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SEKILAS PENATALAKSANAAN NYERI

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Presentation on theme: "SEKILAS PENATALAKSANAAN NYERI"— Presentation transcript:

1 SEKILAS PENATALAKSANAAN NYERI
AWALUDDIN NOOR Kuningan, 9 April 2010

2 Definisi Nyeri (Pain) dari IASP
(International Association for the Study of Pain) 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

3 JENIS NYERI Neuropathic Pain Inflammatory Pain
Pain initiated or caused by a primary lesion or dysfunction in the nervous system (either peripheral or central nervous system)1 Inflammatory Pain Pain caused by injury to body tissues (musculoskeletal, cutaneous or visceral)2 Mixed Pain Pain with neuropathic and nociceptive components 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 Pain due to inflammation Limb pain after a fracture Joint pain in osteoarthritis Postoperative visceral pain Common descriptors2 Aching Sharp Throbbing Examples Low back pain with radiculopathy Cervical radiculopathy Cancer pain Carpal tunnel syndrome 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 ;11-57 LYRICA Neuropathic Pain Slide Kit: February 2005 Update

4 Diagnosis Drug Treatment Acute and chronic pain
NSAIDS (al Meloxicam/ Movi-cox), Opioids, Paracetamol Myofascial pain dysfunction Analgesics (Movi-cox), tricyclics, centrally-acting muscle relaxants, glucocorticoids Neuropathic pain, neuralgias Carbamazepine, phenytoin, baclofen, tricyclics, gabapentin, others?

5 Ascending Pain Transmission Pathway
Ascending Pain Pathway (Purves, 2001). Ascending Pain Transmission Pathway The ascending neural pain pathway is only a 3 neuron relay The major convergence point is the ventral posterior lateral nucleus of the thalamus, which relays the signal to limbic and cortical areas

6 Descending Pain Modulation Pathway
Descending pain pathway (Purves, 2001). Descending Pain Modulation Pathway The Descending Pain Pathway – The Periaqueductal Grey (PAG) is the major convergence point.

7 Targets of Pain Therapies
Pharmacotherapy Non-opioid analgesics Opioid analgesics Nerve Blocks Adjuvant analgesics (neuropathic, musculoskeletal) Acetaminofen Electrical Stimulation Transcutaneous electrical nerve stimulation (TENS) Percutaneous electrical nerve stimulation (PENS) Alternative methods Acupuncture Physical Therapy Chiropractics Surgery (NSAID) Gottschalk et al., 2001

8 Thick, myelinated, fast conducting neurons
Mediate the feeling of initial fast, sharp, highly localized pain. Very thin, unmyelinated, slow-conducting Mediate slow, dull, more diffuse, often burning pain. Rabaan Tekanan

9 Nerve Fibers Class Velocity Function A- Fast Motor A- A-
Touch, pressure A- Intermediate Muscle tone A- Pain, temperature B Small C Pain

10 Nyeri Inflamasi 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.

11 Inflammation biological response to injury or foreign substances
acute and chronic inflammation components: cellular response biochemical mediators

12 Mechanisms of Inflammation Cellular Mechanisms:
Acute inflammation PMN Chronic inflammation lymphocytes monocytes

13 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

14 Mediators of Inflammation
Arachidonic Acid Metabolites Prostaglandins Leukotrienes

15 Generation of Eicosonoids

16 Biological Effects of Prostaglandins

17

18 NSAIDs Selective COX-2 inhibitors
Non-COX selective inhibitors of cyclooxygenase Selective COX-2 inhibitors Leukotriene inhibitors

19 Non-COX Selective NSAIDs
Carboxylic acids [salicylates, meclofenamate, diflunisal] Indoleacetic acids [indomethacin, sulindac] Propionic acids [ibuprofen, fenoprofen, ketoprofen, flurbiprofen] Naphthalene acetic acids [naproxen]

20 Non-COX Selective NSAIDs [cont’d]
Diclofenac Etodolac Nabumetone Oxaprozin Ketorolac

21 COX - 2 Inhibitors Celecoxib Rofecoxib Valdecoxib
Meloxicam (Movi-cox)* *[less COX-2 selective]

22 Golongan Coxib resiko kardiovaskuler + stroke
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.

23 Justification for the Development of COX-2 Selective Inhibitors

24 COX-2 Selectivity: Molecular Basis

25 Chemical Structures of Oxicams and Coxibs
OXICAMS COXIBS Linear, enolic acid Y-shaped, Tricyclic Celecoxib NH2 S O N CF3 H3C CH3 OH O N S N H Meloxicam O CH3 S A linear structure with a terminal acid group is common to all traditional NSAID Remember: Use single finger to represent “linear structure” blocking COX-1 (Careful which finger you use.) Specific COX-2 Inhibitors share a common “Y-shaped”, “tricyclic” (three-ringed) structure thought to be responsible for their COX-2 specifivity The side-chain containing the polar sulfonamide or sulfone group will enter and bind to the polar side-pocket unique to COX-2. The bulky “Y-shaped” structure impedes entry into the narrower COX-1 channel making them “COX-1 sparing” Remember: Use two fingers to represent “Y-shaped” and COX-2 Specificity (Careful which way you turn the fingers in the UK and Oz) OH O N S N H CH3 Piroxicam Rofecoxib

26 COX-2 Selectivity

27 Efficacy as an emerging concern of NSAID used
Potency (strong) Onset of action (rapid) Duration of action (long) Efek samping minimal Harga terjangkau

28 Meloxicam 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)

29 Potency of NSAID milligram basis of active compound for each formula
mg/formula strong Meloxicam Piroxicam 7.5, 15 10, 20 Diclofenac 25, 50, 75 moderate Celecoxib Nimesulide 100, 200 100 Ketorpofen weak Mefenamic acid Naproxen 500 Nabumetone

30 Onset of action of NSAID
T-max (hr) Rapid Diclofenac 0.8 Nimesulide 1.2 – 2.7 Slow Celecoxib 2 – 4 Meloxicam 6

31 Duration of action of NSAID
T-1/2 (hr) short Diclofenac 1.1 Nimesulide 1.8 – 4.7 moderate Celecoxib 11 Naproxen 14 long Meloxicam 20 Piroxicam 57

32 TOXICITY OF NSAIDs Perdarahan GI Mechanism of = Mechanism of
Ototoxic Color blindness Bronchospam CHF Hepatotoxic Perdarahan GI UGIB Nephrotoxic Bleeding Allergy Tocolytic Mechanism of = Mechanism of therapeutic effects adverse effects

33 Percentage per 100 patients/year
Table IV. Incidence of gastrointestinal (GI) adverse events Treatment No. of patients Drug exposure (days) Patients/ byear No. of GI adverse events Percentage per 100 patients/year Placebo 736 56 113 Meloxicam 7.5mg 10158 33 918 3 0.3 Meloxicam 15mg 2960 179 1451 9 0.6 Meloxicam 22.5mg 910 241 600 6 1 Diclofenac 5464 35 524 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): , © 2002 Adis International Limited]

34 Kombinasi OAINS Kombinasi 2 OAINS:
Tidak dianjurkan Efek samping meningkat Tidak menambah efikasi Kombinasi OAINS dan Analgetik: Masih dapat dipertanggungjawabkan Kombinasi OAINS dengan Pelindung Lambung: Ditujukan untuk sedikit mengatasi masalah efek samping terhadap lambung. Dapat diberikan bersama golongan PPI, Misoprostol

35 NSAID +Acetaminophen Greater analgesic effect than either alone
Avoids adverse effects of opioids Similar half lives for many NSAIDS and acetaminophen Over-the-counter Each has analgesic ceiling.

36

37 Pain: A conceptual approach to treatment (Biopsycosocial approach)
Anti-depressants / psychotropics Relaxation Spiritual Cognitive therapies Functional restoration Pain Behaviors Suffering Pain Perception Nociception Opioid Adjuvants NSAIDs? Acetaminophene Neural augmentation Ablative surgery Local block NSAIDs (Movicox ®) Surgery Physical modalities 1. Looser JD, Cousins MJ. Med J aust 1990;216: ; 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: ; 4. Morley S, et al. Pain. 1999;80:1-13.

38 ABC Tx. Nyeri Anamnesa nyeri secara sistematik dan teratur
Berprasangka baik (percaya) terhadap keluhan pasien atau keluarga Carilah metode kontrol nyeri yang nyaman untuk pasien dan keluarga Dilakukan intervensi yang tepat waktunya, logis dan terkoordinasi Edukasi pasien dan keluarga untuk mengatasi nyeri sekuat mungkin

39 HATUR NUHUN


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