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86 Cards in this Set
- Front
- Back
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Pain
-define |
-an unpleasant sensory or emotional experience associated with actual or potential tissue damage or described in terms of such damage
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Pain transmission
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Inciting cause
-transduction (sensory nerve endings, nociceptors) --transmission (sensory nerves) ---Modulation (spinal cord) ----Perception (cerebral cortex) |
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Pain transmission
-part that we want to try and prevent |
-Perception
-not pain unless it can be perceived |
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Dorsal horn Grey Matter
-components |
-Projection neurons
-Propriospinal neurons -Interneurons |
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Projection neurons, Propriospinal neurons, Interneurons
-main function |
-relay sensory information to the brain and activate descending control system
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Propriospinal neurons
-main function |
-transfer information from one segment to the next and ultimately the brain
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Interneurons
-main function |
-modulate (inhibit or excite) and transmit sensory information for a short distance within the spinal cord
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Ventral horn Grey matter
-components -function |
-interneurons
-motor neurons -control skeletal muscle activity |
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Intermediate Zone Grey Matter
-components -function |
-pre-ganglionic neurons of the autonomic nervous system
-control visceral functions and transmit afferent information to the brain |
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Spinal cord receptors
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-Excitatory
-Inhibitory -Neurokinin -Metbotropic |
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Spinal cord receptors
-excitatory receptors |
-AMPA
-KAI -NMDA |
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Spinal cord receptors
-inhibitory receptors |
-GABA
-Glycine |
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Dorsal horn neurotransmitters
-main categories |
-Peptides (substance P)
-Amino acids (excitatory, inhibitory) -Nitric Oxide -Prostaglandins -Adenosine triphosphate -Endogenous opioids -Monoamines (serotonin, norepinephrine) |
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Modulation
-describe pathway |
action potentials are transmitted to the dorsal horn and are amplified or suppressed
-nociception transmits via Adelta and C fibers --transmission to laminae via amino acids (glutamate) and peptides (substance P) ---activation of postsynaptic receptors ----local interneurons modulate and transmit |
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Wind-up
-effect |
-increased gene induction---> upregulation of receptors
--leads to hyperalgesia ---can eventually lead to allodynia |
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Reasons to control pain (sequelae)
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-hypertension, tachycardia
-hypercoagulability -increased metabolic rate -tachypnea, hypoventilation -ileus -immunosuppression -hyperalgesia/allodynia -central sensitization |
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Hypoventilation cause by pain
-due to |
-small breaths
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Central sensitization
-define |
-dynamic changes in dorsal horn neuron excitability which modify and potentially increase their receptive fields for nociception
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Central sensitization
-ways it can occur |
-expansion of receptive field size
-increased magnitude and duration of response -reduction in threshold |
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Is there a behavior pathognomonic for pain?
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-NO
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Pain behavior
-reasons for variability |
-species
-breed -sex -age -duration and intensity of pain |
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Pain behavior
-common behaviors |
-abnormal posture (hunched, guarding, prayer position, not resting in normal position)
-abnormal gait (stiff, non-weight bearing, limp) -abnormal movement (restless, not sleping, thraching, circling) -vocalizing -licking or chewing at area -abnormal facial expression -hiding -lack of grooming -purring -submissive behavior -allodynia or hyperalgesia |
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Causes for delayed recovery after surgery
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-Pain
-Stress response -Nausea, vomiting, ileus -hypoxemia, sleep disturbance -fatigue -immobilization, semistarvation -drains. nasogastric tubes, restrictions, traditions |
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Analgesic drugs
-major classes |
-Opiates
-Alpha-2 agonists -NMDA antagonists -local anesthetics |
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Opioids
-receptor locations |
-CNS
-some peripheral tissue |
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Opioids
-receptors |
-Mu1
-Mu2 -Mu3 -Kappa -Delta |
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Opioids
-Mu1 receptor function |
-Supraspinal analgesia
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Opioids
-Mu2 receptor function |
-respiratory depression
-bradycardia -physical dependence -euphoria |
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Opioids
-Mu3 receptor function |
-hyperpolarization of peripheral nerves induced by inflammation/immune response
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opioids
-Kappa receptor function |
-analgesia
-sedation -miosis |
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Opioids
-Delta receptor function |
-modulation of mu receptor activity
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Opioids
-route of administration |
-Oral (poor bioavailability)
-Intermittent IM/SQ injection -IV (intermittent or CRI) -Transdermal -Transmucosal |
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Opioids
-most frequently used routes of administration |
-Intermittent IM/SQ injection
-IV |
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Opioids
-how to choose which to use |
-Opioids with strong Mu activity are generally better for marked pain
-duration of action -species differences -route of administration -cost |
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One of the most effective opioids
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-Morphine
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Morphine
-administration |
-every 2-4 hrs
-SQ, IM, IV (and CRI) |
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Morphine
-possible negative effects |
-can have increased locomotor activity in horses
-minimal cardiovascular effects -some histamine release |
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Hydromorphone
-effects |
-similar analgesia to morphine
-less sedation? -less vomiting (opioids usually cause vomiting) |
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Hydromorphone
-negative effects |
-can cause hyperthermia in some cats
(general effect of opioids, just more pronounced) |
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Methadone
-effects |
-analgesia similar to morphine
-possible NMDA antagonist effect -less locomotor effects in horses |
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Methadone
-problem with administration |
-cost
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Fentanyl
-effects |
-very potent analgesic
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Fentanyl
-route of administration |
-transdermal (patch)
-CRI |
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Fentanyl
-problem |
-can't really be given by injection due to short duration
- <30 mins |
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Buprenorphine
-receptor |
-partial Mu agonist
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Buprenorphine
-contraindication |
-may not provide same degree of analgesia that pure Mu agonists will in procedures with marked pain (thoracotomies, orthopedic procedures)
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Buprenorphine
-good analgesic for |
-soft tissue Sx
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Buprenorphine
-route of administration |
-transmucosal (good for cats)
-high bioavailability |
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Buprenorphine
-duration |
-long
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Butorphanol
-effect |
-less effective analgesic than morphine and other pure Mu agonists
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Butorphanol
-duration |
-1-6 hrs
-usually less than 1 hr |
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Butorphanol
-indication |
Horses
-minimal locomotor effects -less effects on GI motility |
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Opioid CRI
-drugs |
-Fentanyl
-Morphine |
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Opioid CRI
-benefits |
-plasma levels more constant
-eliminates need for repeat injection |
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Opioid CRI
-disadvantages |
-requires 24 hr monitoring
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Fentanyl transdermal administration
-problems |
-patch was made for human skin which is different from dog skin
-takes up to 24 hrs to start working -skin reactions -nausea -anorexia -potential human exposure -ingestion by the animal -inconsistent blood levels |
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Oral mucosal transfer
-opioid |
-buprenorphine
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Why buprenorphine is good for oral mucosal transfer
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-high bioavailability
-tasteless |
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Tramadol
-receptors causing analgesia |
-opiate
-adrenergic -serotonergic |
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Tramadol
-problem when given with other drugs |
-can cause serotonin toxicosis
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Low-dose ketamine
-mechanism of action |
-antagonize glutamate action at the NMDA receptor
-prevents and treats central sensitization |
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Low-dose ketamine
-route of administration |
-IV
-SQ -epidural |
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Alpha-2 adrenoreceptors
-found where |
-dorsal horn
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Alpha-2 agonists
-presynaptic effects -postsynaptic effects |
Presynaptic
-decreased release of neurotransmitters from C fibers Postsynaptic -on wide dynamic range neurons, preventing hyperpolarization and damping nociceptive transmission through the spinal cord |
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Alpha-2 agonists
-analgesia due to |
-sedative effects from supraspinal effects in the brainstem
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Alpha-2 agonists
-why patient selection is important |
Significant alterations to cardiopulmonary function:
-decreased CO -decreased HR -increased vascular resistance |
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Alpha-2 agonists
-route of administration |
-CRI for sedation and analgesia
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Antiepileptic drugs
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-Gabapentin
-Phenytoin |
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Gabapentin
-Mechanism of action |
-structural analogue of GABA
-analgesia via NMDA antagonism not GABA |
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Antiepileptic drugs
-use in analgesia |
-treat neuropathic pain
-phantom limb pain |
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Phenytoin
-Mechanism of action |
-blocks sodium channels
-reduces ongoing discharge in peripheral nerves |
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Gabapentin
-incombination with what other drugs can giver superior analgesia at lower doses |
-opioids
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Lidocaine CRI
-effects |
-analgesia or sedation?
-decreased requirement for inhalation anesthetic |
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Lidocaine CRI
-mechanism of action |
-blocks sodium channels
-reduce ongoing discharge in damaged peripheral nerves |
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Lidocaine CRI
-negative effect |
-convulsant at high doses
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Lidocaine
-usually combined with |
-ketamine
-morphine |
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NSAIDs
-COX-1 receptor function |
-hyperalgesia
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NSAIDs
-COX-2 receptor function |
-induced with injury (up to 20x)
-most hyperalgesia |
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NSAIDs
-COX-1 & COX-2 inhibition function |
-prevents conversion of arachidonic acid into prostanoids
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NSAIDs
-effect on renal function |
-turn off PGF2a which is required for autoregulation of renal blood flow to the glomerulus
-anesthesia can reduce renal blood flow and arterial pressure -can lead to acute renal failure (have off NSAIDs 2 days before Sx) |
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Blood pressure range where kidneys can autoregulate flow
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60-180 mmHg
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NSAIDs
-contraindications |
-renal/hepatic insufficiency
-low effective circulating volume (dehydration, hypotension) -coagulopathies -current use of corticosteroids or other NSAIDs |
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NSAIDs
-drug examples |
-Carprofen
-Meloxicam -Deracoxib -etc. |
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Acetaminophen
-contraindication |
-cats
*can use codeine syrup |
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Codeine metabolite
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-morphine
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Alternative analgesic therapies
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-hydrotherapy
-physical therapy -acupuncture |
