Bb6

Front 1

Acute pain nocireceptors characteristics

Back 1

Freenerveendings—notanidentifiable
structure as for touch and vibration.
• Respondstoabroadrangeofphysical and chemical stimuli

Front 2

Nocireceptors for acute pain only respond when

Back 2

intensities that are capable of causing damage.
• Activated by injury or tissue damage

Front 3

Some factors that activate acute pain are

Back 3

Bradykinins,prostaglandins,&
potassium.
Release of Substance P from other
branches of the axon.

Front 4

Acute pain nocireceptors stimulate the release of

Back 4

histamine and promote vasodilation.

Front 5

There are 3 main types of peripheral afferent axons

Back 5

A beta (skin)
A alpha (muscle and joints)
A delta (Thinly myelinated)

Front 6

A beta characteristics

Back 6

the largest & most heavily
myelinated

Front 7

A alpha characteristics

Back 7

muscle and joints – thicker and transmit sensory information – posture, motion, position, proprioception.

Front 8

A delta characteristics

Back 8

Thinly myelinated

Front 9

C fibers characteristics

Back 9

unmyelinated

Front 10

A delta and C fibers both send pain signals to the dorsal root ganglion (because thats where their bodies are) how is the signal that each sends)

Back 10

-A delta are thinly myelinated axons that quickly send the first, sharp signals of pain.
-C fibers are unmyelinated and send a slower, dull pain signal.

Front 11

A beta are high treshold mechanoreceptors which mean that they transmit what type of pain

Back 11

Sharp, noxious thermal stimuli

Front 12

C fibers have higher thresholds than
myelinated which means that they react to

Back 12

Nonselective responding – chemical, thermal, mechanical
! Polymodal

Front 13

The nociceptive afferent nerve fibers are “first-order” neurons and synapse in the dorsal horn with the “second-order” neuron (may also be interneurons) which then crosses to the contralateral side and ascends to the brain. And it is a this point that pain signals can be

Back 13

modified at this point by descending fibers from the brain or from simultaneous activity by nonpain neurons, the mechanoreceptors Abeta fibers.

Front 14

A beta fibers can dampen the pain signal how?

Back 14

A signal from the larger mechanoreceptor activates an inhibitory interneuron in the dorsal horn.
! Results in a smaller signal conveyed to the brain.
! Rationale for the use of transcutaneous electrical stimulation (TENS

Front 15

what is sensitization?

Back 15

process in which nociceptors in an area extending beyond a tissue injury exhibits decreased thresholds for activation.

Front 16

sensitization can be initiated by

Back 16

inflammatory mediators such as prostaglandins and leukotrienes.
-spontaneous pain

Front 17

what is allodynia?
what is hyperalgesia

Back 17

- Innocuous (light touch for instance) stimulates nocireceptors
-Exaggerated response to noxious stimuli

Front 18

sensitization can be due to alteration in the threshold for opening of TRP channels, this could be achieved by

Back 18

Second messenger phosphorylation of TRP channels and Na+ channels in pain pathways.

Front 19

What tract allows sensory discrimination of pain?

Back 19

Spinothalamic tract
Signal->Lateral hypothalamus->somatosensory cortex

Front 20

What is pain asymbolia?

Back 20

A person with damage to the parietal lobe develops this condition where they cant localize pain. They only know they are in pain they see some visible cue

Front 21

The intensity of a noxious sensation is carried by

Back 21

The spinoreticular tract or the spinomesencephalic tract
Anterolateral region (spinal cord)->reticular formation, PAG and amygdala

Front 22

Affective-motivational signals of pain "how much does it hurt" activate

Back 22

anterior cingulate cortex, insula cortex, and prefrontal cortex, and the amygdala.

Front 23

Subjects with frank congenital insensitivity to pain are without

Back 23

the peripheral Adelta and C fibers. Lack the sensory-discriminative as well as affective components of pain and are the most at risk for harm and premature death.

Front 24

The number one cause of insensitivity to pain is

Back 24

leprosy

Front 25

brain imaging studies have documented that subjects with less pain tolerance have greater activation of

Back 25

anterior cingulate cortex [ACC], insula cortex, and prefrontal cortex, along with the somatosensory cortex

Front 26

Low COMT activity is associated

Back 26

increased pain sensitivity in experimental pain models and with increased pre- and postoperative pain in acute clinical situations.

Front 27

Endogenous Opioids and Related Peptides that cause analgesia

Back 27

Propriomelanocortin ! Proenkephalin
! Prodynorphin

Front 28

Genes that encode for increase in pain sensation are

Back 28

Orphanin FQ-nocieptin, which Binds to u opioid receptor

Front 29

PAG is part of the descending pain modulating pathway. This is partly

Back 29

opiod depedent and indepedent

Front 30

Descending pathway releases

Back 30

Release of endocannabinoids
! 2-AG
! Anandamide

Front 31

desceding pathway is blocked by

Back 31

CB1 receptor blockers

Front 32

Chronic Back Pain Is Associated with Decreased

Back 32

Prefrontal and Thalamic Gray Matter Density.
Brain gray matter decrease in chronic pain is the consequence and not the cause of pain.

Front 33

What are the systems suspected to be transmit signals relating to motivational and hedonic aspects of both pain and pleasure and, in particular, their interactions

Back 33

The Mu opioidandmesolimbicdopaminesystems

Front 34

Bothpainandpleasurehavebeenshowntoelicit opioid release in

Back 34

orbitofrontal cortex (OFC), the amygdala (Amy), the nucleus accumbens (NAc) and the ventral pallidum (VP).

Front 35

Pleasure and reward expectation are also associated with increased phasic dopamine signaling from

Back 35

ventral tegmental area (VTA) to the NAc and VP, which in turn causes increased -opioid release in the Nac.

Front 36

Pain has been associated with both increases and decreases in

Back 36

mesolimbic dopamine signaling, depending on the type of measurement and pain model that have been used.

Front 37

Naloxone, a u opioid receptor antagonists, reverses

Back 37

pleasure-related analgesia.

Front 38

Morphine a u opioid receptor agonists renables

Back 38

pleasure that has been previously reduced by concomitant pain.

Front 39

Repeated use of addictive drugs produces multiple unwanted changes in the brain that may lead to

Back 39

tolerance, sensitization, dependence and addiction.

Front 40

Unlike natural rewards, addictive drugs have no nutritional, reproductive, or other survival value.
! However, all addictive drugs exert pharmacologic effects that cause release of

Back 40

dopamine.

Front 41

dependence to drugs includes

Back 41

anhedonia, depression, anxiety, and negative emotional states (dependence).

Front 42

Whats structures are implicated in both long term and acute drug effects?

Back 42

Ventral tegmental area and nucleus accumbes
Reduced VTA activity and enhanced NAc activity associated with reduced sensitivity to rewarding effects and dysphoria associated with drug withdrawal.

Front 43

Tolerance to drugs can be in 3 ways

Back 43

behavioral,
pharmacokinetic
neuronal

Front 44

Neuronal tolerance is due to

Back 44

Up-regulation of the cAMP
pathways
! Opiates, cocaine, amphetamine, and ethanol
Up-regulation of CREB
! Regulation of GABAergic and Glutaminergic transmission
! Dynorphin provide negative feedback

Front 45

Mechanismsthatevolvedtomotivatesurvival behaviors, the pursuit of natural rewards, are usurped by the potent and abnormal dopamine signal produced by addictive drugs.
! The result is

Back 45

abrain inwhich drug cues powerfully activate drug seeking, and in which attempts to suppress drug seeking result in intense craving.

Front 46

Thismodeldoesnot,however,reduceaddicted individuals to zombies who are permanently controlled by external cues.

Back 46

Perhapsinadrug-freecontext,perhapswitha good measure of initial coercion, perhaps with family, friends, and caregivers acting as external "prostheses" to strengthen and partially replace damaged frontal mechanisms of cognitive control, and often despite multiple relapses, addicts can cease drug use and regain a good measure of control over their drug taking.