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Anesthesia > Pain Therapies > Flashcards

Pain Therapies Flashcards

1
Q

What are the most common administration forms of acute and chronic pain relievers?

A

ACUTE: injectable, OTM, topical, oral

CHRONIC: oral, OTM, topical, injectable

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2
Q

What are the 4 classic agents used to prevent and treat acute pain?

A
  1. opioids
  2. alpha-2 agonists
  3. anti-inflammatories
  4. local anesthetics
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3
Q

What is the difference between opium, opiates, and opioids?

A

OPIUM = substance derived from the poppy, Papaver sommiferum

OPIATE = drugs derived naturally from opium, like morphine and codeine

OPIOID = exogenous substances, natural and synthetic, that bind to endogenous receptor systems

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4
Q

What is morphine?

A

one of twenty natural alkaloids in opium

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5
Q

What is Simbadol? What are 3 major benefits?

A

buprenorphine injection - Schedule III

  1. post-op pain control day and night for patient
  2. proven efficacy in cats
  3. multidose vial available
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6
Q

What is Recuvrya? When is it indicated for use?

A

transdermal fentanyl solution approved for use in dogs

control of post-op pain associated with moderate to severely painful surgical procedures —> apply 2-4 hours before sx to allow peak plasma concentrations 12-14 hrs later

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7
Q

What is tramadol? What is responsible for its effects?

A

analgesic and antitussive weak mu partial agonist that inhibits serotonin and norepinephrine uptake and has alpha-2 agonist-like effects

metabolite M1 = analgesia

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8
Q

What are 6 oral opioid alternatives?

A
  1. codeine
  2. tylenol*
  3. hydrocodone
  4. oxycodone
  5. morphine (ER)
  6. methadone (cats only)
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9
Q

What side effect is associated with codeine use in dogs? What is it commonly combined with?

A

constipation

tylenol

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10
Q

What are the 4 locations of endogenous opioid receptors? What are the 3 types of receptors?

A
  1. dorsal horn of the spinal cord
  2. brain
  3. peripheral nervous system
  4. non-nervous tissue: GIT, CV system, endorine system

mu, kappa, delta

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11
Q

What substances to opioid receptors commonly interact with?

A

endorphins, enkephalins, dynorphins

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12
Q

What are 6 common effects associated with mu receptor agonism?

A
  1. respiratory depression
  2. euphoria
  3. addiction
  4. analgesia
  5. sedation
  6. miosis
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13
Q

What are 4 common effects associated with kappa receptor agonism?

A
  1. analgesia
  2. sedation
  3. respiratory depression
  4. miosis
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14
Q

What 2 effects are associated with delta receptor agonism?

A
  1. analgesia
  2. motor dysfunction
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15
Q

Opioid receptor effects, agonists, and antagonists:

A
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16
Q

What opioids are considered agonists? Partial agonists?

A

morphine, codeine, fentanyl, meperidine, hydo/oxycodone, etorphine

buprenorphine

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17
Q

What opioids are considered antagonists? Mixed agonist/antagonist?

A

naloxone, naltrexone

butorphanol

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18
Q

What happens when opioid receptors are activated?

A

G-coupled protein receptors catalyze the intracellular formation of second messengers

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19
Q

What do G-proteins couple? What 3 subunits are present?

A
  • cell surface receptors to catalytic units
  • receptor to ion channels

alpha, beta, gamma

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20
Q

What 3 effects do G-proteins have once they opioid receptor is agonized?

A
  1. inhibits cAMP
  2. inhibits voltage-gated Ca and Na channels, resulting in decreased calcium influx, calcium intracellular modulation, and neurotransmitter release
  3. increased K conductance, resulting in hyperpolarization of cells and lessened nerve impulse transmission
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21
Q

What are the 6 primary clinical effects of opioids? What is seen in cats?

A
  1. analgesia
  2. sedation
  3. bradycardia
  4. panting
  5. respiratory depression
  6. ileus, urinary retention

hyperthermia - hydromorphone, buprenorphine

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22
Q

What action of opioids causes analgesia? What are the best opioids for analgesia?

A

inhibits pain transmission in the dorsal horn of the spinal cord at mu receptors (pure mu agonists > mixed, partial)

fentanyl, morphine, hydro/oxymorphone, sufentanil

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23
Q

What are the 4 routes used to deliver opioids? What is avoided?

A
  1. parenteral**
  2. epidural
  3. spinal
  4. local

oral - first-pass metabolism (tramadol)

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24
Q

What are the 3 most potent pure mur agonists?

A
  1. carfentanil
  2. etorphine
  3. fentanyl
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25
Q

What opioid gives the best pain relief?

A

fentanyl

(buprenorphine is a good option in cats)

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26
Q

What opioid gives the best sedation?

A

butorphanol

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27
Q

What 3 respiratory effects do opioids have?

A
  1. decrease tidal volume and rate
  2. decrease responsiveness of respiratory center to CO2
  3. panting due to direct effect on temperature regulating center
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28
Q

In what 2 situations are the respiratory effects of opioids particularly noticeable?

A
  1. combined with other agents, like Acepromazine and Medetomidine
  2. “higher” fentanyls used IV, like carfentanil, remifentanil, sufentanyl

ventilation may be required!

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29
Q

What 3 opioids have anti-tussive effects?

A
  1. codeine
  2. hydrocodone
  3. butorphanol
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30
Q

What 3 effects do opioids have on the CV system?

A
  1. cardio soothing - CO and contractility maintained
  2. increased vagal tone - mild bradycardia, heart block
  3. histamine release - vasodilation
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31
Q

What 2 opioids are associated with histamine release?

A
  1. morphine
  2. meperidine

(vasodilation!)

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32
Q

How do opioids affect pupil dilation in the eyes of dogs and cats?

A

DOG = miosis

CAT = mydriasis

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33
Q

In what patients is mild sedation most commonly seen with the use of opioids?

A

painful animals

  • non-painful = excitement, most commonly in cats and horses
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34
Q

What GI effects are associated with opioid use?

A
  • initial increase in peristalsis
  • GI stasis —> vomiting, nausea, constipation
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35
Q

What 4 effects are associated with continuous use of opioids?

A
  1. opioid hyperalgesia (monotherapy)
  2. increased inflammation
  3. tumor metastasis and angiogenesis
  4. cardiac autonomic non-responsiveness
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36
Q

What antiemetics are commonly coupled with opioids? In what 2 is this not necessary?

A
  • neurokinin antagonist (Maopitant)
  • metoclopramide
  • ondansetron

oxymorphone and methadone

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37
Q

In what patients should opioids be used carefully?

A
  • pre-existing CNS depression
  • pre-existing respiratory depression
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38
Q

What full reversals are used for opioids? Partial reversal?

A

naloxone, naltexone

butorphanol

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39
Q

How do opioid reversals compare to alpha-2 reversals? Why do we use reversals?

A

very short-lived —> animals often “renarcotize”

  • emergency overdose
  • reduce narcosis
  • rouse an animal from too much sedation
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40
Q

What are some pros to using butorphanol?

A
  • minimal opioid side effects
  • respiratory depression
  • urinary retention
  • vomiting
  • great antiemetic
  • GI analgesic in cats and horses
  • very safe
  • can act as a benign filler in premeds
  • minimal expense
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41
Q

What are 5 cons to using butorphanol?

A
  1. minimal analgesia
  2. considered a reversal
  3. short duration of analgesia
  4. disturbed sleep
  5. confusion
42
Q

What are the 5 major results of keeping butorphanol in premeds?

A
  1. less vomiting
  2. sedation
  3. safety and familiarity
  4. less narcosis
  5. pretty good analgesia - not quite as good as pure mu receptors, but close
43
Q

What injectable and OTM opioids are available in cats?

A
  • buprenorphine: 6-8 hr
  • Simbadol (injectable buprenorphine): 24 hr
44
Q

Is tramadol an opioid? How does it act?

A
  • weak mu receptor effect with less affinity
  • structurally related to morphine and codeine

metabolized into active M1, which causes analgesia and serotonin and norepinephrine reuptake inhibition —> serotonin syndrome!

45
Q

What analgesic activity does tramadol have in animals?

A

short half-life, negligible amounts of M1 production

  • inconclusive activity parenteral vs. oral
46
Q

When is opioid hyperthermia especially common in cats? What should be done if this happens?

A

hydromorphone use, especially when combined with ketamine or atropine

  • stop opioid
  • administer fluids, phenothiazines
  • give it time
47
Q

What do fentanyl patches provide? What 3 things does its effect depend on?

A

background analgesia with the use of the most potent opioid (unreliable plasma levels as monotherapy)

  1. skin thickness
  2. skin integrity
  3. temperature (increased heat)
48
Q

What are the 2 most common opioids used in CRIs? What combination is used in fluids?

A
  1. morphine
  2. fentanyl

opioid + ketamine + lidocain —> great multimodal pain relief

49
Q

What are alpha-2 agonists? What 6 effects do they have?

A

potent sedative analgesics that act on endogenous fight or flight receptors

  1. pain relief, sedation, sleep, arousal
  2. blood pressure regulation
  3. renal perfusion
  4. cardiac output
  5. insulin secretion
  6. bronchodilation
50
Q

What are the 7 results of alpha-1 receptor activation?

A
  1. arteriolar constriction
  2. mydriasis
  3. piloerection
  4. salivation
  5. lacrimation
  6. GIT relaxation
  7. sphincter contraction
51
Q

What are the 3 results of alpha-2 receptor activation?

A
  1. negative feedback inhibition of norepinephrine release
  2. platelet aggregation
  3. hyperpolarization of cells in the CNS
52
Q

What alpha-2 agonist has the highest alpha-2:alpha-1 selectivity? How does this affect its action?

A

dexmedetomidine and levometedomidine

provides more sedation and analgesia (alpha-2) compared to vascoactivity (alpha-1)

53
Q

What 6 actions do alpha receptors regulate?

A
  1. smooth muscle contraction
  2. diversion of blood flow to skeletal muscles
  3. pupillary dilation
  4. sphincter contraction
  5. vasoconstriction to skin
  6. negative feedback of NE release
54
Q

What physiological changes are expected with alpha-2 agonists?

A

peripheral vasoconstriction causes hypertension, which results in reflex bradycardia

55
Q

What are 5 benefits to using Dexmedetomidine in premeds?

A
  1. reduced need for induction and inhalant agents
  2. analgesia
  3. anxiolytic (not seen with opioids)
  4. muscle relaxant (not seen with opioids)
  5. maintains blood pressure
56
Q

What are 5 side effects associated with alpha-2 agonists? What route of administration increases risk?

A
  1. high doses decreased gastric motility
  2. vomiting
  3. suppressed insulin release
  4. diuresis
  5. oxytocin-like effect in ruminants

SQ

57
Q

Why is Dexmedetomidine commonly used in premeds?

A
  • sedation, analgesia, anxiolysis, muscle relaxation = most tenets of GA in one drug
  • reversibility
  • maintains vascular tone
58
Q

How are opioids and alpha-2 agonists similar? Why is this significant?

A

receptors found in similar locations in the CNS and are coupled to the same G-proteins

synergism causes supra-additive analgesia vs. additive analgesic effects

59
Q

How can opioid and alpha-2 agonist synergism be avoided?

A
  • smaller doses of both drugs
  • multimodal analgesic approaches
60
Q

In what 5 ways is the synergism of opioids and alpha-2 agonists used?

A
  1. balanced and injectable regimens for anesthesia - kitty magic = Dexmedetomidine + opioid + Ketamine
  2. pre-anesthetic agent before induction and maintains GA - Dex + opioid
  3. sedative for short diagnostic or minor sx procedures - Dex + opioid
  4. intraoperative rescue - microdose Dec
  5. post-op use - Dex + opioid
61
Q

In what 5 situations should use of Dexmedetomidine be avoided?

A
  1. pre-existing severe bradycardia
  2. life-threatening decreases in CO - clinical heart disease
  3. pre-existing hypertension
  4. vasoactive disease
  5. hypercoagulability disorders
62
Q

What are the most common clinical effects of alpha-2 agonists?

A
  • sedation
  • muscle relaxation
  • analgesia
  • decreased HR, CO
  • initial hypertension followed by normotension
  • decreased sensitivity to PCO2
  • decreased tidal volume and RR
63
Q

How does the size of patients alter Dexmedetomidine dose?

A

smaller dogs get larger doses with body SA dosing

  • 16 kg is a pivotal point
64
Q

What is considered a micro and mini dose of Dexmedetomidine? What is a macrodose?

A
  • MICRO = intra and post-op, 0.2-1 mcg/kg
  • MINI = premed with opioid, 1-7 mcg/kg in cats and 1-3 mcg/kg in dogs

label dose used for conscious sedation with opioids

65
Q

How long are the effects of macro, mini, and micro doses of dexmedetomidine expected to last?

A

MACRO = 1-2 hr

MINI = 1 hr

MICRO = 10-20 min

(IV is shorter than IM!)

66
Q

What is the reversal of Dexmedetomidine?

A

Antisedan (atipamazole) - reverses both sedation and analgesia (consider NSAIDs and opioids for pain!)

  • tends to produce abrupt reversal of sedation
67
Q

What OTM use of Dexmedetomidine can be used? What oral alpha-2 agonist can also be used?

A

Sileo - approved for noise aversion, careful with handling!

oral Clonidine

68
Q

What is Trazadone? What additional effect may it have?

A

serotonin 2A antagonist reuptake inhibitor (SARI) typically used as an adjunctive agent in the treatment of canine anxiety disorders

analgesia —> reversed with naloxone!

69
Q

What are 4 important aspects of NSAID pharmacokinetics?

A
  1. highly protein bound
  2. long-term safety and efficacy - Carprofen in dogs!
  3. well-absorbed after oral administration
  4. weak acids with high lipophilicity
70
Q

What is the most important rationale for the pre-op use of NSAIDs?

A

opioid overuse can result in INCREASED inflammation

  • synergistic with opioids
  • treats inflammation associated with sx
  • MAC sparing effects
71
Q

What 2 enzymes are responsible for inflammation? What are the 5 signs if inflammation?

A

breakdown of arachidonic acid by cyclooxygenase and lipoxygenase

  1. redness
  2. heat
  3. swelling
  4. pain
  5. loss of function
72
Q

What is the mechanism of action of NSAIDs?

A

decreases to production of prostaglandins by inhibition of COX, LOX, neutrophils, and metalloproteinase

73
Q

How does COX usually function?

A

prostaglandin synthase that places an O2 on arachidonic acid, which produces mediators or pathology and function

  • thromboxanes
  • prostacyclin
  • prostaglandins E2, F2, D2
74
Q

What are the 2 major isoforms of COX?

A

COX-1 - constitutive in platelets, kidneys, stomach, and reproductive tract; maintains homeostasis, renal blood flow, and gastric mucus secretion

COX-2 - inducible mediator of inflammation and pain in fibroblasts, endothelium, chondrocytes, and macrophages; constitutive in some other tissue

75
Q

What makes the ideal NSAID?

A

inhibit pain and inflammation (COX-2) without interrupting physiological functions (mostly COX-1)

76
Q

What are nonselective NSAIDs? Dual acting?

A

inhibit both, but mostly COX-1 - Aspirin, Flunixin

inhibit COX-1, COX-2, and LOX - Tepaxolin

77
Q

What are preferential NSAIDs? Selective?

A

inhibit both, but mostly COX-2 - Carprofen

inhibit COX-2 only - Deracoxib

78
Q

Why is selecting the ideal NSAID difficult?

A

COX-2 can be a good enzyme and is constitutive in some tissues, like:

  • damaged gastric epithelium
  • hypovolemic and developing renal tissues
  • brain
  • endometrium

(also depends on the presence of isoforms in each separate patient)

79
Q

What causes NSAID side effects? What are the 3 major ones seen?

A

constitutive COX-1 inhibition

  1. interfere with PG of normal gastric homeostasis - increases gastric acid and decreases mucus production
  2. interfere with PG of renal blood flow - reduced renal medullary blood flow and perfusion
  3. inhibits platelet function - inhibits thromboxane A2 responsible for platelet plug formation
80
Q

How does the platelet effects of NSAIDs differ?

A
  • Aspirin = permanent, entire life of the platelet
  • other NSAIDs = temporary, mild
81
Q

What are the 6 most common side effects associated with NSAIDs?

A
  1. gastric irritation and ulceration***
  2. decreased renal perfusion in times of pre-existing hypotension
  3. coagulopathy
  4. bronchospasm
  5. thrombosis and hypertension
  6. reproductive issues
82
Q

What causes GI instability seen with NSAIDs?

A
  • direct irritation of the drug on the GI mucosa
  • COX-1 inhibition in stomach
  • COX-2 inhibition in duodenum (Deramaxx)

mostly occurs due to accidental ingestion or administration of incorrect dose

83
Q

What response helps protect the stomach from the affects of NSAIDs?

A

gastric adaptation by Aspirin-triggered lipoxins (ATLs)

84
Q

What risk factors cause renal-related injury on NSAIDs? Why? What animals are most commonly affected?

A
  • high doses
  • anesthesia
  • dehydration, shock
  • pre-existing kidney disease

both COX-1 and COX-2 are involved in renal blood flow and tubular regulation

CATS

85
Q

How should NSAIDs be used in cats with acute pain?

A

use less than label if needed for 1-3 days

  • LOW RISK = pre or intraoperative Carprofen, Meloxicam, or Onsior
  • HIGH RISK = local blocks, steroids, postoperative Onsior or Meloxicam, laser therapy
86
Q

What are 3 important aspects of using NSAIDs in cats with chronic pain?

A
  1. use least effective dose daily
  2. multimodal plan: Adequan, low dose Gabapentin, photobiomodulation
  3. attempt every other day dosing
87
Q

When should the use of NSAIDs be avoided?

A
  • renal failure
  • dehydration, hypovolemia, hemorrhage
  • severe liver function
  • history of gastric ulceration
  • coagulopathy
  • pregnancy, neonates
88
Q

When should NSAIDs be used at reduced doses or increased dosing intervals?

A
  • renal insufficiency
  • impaired liver function
  • vascular disease
  • thrombotic patients
  • geriatric or asthmatic patients
89
Q

What are 4 other options for anti-inflammation?

A
  1. steroids - Dexamethasone sodium phosphate IV
  2. reduced opioids - lower CRI rate and injection frequency
  3. low level light therapy, laser therapy
  4. local anesthetics - local blocks, IV lidocaine
90
Q

What are 6 effects of laser therapy for anti-inflammation?

A
  1. increased beta endorphins
  2. increased nitric oxide
  3. decreased bradykinin
  4. reduced rate of depolarization of C fibers
  5. increased resting membrane potential of A fibers
  6. increased availability of Ach
91
Q

How are steroids used for anti-inflammation? What does it work best for?

A

switch from NSAIDs without washout period

  • axial pain
  • renal disease
  • inappetent patient
92
Q

When administering a dose of hydromorphone to a pit bull as premedication (along with midazolam) you might notice all of the following effects EXCEPT:

a. Panting
b. Mild bradycardia
c. Nausea exemplified as drooling
d. Increased appetite
e. Heart block

A

D

93
Q

A major area of the spinal cord that is the target/site of action of many major classes of pain relievers is a collection of interneurons known for its ever-changing state. This area is the

a. Intermediate grey area
b. Grey matter
c. Dorsal horn
d. White matter
e. Ventral horn

A

C

94
Q

All of the following are considered reversal agents for opioids EXCEPT

a. Buprenorphine
b. Naltrexone
c.Naloxone

A

A

95
Q

Non steroidal anti-inflammatories work to reduce prostanoids chemicals which cause the classic signs of inflammation via inhibition of which enzymes?

a. Platelet growth factor
b. Tumor necrosis factor
c. Beta amylase
d. Arachidonic acid
e. Cyclooxygenase

A

E

96
Q

Opioids can be used in any ASA class patient because of their ultimate safety profile, but alpha agonists should not be used in all of the following patients EXCEPT:

a. Patients with clinical bradyarrhythmias (fainting or collapsing because of their low heart rate)
b. Patients with preexisting uncontrolled hypertension
c. Patients with hypercoagulable states
d. A Chihuahua with heart failure (on pimobendan, enalapril, and Lasix)
e. Patients with head trauma

A

E

97
Q

Opioids and alpha agonists work well as analgesics because they work

a. Via H transmembrane proteins
b. Via the same receptors
c. In the dorsal horn of the spinal cord via different receptors but the same G protein mechanism
d. In the cerebrum
e. In different areas of the spinal cord

A

C

98
Q

Alpha two agonists provide analgesia via

a. Preventing the uptake of NE being recycled into the terminal axon via connecting to POSTSYNAPTIC Alpha 2 receptors
b. Reduced intracellular calcium cycling
c. Stopping the uptake of NE being recycled into the terminal axon via connecting to PRESYNAPTIC Alpha 2 receptors
d. Inhibition of NE connection to POSTSYNAPTIC Alpha 1 receptors
e. Inhibiting NE contact with the nerve ending

A

C

99
Q

Butorphanol, a Kappa agonist once thought to “reverse” pure Mu agonists such as Morphine, can be combined with pure Mu agonists such as morphine because it would provide all of the following EXCEPT

a. Reduced narcosis from the morphine
b. Antiemetic effect
c. Mildly lessened analgesia compared to the pure Mu Agonist
d. Longer duration of analgesia
e. Prolonged agitation

A

E

100
Q

The mechanism of action of opioids is mediated through a G protein receptor complex wherein neurons become less responsive to pain via

a. Reduced Magnesium flux
b. Alpha agonism
c. Potassium storage
d. Heightened action potential D waves
e. Reduced calcium influx and increased potassium efflux

A

E

101
Q

Antisedan reverses dexdomitor via which mechanism?

a. Lighting a fire in the second order neurons
b. Competitively antagonizing alpha 1 receptors
c. Competitively antagonizing alpha 2 receptors
d. Increasing calcium in the neural cleft
e. Agonizing endorphin D receptors

A

C

Anesthesia (40 decks)

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