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Analgesics Flashcards

1
Q

define: pain

A
  • an unpleasant sensory and emotional experience associated with the application or anticipation of a noxious stimulus
  • may occur with or without inflammation
  • pain happens in the brain
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2
Q

define: analgesia

A
  • is relief from pain
  • provides the patient with a faster return to normal function when ill or injured
  • improves surgical recovery and healing post-operative
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3
Q

common responses to pain:

A
  • increased or abnormal heart and/or respiration
  • vocalization
  • self-mutilation
  • guarding
  • personality changes
  • lethargy, reluctant to move
  • decreased desire to eat
  • lack of self grooming
  • changes in posture
  • weight loss and dehydration over time
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4
Q

what are the 3 types of pain

A
  • visceral pain
  • somatic pain
  • neuropathic pain
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5
Q

describe visceral pain

A
  • pain arising from the disruptive or injury of INTERNAL ORGANS
  • originates from pain receptors located within body cavities (peritoneum)

thorax
abdomen
pelvis

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6
Q

describe somatic pain

A
  • originates from pain receptors in musculoskeletal or body surface tissue that’s activated during injury
  • pain may initially be described as ‘stabbing’ pain or a dull aching pain
  • is usually alleviated by rest and aggravated activity
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7
Q

describe neuropathic pain

A
  • pain caused by spinal cord or peripheral nerve injury
  • the pain itself is sensed at or below the site of the injury
  • can be present in waves of intensity and frequency
  • most likely to be chronic
  • ## Central sensitization: chronic, intractable pain due to overly sensitized spinal cord neurons
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8
Q

what is central sensitization

A

chronic, intractable pain due to overly sensitized spinal cord neurons
- leads to allodynia (pain perceived from a non-painful stimulus)

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9
Q

where does pain sensation arise from

A

nerve ending called Nociceptors

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10
Q

where are nociceptors found

A

all throughout the body
- skin
- joints
- blood vessels
- hollow organs
- the parietal surface of the thorax and abdomen (lungs and heart)

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11
Q

when are nociceptors activated?

A
  • when nerve endings are activated through mechanical, chemical, and thermal stimulation
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12
Q

what are the 4 phases of the pain pathway

A
  1. transduction
  2. transmission
  3. modulation
  4. perceptino
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13
Q

what drugs work on the transduction portion of the pain pathway?

A
  • local anesthetic agents
  • opioids
  • NSAIDs
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14
Q

what drugs work on the transmission portion of the pain pathway?

A
  • local anesthetic agents
  • alpha 2 agonists
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15
Q

what drugs work on the modulation portion of the pain pathway?

A
  • local anesthetic agents
  • opioids
  • alpha 2 agonists
    NMDA antagonists
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16
Q

what drugs work on the preception portion of the pain pathway?

A
  • opioids
  • alpha 2 agonists
  • general anesthetic
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17
Q

describe the transduction part of the pain pathway

A

initial phase of the pain pathway
- begins at the site of injury (nociceptors are engaged)
- electrical impulses are created when nerve endings exceed their threshold for stimulation

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18
Q

describe the transmission part of the pain pathway

A

second phase of the pain pathway
- nerve impulses are transmitted along afferent nerves toward the dorsal horn of the spinal cord
- motor impulses are transmitted along efferent nerves away from the ventral horn of the spinal cord

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19
Q

describe the modulation part of the pain pathway

A

3rd phase of the pain pathway
- occurs in the spinal cord
- involves changing or inhibiting pain impulses in the spinal cord
- leads to an increase or decrease in the transmission of pain impulses

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20
Q

what are neonates not fully capable of?

A

modulation
- will feel things more intensely

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21
Q

describe the perception part of the pain pathway

A

4th phase of the pain pathway
- occurs after the pain process (nociception) begins
- the conscious awareness of pain

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22
Q

list the analgesic drugs

A
  • opioids
  • steroidal anti-inflamatories
  • NSAIDs
  • local anesthetics
  • alpha-2 agonists
  • adjunctive agents
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23
Q

describe opioids in the pain pathway

A
  • great at controlling moderate to severe pain (transduction, modulation, and perception)
  • bind with specific receptors to receive pain
  • inhibit ascending pathways of pain perception and activate descending pathways
  • pre-anesthetic protocols should include opioids to prevent spinal wind-up (stop pain before it starts)
  • varied duration and intensity
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24
Q

butorphanol as an analgesic

A

opioid
- partial agonist/antagonist
- mild pain
- 1-2 hours

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25
Buprenorphine as an analgesic
opioid - partial agonist - moderate pain - 6-12 hours
26
Hydromorphone as an analgesic
opioid - agonist - severe pain 4-6 hours
27
fentanyl as an analgesic
opioid - agonist - for severe pain - 30 min of CRI
28
tramadol as an analgesic
opioid - synthetic agonist - milf to moderate pain 8-12 hours
29
what type of response is inflammation?
a vasular and cellular response of living tissue to injury
30
describe the inflammatory pathway
- damaged cells send out chemical signals that initiate the inflammatory response - counteract the injury by segregating/removing the cause of the damage - body responds with a series of actions that in turn combat inflammation and begin the healing process - Phospholipids in the cells are broken down by phospholipase (enzyme) in to arachidonic acid - Cyclooxygenase and lipoxygenase breaks down the arachidonic acid into prostaglandins and leukotrienes, which cause inflammation
31
what are the nonimmunological factors that can cause an inflammatory response
- the presence of microorganisms and their toxins - the presence of parasites - factors that cause tissue damage (mechanical, thermal, electrical, chemical, radiation)
32
what are the immunological factors that can cause an inflammatory response?
- produced by chemicals arising outside the body or produced in the body (insect bites, drug reaction, chronic disease)
33
what are the cardinal signs of inflammation
- redness - heat - swelling - pain - loss of function (blood cells are rushing to the area)
34
how do the signs of inflammation appear
- the result of vascular, immunological, and cellular reactions 1. trauma 2. blood flow to the area, increased supply of phagocytes, redness, and heat 3. increased blood pressure and vasodilation causes fluid leak, swelling 4. increased pressure on nerve endings, and tissue damage, pain 5. together this impairs the function
35
describe a fever in inflammation
- prostaglandins are formed from substances released from the damaged tissue cells - prostaglandins produced in response to pyrogens (cellular products released from microorganisms) cause the 'thermostat' cells in the hypothalamus to reset at a level above normal - this disrupts the balance body responds by increasing both heat production and heat conservation = fever - increased body heat loss causes body temperature to drop (you have a fever but feel cold) - use an antipyretic drug (blocks the biosynthesis of the causative prostoglandin)
36
name an antipyretic
acetaminophen (Tylenol)
37
what may an exaggerated or prolonged inflammatory response result in
- clinical signs that are debilitating - excessive damage and scar tissue, preventing normal function of a body part
38
what are the 2 classes of anti-inflammatory drugs?
1. steroidal anti-inflammatory 2. NSAIDs
39
COX1 and COX2
- Cyclooxygenase (COX) is an enzyme in the body that comes in 2 forms COX1 COX2 - convert arachidonic acid to prostaglandin resulting in pain and inflammation - most side effects of anti-inflammatory drugs arise from their effects on COX1 (this is why newer drugs are COX2 selective)
40
inhibition of which COX receptor is considered therapeutic?
COX2
41
describe COX-1
maintains functions such as: - renal blood flow - gastric mucosa production - blood clotting
42
describe COX2
- produced as a result of injury
43
Steroidal Anti-inflammatory drugs (corticosteroids)
- adrenal glands secret: Mineralocorticoids Glucocorticoids
44
Mineralocorticoids
- steroidal anti-inflammatory drug - regulate the retention and excretion of sodium, potassium, and water - principal natural one is aldosterone
45
Glucocorticoids
- steroidal anti-inflammatory drugs - potent anti-inflammatory action (blocks phospholipase decreasing the formation of prostaglandins) - influence carbohydrates and protein metabolism some assistance in sodium and water retention - The principal natural one is hydrocortisone
46
where are glucocorticoids/hydrocortisone produced and released?
the adrenal cortex
47
what is the adrenal cortex under the control of?
- hypothalamus - anterior pituitary gland
48
under stressful stimulation, the CNS messages the pituitary gland causing it to release what?
ACTH
49
what effect does ACTH have on the adrenal cortex?
- stimulates it to release hydrocortisone
50
what can the hypothalamus not tell the difference between?
hydricotisone (natural) glucocorticoids (synthetic)
51
list the common glucocorticoids
- dexamethasone (IV, IM, SQ, PO) - flumethasone (IV,IM, SQ) - Prednisone, Prednisolone (PO)
52
what is the precursor to prednisone?
prednisolone
53
what must you always do for patients who receive corticosteroids?
taper the dose
54
glucocorticoid administration
- absorbs well in the GIT - absorbs well IM and SQ - minimal topical absorption - slow movement into joints (results in significant blood levels)
55
possible side effects of corticosteroids
- delayed wound healing - decreased immune response - GI ulcers and bleeding - corneal ulceration - abortion - PU/PD - thinning of the skin - muscle atrophy - diabetes mellitus
56
describe NSAIDs
- modify the inflammatory response by inhibiting cyclooxygenase (COX enzyme) - typically COX 2 is preferential in vet med - COX 1 can affect stomach mucus production and leads to gastric ulceration and interfere with clotting - provide analgesia - decreases fever - decreases inflammation - good for all types of pain - synergistic effect when combined with opioids - readily available - affordable - easy to administer - client friendly dosing schedule
57
NSAID side effects
- often depend on how much they affect COX 1 - GI ulceration and bleeding - hepatotoxicity - nephrotoxicity - bone marrow impression - reduction of platelet aggregation - inhibition of cartilage metabolism
58
when should NSAIDs NOT be used?
- in combination with other NSAIDs or steroids - liver or kidney disease - history of gastric ulceration or a coagulopathy disorder - dehydrated patients - shock
59
list the common NSAID clases
- Salicylates - Nicotinic Acid Derivatives - Pyrazolone Derivatives - Propionic Acid Derivatives
60
Acetylsalic acid
- Salicylate (NSAID) - anti-inflammatory - anti-pyretic - effective in releasing skeletal, muscular, and integumentary pain - rate of metabolism varies (cats are sensitive because they suck at biotransforming the drug)
61
what does acetylsalicylic acid have no effect on?
most visceral pain
62
Flunixin meglumine (Banamine)
- Nicotinic Acid Derivative (NSAID) - anti-inflammatory - antipyretic - recommended for: musculoskeletal pain and inflammation in horses, visceral pain associated with colic, fever in bovines
63
Phenylbutazone
- Pyrazolone Derivative (NSAID) - most common equine NSAID - cannot be used during races because it masks lameness - similar action to salicylates (inhibits the enzyme that biosynthesized inflammatory-response prostaglandins -relieves inflammation in the musculoskeletal system - analgesic and some antipyretic - PO or IV (can cause sloughing)
64
Propionic Acid Derivatives
- NSAID - analgesic - antipyretic - effects on vascular and cellular phases of inflammation - high affinity for inflamed tissue - 3 types
65
what are the 3 types of Propionic Acid Derivatives?
COX non -selective COX-2 preferential COX-2 selective
66
Ketoprofen
- propionic acid derivative - COX non-selective SQ or PO
67
list the COX-2 preferential propionic acid derivatives
- Carprofen - Meloxicam - Deracoxib
68
Carprofen
- propionic acid derivative - COX-2 preferential SQ PO
68
Meloxicam
- propionic acid derivative - COX-2 preferential - licensed for multiple species IV SQ PO
69
Deracoxib
- propionic acid derivative - COX-2 preferential - PO
70
list the COX 2 selective drugs
- Firocoxib - Robenacoxib
71
Firocoxib
- propionic acid derivative - COX-2 selective - PO
72
Robenacoxib
- propionic acid derivative - COX-2 selective - cats and dogs IV SQ PO
73
human over-the-counter analgesics
- aspirin (high incidence of toxicity) - Ibuprofen (AVOID) - Acetaminophen (Tylenol) (used a low dose and less frequently than humans in dogs, fatal in cats)
74
describe alpha-2 agonists
- inhibit the release of excitatory neurotransmitter norepinephrine - great sedation with analgesia - best used as a synergistic adjunct (they really enhance analgesic effects of opioids) - significant cardiovascular effects - use on young healthy patients - shorts duration of action - can be reversed - great for short procedures -
75
what parts of the pain pathway do alpha-2 agonists affect?
2, transmission 3. modulation 4. perception
76
why are alph-2 agonists an excellent choice for short procedures?
- short duration of action - can be reversed best used when combined with an opioid
77
list the alpha-2 agonist drugs (anesthesia)
Dexmedetomidine Xylazine
78
local anesthetics (analgesics)
- block the transduction of nerve impulses (can relieve and/or prevent pain - needs to be placed directly beside the target nerve - must calculate the toxic dose (especially in acts)
79
list the local anesthetic drugs
- lidocaine - Bupivacaine
80
Tranquilizers
- alter the body's perception of pain - alter response to pain, reduce anxiety and fear, relaxes muscles
81
list the tranquilizer drugs
- Phenothiazines eg: Acepromazine - Benzodiazepines eg: diazepam
82
NMDA receptor agonists
- block sensitization of neurons in the spinal cord, especially useful for treating patients who've experienced wind up pain Ketamine
83
list a NMDA receptor agonist
ketamine via CRI
84
Anticonvulsants
- reduce neuropathic pain and central sensitization in chronic pain patients Gabapentin PO
85
list the anticonvulsant drug
gabapentin
86
tricyclic antidepressants
- treat neuropathic pain - great with chronic and cancer pain - inhibit the reuptake of serotonin and norepinephrine
87
list the tricyclic antidepressant drug
amitriptyline
88
muscle relaxants
- decrease the severity of muscle spasms - 2 types, spasmolytic agents and neuromuscular blockers
89
Spasmolytic agents
- muscle relaxant - reduce the excitability of motor neurons or inhibits nerve impulses - allows the muscle to relax Methocarbamol
90
Methocarbamol
- Muscle relaxant - spasmolytic agent
91
Neuromuscular blockers
- muscle relaxant - block the transmission of a neurotransmitter at the end of a neuromuscular junction
92
Atricurium besylate
- muscle relaxant - neuromuscular blocker - ONLY used during sx when mechanical ventilation can be provided
93
Antihistamines
- inhibit the inflammatory effects of histamine released during the allergic process Diphenhydramine
94
what are the 2 good pain management concepts
- pre-emptive analgesia - multimodal analgesia
95
describe pre-emptive analgesia
- the administration of analgesics before anticipated noxious insult to prevent sensitization of neurons and windup
96
describe multimodal analgesia
- the use of multiple drugs from different drug classes or given in different applications, which may act at different levels of the nociceptive pathways to produce optimal analgesia

Pharmacology (7 decks)

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