Pain Physiology Flashcards
what is pain
unpleasant sensory and emotional experience completely subjective and not proportional to the tissue damage
how does pain stimulation of the sympathetic nervous system affect the body
stimulates endocrine and metabolic systems and causes abnormalities
retards recovery from trauma, surgery, and disease
define acute pain
lasts less than 6 months
subsides once healing process is accomplished
define chronic pain
constant and prolonged over 6 months, involves altered anatomy and neural pathways, sometimes for life
why should you treat pain
tissue damage can cause disabling, refractory, chronic situations that pain prolongor outlast the period of healing
what is cousins theory of acute pain
severe unrelieved acute pain results in abnormally enhanced response that cause pronounced and increasing pathophysiology
what are some harmful effects of pain
increased adrenergic stimulation
increase heart rate, cardiac output, and myocardial oxygen consumption
decreased pulmonodayr vital capacity, alveolar ventilation, and functional residual capacity
arterial hypoxemia
suppression of immun functions
what are the pain receptors
free nerve endings
what are the two types of pain neurons
A delta- first pain, sharp (protective)
C- second pain, dull (learning)
what can stimulate these receptors
mechanical damage
extreme temp
chemical irritation
what are the four distinct processes in the pain pathway
transduction
transmission
modulation
perception
what is transduction
local biochemical changes in nerve endigns that generate a signal
what is tranmission
movement of a signal from the site of pain to the spinal cord and brain
what is perceptions
synthesis and analysis in the brain
what is modulation
endogenous systems in place that can inhibit pain at any point along the pathway
what are nociceptors
free nerve endings that can distinguish between noxious and innocuous stimuli
what are some substances released from traumatized tissue that cause pain
bradykinin
serotonin
substance P histamine * inflammation
prostaglandin*
what do the substances released from traumatized tissues cause
sodium influx and depol
facilitates movement of pain impulse to spinal cord
what are two drugs that inhibit transduction
NSAIDS minimize prostaglandin production
corticosteroids inhibit prostaglandins and other inflammatory mediators
how is pain transmitted
damage - nerve - spinal cord - brain stem - thalamus - central structures of brain where processed
describe the a delta pain fibers
large diameter so can be transferred very fast and immediately can withdraw from painful stimulus to prevent further damage
describe the c pain fibers
small diameter slower causes immobilization healing and behavour modification
where is pain perceived
cortical structures
how is modulation mediated
endorphins reduce pain sensation and neurotransmitters
where do endorphins come from
descending fibers in spinal tract and hihger cortical centers released when pain impulse reaches brain binds to receptors in pain pathway to block transmission
what activates the descending pain modulation system
stress fear hunger thirst fatigue prolonged motor activity hypnosis
what drugs block transduction
nsaids antihistamines membrane stabilizing agents local anesthetic cream opioids bradykinin and serotonin antagonists
what drugs block modulation
spinal opiods alpha2 agonists NMDA receptor antagonists anticholinesterases nsaids cck antagonist NO inhibitos k channel openers
what drugs block transmission
local anesthetics
what drugs block perception
parenteral opiods
alpha 2 agonists
anesthetics
what is nociceptive pain
injury
trauma
infection
what is neuropathic pain
damage or dysfunction of peripheral or CNS
what is visceral pain
arises from an internal organ
wht is hyperalgesia
intense pain in response to mildly painful stimulus
what is allodynia
pain in response to completely innocuous stimulus
what are theffect caused by inhibition of prostaglandins by nsaids
analgesic
antipyretic
anit inflammatory
what does cox-1 do
found in many cells constantly maintain stomach lining and many critical functions
what does cox-2 do
induced in immune cells
cause pain inflammation and fever
what are the 3 phases of inflammation
- acute transient -vasodilate, cap permeability
- delayed subacute phase - leukocytes and phagocytes
- chronic proliferative phase - tissue degeneration and fibrosis
what do prostaglandins do upon cell damage
released cause local inflammation and pain
how can prostaglandins be used in birth
cause uterine cramping to injection to abort and inibitos to delay delivery
what other effects do prostaglandins have
platelet aggregation formation of clots - ASA
modulate stomach acidity and mucous lining - NSAIDS
how does aspirin work
irreversibly acetylates COX enzymes so effect lasts as long as it takes to replace the enzyme
how is caffiene used as a coanalgesic
60-120mg will increase the analgesic effect of all non opiod analgesic drugs
what are signs and symptoms of salicylate overdose
tinnitus***
increase in metabolic rate burns glucose and oxygen causing increased co2 - initial hyperventilation, metabolic acidosis, sever hypoglycemia
what are the immediate dangers of salicylate overdose
hyperthermia
deydration
hypoglycemia
treatment of salicylate overdose
parenteral fluids and glucose
keep cool
salycilates
methylsalicylate - oil of wintergreen bismuth salicylate (peptobismol) aspirin
proprionic acids
ibuprofen
naproxen
diclofenac
high potency and GI bleed risk
prescriptions for inflammation pain such as arthritis
indomethacin
gout pain and swelling
less common for chronic conditions
GI side effects
cox- 1 makes PGE2 and PGI1 which suppresses acid production, increases gastric blood flow, and increases secretion of mucin so non selective cox inhibitors increase acid and reduce mucous
misoprostol
prostaglandin analog that supplies stomach with prostaglandin effect lost with non sleective COX inhibitors - not very effective and more likely to cause diarrhea
what is reyes syndrome
fetal hepatic encephalopathy (liver induced brain disease) in children with viral infection, associated with SAS
nsaids and hypertension
increase in circulating volume
nsaids and bleeding disorders
inhibition of COX decreases ability to make clots
interferes with alcohol and warfarin
what were the results of a cox2 selective inhibitor
strokes and heart attacks due to the inhibition of prostocyclin
how is acetaminophen different
centrally acting analgesic
no ceiling effect
not anti-inflammatory
what happens in acetaminophen overdose
metabolized by GSH an antioxidant and at high levels depletes it causing oxidative damage to liver cells and direct damge to liver from the highly reactive intermediate
signs of tylenol overdose
elevated serum transaminase levels
hepatic encephalopathy
jaundice - too late
symptoms of migraine
throbbing!
nausea
preceded by aura
variable duration and incidence
whos more prone to migraines
more common in boys than girls adn reverses after puberty
triggers of migraines
weather missing a meal stress alcohol food menses
phases of a migraine
prodrome - feeling
aura - visual
headache and associated features
postdrome - exhausted
how do you treat an acute headache
nsaids
combo with caffiene and ice water
try avoid triggers
ergot alkaloid cautions
serotonin agonists liver disease rebound headache cadriovascular disease - vasoconstrict poor peripheral circulation
what are the triptans
agonists at serotonin receptors
side effect similar to ergot alkaloids
relieve nausea and headaches
why cant you take triptans with antidepressants
serotonin syndrome both increase serotonin
restless, twitches, sweatingm shivering, tremor
how can beta blockers be used in migraine prevention
propanalol regulates blood flow, reduces blood pressure
may cause tiredness, dizzyness
how can you use amitryptiline for migraine prevention
lower doses than in depression
may cause dry mouth and eyes, drowsiness
drugs for migraine prophylaxis
beta bloackers TCAs gabapentin candesartan some dietary supplements
