Behavioral science - Pain Flashcards
What is transference?
The patient attributes beliefs and expectations of the MD-PT relationship onto the doctor. Can be positive or negative transference but always pathological
EXAMPLE: assuming that Dr. can’t or won’t help and will likely not listen, be short and possibly rude
What is countertransference?
The doctor attributes beliefs and expectations of the MD-PT relationship onto the patient. Can be positive or negative transference but always pathological
EXAMPLE: you (Dr.) likely will be stressed, irritated, short and rude as these patients don’t follow the medical rules
Acute pain vs chronic pain time cutoffs for Dx
Acute pain – 1 week or less
Chronic pain – Considered an autonomous disease by many physicians; at least 6 months
Pathway for endogenous opioid synthesis (what is most important endogenous opiod? What receptor does it act on?)
POMC > beta-lipotropin > beta-endorphin
beta endorphin
mu opioid receptors
What CSN structures are involved in descending pain circuit?
amygdala, mesencephalic reticular formation, PAG, rostral ventral medulla
Where are mu opioid receptors expressed?
Descending pain circuit
How do endogenous opioids work?
Involved at inhibiting GABA and thus disinhibiting dopamine
Where in the PNS are mu opioid receptors?
Primary Afferent Neurons, Peripheral Sensory Nerve fibers, Dorsal Root Ganglia
how do mu opioid receptors work in PNS?
Inhibition of substance P and other tachykinin release
What triggers endorphin release in the PNS?
stress and ACTH co-release
Where are endorphins involved in PNS release synthesized?
Corticotrophs in the anterior pituitary synthesize ACTH and β-endorphin in equimolar amounts
What triggers central endorphin release
activation of nociceptive circuits in the hypothalamus, midbrain, and rostral medulla
Where are centrally released endorphins synthesized?
Cell bodies of opioidergic neurons in the median eminence of the hypothalamus
In response to pain the peripheral nociceptive pathways trigger co-release of endorphins and ATCH from the anterior pituitary. What agents trigger release?
5-HETE, LTA4, LTB4, and other lipoxygenase products
Angiotensin-II
Serotonin
What receptors and signalling pathways are involved in release of endorphins?
β-adrenoreceptor activation
Gs: adenylate cyclase activated, cAMP
How is glutamate signaling involved in opioid pain inhibition?
glutamate receptor antagonists block effect of opioid suggesting glutamate signaling facilitates opioid effects
Are high-dose opioids usually helpful for chronic non-malignant pain?
no
What should cut-off be for opioid prescription be for non-malignant chronic pain?
longer than 1 months should be reconsidered
MOA for NSAIDS
inhibit cyclooxygenase (COX), enzyme for conversion of arachidonic acid to prostaglandins and thromboxane, which provoke tissue inflammation
Why do some NSAIDS cause GI irritation?
Inhibit prostaglandin production - Prostaglandins protect the stomach lining from acid
How can GI irritation be circumvented?
COX-2 specific inhibitors; celecoxib and low dose meloxicam (7.5 mg/day) cause less gastric irritation
What is the only NSAID that causes irreversible inhibition of COX
aspirin
What else do NSAIDS do?
reversibly inhibit renal blood flow decrease fever (PGE2 causes fever)
Which drugs should be used to treat neuropathic pain?
anticonvulsants, tricyclics
