Chronic Pain Flashcards
any time you see central sensitization or “wind-up phenomenon” you want to think:
WDR neuron (wide dynamic range) neuron NMDA receptor (plays a big role in pain) treat with ketamine
conversion of nociceptor specific neurons to sensitized WDR neuron:
light touch, stubbing toe all horrific pain
complex regional pain syndrome:
pain history mnemonic: p provokes q uality r reduction s everity t ime
morphine and end stage renal disease patients:
morphine is broken down and the metabolites can build up and cause:
delirium, seizures, psychosis, respiratory failure:
NOT THE FIRST CHOICE FOR DIALYSIS PATIENTS
Complex regional pain syndrome:
roots based in the over activity of the sympathetic nervous system: this makes it the target for intervention
TREAT WITH INJECTIONS INTO THE STELLATE GANGLION BLOCK: CAUSE INSTANT HORNERS
Goal of treating chronic pain:
improve functionality
TREATMENT OF CHRONiC PAIN INCLUDES:
WHO step ladder of increasing treatment:
NMDA antagonist: KATAMINE
ANTICONVULSANT: PREGABALIN GABAPENTIN to treat NEUROPATHIC PAIN
diabetic neuropathy:
snri or tca
of all the side effects of opiods, the one side effect that you never develop a tolerance for is:
constipation
what is one of the best treatments for someone who is alerady taking medication (norco) and is now reaching the top of the WHO step ladder of pain treatment?
PT, TCA amytryptaline, nortryptaline, gabapentin, anticonvulsants, bupor patch, spinal cord stimulatoor, stellative ganglion block
Which of the following are appropriate for the treatment of this patient with Complex Regional Pain Syndrome?
Start Amitriptyline
Refer patient to physical therapist to learn desensitization exercises
Assess her risk of developing addiction to opioid medications
All of the above
all the above
if you have a patient that has a TENS unit (low voltage electrical stimulus to the spinal cord and this overwhelms the sensory nerve fibers that usually carry back sensation of pain) or similar treatment for chronic pain. This is thought to work via the gate control theory of pain suggests that the nerve stimulous is reducing the chronic pain, so one of the mechanisms of action of the gate controlled theory of pain would be:
activation of alpha beta fibers, which reduces the ability of pain inputs in the spinal thalamic tract
if you have a patient on codeine (different than morphine bc it has to be metabolized to be effective) if you have a paitent that is not getting good pain relief on codeine. How is codeine matabolized?
its metabolized to morphine by deacetylating enzymes in the brain
if you have a patient with a spinal cord stimulator, one of the ways it’s thought to reduce pain is by:
activating the body’s endogenous peptides that are important in pain relief, and one of these is encephlin (an endogenous peptide releasd by the body as a response to injury and inflammation, enkephlin also binds to opiod receptors, and it inhibits further neurotransmitter release to reduce pain
you have a patient in the ED that is overdosing, he has pinpoint pupils and tracks, he is overdosing on ______ and should be given_______. How does this work?
morphine, IV NALOXONE (aka narcan, naltrexone), is an antogonist of opiates at the receptor site and acts by displacing it from the opiod from its receptor