Week 10: Pain Management Flashcards
consequences of untreated pain
catabolism wasting immune system suppression inflammation delayed wound healing anesthetic risk/increased dose patient suffering
neuroendocrine/catabolic wasting
ACTH release
elevated cortisol, norepinephrine, epinephrine
decreased insulin
sympathetic stimulation can result in cardiac arrhythmias
vasoconstriction
increased myocardial work
increased myocardial oxygen consumption
nocioception
detection of nervous system for potential or actual tissue injury
physiological pain
ouch pain
little or no tissue injury
protective response
pathologic pain
follows tissue injury
acute or chronic
visceral pain
originates from organs
somatic pain
originates from musculoskeletal system
superficial pain-skin
deep pain-muscle, bone, joint
hyperalgesia
hypersensitivity to painful or even normally non panful stimuli
secondary hyperalgesia
CNS hypersensitivity wind up further away from site of injure spinal cord neuron stimulation modulated by NDMA receptors
pain pathway
transduction
transmission
modulation
perception
transduction
electrical signals
inhibited by NSAIDs, local anesthetics, opioids
transmission
spinal cord
reduced by local anesthetics and alpha 2 agonists
modulation
neurotransmitters
influenced by local anesthetics, alpha 2 agonists, opioids, NSAIDs, tricyclic antidepressants, selective serotonin, reuptake inhibitors, NDMA receptor agonists
percdption
brain
alpha 2 agonist
opiods