Professional Documents
Culture Documents
Pain (Nyeri) adalah suatu pengalaman sensorik dan emosional yang berkaitan dengan kerusakan jaringan atau diduga ada kerusakan jaringan
Nyeri adalah
pengalaman sensorik yang berkaitan dengan aktivasi nociceptor dan lintasan nyeri Nyeri adalah suatu pengalaman emosional Kerusakan jaringan tidak mesti ada
JENIS NYERI
Neuropathic Pain
Pain initiated or caused by a primary lesion or dysfunction in the nervous system (either peripheral or central nervous system)1
Mixed Pain
Pain with neuropathic and nociceptive components
Inflammatory Pain
Pain caused by injury to body tissues (musculoskeletal, cutaneous or visceral)2
Examples Peripheral Post herpetic neuralgia Trigeminal neuralgia Diabetic peripheral neuropathy Postsurgical neuropathy Posttraumatic neuropathy Central Posts troke pain Common descriptors2 Burning Tingling Hypersensitivity to touch or cold
Examples
Examples
Pain due to inflammation Limb pain after a fracture Joint pain in osteoarthritis Postoperative visceral pain
1. International Association for the Study of Pain. IASP Pain Terminology. 2. Raja et al. in Wall PD, Melzack R (Eds). Textbook of pain. 4th Ed. 1999.;11-57
Diagnosis
Acute and chronic pain
Drug Treatment
NSAIDS (al Meloxicam/ Movi-cox), Opioids, Paracetamol
Analgesics (Movi-cox), tricyclics, centrally-acting muscle relaxants, glucocorticoids Carbamazepine, phenytoin, baclofen, tricyclics, gabapentin, others?
Acetaminofen
Electrical Stimulation
Transcutaneous electrical nerve stimulation (TENS) Percutaneous electrical nerve stimulation (PENS)
Alternative methods
(NSAID)
Gottschalk et al., 2001
Thick, myelinated, fast conducting neurons Mediate the feeling of initial fast, sharp, highly localized pain.
Very thin, unmyelinated, slowconducting Mediate slow, dull, more diffuse, often burning pain.
Rabaan Tekanan
Nerve Fibers
Class A- A- A- A- B C Velocity Fast Fast Intermediate Intermediate Small Small Function Motor
Touch, pressure Muscle tone Pain, temperature
Motor Pain
Chemical mediators are released from damaged tissue and inflammatory cells. Some inflammatory mediators directly activate nociceptors, while others act together to sensitize the pain pathway.
Inflammation
biological response to injury or foreign substances l acute and chronic inflammation l components:
l
cellular response biochemical mediators
Mechanisms of Inflammation
Biochemical Mediators
vasoactive amines plasma proteases (complement, kinins) arachidonic acid metabolites (PG, LT) lysosomal constituents oxygen derived free radicals cytokines growth factors
Mediators of Inflammation
Arachidonic Acid Metabolites
Prostaglandins Leukotrienes
Generation of Eicosonoids
Phospholipids
Phospholipase
Arachidonic Acid
5-lipoxygenase cyclooxygenase
5-HPTE
peroxidase
LTB4
Renal function
COX - 2 Inhibitors
l l l l
resiko kardiovaskuler +
Physicians prescribing celecoxib or valdecoxib should consider the emerging cautionary data "when weighing the benefits against risks for individual patients." The most appropriate candidates for coxib therapy are patients at a high risk of GI bleeding or who have a history of intolerance to "or are not doing well on" nonselective NSAIDs. "Individual patient risk for cardiovascular events and other risks commonly associated with NSAIDs should be taken into account for each prescribing situation." Consumers should use all over-the-counter analgesics, "including NSAIDs," strictly according to the label instructions and consult a physician if using them for longer than 10 days.
Meloxicam
Celecoxib
N N
OH
O N H
S O
N CH3 O
CF3
H3C CH3 O S O
O
N H N
Piroxicam
OH
Rofecoxib
S N
O
CH3
O
COX-2 Selectivity
DRUG Rofecoxib Celecoxib Meloxicam Diclofenac Indomethacin COX-2 IC50/COX-1 IC50 .013 .080 .200 .170 1.500
Meloxicam (MOVI-COX) was approved recently by the FDA for use in osteoarthritis. The recommended dose for meloxicam is 7.5 to 15 mg once daily for osteoarthritis and 15 mg once daily for rheumatoid arthritis. Meloxicam demonstrates roughly tenfold COX-2 selectivity on average in ex vivo assays. However, this is quite variable, and a clinical advantage or hazard has yet to be established. There is significantly less gastric injury compared to piroxicam (20 mg/day) in subjects treated with 7.5 mg/day of meloxicam, but the advantage is lost with 15 mg/day
(Goodman & Gilman, 2006)
Potency of NSAID
milligram basis of active compound for each formula
potency
NSAID
mg/formula
7.5, 15 10, 20 25, 50, 75 100, 200 100 100, 200 500 500 500
strong Meloxicam Piroxicam Diclofenac moderate Celecoxib Nimesulide Ketorpofen weak Mefenamic acid Naproxen Nabumetone
TOXICITY OF NSAIDs
Ototoxic Color blindness
Bronchospam
CHF
Hepatotoxic
Bleeding
Allergy
Tocolytic
0 0.3
Meloxicam 15mg
Meloxicam 22.5mg Diclofenac
2960
910 5464
179
241 35
1451
600 524
9
6 9
0.6
1 1.7
Naproxen
243
117
78
1.3
Efficacy and Tolerability of Meloxicam, a COX-2 Preferential Nonsteroidal Anti-Inflammatory Drug [Clin Drug Invest 22(12):799-818, 2002. 2002 Adis International Limited]
Kombinasi OAINS
Kombinasi 2 OAINS:
Ditujukan untuk sedikit mengatasi masalah efek samping terhadap lambung. Dapat diberikan bersama golongan PPI, Misoprostol
NSAID +Acetaminophen
Greater
alone Avoids adverse effects of opioids Similar half lives for many NSAIDS and acetaminophen Over-the-counter Each has analgesic ceiling.
Anti-depressants / psychotropics
Relaxation Spiritual
Opioid
Pain Perception
Adjuvants
NSAIDs? Acetaminophene Neural augmentation
Nociception
Local block
NSAIDs (Movicox )
Surgery Physical modalities
Ablative surgery
1. Looser JD, Cousins MJ. Med J aust 1990;216: 153-208; 2. van den Hout JH, et al. Clin J Pain. 2003;19:87-96.; 3. Mynors-Wallis L, et al. Br J Psychiatry. 1997;170:113-119.; 4. Morley S, et al. Pain. 1999;80:1-13.