obat antinyeri, 2010 [compatibility mode]

8/18/2019 OBAT ANTINYERI, 2010 [Compatibility Mode]

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O

Fakultas Kedokteran

Farmakologi

AT ANTI NYERIFathiyah Safithri

Laboratorium Farmakologi

niversitas Muhammadiyah Malang

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DEFINISI NYERI

= Pengalaman sensorik dmenyenangkan akibat

aktual maupun potensia

dalam bentuk kerusaka

MEKANISME PRMEKANISME PR

(berfungsi melindungi &

n emosional yang tidakerusakan jaringan, baik

l, atau yang digambarkan

tersebut

TEKSI TUBUHTEKSI TUBUH

memberi tanda bahaya)




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JENIS

Menurut Sumber Nyeri : NYERI NOSISEPTIF / NYE

- adanya kerusakan / inflamasi janyeri

NYERI NEUROPATIK

- berhub dg lesi sist syaraf perifer- mis. Neuropatik DM, kompresi s

NYERI NOSISEPTIF-NEUR

Menurut lamanya,☻ AKUT

- terjadi segera setelah trauma, o

☻ KRONIK- terjadi kontinu (minimal 3 bulan)

NYERI

I INFLAMASI

ingan ujung saraf menerima rangsang

/ sentral

rabut saraf, neuroma

OPATIK

erasi, atau lesi saraf




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PROSES TIMB

STIMUL

KERUSAKA

MEDIATO

(HISTAMIN, PG, BRADIKININ,

RESEPTO

SARAF SE

MEDULA S

THALAMUS /

Transmisi

Modulasi

Persepsi

Transduksi

LNYA NYERI

US

JARINGAN

NYERI

LEOKOTRIEN, SEROTONIN DLL)

NYERI (nociceptor)

SORIS

INAL

ORTEKS PUSAT NYERI




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TRANSDUKSI




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JALUR TRA Smisi NYERI




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FAST & SLOW P IN PATHWAY




8/88

JALUR TRANSMISI N YERI


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Stimuli : panas, bhn kimia, mekanikTujuan tubuh menimbulkan reaks

1. Menetralkan dan menghancurkan bberbahaya

2. Mencegah penyebaran bahan berba3. Memperbaiki kondisi yang rusak

Proses yang terjadi :

kerusakan mikrovaskular

peningkt permeabilitas kapiler

migrasi lekosit ke jar radang.

Mediator kimiawi yang dilepas se

histamin, 5 HT, bradikinin,PAF, sP, tromboksan, proton, radikal bleukotrien, prostaglandin

INFLAMASI / R

i radang :

han

aya

cara lokal

ubstancebas,

DANG

Tanda radang

cardinal signs :

rubor

calor

tumor,

dolor

functiolaesa




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Suhu tubuh diatur oleh keseimba

oleh hipotalamus (normal termos

termoreg

Demam : Ada gangguan keseim

pelepasan zat pirogen (sitokin

hipotalamus)

DEMAM /

ngan produksi dan hilangnya panas

at mengatur pd setpoint 37o C )

lator

angan pengaturan panas akibat

IL-1 , memicu peningkatan PG di

PANAS




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FEBRIS




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Terapi NY

A. TERAPI FARMAKO

1. Menghambat me(transduksi): analgesik non nark

NSAID

Anti inflamasi steroi

2. Menghambat tran anestesi lokal

3. Blokade pusat nye Analgesik narkot ik

Anestesi umum

B. TERAPI NON FAR

RI

LOGI

iator nyeri

tik

misi nyeri

ri di SSP (Persepsi)

AKOLOGI




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(Golanet al., 2008)




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TerapiTerapi





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Terapi Nyeri Non-farm

Cognitive-Behavioral

• Relaxation

• Preparatory information

• Hypnosis

Physical Agents

• Application of superficial hea

• Massage

• Exercise

• Immobilization

• Electroanalgesia (eg, TENS=

stimulation )

• Acupuncture

Carr DB, et al. AHCPR Pub. No. 92-0032. 1992.

akologik

t and cold

ranscutaneous electrical nerve


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22/88

0 1 2 3 4Mild Mod

Pain threshold

Pain tolerance

Pain RatiPain Rati

6 7 8 9 10rate Severe

g Scalesg Scales


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Choosing pain killerChoosing pain killer

10 Pain Intensity Scale

0 1 2 3 4

Mild Mo

paracetamol

or/+

NSAIDNSAID

±adjuvant

analgesic

NN

wea

adj

ana

and its combinations and its combinations

5 6 7 8 9 10

erate Severe

Strong opioid

±

NSAID

±adjuvant

analgesic

AID AID

±

opioid

±vant

lgesic




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Current view in selecti

inflammatory drugs

Efficacy (indication) Safety (side effect)

Not only GI toxicity Cardiovascular toxi Renal toxicity Bleeding Bone healing impai

Suitability (contra-indic

Availability Pharmacokinetics and Daily cost Evidence based medici

g analgesic and anti-

ity

ment etction)

rug interaction

e




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ANAL ESIK NON OPIOID




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Analgesic Non Opi

– Acetaminophen

– NSAID

• Non selective CO

–Salicylic acid (a

–Asetic acid (inddiclofenac)

–Propionic acid (

–Anthranic acid (

–Enolic acid (pir • Selective COX – 2

–Rofecoxib

–Celecoxib

–Etedolac

id Drugs

inhibitor

pirin)

methacine, ketorolac,

etoprofen)

efenamat)

xicam) Inhibitor


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Analgesik Non-o

Acetaminoph

Mekanisme kerja hamb sintesa

hipotalamus,

Efek samping Hepatotoksik

Sisson CB. In: Benzon HT, et al, eds. Essentials of

1999:59–62.

pioid

n Tramadol

G sintetik weak -opioid

inhibisi re-uptake

norepinephrine dan

serotonin (5-HT3)

Opioid-like effects

Pain Medicine and Regional Anesthesia;




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Acetaminophen

A c eto m in o p h e A c eto m in o p h e A c eto m in o p h e

A c A c --g l u c u r o n i d eg l u c u r o n i d e A c A c

React i veReact i ve elel

c o m p o uc o m p o u

GSHGSH

G SG S -- A c * A c *

A c A c --m ercap tu ra tm ercap tu ra te

Good

Metabo l i smMetabo l i smMetabo l i sm

A c A c -- su l f a tesu l f a te

y t o c h r o m ey t o c h r o m e PP --450450

c t roph i l i cc t roph i l i c

d (Ac* )d (Ac *)

A c * A c * --p ro te inp ro te in

Hepat ic c e l l d eathHepat ic c e l l d eath

Bad




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(NON STEROID NSAID L ANTI INFLAMMATORY DRUG)




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PGD2inhibits platelet

aggregation,

vasodilator

PGE2vasodilator,

hyperalgesia

Pbronch

myom

hyp

PGI2inhibits platelet

aggregation,

vasodilator ,

hyperalgesia

Tstimula

aggr

vasoc

cyclicendoperoxides

phosp

arachid

COXCOX-1COX-2

F2alfaconstriction

etrial contr.

ralgesia

A2es platelet

gation,

nstriction

5-HPETE

LTA4

LTB4chemotaxis

LTC4

LTD4

LTE4

brochoconstriction

increase

vascular

permeability

olipids

nic acid

LOX




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10/02/2010 Ngatidjan, NS AIDs - GOUT 32

(Nijkamp et al., 2

zafirlukast

montelukast

zilueton




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NSAID

Effects :

Analgesics

Antiiflammation (most) Antipyretics (most)

Uricosuria (some)




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NS

Mekanisme kerja :Menghambat sintesa PG m

COX 1 dan atau COX 2

– NSAID konvensional men

– Inhibisi COX-1

gastroto – Obat baru hanya mengha

Efek : secara umum = anal

Dosis antipiretik >>> dosis

Efek terapi atau efek sampi

penghambatan biosintesis

synthetase menurunkan infl

mengurangi nyeri.

ID

lalui penghambatan enzim

hambat COX-1 dan COX-2

sik,

agregasi plateletbat COX-2 pada dosis terapi

etik, antiinflamasi, antipiretik

nalgetik, antiinflamasi

ng NSAID tergantung pada

rostaglandin. Inhibisi PG

amasi dan selanjutnya




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PROSTAGLANDIN

Merup autakoid, terdapat diaktivitas yg bervariasi

Fungsi :

– Inflamasi sebagai mediat

– Homeostatic COX 1, terd

mucosa bronkus dan ginjal

(PG)

semua jaringan dg spektrum

r COX 2

pat di lambung, usus, platelet,




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10/02/2010 Ngatidjan, NS

COX1-thrombocyte

•TX-A2synthesis(stimulate thrombocyte aggregation)

• COX1 can not be synthesized instantly

C

(cyclooxyg

ASA

low dose acetosaleffectively inhibit COX1 thrombocyte

thrombocyte aggregation

ASA

AIDs - GOUT 37

blocks

COX1-endothel

- prostacyclin synthesis

inhibit thrombocyte aggregation

(antithrombotic properties)

- new COX-1 can be synthesized

1

enase-1)

low dose acetosalineffective in COX1 endothel inhibition

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Summary of analgesic anti inflammatory and



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Summary of analgesic, anti-inf

antipyretic activity of NSAIDs (

0

10

20

30

40

50

60

anti

ketorolac ind

naproxen ibu

0

20

40

60

80

100

120

analgesic

ketorolac indomethacin diclofenac

naproxen ibuprofen piroxicam

NSAID Analgesic

ketorolac 0.7

indomethacin 3

diclofenac 8

naproxen 13

ibuprofen 45

piroxicam 100

tenoxicam 100

aspirin 228

lammatory and

ED50 in mg/kg)

inflammatory

omethacin diclofenac

profen piroxicam

0

1

2

3

4

5

6

7

8

antipyretic

ketorolac indomethacin diclofenac

naproxen ibuprofen piroxicam

Anti -inflammatory Antipyretic

2 0.9

4 2.1

7 0.4

56 0.5

10 7

3 1.7

5 1.7

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Ibup

Keto

Acetosal

Ketorolac

Indomethacin

Piroxicam

nsele

Cinhi

COX-1selectiveinhibitor

preferentially

COX-1

selectiveinhibitor

analgesic

ant

More GI side effects

ofen

rofen

Diclofenac

Meloxicam

Nimesulide

Celecoxib

Rofecoxib

Valdecoxib

n-tive

Xitor

preferentially

COX-2

selectiveinhibitor

COX-2selectiveinhibitor

COXIB

-inflammatory

Less GI side effects




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41/88




42/88

(Finkel et al., 2009)




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NALGETIK OPIOID




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• “opioid” is a natural orsynthetic drug that binds

to opioid receptors

producing agonist effects

• RESEPTOR OPIOID : Mu

( ), Kappa ( ) & Delta ( )

• Resept delta : regulasi

aktifitas resept Mu

• Sangat efektif

• Efek samping sering

D

esponse Mu-1 Mu-2 Kappa

nalgesia

espiratory

epression

Euphoria

ysphoria

ecrease GI

motility

Physical

ependenc

e




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Aktivasi Reseptor Opioidmenyebabkan :

- Me konduktansi ion K

- Hiperpolarisasi

- Aksi potensial

terhambat

- Release

neurotransmitterterhambat




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Efek Farmakologis Anal

• Sedation and anxiolysis – Drowsiness and lethargy

– Apathy

– Cognitive impairment

– Sense of tranquility

• Depression of respiration – Main cause of death from

– Combination of opioids adangerous

• Cough suppression

– Opioids suppress the “co• Pupillary constriction

– pupillary constriction in thcharacteristic of opioid us

etik Opioid

opioid overdose

d alcohol is especially

gh center” in the brain

e presence of analgesics ise




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Efek Farmakologis Anal

• Nausea and vomiting – Stimulation of receptors i

the chemoreceptor triggevomiting

– Unpleasant side effect, b

• Gastrointestinal symptom – Opioids relieve diarrhea

on the intestines

• Urine Retention

• Other effects

– Opioids can release histasevere allergic reactions i

– Opioids can affect whitefunction

getik Opioid

an area of the medulla calledzone causes nausea and

t not life threatening

(constipation) s a result of their direct actions

mines causing itching or morencluding bronchoconstriction

lood cell function and immune


O



49/88

Analgetik Opioid

• Indicated for musculoskeletal pain :

- Severe injury

- Oncogenic pain

- Pain that is not alleviated by NSAIDs

• Contraindicated for :

- Patients with respiratory problems

• Chronis usage of the drugs may caus

- Tolerancedecrease of the effect

- Addiction need to a compulsive u

- Dependency(physically or psycholo

r other analgesics

:

e

gically)




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Multimodal Analge

Kehlet H, Dahl JB. Anesth Analg. 1993;

MorfinMorfin

NSAIDs,acetaminophen,

blok saraf

NSAIDs,acetaminophen,

blok saraf

PotensiasPotensias

ia

7:1048–1056.

• Pengurangan dosistiap analgesik

• Meningkatkanantinociception karenaefek sinergistik

• Mengurangi efeksamping tiap obat

ii




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AN LGETIK ADJUVANt




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= Obat yang dikombinasikan popioid / opioid) untuk me

menyeimbangkan efek & ef

- Sering dipakai untuk terapi n

Yang termasuk adjuvant :

Kortikosteroid

Neuroleptik

Benzodiazepin

Antidepressan (TCA : amitri

desipramin, nortryptilin )

Antikonvulsan (karbamazep

valproate, Gabapentin)

Klonidin

da obat analgetik utama (nonfek analgetik,

k samping

eri neuropatik

tilin, doxepin, imipramin,

n, Phenitoin, Sodium




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OBAT A ESTESI LOKAL


OBAT LOKAL ANE TESI



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OBAT LOKAL ANE

• Obat Lokal Anestesi- - - > obat yg m e ja lu r sar af pusat m aupun per if er sec

• Dibedakan 2 golongan :1. Amida(Bupivacaine, Nuper c aine, Et id

Mepivacaine, Prilocaine, Ropivacaine

2. Ester(Chlor opr ocaine, Coc aine, Pr o

TESI

yebabkan blokade konduksi im puls di sepanjangr a r ever sibel setelah anest esi r egional

oc aine, Lidoc aine,

)

aine, Tet r acaine)


Mekanisme kerja obat ane tesi lokal



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Mekanisme kerja obat ane

• Obat lokal anes t es i m encegah pr oses dmemblok aliran ion Na ham bat an t

• Kualit as ham bat an t er jadi set elah pem

ka rakte r i st i k oba t yai t u po tens i (d it entuko leh pKa ) dan dur as i (d it entukan o leh i ka

penambahan vasokonstr ikor (epinephr in)memperpanjang efek durasi

lokasi penyuntikan

kecepatan penyuntikan

posisi dan kondisi pasien

tesi lokal

polar isasi mem br an sar af denganansm isi im puls sar af (blokade konduksi)

er ian sangat ter gantung pada :

an oleh kelarut an dalam lemak); onset (di tentukanan pr otein), volume konsentr asi yang dipakai

: memperlambat penyerapan dananestesi 60%.




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C P tik



57/88

Cara Penyuntikan

• Infi ltrasi anestesi :

Penyuntikan lokal ane

dianestesi.

• Blok anestesi:Menyuntikkan lokal an

yg jaraknya jauh dari lo

tesi ke lokasi yg akan

stesi di sekitar saraf utama

kasi yg akan dianestesi.


K it i id l b t t i l k l



58/88

Kriteria ideal obat a

1. Ons et c epat

2. Dur asi panjang

3 . Dapat dit i t r asi

4. Toksisit as r endah5 . Tem pat ker ja ter lokal is ir

6 . Khusus menghambat nyer

t idak ber efek pada fungs

7. Dos is r elat if kec il8 . Efek s amping m inimal

9 . Rever sibel

estesi lokal

i,

i motor ik


OBAT ANESTESI L KAL



59/88

OBAT ANESTESI L

OBAT

Prokain

Lidokain

MepivacainePrilokain

Bupivakain

Ropivakain (Naropin)

(Levobupivakain) Chirokain

KAL

% DURASI MAX

2-4%

1-2%

1-2%1-2%

0,5%

,5-7,5%

1½ jam

1-2 jam

1-2 jam1-2 jam

5-7 jam

6-8 jam

1000 mg

500 mg

500 mg500mg

200 mg


LIDOK

IN



60/88

Mekanisme Kerja :

cegah transmisi impuls saraf at

hambat lintasan ion sodium me

saraf

Farmakokinetik :

• Absorbsi & distribusi dipengaruepinephrine dan sifat farmakol

• Faktor terkait : usia, status ka

• Eliminasi metabolisme hepa

LIDOK

au blokade konduksi mel

lalui kanal Na di membran

hi tempat injeksi, dosis,gi.

diovaskuler dan fungsi hepar.

IN




61/88

NESTESI UMUM


GENERAL ANAEST ETICS



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GENERAL ANAEST

THE FIRST GENERAL ANAESTHETICS

• Nitrous oxide, 1880,Laughing gas

• Ether, 1846, explosive

• Chloroform, 1847,Toxic to the liver

ETICS

THEORIES OF ANAESTHETIC ACTION

• LIPID THEORY– Anaestheticsdissolve in lipid part of cellmembranes and depressmembrane activity

• PROTEIN THEORY– Anaestheticsbind to hydrophobic protein sitein membranes and depressactivity

• Depression of transmitter release

rather than nerve conduction.Not via receptors

• We don’t really know how they


FOUR STAGES OF ANAESTHESIA



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1. Analgesia2. Delirium

– loss of consciousness,

– delirious excitement

– reflex activity

3. Surgical anaesthesia

– deep unconsciousnes

– respiratory depression – muscle relaxation

4. Medullary paralysis

– respiratory & cardiova

FOUR STAGES OF A

,

cular, depression, death

NAESTHESIA




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ADVERSE EFFECTS

• Respiratory & cardiac depre• Sensitisation of heart to cat

• Malignant hyperthermia

• Aspiration of gastric conten

• Hepatotoxicity• Renal toxicity

sion cholamines

s – use endotracheal tube




65/88

ADJUNCTS TO ANAESTHE

(Preanaesthetic medications)• Benzodiazepines/ Barbitur

– Reduce anxiety & produce• Opioids

– Analgesia,– Depression of cough

• Anticholinergic drugs– Decrease risk of bradyca

• Neuromuscular blocking age

– Paralysis

IA

tes sedation

dia ts


ANESTESI INHAL SI



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ANESTESI INHAL SI

• Enflurane ( Ethrane ).• Halothan ( Fluothane )

• Isoflurane (Forane ).

• Desflurane.

• Sevoflurane.




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OBAT ANTI GOUT


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(Finkel et al., 2009)


Drugs used i Gout and



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Hyperuri

• Allopurinol : prevents orUric acid is formed by pur

enzyme xanthine oxidase.

formation by inhibiting xa

• Colchicine : used to treatgout. Drug of choice for a

inflammation by affecting

• Probenecid : increases

Not effective in acute atta

• Sulfinpyrazone : uricosu

for acute attacks.

emia

reats hyperuricemia ne metabolism and an

Allopurinol prevents

thine oxidase.

or prevent acute attacks ofute attacks. Decreases

eukocytes.

rinary excretion of uric acid.

ks.

ic similar to Probenecid. Not


Guidelines for reating Gout



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Guidelines for

• in accute attack – analgesic NSAIDs – uricosuric agent

– colchicin

– glucocorticoids (if nec

• Maintenance drugs are Allop

Sulfinpyrazone

• Colchicine needed for severawhile serum levels are being

• Need high fluid intake, alkali

reating Gout

ssary)

rinol, Probenecid, and

l weeks to prevent acute attacksowered

e urine to prevent renal calculi




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Migraine



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Migraine

• Migraine: a neurological disof headache, photophobia,

• 3 times more common in wo

• Up to 28 million people in th

ease characterized by attackshonophobia, and nausea.

men than men

US are affected


The 4 phases of a igraine



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The 4 phases of a

• Prodrome

– Occurs hours to days beforemigraine without headache

• Aura

– Neurological phenomena such

disturbance of vision just beforheadache

• Pain phase

– Headache on one side of headwith nausea, photophobia and

other classic migraine sympto• Postdrome

– Exhaustion, irritability, depress

igraine

as

s

ion


C ausesof M igraine



75/88

C auses of M igraine

• Increased excitability of CNS

• Meningeal blood vessel dilatio

• Activation of perivascular sen

nerves

• Pain impulses• Vasoactive neuropeptides con

– substance P

– calcitonin gene-related pe

– neurokinin A

• combination of increased pain

tissue and vessel swelling, an

n

ory trigeminal

ain:

tide (CGRP)

sensitivity,

inflammation




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Evidence for vascularcause:

1. During the aura phase,there is a decrease incerebral blood flow(indicating that ischaemiamaybe causing the aura)

2. During a throbbingheadache, there iscerebral vascular dilation(the stretch of the vesselstriggers nerve endingsaround the vessels)

3. Headache can be triggeredby vasodilators (e.g.. GTN)and reversed byvasoconstrictions

1. Pain sensitive trigeminalnerves innervate cerebralvessels

2. Trigeminal nerves release

a peptide CGRP (calciumgene related peptide)3. CGRP is elevated during a

migraine4. Sumatriptan inhibits the

release of CGRP (also actsas a 5HT1D agonist)

Evidence for neuralcauses :


Pathophysiol gy:Triggers



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Pathophysiol

Trig

EmotionalPhysical

Vasoconstriction

Release of NE

Locus CerulusSympathetic System

Vasocon

stimluation of 5-

gy:Triggers

ers

Chemical

Dorsal Raphe

Release of 5-HT

striction

HT 2B or 5Ht 7

Nausea & vomiting

stimulates chemo center




78/88


A t T t t D Th



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Acute Treatment: D

• Analgesics/combin• NSAIDs

• Opioids

• Neuroleptics/antie

• Migraine specific

– Triptans

– Ergotamines

ug Therapy

tion analgesics

etics


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P h l i Th



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Prophylaxis Therapy

• Anticonvulsants: topiKeppra, gabapentin• Tricyclics

– Amitriptylene, nortript

• Beta Blockers – Timolol, propranolol, n• Calcium channel bloc• ACE inhibitors

• SSRI’s• Atypicals

amate, valproate,

lene, trazodone

adolol

er – verapamil




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Severity Migrain



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lastseverity


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• Simple analgesics

• NSAIDs

• Isometheptene (Midrin, etc.)

• Metoclopramide (Reglan) maand enhance drug absorption

Moderately severe migraine

• NSAIDs

• Isometheptene

• Ergotamine, oral or intranasa

• Sumpatriptan (Imitrex), oral

• Zolmitriptan (Zomig), oral• Naratriptan (Amerge), oral

• Rizatriptan (Maxalt), oral

• DHE, intranasal

• With oral agents, metoclopra

be added to reduce nausea

l

r intranasal

ide may be added to reduceCreate PDF files without this message by purchasing novaPDF printer (http://www.novapdf.com)



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Severe migraine

• Ergotamine plus an antie

suppository• Sumatriptan, subcutaneo

oral

• Zolmitriptan, oral

• Naratriptan, oral• Rizatriptan, oral

• DHE, intramuscular or int

Extremely severe migrai

• Ketorolac (Toradol), 60

• DHE, intravenous, plus m

• Dopamine antagonist

• Opioids

etic, both administered by

s injection, intranasal or

anasal

e

g intramuscularly

toclopramide




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obat antinyeri, 2010 [compatibility mode]

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