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PAIN

MANAGEMENT
Oleh:
Ema Pristi Yunita,
M.Farm.Klin., Apt.

DEFINITION
Pain is an unpleasant
sensation that can negatively
affect all areas of a person's
life, including comfort,
thought, sleep, emotion, and
normal daily activity
Pain is defined by the
International Association for
the Study of Pain (IASP) as an
unpleasant sensory &
emotional experience
associated with actual or
potential tissue damage or
described in terms of such
damage

TYPES OF PAIN
The IASP classification system describes pain
according to five categories: (1) duration and
severity, (2) anatomical location, (3) body
system involved, (4) cause, and (5) temporal
characteristics (intermittent, constant, etc.)
Duration and severity :
1. Acute pain
2. Chronic Pain
a. Inflammatory pain
b. Neuropathic pain

PAIN PATHWAYS
Specialized receptors = free nerve
endings
Stimulation
Mechanical damage
Extreme temperature
Chemical irritation

Two types of neurons


A-delta fibers: first pain, sharp
C-fibers: second pain, dull

Four distinct processes


Transduction, transmission, modulation,
perception

Transduction
Process by which noxious stimuli are translated into
electrical signals at peripheral receptor sites. This
begins when nociceptors (free nerve endings located
throughout the skin, muscle, and viscera) are exposed
to a sufficient quantity of mechanical, chemical, or
thermal noxious stimuli.
In addition, a variety of chemical compounds (e.g.,
histamine, bradykinin, serotonin, prostaglandins and
substance P) are released serially from damaged
tissues and can activate or sensitize nociceptors.
Serotonin has the additional action of modulating the
peripheral release of primary afferent neuropeptides
that are responsible for neurogenic inflammation.
These neuropeptides include substance P, calcitonin
gene-related peptide, and neurokinin A.

Transmission

Transmission continued ...


Transmission involves the propagation of an electrical
signal along neural membranes.
Stimuli, such as prostaglandins and inflammatory
mediators, change the permeability of the membrane,
producing an influx of sodium and an efflux of potassium,
thereby depolarizing neuronal membranes. Electrical
impulses are transmitted to the spinal cord via two
primary afferent nerve types: myelinated A-fibers and
unmyelinated C-fibers.
The A-delta fiber is responsible for rapidly conducting
electrical impulses associated with thermal and
mechanical stimuli to the dorsal horn of the spinal cord.
A-delta fibers release excitatory amino acids, such as
glutamate, which activate AMPA (-amino-3-hydroxy-5methylisoxazole-4-propionic acid ) receptors located on
dorsal horn neurons.
Transmission of signals along these fibers results in sharp
or stabbing sensations that alert the subject to an injury or

Modulation
Modulation of nociceptive information occurs
quickly between descending inhibitory
pathways from the thalamus and brainstem
and interneurons in the dorsal horn.
Neurons from the thalamus and brainstem
release inhibitory neurotransmitters, such as
norepinephrine, serotonin, -aminobutyric
acid (GABA), glycine, endorphins, and
enkephalins, which block substance P and
other excitatory neurotransmitter activity on
primary afferent fibers.

Perception
The conscious awareness, or perception, of pain is
the end result of this complex cascade of actions.
The perception of pain involves not only
nociceptive processes, but also physiologic and
emotional responses, which contribute
significantly to the sensation that is ultimately
experienced by the person. The perception of pain
may be influenced by abnormal generation or
processing of electrical pain signals and by the
psychological framework created by the patient's
temporal affective state or from previous painful
experiences.
Therefore, treatment that includes drug
therapy to alter the nociceptive and
physiologic responses, in addition to
cognitive-behavioral strategies (e.g.,
distraction, relaxation, and imagery) to
alter the psychological response, may be
more effective together than if either

Tissue Damage
Release of chemical substances and
enzymes (mediators) that alter the
activity and sensitivity of sensory
neurons
Prostaglandins, leukotriens: sensitization of
receptors
Bradykinin and PGs: stimulate the neurons
directly
Histamine: pain, itching

Result
Increase in nociceptor activity
Hyperalgesia
Neurogenic edema

calcitonin gene-related peptide (CGRP)

Injury
stimulates
peripheral
nociceptors,
which synapse in the
dorsal root ganglion to
send signals of pain to
the brain inflammatory
mediators are released
which again stimulate
the nociceptors, which in
turn release substance P
to create mast cell
degranulation
and
peripheral vasodilation

Dorsal Horn
Neurotransmittors
causing enhanced
excitability and
sensitization of dorsal
horn cells
Persistent changes
Cause of allodynia
(touch becomes pain)
Prevented by pretreatment with e.g
opioids

calcitonin gene-related peptide (CGRP)

Excitation of the nociceptors


in an organ then triggers
pain sensations in those
areas of the skin whose
afferents make connections
in the same spinal cord
segment (referred pain). In
myocardial infarction, for
example, pain radiates into
the left shoulder and left
arm (Heads zones)
Projected pain is produced
by stimulation of a nerve
(e.g., of the ulnar nerve in
the ulnar sulcus). The
perception of pain is
projected to the innervation
area of the nerve

Wong-Baker FACES Pain


Rating Scale

Explain to the person that each face is for a person who feels happy
because he has no pain (hurt) or sad because he has some or a lot of
pain. Face 0 is very happy because he doesnt hurt at all. Face 1 hurts
just a little bit. Face 2 hurts a little more. Face 3 hurts even more. Face 4
hurts a whole lot. Face 5 hurts as much as you can image, although you
dont have to be crying to feel this bad. Ask the person to choose the
face that best describes how he is feeling.
Rating scale is recommended for persons age 3 years and older.
Point to each face using the words to describe the pain intensity. Ask the
child to choose
face that best describes own pain and record the appropriate number.

010 Numeric Pain Rating


Scale

Visual Analog Scale

Verbal Pain Intensity Scale

Pharmacological
Treatment of Pain

Periphery-along axons-CNS
Single treatment/polymodal
Continuosly/intermittently
1.
2.
3.
4.
5.
6.

Regional anesthesia
NSAIDs
Opioids
NMDA-receptor antagonists
Alpha-2-receptor agonists
Other agents

1. Regional Anesthesia
Lidocaine (lignocaine): Xylocain
Bupivacaine: Marcain
Tricaine: MS-222
Preoperatively and postoperatively
Underuse in small species
Na+channels inhibitor

2. NSAIDs
Non-steroidal anti-inflammatory drugs
Reduce synthesis of PGs
COX inhibitors (cyclooxygenase)
Diminish nociceptor activation
Block peripheral sensitization
Antipyretic
Anti-hyperalgesic
No sedation

2. NSAIDs continued ...

Salicylates (aspirin)
Ketoprofen: Romefen
Carprofen: Rimadyl
PO, SC, IM
Gastrointestinal ulceration
and renal function disturbances,
embryotoxic, prolong bleeding

3. Opioids
Spinal cord
Decreasing neurotransmitter release
Blocking postsynaptic receptors
Activating inhibitory pathways

Receptor subtypes
mu > delta > kappa

Supraspinal analgesia
Peripheral analgesia (prevent
nociceptor sensitization)

3. Opioids continued ...

Morphine
Fentanyl: Leptanal, Hypnorm
Sufentanil
Burprenorphine: Temgesic
Sedation
PO, SC, IM, IP
Side effects:
respiratory depression, severe
bradycardia, decreased gastric HCl
secretion

4. NMDA-receptor
antagonists
(N-methyl-D-aspartate)
Spinal cord receptors
Repetitive C-fiber activation
Central hyperalgesia

Not effective against acute


inflammatory pain
Effective against prolonged
inflammatory pain
Neuropathic and cancer pain
Abolish the wind-up phenomenon
Work in synergy with opioids
Contoh: ketamine, tiletamine

5. Alpha-2-agonists

Xylaxine: Rompun
Medetomidine: Domitor
Receptors in the spinal cord and brain
Activated by descending noradrenergic pathways
Inhibit pre-synaptic calcium influx and
neurotransmitter release
IM, SC, IP, IV
Sedation, analgesia, muscle relaxation and anxiolysis
Side effects
Initial hypertension
Hypotension
Bradycardia
Decreased cardiac output
Depress insulin release
Diuresis
Hypothermia

6. Other agents
Sedatives and tranquillizers

Diazepam, acepromazine, fluanisone


Relieve anxiety, decrease stress
Minimal respiratory and cardiovascular effects
Hypotension, hypothermia
GABA (enhancement), dopamine (blockade)
Antagonist benzodiazepine (flumazenil) to
reserve sedative effects of BZD
SC, IM, IV

Tricyclic antidepressants
Amitryptilline
GABA: gamma-aminobutyric acid

Pain Management
Prevention: preemptive
approach
Recognition of pain
Choice of substance
Drug dose and duration

TUJUAN TERAPI
1. Menghilangkan nyeri
2. Menghambat perkembangan nyeri
akut menjadi nyeri kronik
3. Meningkatkan kualitas hidup
pasien

Non farmakologis
Cognitive behavioral therapy
(CBT)
Transcutaneous electrical nerve
stimulation (TENS)
Spinal cord stimulation (SCS)
Akupuntur dan pemijatan
Farmakologis

HOLISTIK

adjuvant

Nonopioid adjuvant

Pain

95
04
1

Weakopioid+nonopioid

W
H

Strongopioid+
nonopioid

adjuvant

This three-step approach of administering the right drug in


the right dose at the right time is inexpensive and 80-90%
effective
WHOhasdevelopedathreestep"ladder"forcancerpainrelief(1986)
WHONationalCancerControlprogram,PoliciesandManagerialGuidelines(2002)
The Joint Commission of Health Care Organizations Declaration of the present decade as the
decade of pain control and research (2001)

Efficacy

Time to peak
concentration
(h)

Analgesic
duration
(h)

Class

Agent

Paraaminophenol

Acetaminophen (Tylenol)

Good

0.5-2

3-6

NSAID

Salicylates
Asetylsalisylic acid (Aspirin)
Choline /Mg salicylate
(Arthropan)
Diflunisal (Dolobid)

Excellence

0.25-2
1.5-2

3-6
4

2-3

8-12

Fenamates
Mefenamic acid (Ponstan)
Meclofenamate (Meclomen)

Excellence
2-4
0.5-2

4-6
3-6

Pyranokarboxylic acid
Etodolac (Lodine)

Excellence

6-8

Acetic acid
Diklofenak Na/K
(Voltaren/Cataflam)

Excellence
1

6-8

Class

NSAID

Agent

Efficacy

Time to peak
concentration
(h)

Propionic acid
Ibuprofen (Motrin)
Fenoprofen (Nalfon)
Ketoprofen (Orudis)
Naproxen (Aleve)

Excellence

Pyrolizine carboxylate acid


Ketorolac (Toradol)

Excellence

COX 2 inhibitor
Rofecoxib (Vioxx)
Celecoxib (Celebrex)

Excellence

Analgesic
duration
(h)

1-2
1-2
0.5-2
2-4

4-6
4-6
4-6
4-8

0.5-1

2-3
3

up to 24
12-24

Class

Opioid

Agent

Efficacy

Morphine-like agonis
Morphine (MS Contin)
Hydromorphone (Dilaudid)
Levorphanol (Levo-dromoran)
Codein
Oxycodone (Oxy contin)

Excellence

Meperidine-like agonis
Meperidine (Demerol)
Fentanyl (Duragesic)

Excellence

Others
Tramadol (Tramal)

Excellence

Time to peak
concentration
(h)

Analgesic
duration
(h)

0.5-1
0.5-1
0.5-1
0.5-1
0.5-1

3-5
3-5
5-8
4-6
4-6

0.5-1
0.1-0.5

2-5
1-2

2-3

4-6

Analgesik non-opioid
Acetaminophen
Aspirin
Choline / Mg salicylate
Diflunisal
Mefenamic acid
Meclofenamate
Etodolac
Diklofenak Na/K
Ibuprofen
Fenoprofen
Ketoprofen
Naproksen
Ketorolac
Rofecoxib
Celecoxib

GI
Irritation

CNS
Effects

Hepatic
Toxicity

Renal
Toxicity

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++
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+
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++

Analgesik Opioid

Potency
(po)*

Sedation

Nausea
and
vomiting

Constipa
tion

Respiratory
Depression

Codeine
Dihydrocodeine
Tramadol
Pethidine (Meperidine)
Morphine
Diamorphine
Oxycodone
Phenazocine
Levorvanol
Hydromorphone
Buprenorphine
(sublingual)
Fentanyl (transdermal)

0.05
0.1
0.1
0.1
1.0
1.0
2
5
5
7.5
50

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++
+

150

Neuropathic Pain

Dosis
(mg/hari)

Frek/
Rute

Carbamazepin
Gabapentin
Lamotrigin
Pregabalin
Baclofen

100-1000
900-3600
150-500
5

bid to qid
tid
bid
bid

-Penghambat
neurotransmiter eksitatori
(asam amino glutamat)
-Menghambat voltage
gated cation channel

Antidepresan

Amitriptilin
Imipramin
Venlafaxine

10-200
10-200
37.5-340

qd
qd to bid
tid to bid

-5HT release
-Noradrenergic pathway

Anestetik

Lidocain

0.25-2

Continuous
iv

Anti aritmia

Mexiletine
Clonidin

50
50

bid
tid

Ketamin
Memantin

0.25-0.5

IV or IM

Kelompok
Antikonvulsan

NMDA
Antagonis

Analgesik

Mekanisme

-Sodium channel
blocking effect
-Local anestetic
-Noradrenergic pathway
-Menghambat sistem
eksitatori

- NMDA blocking

Recommended first-line
treatments for patients with
neuropathic pain

Algorithm for pain management in


oncology patients

Migrain dan
Headache Type
Tension

The International
Classification of
Headache Disorders

MIGRAIN

Sakit Kepala Migrain vs


Tegang Otot (tension
headache)

DEFINISI & KLASIFIKASI


MIGRAIN
Migrain = suatu kondisi kronis yang
ditandai oleh sakit kepala episodik
dengan intensitas sedang berat yang
berakhir dalam waktu 4 72 jam
(International Headache Society)
Migrain diklasifikasikan menjadi :
a) Migrain dengan aura (disebut
"classic" migraine) 20%
b) Migrain tanpa aura (disebut
"common" migraine) 80%
c) Status migrain yang tidak sembuh
sendiri, bertahan > 72 jam

GEJALA MIGRAIN
Bervariasi antar individu maupun antara kejadian
migrain pada individu
Ada lima gejala yang dapat diidentifikasi:
a) Prodrome: suatu rangkaian peringatan sebelum
terjadi serangan meliputi perubahan mood,
perubahan perasaan atau sensasi (bau atau rasa),
atau lelah dan ketegangan otot
b) Aura: gangguan visual yang mendahului serangan
sakit kepala
c) Sakit kepala: umumnya satu sisi, berdenyut-denyut,
disertai mual dan muntah, sensitif terhadap cahaya
dan suara terjadi antara 4 72 jam
d) Berhentinya sakit kepala: meskipun tidak diobati,
nyeri biasanya akan menghilang dengan tidur
e) Postdrome: tanda-tanda setelah serangan migrain
seperti tidak bisa makan, tidak bisa konsentrasi,
kelelahan

PATOFISIOLOGI
MIGRAIN
Menurut teori/hipotesis vaskular : aura disebabkan
oleh vasokonstriksi intraserebral diikuti dengan
vasodilatasi ekstrakranial
Aura mungkin merupakan manifestasi penyebaran
depresi, suatu peristiwa neuronal yang ditandai
oleh gelombang penghambatan yang menyebabkan
turunnya aliran darah otak sebesar 25-35%
Nyeri disebabkan karena aktivitas sistem trigeminal
yang menyebabkan pelepasan neuropetida vasoaktif
vasodilatasi, plasma neurogenik ekstravasasi, dan
nyeri
Aktivitas di dalam sistem trigeminal diregulasi oleh
saraf noradrenergik dan serotonergik
Reseptor 5-HT, terutama 5-HT1 dan 5-HT2 terlibat
dalam patofisiologi migrain

SARAF TRIGEMINAL
Nervus Trigeminus /saraf
trigeminal merupakan
saraf kranial terbesar
Nervus ini disebut
nervus trigeminus,
karena mempunyai tiga
cabang yaitu
n.optalmikus, n.
maksilaris, dan
n.mandibularis
Nervus trigeminus terdiri
dari serabut sensoris
maupun serabut motoris

Lanjutan PATOFISIOLOGI
MIGRAIN ..
Stimulasi
Stimulasi pd
pd saraf
saraf trigeminal
trigeminal

Melepas
Melepas substansi-P,
substansi-P, CGRP,
CGRP, neurokinin-A
neurokinin-A dari
dari
sensory
sensory C-fiber
C-fiber

Substansi-substansi
Substansi-substansi tsb
tsb menyebabkan
menyebabkan inflamasi
inflamasi
neurogenik
neurogenik

Berinteraksi
Berinteraksi dgn
dgn dinding
dinding pembuluh
pembuluh darah
darah shg
shg
terjadi
terjadi dilatasi,
dilatasi, ekstravasasi
ekstravasasi plasma,
plasma, inflamasi
inflamasi
Ekstravasasi
Ekstravasasi neurogenik
neurogenik plasma
plasma dpt
dpt dihambat
dihambat oleh
oleh 55HT1
HT1 agonis,
agonis, neurosteroid,
neurosteroid, prostaglandin
prostaglandin inhibitor,
inhibitor,
antagonis
antagonis substansi-P,
substansi-P, antagonis
antagonis endotelin
endotelin

FAKTOR PEMICU
MIGRAIN
Faktor psikologis
Stress, depresi
Faktor lingkungan
Rokok
Bau menyengat
Perubahan cuaca
Cahaya atau suara
Faktor makanan
Yg mengandung tiramin
Food additive (MSG, aspartam)
Coklat, kopi
Jeruk

Obat-obatan
Simetidin
Kokain
Fluoksetin
Indometasin
Nikotin
Nifedipin, dll
Faktor hormonal
Menstruasi
Hamil, menopause
Gaya hidup
Kurang atau kebanyakan tidur
Terlambat makan, dll

TUJUAN TERAPI

TUJUAN TERAPI JANGKA


PANJANG

Terapi bertujuan
menghilangkan
gejala/nyeri pada
saat serangan
(terapi abortif)
atau mencegah
serangan (terapi
profilaksis)

Mengurangi frekuensi dan


keparahan serangan
Mengurangi patient disability
selama serangan
Memperbaiki kualitas hidup
pasien
Mencegah serangan
berikutnya
Menghindarkan penggunaan
obat yang makin bertambah
Dan mengedukasi pasien utk
dapat menatalaksana
penyakitnya

STRATEGI TERAPI

Menghindari
atau
menghilangk
an pemicu

Terapi
abortif
dimulai pada
saat
terjadinya
serangan

Terapi
Terapi profilaksis
profilaksis

dimulai
dimulai jika
jika serangan
serangan
terjadi
terjadi >
> 2-3
2-3 x/bln,
x/bln,
serangan
serangan berat
berat dan
dan
menyebabkan
menyebabkan gangguan
gangguan
fungsi,
fungsi, terapi
terapi simptomatik
simptomatik
gagal
gagal atau
atau menyebabkan
menyebabkan
efek
efek samping
samping yang
yang serius
serius

Algoritma
Terapi pada
Migrain

Midrin: kombinasi PCT,


isometheptene mucate
(simpatomimetik amin)
& dikloralfenazon
(turunan kloralhidrat)

TERAPI ABORTIF VS
PROFILAKSIS
Pembeda

Terapi Abortif

Terapi Profilaksis

Melibatkan
analgesik

Ya

Tidak

Waktu

Saat serangan

Setelah serangan

Tujuan

Meredakan rasa
nyeri ketika
serangan terjadi

Memperbaiki
pengaturan proses
fisiologis yang
mengkontrol aliran
darah dan aktivitas
sistem saraf

TERAPI ABORTIF
Analgesik
& NSAID

Antiemeti
k

Golongan
Triptan

Alkaloid
ergot &
turunann
ya

Analgesik

Analgesik ringan : aspirin (drug of


choice), parasetamol
NSAIDs: menghambat sintesis
prostaglandin, antiagregasi platelet,
dan pelepasan 5-HT; Naproksen
terbukti lebih baik dari ergotamin;
Pilihan lain: ibuprofen, ketorolak
Analgesik opiat

Gol.
Triptan

Agonis reseptor 5-HT1D menyebabkan


vasokonstriksi di kranial vasodilatasi
pembuluh darah di kranial dapat dihambat
inflamasi neurogenik terhambat
Contoh: sumatriptan, zolmitriptan,
naratriptan, dll
Efikasinya setara dengan dihidroergotamin,
tetapi onsetnya lebih cepat
Sumatriptan per oral lebih efektif
dibandingkan ergotamin per oral

Alkaloid
ergot &
turunann
ya

Menstimulasi reseptor 5-HT1 presinaptik


vasokonstriksi di vaskular intrakranial
vasodilatasi dapat dicegah blokade
inflamasi neurogenik
Pemberian IV dapat dilakukan untuk
serangan yang berat
Contoh: ergotamin tartrat &
dihidroergotamin

Antiemet
ik

Contoh: metoklopramid, klorpromazin,


proklorperazin
Digunakan untuk mencegah mual muntah
Diberikan 15-30 menit sebelum terapi
antimigrain, dapat diulang setelah 4-6 jam

Algoritma Terapi untuk


Pencegahan Migrain

TERAPI PROFILAKSIS
Beta blocker
Merupakan drug of choice untuk prevensi migrain
Kemungkinan dpt meningkatkan ambang batas /
treshold dengan menurunkan transmisi saraf
adrenergik atau serotonergik di kortikal atau
subkortikal
Contoh: propranolol, timolol, atenolol,
metoprolol, nadolol
Antidepresan trisiklik
Kemungkinan menyebabkan downregulation dari 5-HT2
di sentral aktivitas serotonergik di sentral menurun
Contoh: amitriptilin, doxepin, nortriptilin, protriptilin,
dan imipramin
Sebaiknya digunakan pd malam hari ada ES sedasi
(mengantuk)
Punya efek antikolinergik, tidak boleh digunakan

TERAPI PROFILAKSIS
Methysergide
Merupakan senyawa ergot semisintetik, antagonis
5-HT2 yang poten menghambat aktivitas
serotonergik pada saraf trigeminal memblok
inflamasi neurogenik
Kompetitif serotonin antagonis di perifer &
serotonin agonis di SSP
Asam-Valproat / Na-Valproat
Diduga meningkatkan aktivitas inhibisi melalui
GABA, memodulasi neurotransmiter eksitatori dan
hambatan aktivitas kanal ion natrium dan kalsium
Dapat menurunkan keparahan, frekuensi dan
durasi pada 80% penderita migrain

Sakit Kepala Tegang


Otot
(Tension Headache)

DEFINISI
Merupakan jenis yang paling banyak dijumpai,
disebabkan karena kontraksi otot di kepala
Rasa nyeri tumpul yang konstan, atau perasaan
menekan yang tidak enak pada leher, pelipis,
dahi, atau di sekitar kepala, leher terasa kaku
Umumnya terjadi secara bilateral (terjadi pada
kedua belah sisi pada waktu yang sama)
Episodic tension-type headaches frekuensi
nyeri sedikitnya 10 x sakit kepala yang lamanya
berkisar 30 menit 7 hari, dan terjadi kurang dari
180 kali setahun
Chronic tension-type headache frekuensi
rata-rata 15 hari dalam sebulan selama 6 bulan

GEJALA
Rasa menekan/berat yang berlokasi di
kedua belah sisi kepala
Sakit dengan intensitas ringan sampai
sedang
Tidak bertambah berat dengan aktivitas
fisik rutin
Tidak mual atau muntah
Mungkin sensitif terhadap cahaya atau
suara, tapi tidak keduanya

TERAPI NONFARMAKOLOGI
Melakukan latihan peregangan leher atau otot
bahu sedikitnya 20 - 30 menit
Perubahan posisi tidur
Pernafasan dengan diafragma atau metode
relaksasi otot yang lain
Penyesuaian lingkungan kerja maupun
rumah: Pencahayaan yang tepat untuk
membaca, bekerja, menggunakan komputer,
atau saat menonton televisi
Hindari paparan terus-menerus pada suara
keras dan bising
Hindari suhu rendah pada saat tidur pada
malam hari

TERAPI FARMAKOLOGI
Menggunakan analgesik atau analgesik plus
adjuvant sesuai tingkat nyeri Contoh : obatobat OTC seperti aspirin, acetaminophen,
ibuprofen atau naproxen sodium
Produk kombinasi dengan kafein dapat
meningkatkan efek analgesik
Untuk sakit kepala kronis, perlu assesment yang
lebih teliti mengenai penyebabnya, misalnya
karena anxietas (cemas, gelisah) atau depresi
untuk antianxietas dpt digunakan diazepam
atau chlordiazepoxid
Pilihan obatnya adalah antidepresan, seperti
amitriptilin, trifluoroperazin atau
antidepresan lainnya
Hindari penggunaan analgesik secara kronis

SELAMAT
BELAJAR