5. Perioperative Pain Management Flashcards
- Identify the 5 steps of the pain pathway and types of pain
transduction, transmission, modulation, projection, perception
Types: somatic v. visceral; acute v. chronic(pathologic)
- Be aware of options for assessing pain in small animals
- get pre and post op pain scores
- many systems: simple descriptive, numerical, visual analog (have the same trained observer score the pain for these 3)
- Also glascow (multidimentional), CSU feline acute pain scale (non verified yet)
- Know common drugs and MOA used for small animal analgesia
- Opioids - (modulation, dorsal horn) full mu, partial, ag/antag
- NSAIDs - block COX (transduction and modulation)
- local anesthetics - Na channel blockers (Transmission) (Also systemically, MOA unknown)
- NMDA antagonists (modulation) help with chronic/neuropathic pain, and prevent windup
- alpha 2 agonists - (modulation) alpha 2 receptor in cord, brain, and periphery, may have local anesthetic effects
- Define Multimodal analgesia and be able to develop an analgesic plan for perioperative patient care
use different MOA drugs to cover multiple parts of pain pathway
- some drugs work synergistically to decrease doses, cost, drug consumption
side effects of full mu agonists
respiratory depression, bradycardia, dec. GI motility
partial my agonists
buprenorphine, tramadol, has a ceiling effect
agonist-antagonist opioids
not very effective
alpha 2s in small animals v. other species
not good enough for primary method of pain control in small animals, adjunctive only.
nmda antagonists
ketamine
amantadine - oral
methadone (nmda and full mu)
adjunctive agents for pain control
- gabapentin (modulation - CNS Ca channels) neuropathic/chronic pain
- Acetaminophen (COX3, maybe cannabinoid receptors)
NOT IN CATS -> MetHbemia - Maropitant - NK1 antag, may do some visceral analgesia
What happens to arachadonic acid after tissue injury?
broken to thromboxanes, PGFs from COX
COX1
constitutive enzyme, always there
produces PGE2, I2, TXA2 (prostanoids for homeostasis in kidneys, GI, platelets)
COX2
Inducible Enzyme, upregulated with inflammation (though technically still constitutive)
produces PGE2, PGI2, also for homeostasis (GI ulcer healing, renal BF)
COX constitutive enzymes?
Both of them!!! They’re both needed, both important for homeostasis
Inhibitory Ratio of nsaids
plasma concentration needed to inhibit Cox1:cox2
Because it was thought to minimize side effects by targeting COX2
Which drugs target Cox2?
the ones that end in -oxib are actually cox2 preferential
(carprofen only mildly cox2 preferential)
BUT THEY STILL BLOCK COX1 SOME
Basic pharmacokinetics of NSAIDs
- good bioavailability PO, but feeding alters (give carprofen with food, robenacoxib fasted)
- heavily protein bound (reduce dose in hypoproteinemic)
plasma concentration of nsaids ________ reflect analgesic property
do not
GI side effects of nsaids
cox1 - maintains cellular integrity
cox2 - repairs GI mucosa
- inappetance, v/d, inflam, melena, ulceration, perforation
** most common reason to discontinue nsaids
risk factors for GI injury with NSAIDs
- inappropriate dosing
- given with steroids
- given with pre-existing GI disease
risk factors for GI injury with NSAIDs
- inappropriate dosing
- given with steroids
- given with pre-existing GI disease
Tx for GI side effects nsaids?
- discontinue
- palliative (fluids, bland diet)
- give H2 blocker/Famotidine or PPI/omeprazole, pantaprozole (if signs of ulceration, like melena)
- misoprostol (PGE1 analog for GI integrity)
- use different nsaid in future
- alternative analgesia
renal effects of nsaids
not directly nephrotoxic but can cause AKI. regulate BF to kidney and amount of diuresis
use nsaid in cats with mild/mod chronic renal disease?
yes with oral low dose