Rangsang Nyeri

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Rangsang Nyeri PSIK Block 1.3 Year 2009 Andreanyta Meliala, Dr.,Ph.D Dept. of Physiology (Med.F-GMU)

Transcript of Rangsang Nyeri

Rangsang Nyeri

PSIK Block 1.3 Year 2009

Andreanyta Meliala, Dr.,Ph.D

Dept. of Physiology (Med.F-GMU)

Nyeri….Terjadi oleh karena gangguan keseimbanganeksitasi dan inhibisi

Eksitasi Inhibisi

Low intensity stimulus

High intensitystimulus

Lowthreshold

A betafibre

High thresholdA deltaand Cnociceptor

PNSCNS

Cortex

Non-painful sensation PAINStubhaug, 2002

Modifikasi Meliala, 2003

HEAT

CHEMICAL

PRESSUREBRAINPANASPEGELPERIH

Modifikasi Meliala, 2003

Activation

External

Stimuli

Heat

Mechanical

Chemical

VR1

Ca2+

mDEG

P2X3

Generator potentials

action potentials

Voltage gated sodium channels

Pain and auto-sensitization

Woolf & Mitchel, 2001

TRANSDUCTION

ATP

Na+

Modifikasi Meliala, 2003

PAINPAIN

Pemeriksaan Neuromuskuloskeletal (5 menit)

OA, RA, Trigger OA, RA, Trigger fingerfinger

De QuervainDe Quervain

Tennis ElbowTennis Elbow

Frozen shoulderFrozen shoulderSindrom Sindrom servikalservikal

Low back Low back painpain

IschialgiaIschialgia

OA lututOA lututFasciitis Fasciitis plantarisplantaris

TendinitisTendinitis

Anger

Fear

Anxiety

Depression

Noxious Stimuli P

SY

CH

OL

OG

ICA

L

NOCICEPTIVE

A

B

MELIALA 2004

Glu

C-fiber terminal

GABA Badenosine

AMPAKAI

NMDA

K+

NK1mGluR TrkB

VGCC NSC GABA-A GLY

Inhibitory interneuron

Gly/GABAGABA B

Adenosine

NociceptiveDorsal horn neuron

Activation: AMPA/KAI receptor fast EPSPs

HIPERSENSITIFITAS : Sensitisasi Perifer (Modulasi)

Woolf & Mitchel, 2001Modifikasi Meliala, 2003

K+

K+K+

Glu

Ca2+

Glu SP

C-fiber terminal

GABA Badenosine

AMPAKAI

NMDA

K+

NK1mGluR TrkB

VGCC NSC GABA-A GLY

Inhibitory interneuron

Gly/GABAGABA B

Adenosine

Woolf & Mitchel, 2001Modifikasi Meliala, 2003

K+

K+K+

Glu

Ca2+

Ca2+

IP3

Ca2+ Na2+

Activation: Slow EPSPs, plateau potentials, summation & wind-up

HIPERSENSITIFITAS: Sensitisasi sentral

P2XNMDA

Ca2+

Ca2+

Ca2+ Na2+

Ca2+

Ca2+Ca2+

Mg2+

Beydoun, 2002

TERAPI BERDASAR MEKANISME

MedulaSpinalis

Sensitisasi perifer ion Na

PAINTPAINTBRAIN

InhibisiDescenden

NE/SHT

ReseptorOpoid

Modifikasi Meliala, 2003

Beydoun, 2002

TERAPI BERDASAR MEKANISME

MedulaSpinalis

Sensitisasi perifer ion Na

CBZOXCPHTMEXILETINLIDOCAINDLL

TX

CBZOXCPHTMEXILETINLIDOCAINDLL

PAINPAINBRAIN

InhibisiDescenden

NE/SHT

ReseptorOpoid

NO PAINNO PAIN

Modifikasi Meliala, 2003

Beydoun, 2002

TERAPI BERDASAR MEKANISME

MedulaSpinalis

Sensitisasi perifer ion Na

PAINPAINBRAIN

InhibisiDescenden

NE/SHT

ReseptorOpoid

NO PAINNO PAIN

SensitisasiSentral

(NMDA,Calcium)

TX

GBPOXCLTGKetaminDextroMetorphanDLL

GBPOXCLTGKetaminDextroMetorphanDLL

Modifikasi Meliala, 2003

Beydoun, 2002

TERAPI BERDASAR MEKANISME

MedulaSpinalis

Sensitisasi perifer ion Na

TCATramadolOpioidDLL

TX

TCATramadolOpioidDLL

PAINPAINBRAIN

InhibisiDescenden

NE/SHT

ReseptorOpoid

NO PAIN NO PAIN

Modifikasi Meliala, 2003

Disc

Nucleus

Annulus

PosteriorLongitudinalligament

Spinousprocess

Ligamentumflavum

JointCapsule

Spinal cord and sheath(Dura)Nerves

JARINGAN DENGAN SENSOR NYERI

Disc bulging

Osteophytes (trapping nerve)

JointCapsule

TITIK TEKAN DISEKITAR ARTIKULASIO SPINALIS

Longissimuscapitis

Spinalisthoracis

Longissimus

Keterangan : Otot pendek berfungsi sebagai stabilisator dan otot panjang untuk pergerakan

GAMBAR OTOT PUNGGUNG

Longissimuscervicis

Spinaliscervicis

Iliocostalislumborum

Iliocostalisthoracis

Multifidus

Intertransversarii

Iliocostaliscervicis

Penurunan fungsi oleh usia

Epesode akut dengan pengobatan yang baik

Pengobatan tidak adekuat menyebabkan NPB kronik

Pengobatan Nyeri yang baik memungkinkan rehabilitasi

Keku

ata

n/S

tabili

tas/

Fungsi

WaktuKeterangan :

2.3.

4.5.

Histamin

Sel Mast

DRG

Medulaspinalis

Pembuluhdarah

Lesi

1.

1.

BRAIN

Meliala, 2005

Mekanisme Proteksi Nyeri spasme otot

I

II-IV

III-IV

Ia

Joint receptor (nociceptor)

Joint dysfunctionor pain

Nociceptor

Muscle painA

B

Muscle spindle

-Motoaxon

-Motoaxon

Descending influencesCSpinothalamic

tract

I

Eperison

PAINNO PAIN

Diabetic foot ulcer in typical location

Medscape http://www.medscape.com

Semmes-Weinstein monofilament being used to

test sensation in a diabetic patient

Medscape http://www.medscape.com

Measuring temperature sensation thresholds using

the CASE IV quantitative sensory testing device.

Medscape http://www.medscape.com

Measuring vibratory sensation thresholds using the

CASE IV quantitative sensory testing device

Medscape http://www.medscape.com

Medscape http://www.medscape.com

Polyneuropathy is caused by the degeneration of axon terminals and results in symmetric distal sensory loss with shading to normal sensation. A compression neuropathy often results in demyelination with the axon left relatively intact. Sensory loss follows a radicular pattern. When the neuronal cell body dies the condition is called "neuronopathy." If the cell body is in the sensory ganglion the condition is often referred to as "ganglionopathy." The pattern is usually random

Axonal polyneuropathy Demyelinating Neuropathy Neuronopathy (Ganglionopathy)

• Pain in a patient with no pre-existing chronic painful condition

• Pain in patient with a chronic painful condition, not related to the pre-existing problem.

• Pain due to an exacerbation of a chronic painful condition.

TYPES OF ACUTE PAINTYPES OF ACUTE PAIN

CLASSIFICATION OF PAIN

PAIN TYPEPAIN RECEPTORS

INVOLVED

STATUS OF NERVOUS SYSTEM

SYMPTOMS

Somatic

Visceral

Peripheral nociceptive and somatic sensory efferent nerves

Visceral nociceptive and efferent nerves

Undamaged

Undamaged

Ussualy well localized

Poorly localized,deep aching,

cramping

Nociceptive

Neuropathic NoneDamaged due to injury or disease

Burning sensation

PAIN MANAGMENTNoninvasive• Physical

– Physical therapy– Occupational therapy– Activity modification– Brancing

• Cognitive-behavioural– Relaxation therapy– Psychological/psychiatric management

• Pharmacological

Invasive• Blocks

– Diagnostic– Therapeutic– Implanted devices– Medication pumps– Spinal-cord stimulators

• Surgery

ANALGESIC MEDICATIONSPRIMARY ANALGESICS• Acetminophen• Prostaglandin synthesis inhibitors

– Salicylates– Traditonal NSAIDs– COX-2-selective NSAIDs (coxibs)

• Tramadol• Opioids

– Traditional– Mixed

ADJUVANT MEDICATIONS• Antidepressants• Anticonvulsants• Local anesthetics• Miscellaneous agents

PERCEPTION

MODULATION

TRANSMISSION

TRANSDUCTION

PAIN – SERIES OF EVENTS

PAIN

V. PRINCIPLES OF PAIN MANAGEMENT WITH ANALGESICS

See text

Andreanyta Meliala, Dewanto Husodo, Benaia Decitta Husodo, Jedidia Suksmatatya Husodo

Picture taken: May, 2007