Pain Flashcards

1
Q

what is pain

A

an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage

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2
Q

purpose of pain

A

prevents serious injury
teaches avoidance
prevents permanent damage

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3
Q

pain is classified in two ways - list those two

A

based on location and. based on duration

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4
Q

two classifications of pain on location

A

somatic pain
visceral pain

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5
Q

two classifications of pain based on duration

A

acute pain and chronic pain

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6
Q

somatic pain

A
  1. superficial pain (outside our body)
  2. arises from nocieptive receptors in the skin
  3. it is localized, fast or slow onset, feels like sharp burning or prickling and is constant
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7
Q

visceral pain

A

poorly localized
originates from internal organs
activates nociceptors on internal organs
feels like an achy and dull sensation

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8
Q

acute pain

A

short lived and adaptive pain resposne
occurs in response eto injury or illness
responds well to interventions
produces behavioural change that promotes healing.

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9
Q

chronic pain

A

mismanaged acute pain turns into chornic pain
pain persists beyond the normal healing period

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10
Q

pain classification based on mechanism (list 3)

A

nociceptive (acute), neuropathic (chronic), nociplastic (mix)

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11
Q

nocicepetive pain - cause, subtypes, duration

A

relatex to damage or the threat of damage to non neural tissues
somatic, visceral
less than three months

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12
Q

neuropathic pain - cause subtypes, duration

A

injury or disease of the peripheral or central nervous system
sensory abnormalities cause varying degrees ofpain sesnations from numbness to hypersensitivity, in which pain receptors react to non-painful stimuli. e.g. allodynia and hyperalgesia.
lasts more than three months

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13
Q

nociplastic pain - cause subtypes, and dudration

A

abnormal processing in the CNS with no actual threatened tissue damage and no damage or disease of the nervous system - e.g., fibr0myalgia, IBS
non nocicepetive and non neuropahic pain.
as - associated with central sensitization or psychological disttress or ongoing inflammation.
activation and sensitization of nociceptive pain pathway by mediators released at a site.

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14
Q

Modulation of Pain sensation steps (5)

A
  1. nocicepetors detect harmful signal
  2. Message passes from the site of injury to spinal cord through adelta and c fibers (which are the first order sneory afferents coming into the gate at the dorsal horn of hte spinal cord.
  3. message is relayed to second order neurons whose fibers asccent to the thalamus
  4. third order afferents project it to higher brain centers of hte limbic system, the frontal cortex, and the primary sensory cortex
  5. the electrical communication between these regions gives rise to the feelling of pain.
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15
Q

transduction

A

first and second order neurons, detect noxious stimuli from somatic and visceral tissue. this painful stimuli is converted to energy, and sends the impulse across peripheral nerve fibers

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16
Q

transmission

A

nociceptive message is transmitted to the CNS of actual or impending tissue injury
a delta fibers send sharo, localized sensations, c fibers relay impulses that are poorly localized.

17
Q

perception

A

person is aware of the pain
somatosensory cortex identifies the location and intenisty

18
Q

modulation by body

A

excitatory transmitter mediate synaptic transmission to the dorsal horn
inhibiotry NT work to inder pain

19
Q

excitatory NT , inhibitory NT

A

E - Glut, Substance P, CGRP
I - GABA, Glycine, Enkephalins, Dynorphin, NOradreanline

20
Q

Types of NOciceptors and their functino

A

mediate potentially harmful stimuli
1. thermal receptors are activated by temperatures above 42 degrees or severe cold
2. mechanical nociceptors respond to strong pressure
3. chemically sensitive respond to various chemicals such as bradykinin, histamine, high acididty
4. polymodal ones respond to a combo

21
Q

Nociceptor activation

A
  1. tissue injury releases bradykinin and prostaglandins that sensitize or activate nociceptors, which in turn release substance P and CGRP
  2. Substance P acts on mast cells to cause degranulation and release histamine, which activates nociceptors
  3. Substance P causes plasma extravasation and CGRP dilates blood vessels, the resulting edema causes additional release of bradykini
  4. 5HT is released from platelets and activates nociceptors.
22
Q

how does thickness of a nerve fiber correlate to speed with which info transfers

A

thicker the nerve (a delta), fasater the info
slow pain - c nerve fibers

23
Q

neospiniothalamic tract transmission

A

a delta fibers takes info through the DRG, synapse onto second order neurons which carry the signal all the way to the thalamus

24
Q

paleospinothalamic tract

A

The C fibers synapse on the second order neurons which carry the signal to the reticular formation and midbrain and hten go to the thalamus.

25
Q

what happens in between the first and second order neuron?

A

first order release NT glutamate, Substance P, CGRP, NO, and PG and BDNF.
Glutamate b inds to metabotropic glutamate specific receptors and ionotropic AMPA receptors.
SP and BDNF bind to the G-protein coupled NK1 receptor and Tyrosine kinase receptor B.
Prostaglandins bind to the EP1 receptor.
THe binding of these causes a sensitized state

26
Q

in the sensitized state, the second order neuron

A
  1. ligand gated ion channels like NMDA are up regulated, mg plug removed, increase in glutamate sensitivity to signalling is intensified
  2. An increase in intracellular Ca concentrations leads to a potentiation in activity via AMPA receptors results in transmission of the nerve signal from second order neurons
27
Q

second order neurons are iether

A
  1. nociceptive specific
  2. wide dynamic range (receive non noxious afferent input as well)
28
Q

How is pain cut off

A

inhibitory pathways descending from the brainstem release NT in the spinal cord such as 5HT and NA, or activate small opioid containing interneuronsin the spinal dorsal horn to release opioid peptides. this slows down transmission - ucts down the signal to the brain.

29
Q

what does the activation of the opioid receptors lead to

A

Reduced cyclic AMP, coupled to inhibiotry G protein.
Reduces neuronal cell excitation and transmission, closesCa channels, stimulation of K+ efflux - hyperpolarization.
can lead to euphoria - involves dopaminergic pathways.

30
Q

what to opioids do

A

bind to enkaphalin receptors, mimicking the pain supressing effects of teh endogenous opiate enkephalin.

31
Q

what do enkaphalin containing interneurons normamlly do

A

synapse with the terminals of pain fibers and inhibit the release of substance P thus fewer pain impulses to the brain.