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Adv. Pharm > Quiz 2 - Pain > Flashcards

Quiz 2 - Pain Flashcards

1
Q

Define pain

A

an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage

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2
Q

4 steps in the gate control theory of pain

A
  • transduction
  • transmission
  • modulation
  • perception
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3
Q

Epidural opioids act on which part of the pain pathway?

A

modulation

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4
Q

Non-steroidals act on which part of the pain pathway?

A

transduction

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5
Q

LAs act on which part of the pain pathway?

A

transduction and transmission

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6
Q

Systemic opioids act on which part of the pain pathway?

A

perception (cerebral cortex and thalamus)

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7
Q

2 natural opioids

A

morphine and codeine

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8
Q

2 semi-synthetic opioids

A

oxycodone and hydromorphone

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9
Q

2 synthetic opioids

A

meperidine and fentanyl

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10
Q

List the phenanthrenes

A
  • codeine
  • morphine
  • oxycodone
  • hydromorphone
  • hydrocodone
  • oxymorphone
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11
Q

What effect does activation of codeine have on receptor binding?

A

activation to morphine increases receptor binding potency by 300-7000x

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12
Q

3 phenanthrene antagonists

notable difference in structure?

A
  • nalorphine
  • naloxone
  • naltrexone
    (large nonpolar fxnl group on the N)
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13
Q

2 phenylpiperazines

A

meperidine and fentanyl

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14
Q

(ionized/nonionized) drugs are less likely to get into the CNS

A

ionized

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15
Q

Describe the spread of fentanyl along the spinal canal and why?

A

minimal spread because fentanyl is very lipophilic - it quickly crosses the BBB and leaves the epidural space

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16
Q

Describe the spread of morphine along the spinal canal and why?

A

significant spread because morphine is very hydrophilic - it does not get into the CSF as quickly –> longer DOA

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17
Q

Precursors to endogenous opioids

A
  • proenkephalin –> enkephalin
  • proopiomelanocortin –> endorphin
  • prodynorphin –> dynorphin
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18
Q

Describe the pharmacology of exogenous opioids:

A

they mimic the actions of endorphins by binding to opioid receptors, resulting in activation of a pain modulating system - inhibits release of NT responsible for pain
- work primarily centrally
- NO ceiling effect
- YES specific antagonist

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19
Q

What type of receptors are opioid receptors? Describe the effects:

A
  • G-protein-coupled receptors
  • Ginhibitory; decrease cAMP –> decrease Ca2+ –> decreased release of pain NT
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20
Q

3 opioid receptor types and their activity

A

1) mu: supraspinal analgesia, euphoria, resp depression, bradycardia, physical dependence
2) delta: modulate mu receptor activity
3) kappa: analgesia with little to no resp depression

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21
Q

Action of opioid agonist:

A

affinity and efficacy at mu receptor

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22
Q

Action of opioid partial agonist:

A

partial activation of mu receptor w/ or w/o kappa activity

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23
Q

Action of opioid agonist/antagonist:

A

agonist at kappa receptor and antagonist at mu receptor

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24
Q

Action of opioid antagonist:

A

affinity without efficacy at any opioid receptor

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25
Q

Advantages of opioid partial agonists and agonist/antag:

A
  • good if pt is hyperreactive to opioids
  • used for partial reversal
  • better SE profile
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26
Q

Disadvantages of opioid partial agonists and agonist/antag.:

A
  • not very effective d/t ceiling effect
  • opioid SE
  • reversal is problematic if pure agonist also given
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27
Q

MOA of Tramadol:

A

weakly binds to mu receptor and inhibits reuptake of serotonin and NE

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28
Q

Advantages & disadvantages of Tramadol:

A

Advantages:
- new alternative to pain therapy
- not a controlled substance

Disadvantages:
- expensive
- no more effective than Tylenol + Codeine
- sz reported

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29
Q

MOA of Tapentadol:

A

weakly binds to mu receptor and inhibits reuptake of serotonin and NE (same as Tramadol)

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30
Q

Advantages & disadvantages of Tapentadol:

A

Advantages:
- new alternative to pain therapy
- improved SE over opioids

Disadvantages:
- Class II controlled substance
- expensive
- less effective than other opioids

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31
Q

Advantages & disadvantages of Codeine/Hydrocodone/Oxycodone:

A

Advantages:
- good 1st line agent if NSAIDS ineffective
- good for breakthrough pain

Disadvantages:
- SE
- PO Codeine = nauseating
- monitor Tylenol intake

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32
Q

Advantages & disadvantages of Morphine:

A

Advantages:
- good analgesia
- good maintenance for acute and long-term pain
- + effect on preload post-MI
- staff familiarity

Disadvantages:
- long onset
- SE
- morphine-6 glucoronide metabolite accumulation (esp renal)

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33
Q

Methadone used to treat what type of pain?

A

severe & opioid withdrawal

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34
Q

Advantages & disadvantages of Methadone:

A

Advantages:
- good analgesic
- long half-life for chronic pain
- d-isomer has NMDA antagonist effect that lowers tolerance

Disadvantages:
- accumulates
- opioid SE
- difficult to manage long-term

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35
Q

Advantages & disadvantages of Meperidine:

A

Advantages:
- OK for morphine allergic pts
- less effect on biliary spasm
- efficacious for chills

Disadvantages:
- long onset
- accumulation of nor-meperidine metabolite (esp renal)
- SE

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36
Q

Advantages & disadvantages of Fentanyl:

A

Advantages:
- rapid onset
- OK for morphine allergic pts
- effective analgesic

Disadvantages:
- SE
- chest wall rigidity
- fast on/off d/t redistribution

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37
Q

5 most important opioid SE

A

1) resp depression
2) decreased GI motility
3) biliary tract spasm
4) histamine release
5) N/V

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38
Q

Opioid-associated histamine release has a particularly strong effect on what patient population?

A

hypovolemic

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39
Q

List the 6 emesis receptors that affect the CTZ:

A
  • histamine
  • muscarinic
  • 5HT3 (serotonin)
  • opioid
  • CN VIII (vestibulocochlear)
  • dopamine
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40
Q

Opioids directly stimulate which CN? Why is this relevant?

A

CN VIII - also concurrently stimulates the CTZ

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41
Q

Which opioid SE do patients NOT develop a tolerance to?

A
  • miosis
  • constipation
  • convulsions
  • antagonist actions
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42
Q

Which opioid SE do patients develop a moderate tolerance to?

A

bradycardia

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43
Q

Which opioid SE do patients often develop a tolerance to?

A
  • analgesia
  • euphoria/dysphoria
  • mental clouding
  • sedation
  • resp depression
  • antidiuresis
  • N/V
  • cough suppression
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44
Q

MOA of Naloxone

A

competitive inhibitor of mu, kappa, and delta receptors

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45
Q

Onset/duration of Naloxone:

A
  • onset 1-2 min
  • duration 30-90 min
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46
Q

Dose and frequency of Naloxone:

A

0.05-0.1 mg IV repeated every 2-3 min

titrate up depending on clinical response and desired effect (OD - big dose fast, decreased RR - small dose)

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47
Q

SE of Naloxone administration:

A
  • sudden and complete antagonism may cause severe HTN
  • ventricular arrhythmias
  • acute pulm edema d/t huge sympathetic outflow
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48
Q

Sedative-hypnotics + opioid interactions:

A
  • increased CNS depression
  • resp depression
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49
Q

Antipsychotic tranquilizers + opioid interactions:

A
  • sedation
  • resp depression
  • CV effects
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50
Q

MAOIs + opioid interactions:

A
  • hyperpyrexic coma
  • HTN
  • serotonin syndrome w/ phenylpiperidines (esp Meperidine)
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51
Q

Recommended agents for neuropathic pain:

A

TCAs (Imipramine, Doxepin, Duloxetine), Trazodone, Fluoxetine

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52
Q

Negative SE of TCAs and non-TCAs for neuropathic pain:

A

anticholinergic SE, sedation

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53
Q

Most NSAIDS are (acids/bases)?

A

acids

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54
Q

MOA of NSAIDS:

A

produce analgesia through inhibition of the enzyme cyclooxygenase, resulting in a decreased synthesis and release of prostaglandin

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55
Q

NSAIDS work (centrally/peripherally)

A

peripherally

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56
Q

Do NSAIDS have a ceiling effect?

A

yes

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57
Q

What effect does inhibition of prostaglandins have on the nerve cell?

A

decreased sensitization of nociceptors

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58
Q

List the alogenic mediators:

A
  • K+
  • serotonin
  • bradykinin
  • histamine
  • prostaglandins
  • leukotrienes
  • substance P
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59
Q

Prostacyclin is associated with which 2 effects?

A
  • vasodilation
  • decreased PLT stickiness
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60
Q

Thromboxane A2 is associated with which 2 effects?

A
  • vasoconstriction
  • increased PLT stickiness
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61
Q

3 types of eicosanoids:

A
  • prostaglandins
  • thromboxanes
  • leukotrienes
62
Q

What are eicosanoids?

A

oxygenation products of polyunsaturated long chain fatty acids
(LARGE molecules)

63
Q

Advantages & disadvantages of NSAIDS:

A

Advantages:
- reduce inflammation
- lower CNS effects
- no physical dependence
- able to combine with opioid tx

Disadvantages:
- hematological effects
- renal
- hepatic

64
Q

4 effects of Aspirin:

A
  • anti-inflammatory
  • analgesic
  • antipyretic
  • antiplatelet
65
Q

The antiplatelet effect of Aspirin is (reversible/irreversible)

A

irreversible

PLT have no nucleus and cannot make anything new when affected; must be regenerated

66
Q

Inflammation is more associated with (osteoarthritis/rheumatoid arthritis)

A

RA

67
Q

Compare the pathogenesis of osteoarthritis and RA:

A

osteoarthritis = biomechanical and leads to the loss of cartilage matrix
RA = autoimmune and leads to joint destruction

68
Q

SE of NSAIDS

A
  • GI disturbances
  • renal dysfxn
  • inhibition of PLT aggregation
  • hypersensitivity
  • inhibits uterine motility
  • CNS effects
69
Q

What effect can long-term NSAID use have on the renal system?

A

renal papillary necrosis
- renal toxicity in pts that rely on renal prostaglandins for maintenance of renal perfusion
(COX-2 selective and non-selective)

70
Q

Describe how use of NSAIDS and ACE inhibitors affects GFR:

A
  • NSAIDs inhibit prostaglandins that typically would dilate the afferent arteriole
  • ACE inhibitors prevent production of angiotensin II what would typically constrict the efferent arteriole
  • together these drugs decrease GFR by decreasing pressure through the glomerulus and decreasing renal filtration
    BIG problem in hypovolemic patient
71
Q

Which patients are at greatest risk for adverse effects of NSAIDs?

A
  • impaired renal fxn
  • HF
  • impaired hepatic fxn
  • taking diuretics and ACE inhibitors
  • elderly
72
Q

Equation for GFR:

A

(140-age) (weight in kg) / 72 x serum creat

*0.85 for women

73
Q

Where is COX-1 located in the body?

A

everywhere (housekeeping enzyme)
- found in the GI tract where it produces prostaglandins
- also found in kidneys and PLT

74
Q

Where is COX-2 located in the body?

A

sites of inflammation

75
Q

COX enzymes are derived from what substance?

A

arachidonic acid

76
Q

Why was the Rofecoxib drug trial stopped?

A

twice the increased risk of MI and stroke

77
Q

MOA of Acetaminophen:

A

thought to be similar to NSAIDs but more central effect; no effect on inflammation OR PLTs

78
Q

Disadvantage of Acetaminophen:

A

potentially fatal hepatic necrosis (no more than 4g/day) – most recommendations are now less than 3.25g

79
Q

How is Acetaminophen metabolized?

A
  • sulfination conjugation
  • glucoronidation conjugation
  • CYP3A4 & CYP2E1
80
Q

What happens to Acetaminophen that is metabolized via CYP3A4/CYP2E1 enzymes?

A

becomes NAPQI
- glutathione conjugation
OR
- reaction with proteins that causes toxicity

81
Q

What accounts for half of all cases of acute liver poisoning?

A

acetaminophen poisoning

82
Q

Describe the sequence of events leading to Acetaminophen toxicity:

A
  • CYP metabolism to a reactive metabolite (NAPQI)
  • glutathione depletion
  • metabolite binds to proteins
  • changes in mitochondrial permeability leading to oxidative stress, loss of mitochondrial membrane potential, and loss of ability of ability to synthesize ATP
83
Q

Dosage adjustment of Acetaminophen for severe renal impairment:

A

increase dosing interval to Q8h

84
Q

Dosage adjustment of Acetaminophen for moderate renal impairment:

A
  • increase dosing interval to Q6h for adults
  • normal or age-based dose for peds
85
Q

Is IV Tylenol more effective?

A

no - equivalent plasma concentration is reached, IV just works faster

86
Q

Effects of NSAIDs + Tylenol:

A

greater analgesia without significant increase in adverse effects associated with opioid-containing combos

87
Q

MOA of Methotrexate:

A

immunosuppressive cancer chemotherapeutic

88
Q

MOA of Hydroxycholoroquine:

A

antimalarial agent that suppresses T lymphocytes and leukocytes

89
Q

MOA of gold for antirheumatism:

A

decrease bone and articular destruction

90
Q

MOA of Penicillamine:

A

interferes with DNA synthesis and suppresses the immune system

91
Q

MOA of Sulfasalazine:

A

metabolized to 5-ASA (mechanism for UC) - may work on B cell fxn

92
Q

5 meds to treat gout:

A
  • colchicine
  • indomethacin
  • allopurinol
  • probenecid
  • sulfinpyrazone
93
Q

How is allopurinol used to treat gout?

A
  • xanthine oxidase inhibition that prevents more gout
94
Q

Presence of a charge (H+) on local anesthetics makes the molecule more (hydrophilic/lipophilic)

A

hydrophilic

95
Q

Amide LAs are metabolized ___

A

by enzymes (CYP450) in the liver

96
Q

Ester LAs are metabolized ___

A

by ester hydrolysis in the plasma

97
Q

List some ester LAs

A

(one i in the names)
- Cocaine (medium)
- Procaine (short)
- Tetracaine (long)
- Benzocaine (surface use only)

98
Q

List some amide LAs

A

(2 i in the names)
- Lidocaine (medium)
- Mepivacaine (medium)
- Bupivacaine (long)
- Prilocaine (medium)
- Ropivacaine (long)

99
Q

3 physiochemical properties that affect absorption of LAs

A

pKa
pH
lipid solubility

100
Q

3 physiologic conditions of the site of injection that affect absorption of LAs

A

pH
CO2 levels
temperature

101
Q

In LAs, the + charged quaternary amine is (ionized/unionized) and the uncharged tertiary amine is (ionized/unionized)

A

quaternary = ionized
tertiary = unionized

102
Q

For LAs to cross the epineurium, they must be _____.

For LAs to bind and block the Na+ channel, they must be _____.

A

unionized

ionized

103
Q

A drug with a low % unionized and a (low/high pKa) will have a (shorter/longer) onset

A

high pKa and longer onset d/t a smaller amount of the drug is able to cross the membrane

104
Q

A drug with a high % unionized and a (low/high pKa) will have a (shorter/longer) onset

A

low (close to physiologic pH) pKa and shorter onset d/t a larger amount of the drug is able to cross the membrane

105
Q

Describe what happens when sodium bicarbonate is added to a LA

A
  • raises pH of the solution
  • increases amount of unionized LA
  • faster diffusion of agent across the membrane
  • faster onset of nerve blockade
106
Q

Local anesthetics work on which parts of the pain pathway?

A

transduction & transmission

107
Q

MOA of LAs:

A

block voltage-gated Na+ channels and decrease the ability to generate an AP

108
Q

4 factors that contribute to a LA nerve blockade

A

1) myelination
2) fiber placement
3) fiber size
4) blood flow to the area

109
Q

Describe how blood flow affects a nerve blockade

A

Areas with high blood flow will have increased diffusion and less of the LA staying at the site of action to block the Na+ channels

110
Q

What impact does the refractory period of neuronal axon depolarization have on the impulse?

A

blocks another depolarization in that direction, forcing the impulse to only travel in one direction

111
Q

MOA of TTX (tetrodotoxin)

A
  • selective blockade of Na+ channel from the outside
  • blocks the AP of nerve and skeletal muscle leading to respiratory paralysis
  • made by bacteria in the puffer fish
  • no reversal agent
112
Q

Describe a frequency dependent block

A

Nerves firing at greater frequency have channels which open at a higher rate and will block faster d/t the agent entering the channel more quickly

113
Q

(Smaller/Larger) fibers block more quickly

A

smaller

114
Q

(Myelinated/Unmyelinated) fibers block more quickly

A

unmyelinated (C fibers)

115
Q

2 types of nerve fibers associated with pain

A

A-delta and C fibers

116
Q

LA can only block myelinated nerves at ____ and (#) are required for a differential nerve block to be effective

A

nodes of Ranvier

3 are required

117
Q

4 physical characteristics that affect a differential nerve block

A

1) placement
2) size
3) diameter
4) internodal distance

118
Q

(Small/Large) nerve fibers promote faster conduction

A

Large

small=slow conduction

119
Q

Describe how temperature affects frequency of neuron firing

A

frequency increases as T increases

120
Q

Sensations are blocked in the following order:

A
  • pain
  • cold
  • warmth
  • touch
  • deep pressure
  • motor
121
Q

Sensation is recovered in the following order:

A
  • motor
  • deep pressure
  • touch
  • warmth
  • cold
  • pain
122
Q

Type of LA and profile of Procaine:

Used for:

A
  • type: ester
  • profile: slow onset, short duration, low tox
  • use: local infiltration & spinal
123
Q

Type of LA and profile of Chloroprocaine:

Used for:

A
  • type: ester
  • profile: very fast onset, short duration, very low tox
  • use: local infiltration, nerve block, epidural
124
Q

Type of LA and profile of Tetracaine:

Used for:

A
  • type: ester
  • profile: slow onset, long duration, moderate tox
  • use: spinal
125
Q

Type of LA and profile of Lidocaine:

Used for:

A
  • type: amide
  • profile: fast onset, moderate duration, moderate tox
  • use: all types of regional
126
Q

Type of LA and profile of Bupivacaine:

Used for:

A
  • type: amide
  • profile: slow onset, very long duration, high tox
  • use: most types of local and regional
127
Q

Type of LA and profile of Etidocaine:

Used for:

A
  • type: amide
  • profile: fast onset, very long duration, moderate tox
  • use: nerve blocks, epidural
128
Q

Type of LA and profile of Ropivacaine:

Used for:

A
  • type: amide
  • profile: slow onset, very long duration, moderate tox
  • use: similar to Bupivacaine; most types of local and regional; less cardiac toxicity
129
Q

4 major factors involved in distribution of LA:

A

1) site of administration - vascularity, fat content
2) vasoactivity
3) tissue binding - Vd, plasma protein binding
4) patient conditions - age, dz state, pregnancy

130
Q

A 1% solution of any drug contains…

A

1 g of drug per 100mL of solution

131
Q

A 1% lidocaine solution contains ___ mg/mL

A

10 mg/mL

132
Q

A 1 mg ampoule of 1:1000 epinephrine soln contains ___ mg/mL

A

1 mg/mL

133
Q

A 1:100,000 soln of epi contains ___ mg/mL

A

10 mcg/mL

134
Q

A 1:200,000 soln of epi contains ____/mL

A

5 mcg/mL

135
Q

Epi should not be added to LA that are administered to which body parts?

A

end organs (fingers, toes, penis, nose, ears)

136
Q

Max safe dose of Epi =

A

4 mcg/kg

137
Q

What s/s are you watching for when injecting large volumes of LA?

A

tachycardia

138
Q

Recommended dose of sodium bicarb:

A

1 mL of 8.4% sodium bicarb per 10 mL of LA

139
Q

There is little advantage in adding sodium bicarb to which LAs?

A

Bupivacaine or Ropivacaine

140
Q

First clinical sign of Lidocaine toxicity:

A

circumoral and tongue numbness
THEN
tinnitus, lightheadedness

141
Q

Allergic reactions to LA are most commonly to…

A

esters (PABA metabolite)
or a preservative

142
Q

Which LA solutions should never be given spinally, epidurally, or via Bier block?

A

those with preservatives = acts as a neurotoxin

143
Q

An NSAID that is least likely to cause a GI bleed is _______

A

selective COX-2 inhibitor (….coxib)

144
Q

Describe the cardiovascular toxicity hypothesis:

A

NSAID-related hyperthrombotic state is d/t decreased prostacyclin and no effect on thromboxane

145
Q

MAOIs + which drug class is associated with serotonin-reuptake and can cause serotonin syndrome?

A

phenylpiperidine opioids (esp Meperidine)

146
Q

Parecoxib has a ceiling effect at what dose?

A

20mg (per the graph, it demonstrates a less significant effect at the next highest dose)

147
Q

List some NSAIDS

what is one important thing to know about dosing?

A
  • Ibuprofen
  • Indomethacin
  • Naproxen
  • Diclofenac
    ceiling effect
148
Q

Common SE of Fentanyl

A

chest wall rigidity

149
Q

Which opioid has the greatest effec ton SVR? Why?

A

Morphine d/t the histamine release

150
Q

Fentanyl + Midazolam interact when it comes to hypoxemia/apnea. Describe this relationship.

A

synergistic effect
1+1=3

151
Q

Drug that is most likely to be associated with Stevens-Johnson syndrome:

A

Valdecoxib - a sulfonamide

Adv. Pharm (5 decks)

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