Pain Patho Flashcards
Pain as a subjective experience
It is what the patient says it is; phys, cognitive, emotional, spiritual, environmental combo
Afferent pathway
Begins in PNS and impulses ascend thru base of spine
Interpretive centers
Cortical and subcortical areas of the brain and cortex that interpret sensations as pain
Efferent pathways
Send messages from the interpretive centers back to the PNS and elicit a response
3 parts of NS messaging
Sensation, perception, response
Nociceptors
Pain receptors; free nerve endings in afferent peripheral systems that cause nociceptive pain when stimulated by stimuli of certain intensities or that are close to causing tissue injury
Target for pain meds
Nociceptors
Nociceptors location
Dental pulp, skin, meninges, internal organs, periosteum, few in brain, alveoli, deep tissue
NTs role in pain
Control transmission of pain impulse; excitatory or inhibitory
Endorphins
Endogenous opioids that aid in inhibition of pain response; mediate pre-synaptic transmission
What do excitatory NTs do?
Enhance, increase pain response in injury or chronic inflammation
What do inhibitory NTs do?
Block pain (GABA is the main)
4 stages of pain processing
Transduction, transmission, perception, modulation
Transduction
Painful stimuli are converted to APs at sensory receptor; occurs along a-delta and C fibers; NTs released from direct injury and inflammation cause APs
Prostaglandin
Important mediators that lowers the pain threshold when activated; promote inflammation, pain, fever, blood clotting, protecting the stomach lining from acid, kidney function; dilate BVs that lead to kidneys; what we target with pharmacotherapy
A-delta fibers
Small, myelinated fibers that cause stinging, sharp, cut, pinch feeling; LOCALIZED pain
C fibers
Unmyelinated, slower, small diameter, dull pain, burn, ache, poorly localized; workout ache
A-alpha and A-beta fibers
Larger diameter nerve fibers that don’t transmit pain; activated in the gate control theory
Transmission
APs move from peripheral receptors to spinal cord and brain via the dorsal horn located in the spinal cord; end up in thalamus; A-delta and C fibers carry
Pain perception is influenced by…
Influenced by fatigue, attention, distraction, fear, anxiety, previous expectations and experiences, age, concept of health, education, gnetics
Pain tolerance
Greatest intensity a person can handle; varies with time (ex: women’s is higher at childbirth but they can’t feel that pain all the time—unreasonable)
Pain threshold and influencing factors
Lowest intensity of pain a person can recognize; influenced by sleep, injury, frustration/emotions; when these are worsened the threshold is decreased
Opioid tolerance and pain threshold
Opioid tolerance can decreased with time—neuro synapses change with long-term use
Perceptual dominance occurs when…
Pain in 1 area is worse so it masks pain in another area
What increases pain threshold?
Alcohol, hypnosis, strong faith, acupuncture, sex, exercise
Modulation
Synaptic transmission of pain signals can be altered or dampened by pain meds and endorphins
Gate control theory
Blocking the pain before it gets to the brain by stimulating A-alpha and A-beta fibers which inhibit C and A-delta fibers, lowering pain perception; touch, rub, get active which decreases excitation and pain by inhibiting nerve impulses before they reach the thalamus; works for mild or chronic pain
Where does the gate control theory work?
Substantial geltianosa
What produces s/s or inflammation?
Prostaglandins—Chemical mediators in the plasma that are activated by tissue injury (ex: arachidonic metabolites which causes production of prostaglandins)
Acute pain
Nociceptive, normal and protective; sudden and resolves when chemical mediators leave; transient—seconds to months; lasts under 3 months; stims ANS which causes physical response to pain (HR, BP, diaphoresis, diluted pupils)
Chronic pain
Lasts beyond expected healing time (over 3-6 months); no purpose and out of proportion to observable tissue damage; ongoing or intermittent; change in PNS or CNS that causes dysregulation of nociception and pain modification; often no ANS and associated with psychosocial problems
Nociceptive pain
Acute pain that rises from peripheral pain receptors or nociceptors; response to actual tissue damage; ache/gnaw/pound
Neuropathic pain
Results from direct injury to peripheral nerve; does not respond to usual pain meds, involves nerves or abnormal sensory input, shooting, burning, numb, shock, abnormal sensation (ex: diabetic neuropathy, phantom limb pain); poorly localized; tx with adjuvant analgesics
Visceral pain
Involves organs, sometimes, inflammation, poorly localized, diffuse, deep; often referred pain; kidney stones, diaphoresis, cramping, splitting, N/V (appendicitis, bladder spasm, constipation, heart attack)
Idiopathic pain
Chronic pain without a cause; exceeds typical pain levels; associated with conditions—cause apathy, insomnia, anorexia
Cutaneous/somatic pain
A-delta usually; sharp, localized, constant, achy, well-localized in skin and SQ tissue, muscle, BVs and connective tissue
Referred pain
Felt at a distance from actual pathology (ex: radiating arm pain from heart attack)
Phantom pain
Felt from amputation, brain sense something not there, constant, most intense right after amputation, resolves with time
Atypical meds
Adjuvants
Tramadol (Ultram) class and MOA
Centrally acting analgesic; binds weakly to mu opioid receptor, inhibits reuptake of NOR and Sr
What is tramadol for
Moderate-severe pain
Tramadol SE and NC
SE: none often, drowsy, dizzy, headache, nausea, constipation, resp dep; seizures and CNS dep (rare)
NC: Can be given with Tylenol, not best for people who get seizures; schedule 4
Gabapentin (Neurontin) and pregabalin
Anticonvulsants that spontaneously suppress neuronal firing
gabapentin and pregablin SE and NC
SE: drowsy, dizzy, vision problems; Can be partially reversed with Narcan; no ceiling effect; schedule 5
Aspirin (ASA) class and MOA
NSAIDS; non-selective COX inhibitor; Dec formation of thromboxine which causes less clotting
Aspirin SE and NC
GI ulcers, GI bleed, rash, edema, kidney failure, increased BP, decreased platelet aggregation, SOB with asthma; salicylate poison/toxicity; Not best for people with asthma; black box for GI issues—don’t give to elderly and people with past hx, must eat first; NEVER GIVE TO KIDS WITH VIRAL INFX—cause Reye’s sx (severe brain and liver damage, high mortality); Is Excedrin when combined with caffeine, don’t give to; sal tox from acute use—edema, N/V, seizure; sal tox from chronic use—N/V, tinnitus, hearing loss
What do nociceptors respond to?
Hot/cold, sharp, electric
Ceiling effect
The phenomenon when increasing a dose of medication does not increase its effectiveness
When does acute pain end?
When chemical mediators leave
Tx for nociceptive pain
Opioids and analgesics
Tx for chronic pain
Adjunct analgesics? (Neuropathic)
