________ 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

A

S(+); racemic

137
Q

MOA of ketamine

A

NMDA antagonist of glutamate

pharm II: opioids, drugs of abuse, genomics (4 decks)

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