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PAIN

PHYSIOLOGY
FIFTEEN APRILA FAJRIN
BAG FKK-FFUJ

Learning Object???

DeniBon
Nociceptor
Nerves types
Pain types
Allodynia vs Hyperalgesia
Pain pathway

Pain DeniBon?

An unpleasant sensory and emoBonal


experience associated with actual or
potenBal Bssue damage or described in
terms of such damage
(The InternaBonal AssociaBon for the Study of Pain/
IASP)

Why Pain is Important?


Pain protects humans by warning of
occurrence of biologically harmful
processes
Pain can interfere with daily
funcBoning of a person when it
prevents people from performing their
social roles,
vocaBonal roles, and
impacts their psychological well-being.

Noxious
SBmulus?
Pain causing
Chemical
Mechanical
Thermal
Heat (>42 oC)
Cold (<10 oC)

Nociceptor
Pain detecBng
Found throughout the body
NOCICEPTION the detecBon of Bssue damage by
specialised transducers a^ached to nociceptor (A delta and C
bres)

stances, which are produced or released when there is


cellular damage (Table 1). These mediators influence the
degree of nerve activity and, hence, the intensity of the
pain sensation. Repeated stimulation typically causes
sensitization of peripheral nerve fibers, causing lower Nociceptors are unspecialized, free, unmyelinated nerve endings that
ing of pain thresholds and spontaneous pain, a mechaconvert (transduce) a variety of sBmuli into nerve impulses, which the
nism that can be experienced as cutaneous hypersensibrain interprets to produce the sensaBon of pain.
tivity, e.g., in skin areas with sunburn.

Nociceptor

Dierent types of nociceptors have been idenBed that respond to


dierent causes
Released by
A-delta dan C
tissue damage:
Skin

Bradykinin
K+
Prostaglandins

C fibers
Injury

Histamine

A fibers

To spinal cord

Mast
Cell

Fig. 1. Some chemicals released by tissue damage that stimulates


nociceptors. In addition release of substance-P, along with histamine, produce vasodilation and swelling.

patien
b)
wheth
shoul
not b
neuro
c)
lus th
increa
patien
bation
centra
d)
tion,
neous

sitiza
act sp
can b

Cen

The s

Aerent
(sensory)
A Beta sensory,
large diameter with
myelin (30-50 m/s
Fastest)
A Delta pain
bers, smaller with
less myelin (5-25
m/s)

C pain, smallest,
non myelinated (<2
m/s), slow pain

Nerve Types

Eerent
(motory)
Gamma motor
neuron

A
beta

A
delta

CNS
Note: First pain is from
A delta (faster), second
pain is C

Allodynia vs Hyperalgesia
Allodynia pain due to a sBmulus that does not
normally provoke pain
Hyperalgesia An increased response to a sBmulus
that is normally painful.

Intensity
The intensity of pain oers perhaps the least
desirable system for classifying pain, because
intensity varies for most paBents over Bme and is
uniquely subjecBve.
A paBent might rate the experience of pain
resulBng from some pathologic condiBon as a 10,
whereas another paBent with the same pathology
might describe the intensity of pain only as a 5,
both using a 0 to 10 scale (with 0 signifying no
pain at all and 10 represenBng the worse pain
imaginable)

Pain CHART

Remember???
Cell body (in ganglion)
nucleus
Body
Dendrites

Synapse

axon

Dendrite

Chronic
Acute

PAIN

Acute and Chronic Pain


CharacterisBc
Karakteris)k

Nyeri akut

Nyeri kronik

Lama

Singkat (maksimal 1 Hingga 6 bulan/>


bulan)

Peredaan nyeri

Sangat diinginkan

Sangat diinginkan

Ketergantungan
thd obat

Tidak biasa

sering

Komponen
psikologis

Umumnya Bdak
ada

Sering merupakan
masalah utama

Kontribusi
lingkungan dan
keluarga

Kecil

signikan

Insomnia

Jarang

sering

Tujuan pengobatan Kesembuhan

fungsionalisasi

Acute vs Chronic Pain???


First pain: carried in A-delta bers, larger diameter
bers contain myelin, reex to get o source, goes
to cogniBve level (more discrete - very localized)
Second Pain: carried in C bers, smaller diameter,
non myelinated, slower. (less discrete - more
diuse)
Acute A-delta and C bers
Chronic C bers

Inammatory
NocicepBve

PAIN
NeurophaBc

NocicepBve Pain

ossibility of Mechanism-Specific Pharmacologic Management of Pain

ary types of pain.

This nocicepBve pain system is a key early warning device,


an alarm system that announces the presence of a
potenBally damaging sBmulus.

Inammatory Pain

In this state, sensiBvity is increased such that sBmuli to the


aected part that would normally not cause pain now do so.
As a result, we prevent contact with or movement of the injured
part unBl repair is complete, minimizing further damage.
Inammatory pain typically decreases as the damage and
inammatory response resolve

Neuropathic Pain

Neuropathic pain may result from lesions to the peripheral


nervous system, as in paBents with diabeBc or AIDS
polyneuropathy, post-herpeBc neuralgia, or lumbar
radiculopathy, or to the central nervous system, such as in
paBents with spinal cord injury, mulBple sclerosis, or stroke

General Mechanism of Pain


NOCICEPTION
TransducBon
Transmission
ModulaBon
PercepBon

NocicepBon-TransducBon
- the conversion of a
noxious sBmulus into
electrical acBvity in the
peripheral terminals of
nociceptor sensory
bers.
- Mediated by specic
receptor ion channels
expressed only by
nociceptors
- Noxious sBmulus
converted into Ca2+
mediated electrical
depolarizaBon

eurons to pain.

Nociceptor AcBvators

Nociceptor AcBvators

TRP transient receptor potential

NocicepBon-Transmission
- The passage of acBon
potenBals from the
peripheral terminal
along axons to the
central terminal of
nociceptors in the
central nervous system
- The synapBc transfer
- Release of
neurotransmi^er-
induced pain
Glutamate, substance P

NocicepBon-ModulaBon
Balancing between exitatory
mediators and the inhibitory
eect of endogenous
analgesics
Adjust K inux and Na eux
Endogenous analgesics,
including enkephalin (ENK),
norepinephrine (NE), and -
aminobutyric acid (GABA),
acBvate opioid, alpha
adrenergic, and other
receptors that either inhibit
release of Glu

NocicepBon-PercepBon

the conversion of a noxious thermal,


mechanical, or chemical sBmulus
into electrical acBvity in the
peripheral terminals of nociceptor
sensory bers

A-delta ber
C ber
Spinal cord

Brain

Response aduhhh
tarik tangan

Drug
target
for
Pain

-To be continued guys-

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