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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
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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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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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(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
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O
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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
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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)
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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
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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.
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K it i id l b t t i l k l
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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
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OBAT ANESTESI L KAL
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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
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LIDOK
IN
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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
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NESTESI UMUM
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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
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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
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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
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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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(Golan et al ., 2008)(Golan et al ., 2008)Create PDF files without this message by purchasing novaPDF printer (http://www.novapdf.com)
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(Finkel et al., 2009)
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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
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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
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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
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C ausesof M igraine
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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 :
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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
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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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