Principles Of Pain & Analgesia Flashcards

0
Q

Pain results when nocieptors detect this

A

A noxious stimulus

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1
Q

What is pain?

A

Unpleasant sensory or emotional experience associated with actual or potential tissue damage

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2
Q

Nerve cells in the skin or deep tissues that detect pain

A

Nocieptors

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3
Q

What are the 2 types of sensory neurons that detect and transmit pain?

A

A Delta Fibers

C Fibers

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4
Q

Sensory neurons that are large ad myelinated

A

A Delta Fibers

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5
Q

Sensory neurons that are small and non myelinated

A

C Fibers

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6
Q

A Delta Fibers transmit this type of signals

A

Transmit sharp, discrete pain signals that allow the patient to localize the source of pain

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7
Q

C Fibers transmit this type of signals

A

Transmit dull, aching, throbbing pain that cannot be easily localized

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8
Q

A Delta Fibers transmit this type of pain

A

Somatic pain

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9
Q

C Fibers transmit this type of pain

A

Somatic & Visceral pain

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10
Q

The Pain Pathway

A

Transduction
Transmission
Modulation
Perception

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11
Q

Transduction

A

Transformation of pain stimuli into electrical signals (called action potentials)

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12
Q

Transmission

A

The sensory impulses (electrical signals) are conducted to the spinal cord

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13
Q

Modulation

A

In the spinal cord, the impulses can be altered by neurons, making pain better/worse

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14
Q

Perception

A

The impulses are transmitted to the brain, where they are processed and recognized

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15
Q

Multimodal

A

Use different category of drugs to achieve better pain relief analgesia

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16
Q

Somatic Pain

A

Arises from the skin, soft tissues, muscles, bones, or joints
(Easily localized through stabbing, throbbing, or aching)

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17
Q

Visceral Pain

A

Arises from internal organs

Not easily localized and is characterized by cramping or burning

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18
Q

Referred pain

A

Term used to describe the pain that is felt in a body part other than where the actual pain stimulus is coming from

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19
Q

Hyperalgesia

A

Increased sensitivity to a stimulus (to pain)

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20
Q

Neuropathic pain

A

Arises from direct damage to peripheral nerves or the spinal cord
(May be shooting, sharp, or tingling)

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21
Q

Phantom Limb or Stump pain

A

Sensation or pain arising from the missing body part

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22
Q

Acute pain

A

Pain has abrupt onset and a relatively short duration of action

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23
Q

Chronic pain

A

Has slow onset, and duration of several months to years

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24
Q

This type of onset/duration of pain is effectively treated with analgesic drugs

A

Acute

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25
Q

This type of onset/duration of pain may be unresponsive to drug therapy

A

Chronic

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26
Q

Myths about pain in animals

A
  • Pain can be beneficial for healing/recovery
  • Animals don’t feel pain
  • Animals tolerate pain better than humans
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27
Q

The 5 freedoms of acceptable animal welfare

A
  1. Freedom from hunger
  2. Freedom from physical and thermal discomfort
  3. Freedom from pain, injury, and disease
  4. Freedom to express normal behavior
  5. Freedom from fear and distress
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28
Q

Simple pain assessment scale

A

No pain
Mild pain
Moderate pain
Severe pain

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30
Q

Respiratory consequences of untreated pain

A

Increased RR

Decreased ventilation

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31
Q

GI consequences of untreated pain

A

Paralytic ileus

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32
Q

Urinary consequences of untreated pain

A

Urine retention

Na/ H2O retention

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33
Q

Metabolic consequences of untreated pain

A

Break down on muscle, fat, glucose (delay in wound healing)

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34
Q

Analgesia

A

The absence of the awareness of pain, achieved through the use of drugs or other modes of therapy. It applies to the relief of pain without the loss of consciousness.

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35
Q

What are the goals for pain control?

A
  • Control pain at every stage
  • To administer analgesics before the patient has an awareness of pain
  • To prevent windup
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36
Q

Preemptive analgesia

A

The administration of analgesics before the patient has an awareness of pain

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37
Q

Preemptive analgesia decreases this

A

Decreases the analgesic requirements and CNS sensitization

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38
Q

Windup

A

Event caused by a buildup of chemical mediators that intensify the pain response

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39
Q

Where does windup occur?

A

Spinal cord (modulation step)

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40
Q

What triggers the Stress Response?

A
  • Anxiety, Infection, Pre-existing disease

* Anesthesia Trauma

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41
Q

What does the Stress Response cause?

A
  • Sympathetic activity

* Release hormones : Cortisol, ACTH, Catecholamines (epi)

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42
Q

Methods of pain control without analgesia

A
  • Endorphins

* Nursing care

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43
Q

Natural pain reliever

A

Endorphins

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44
Q

Endorphins

A

Endogenous compounds produced by the pituitary gland and hypothalamus that bind to opioid receptors during situations of trauma or stress. They resemble opiates.

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45
Q

Other therapies to control mess without meds

A
Heat/cold compress
Hydrotherapy
Acupuncture 
Music
Essential oil
Pet them
Talk soothing 
Favorite toy available 
Clean dry bedding
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46
Q

Methods of pain using meds

A
  • Opioids
  • NSAIDS
  • Local Anesthetics
  • Alpha2 agonists, ketamine, steroids
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47
Q

Classic K9 Stress Leukogram

A

Mature neutrophilia
Lymphopenia
Eosinopenia
Monocytosis

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48
Q

Classic Feline Stress Leukogram

A

Epinephrine release -

Neutrophilia, Lymphocytosis

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49
Q

What 4 receptors in the brain and spinal cord do opioids act on?

A

Mu
Kappa
Delta
Sigma (cause hallucination, euphoria/dysphoria)

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50
Q

What do opioids act as at each receptor?

A

Agonist or Antagonist

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51
Q

Agonist means?

A

Stimulating agent

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52
Q

Antagonist means?

A

Blocking agent

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53
Q

Some opioids are considered both agonist and antagonist because?

A

They block one type of receptor and stimulate another

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54
Q

Some opioids are considered partial antagonist meaning?

A

They only partially stimulate some opioid receptors

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55
Q

When opioid agents bind to the receptors it can result in these effects

A

Analgesia
Respiratory depression
Sedation
Dysphoria

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56
Q

Pure Antagonist

A

Naloxone

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57
Q

It’s also possible to reverse the effects of pure agonists with these drugs

A

Butorphanol

Buprenorphine

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58
Q

Agonist/Antagonist

A

Butorphanol

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59
Q

Partial Agonist

A

Buprenorphine

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60
Q

Are opioids controlled?

A

Yes

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61
Q

Pure Agonist

A

Morphine

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62
Q

Pure is aka

A

Full

Pure agonist = Full agonist

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63
Q

This drug reverses opioids

A

Naloxone

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64
Q

Morphine is great for…?

A

Moderate to severe pain

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65
Q

This drug causes excitement in cats (use lower doses)

A

Morphine

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66
Q

Morphine often results in this due to its effect on the CRTZ

A

Vomiting

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67
Q

Why should you give morphine slowly IV?

A

Severe histamine can occur leading to hypotension and pruritis

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68
Q

Other full agonists aside from morphine

A

Oxymorohone
Hydromorphone
Fentanyl

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69
Q

CRTZ

A

Chemoreceptor Trigger Zone

70
Q

Histamine release causes this

A

Allergic or anaphylactic reactions!

71
Q

Fentanyl is this kind of drug

A

Full agonist

72
Q

Full/Pure agonists do this

A

Stimulate all 4 receptors

73
Q

This drug is commonly used as a transdermal skin patch

A

Fentanyl

74
Q

How long does it take a Fentanyl patch to reach therapeutic levels in cats?

A

4-12 hours

75
Q

How long does it take a Fentanyl patch to reach therapeutic levels in dogs?

A

12-24 hours

76
Q

Fentanyl patches allow blood levels to remain at therapeutic levels for how long in cats?

A

5 days

77
Q

Fentanyl patches allow blood levels to remain at therapeutic levels for how long in dogs?

A

3 days

78
Q

Methadone targets this receptor

A

Mu receptor

79
Q

This drug has the lowest likelihood of causing vomiting

A

Methadone

80
Q

Methadone is an Antagonist of this receptor

A

NMDA receptor

81
Q

NMDA Receptor

A

Receptor found in the spinal cord and is responsible for “windup”

82
Q

Methadone is favorable for treating pain when this is present

A

Central Sensitization

83
Q

Routes Methadone can be given

A

IV
IM
SQ

84
Q

What is the onset/ duration of the injectable form of Fentanyl?

A

Onset of action is: 2 min

Duration of action is: 20-30 min

85
Q

How long can Methadone last?

A

4 hours

86
Q

Synthetic opioid that has Agonist effects

A

Methadone

87
Q

Synthetic opioid that has Full Agonist effects

A

Meperidine (Pethidine)

88
Q

Meperidine is aka

A

Pethidine

89
Q

Meperidine primarily targets these receptors

A

Mu and Delta

90
Q

This drug has weak analgesic properties lasting

A

Meperidine

91
Q

Meperidine lasts this long

A

1-2 hours
Can last up to 6 hours
(Short acting overall)

92
Q

Meperidine is most useful as this

A

Part of the pre-anesthetic protocol

93
Q

Buprenorohine targets this receptor

A

Mu

94
Q

Buprenorphine is aka

A

Bupi

Buprenex

95
Q

Buprenorphine onset/duration of action

A

Delayed onset: 40min IM, 15min IV

Duration onset: 6-8 hours

96
Q

Buprenorphine is best used for this

A

Mild to moderate pain

97
Q

How is Buprenorphine administered to cats?

A

Given orally

Applied to the gingiva, under the tongue, or in cheek pouch

98
Q

Butorphanol affects these receptors

A

Agonist on Kappa and Sigma

Antagonist on Mu

99
Q

Butorphanol is aka

A

Torb

Torbugesic

100
Q

Butorphanol is best used for this

A

Mild to moderate pain

101
Q

This drug is commonly used as a cough suppressant

A

Butorphanol

102
Q

Butorohano is commonly combined with a sedative such as these

A

Desmedetomidine or

Acepromazine

103
Q

The potent opioids most commonly used for acute pain

A
Morphine
Oxymorohone
Hydromorphone
Methadone
Fentanyl
104
Q

Non opioid drug that has Antagonist activity

A

Tramadol

105
Q

Tramadol affects this receptor

A

Mu receptor

106
Q

Useful post operative pain med in dogs and cats

A

Tramadol

107
Q

Is Tramadol controlled?

A

Yes

108
Q

What is the mechanism of NSAIDS

A

Inhibit the synthesis of prostaglandins by blocking the enzyme cyclooxygenase

109
Q

Cox 1

A

Leads to production of beneficial prostaglandins

110
Q

Cox 2

A

Leads to production of harmful prostaglandins that are present during tissue damage and inflammation

111
Q

Cyclooxygenase

A

Enzyme that produces prostaglandins and assists in producing thromboxanes

112
Q

Benefits of NSAIDS

A
Not controlled
Little abuse potential
Effective when given orally
Antipyretic effects 
No sedative, cardiovascular, or respiratory effects
113
Q

Antipyretic effects

A

Reduces fever

114
Q

Side effects of NSAIDS

A

GI upset/ulcers due to inhibition of prostaglandins
Hepatic toxicity
Renal toxicity
Inhibits platelet aggregation

115
Q

Do not use NSAIDS concurrently with this

A

Steroids

116
Q

Why should NSAIDs be used with steroids?

A

Steroids also block beneficial prostaglandins

117
Q

The 3 NSAIDs we use

A

Rimadyl
Metacam
Onsior

118
Q

Rimadyl is aka

A

Carprofen

119
Q

NSAID approved for use in dogs only

A

Rimadyl

120
Q

NSAID approved for use in both cats and dogs

A

Metacam

121
Q

NSAID approved for use in cats only

A

Onsior

122
Q

Rimadyl, Metacam, and Onsior are Cox 1 or 2 selective?

A

Cox 2 selective

123
Q

NSAIDs given in tablet form

A

Rimadyl and Onsior

124
Q

NSAIDs given oral AND injectable

A

Metacam

125
Q

Metacam is aka

A

Meloxicam

126
Q

Onsior is aka

A

Robenacoxib

127
Q

These drugs are Alpha-2 Agonists

A

Dexdomitor

Xylazine

128
Q

Alpha-2 agonists duration of action

A

~90 min

129
Q

What do Alpha-2 agonists cause aside from pain control?

A

Profound sedation

Bradycardia

130
Q

Alpha-2 agonists are commonly combine with this drug

A

Butorohanol

131
Q

Are Alpha-2 agonists reversible?

A

Yes

132
Q

How does Ketamine work?

A

Works by antagonizing NMDA receptors in the spinal cord

133
Q

Duration of action of Ketamine

A

Short duration: 30 min

134
Q

Ketamine is effective for this type of analgesia

A

Intraoperative

135
Q

What is local anesthesia?

A

The use of a chemical agent on sensory neurons to produce a disruption of nerve impulse transmission, leading to temporary loss of sensation

136
Q

Local Anesthetics exert their effects on neurons located here

A

In the peripheral nervous system and spinal cord that control pain, heat, cold, and pressure

137
Q

Local anesthesia is safe for this surgical procedure

A

C-sections

138
Q

Local Anesthetics have few effects on this

A

The cardiovascular and respiratory systems

139
Q

Local Anesthetics routes of administrations

A

Topical (short dur. Less pain relief)

Injection (site clipped&cleaned)

140
Q

Some local anesthetic drugs are combined with this drug

A

Epinephrine

141
Q

What does epinephrine cause?

A

Vasoconstriction

142
Q

Local anesthesia cannot be given here

A

Cannot be given in inflamed tissues

143
Q

Nerve blocks

A

Injection of a local anesthesia in the proximity of a specific nerve to desensitize a specific anatomic location

144
Q

Ring block

A

Block nerve that goes around anatomical part

145
Q

Lidocaine onset/duration duration

A

Onset: 15 min
Duration: 1 hour

146
Q

Bupivacaine onset/duration action

A

Onset: 40 min
Duration: 6 hours

147
Q

Why does lidocaine and bupivacaine get mixed together?

A

Better pain relief

Add Buprenorphine for 2 extra hours of pain relief

148
Q

This drug is toxic if given IV

A

Bupivacaine

149
Q

What drug is used for epidurals?

A

Lidocaine (or any other local anesthetic)

Morphine (last several hours)

150
Q

2 Nerve blocks

A

Line blocks

Ring blocks

151
Q

Intraarticular (local anesthetic route)

A

Injecting local Anesthetics directly into a joint usually after surgery of the joint, immediately after closure of the joint capsule

152
Q

Epidural

A

Blockage of sensory and motor nerves in the rear, abdomen, pelvis, tail, hind limbs, and perineum

153
Q

Where is an epidural injected?

A

In between L7 and S1

154
Q

Side effects of local Anesthetics

A
Allergy
Systemic toxicity
Infection
Cranial infiltration
Death
155
Q

Neuromuscular Blocking Agents are aka

A

Muscle-paralyzing agents

156
Q

How do neuromuscular blocking agents work?

A

These agents act by interrupting normal transmission of impulses from motor neurons to the muscle synapse

They basically send signals telling the muscle to contract

157
Q

Site of action for neuromuscular blocking agents

A

Neuromuscular junction

158
Q

Neuromuscular junction

A

This is where acetylcholine is real eased by the neurons to attach to muscle end plates

159
Q

The 2 ways for neuromuscular blocking agents to disrupt the nervous system

A

Depolarization agents

Non-depolarization agents

160
Q

Depolarization agents

A

Cause a single surge of activity at the neuromuscular junction, followed by a refractory period

161
Q

Refractory period

A

Unable to contract again

162
Q

Non depolarization agents

A

Block the receptors and the end plate

No initial surge of activity at neuromuscular junction, no muscle movements

163
Q

What can the neuromuscular blocking agents be reversed with?

A

Neostigmine or Edrophonium

164
Q

Special technique not commonly used in Veterinary medicine

A

Neuromuscular blocking agents

165
Q

Special Techniques

A

Neuromuscular Blocking Agents

Mechanical Ventilation

166
Q

Neuromuscular B agents allow relaxation of only these muscles

A

Voluntary muscles

167
Q

Skeletal muscles are affected in this order

A
  1. Facial, neck paralysis
  2. Tail, limb, abdominal muscles
    Last: intercostal muscles, diaphragm
168
Q

How are Neuro M B agents administered?

A

Slowly IV

169
Q

Onset/duration action of Neuro M B agents

A

Onset: 2 min
Duration: 10-30 min

170
Q

Animals on Neuromuscular Blocking Agents require this

A

Manual or Mechanical ventilation

171
Q

What is the patient’s breathing controlled with when using Mechanical Ventilation

A

Patient’s breathing is controlled by Ventilator rather than reservoir bag

172
Q

CV consequences of untreated pain

A

Increased HR, BP, CO, Arrythmia