Ch. 14 Flashcards
Pain
Dysfunctions of general or spectifc senses
Pain characteristics
-Unpleasent but productive phenomnenon
-Can’t be defined, identified or measured by others
Complex characteristics of pain
interactions between, physical, cognative, and emotions
McCarffery Definition of pain
Whatever experiencethe person says it is, exhisting when they say it does
Temperature variations
-Signal disease
Manefestations of temperature functions
-Fever
-symptom of infectious or inflammatory conditions
Theories of pain
-Specificity theory
-Gate control theory
-Neuromatrix theory
Specific theory
-Injury activates specific pain receptors
-Intensity of pain is directly related to associated tissue injury
Example of specificity theory
-Pricking a finger: Minimal pain
-Cutting hand: Higher pain
Problem with specificity theory
Doesn’t account for persistant, emotional pain
Gate control theory
-Combines theories to explain multidimensionl aspects
-transmission altered by a balance of signals sent to s.cord: cells work as a “Gate”
Spinal gate
controls pai transmission to centers in the CNS
Neuromatrix theory
-Brain produces patterns of nerve impulses drawn from various inputs, including genetic, psychological, and cognitive experiences
Can pain be felt with out ecperiencing it?
Yes
-Phantom limb
-Neuromatrix theory
Neuromatrix theory stimuli
trigger patters but don’t make them
Pain pathway
3 parts of NS responsable for perception, sensation, and response
-Afferent pathways
-Interpretive pathways
-Efferent pathways
Nocioception
Processing of harmful (noxious) stimuli through NS
Nociocepters
Pain receptions
-Free nerve endings in afferent PNS
2 types of Nociocepters
- A delta fibers
-C fibers
A Delta fibers
-Large myelinated
-access large tracts in S.cord
C fibers
-Smaller unmylenatied
-Access smaller tracts in S.cord
Fast sharp pain is percieved by
A Delta fibers
Dull throbbing pain
C FIbers
Transduction
Activation of nociocepters
Transmission
Conduction to dorsal horn and up spinal cord
Transducer
Device that converts varations into an electric signal
Perception types
-Sensory-descriminative
-Motivational-affective
-Cognitive-evaluative
Sensory-discriminative
identifies presence, location, and intensity
(Somato sensory cortex)
Motivational-affective
determines avoidance and emotional responses
(Reticulat formation, limbic system)
Cognitive-Evaluative
Learned pain experience
(Can modulate perception of pain)
Pain perception
consoius awareness of pain (reticular and limbic system)
Pain threashold
lowest intensity of pain that a person can recognize
Pain tolerence
-Highest intensity of pain endurance
-Varies greatly among people and in same person over time
-Pain tolerence decreases with repeated exposure
Perceptual dominance
intense pain at one location may increase threashold in another location
Pain modulation
different mechanisms act to increase or decrease pain transmission through nervous system
Perpheral triggoring mechanism
initiates exitatory neuro thransmitters include tissue injury and chrinic inflammation
Excitatory NT
-Substance P, Glutamate, Histamine, Prostaglandins
-Reduce nocioceptior activation threashold
What increases nocioceptor responsiveness
Exciatatory NT
Inhibitory NT
-Opioides, GABA, Cannabinoids, serotonin, norepinepherine
What inhibits/reduces transmission of pain signal
Inhibitory NT
Decending pathway and endorphin response
-decending inhibitory impulses transmitted from brain to inhibit pain signal
Endorphins
Combination of “endogeneous” and “morphine”
Opiates receptors
Gprotein receptors coupled receptors for endorphins which are opiate neuropeptides
Morphine-like neuropeptides
-Bind with opioid receptors throughout the body to inhibit pain impulese in periphery, s.cord, and brain
Whats responsible for sensations of well being
Morphiene-like neuro peptides
Cannabinoids
-Canabis (marajuana) produces resin containing cannabinoids
Analgesic cannabinoids
relieve pain in humans
Drawbacks to anagelisic cannabinoids
psychoactive and addictive properties
-Legalized in 2020
Endocannabinoids
-synthesized in body from phospholipids
-modulate pain and other functions
Alcohol pain reduction
functions by depressing CNS
-Slows down brain and NS
-Delivers some pain relief
dwale
-potion anesthetic used from 1200-1500
-alcohol, bile, opium, lettuce, hemlock (toxic plant) and vinegar
1840
ether created
1846
first pain-free surgery performed in amphitheater of Massachusetts general hospital
Acute pain
-nociceptive pain
-protective mechanism
-pain last minutes to weeks
how is acute pain protective
alerts to harmful condition and mobilizes person to relieve it
types of acute pain
-Somatic
-Visceral
-Referred
Somatic pain
-skin, joints, muscles
-sharp and localized =delta fibers
-dull throbbing= C fibers
Visceral
-internal organs and lining of body cavities
-poorly localized, aching, throbbing quality to pain
-C fibers
Referred pain
-felt distant to place of origin
-cutaneous and visceral receptors converge on same ascending neuron
-brain can’t distinguish between the two
-skin has more receptors so pain is often referred to skin area
Persistent pain
-intractable pain
-lasts more than 3-6 months
-serves no purpose/poorly understood
-ongoing(back pain) or intermittent(migraine headache)
studies of persistent pain show
change in brain = reduced ability to cope with pain
Neuropathic pain cause
dysfunction of nervous system = long term changes in pain pathway and abnormal processing
neuropathic pain
-chronic/amplification of pain
-described as burning, shooting, or tingling
neuropathic pain characterization
increased sensitivity to painful and nonpainful stimuli with hyperalgesia
hyperalgesia
increased capacity to feel pain
analgesia
absence of pain
Fever
temporary resetting of hypothalamic thermostat to a higher level in response to exogeneous or endogenous pyrogens
pyrogen
substance that produces fever when released into blood
exogeneous pyrogens
(pathogens) cause release of endogenous pyrogens
(TNF-a, IL-1,IL-6)
pyrogens job
raise thermal set point by inducing hypothalamic synthesis of prostaglandin E2 (PGE2)
PGE2
prostaglandin E2
prostaglandins effect
increase temperature through increased heat production and conservation
How individuals feel from prostaglandins effects
-feel colder, fetal position to decrease surface area, go to bed to get warm
cause of how individuals feels
heat conservation though cutaneous vasoconstriction
how long is the increased fever temp maintained
until fever breaks and original set point is reinstated
returning to original set point
individual feels warm, throws off covers, and stretches out
fever benefits
-kills MO
-decreases minerals needed for bacterial replication
-breaks down lysosome, prevents viral replication
-facilitates immune response
-enhanced phagocytosis
suppression of fever
can be effective but used with caution
hyperthermia
-elevation of body temp w/o an increase in hypothalamic set
-can cause nerve damage, coagulation of cell proteins, and death
Heat cramps
-Severe spasmodic cramps in abdomen and extremities
-follows prolonged sweating and associated Na loss(40-60mmol/L of swear)
-common in those not accustomed to heat or hard work in hot climates
SS of heat cramps
increased core temperature, rapid pulse, and increased bp
Heat exhaustion
-result of prolonged high core or environment temp
-profound vasodilation and profuse sweating = dehydration and tachycardia
manifestations of heat exhaustion
dizziness, weakness, nausea, confusion
Heat stroke
-potentially lethal
-41C (nerve damage, convulsions)
-43C (Death)
Hypothermia
-body temp less then 35C
-produces ice crystals in cells= cells rupture
Tissue hypothermia
-slows cellular metabolism rate
-increases blood viscosity
-facilitates blood coagulation and vasoconstriction
therapeutic hypothermia
-used to slow metabolism= preserve ischemic tissue during surgery
