PAIN & ANALGESIC DRUGS. Marta Jóźwiak-Bębenista marta.jozwiak-bebenista@umed.lodz.pl Department of Pharmacology Medical University of Lodz
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1 PAIN & ANALGESIC DRUGS Marta Jóźwiak-Bębenista Department of Pharmacology Medical University of Lodz
2 Pain and Analgesia PAIN IS - unpleasant sensory or emotional experience associated with actual or potential tissue damage or described in terms of such damage - individual and subjective - more than a symptom `
3 PAIN Pain is caused by the stimulation of pain receptors which are free nerve endings. Nocireceptors are pain receptors that are located outside the spinal column in the dorsal root ganglion and are named based upon their appearance at their sensory ends. These sensory endings look like the branches of small bushes There are two types of nocireceptors that mediate fast or slow pain signals The perception of pain is when these receptors are stimulated and they transmit signal to the central nervous system via sensory neurons in the spinal cord.
4 DIFFERENT KINDS OF PAIN Pain can be categorized according to several variables, including: its duration, its pathophysiologic mechanisms, its clinical context (eg, postsurgical, Malignancy related, neuropathic, degenerative). Neuropathic Pain Nociceptive Pain Physiologic pain Visceral Pain Somatic pain Phantom pain Acute pain Chronic pain > 3 months
5 Somatic pain arises from injury to skin, bone, joint, muscle and connective tissuse; localized to the site of injury Visceral pain involves injury to nerves on internal organs; present as diffuse, poorly differentiated and often referred pain.
6 CLINICAL DIFFERENTIATIONS BETWEEN ACUTE AND CHRONIC PAIN Acute Pain Usually obvious tissue damage Distinct onset Short, well characterized duration Resolves with healing Serves a protective function Effective therapy is available Chronic Pain Multiple causes (malignancy, benign) Gradual or distinct onset. Persists after 3 6 months of healing Can be a symptom or diagnosis. Serves no adaptive purpose May be refractory to treatment
7 LEXIS Analgesia absence of pain despite presence of stimuli that should be perceived as painful Hyperalgesia increased sensitivity to a normally painful stimulus Allodynia pain from a stimulus not normaly painful Analgesic drug which produces analgesia without impairing other sensory stimuli Opioid analgesic analgesic which binds to opioid receptors Opiate Opioid (phenantrene alcaloids) derived from opium (poppy) Equianalgesic dose Dose of opioid which causes the same analgesic action as 10 mg of morphine
8 THE MAIN GROUPS OF ANALGESICS: NSAIDs Opioids Local anesthetics Others: - Antidepressants: (TCA`s amitriptyline; SNRI`s duloxetine) neuropathic pain - Neuroleptics: haloperidol, prochlorperazine - Anxiolytics: diazepam, hydroxyzine - Anticonvulsants : pregabalin; carbamazepine - trigeminal neuralgia - Triptans, ergot alkaloids - migraine headache
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10 NSAIDS (NON-STEROIDAL ANTI- INFLAMMATORY DRUGS) Marta Jóźwiak-Bębenista Department of Pharmacology Medical University of Lodz
11 MECHANISM OF ACTION OF NSAIDS inhibiting the synthesis of prostaglandins
12 BENEFICIAL EFFECTS OF PROSTANOIDS GI tract PGE2, PGI2 maintenance of microvascular integrity cytoprotection enhanced blood flow through mucosa protection of gastric mucosa stimulate mucous production secretion of phospholipids and surfactants gastric acid secretion and intestinal fluid secretion Endothelium PGD2, PGI2 vasodilation platelet aggregation Kidney PGI2, PGE2 renin release glomerular filtration reabsorption of Na+ and Cl-
13 ACTION OF TROMBOXAN A2 (TXA2) platelet aggregation contraction of blood vessels bronchial constriction
14 ROLE OF PROSTANOIDS IN INFLAMMATION, PAIN, FEVER PGE2, PGI2 released by endothelial cells and inflammatory cells; PGD2 released by mast cells; monocytes and macrophages release PGE2 and TXA2 vasodilation, blood flow and redness synergize with histamine and bradykinin to vascular permeability, fever and pain 1. Rubor (redness) 2. Calor (heat) 3. Tumor (swelling) 4. Dolor (pain) PGE2 febrile effect
15 COX-1 & COX-2 ISOENZYMES
16 CLASSIFICATION OF NSAID`S BASED ON COX SELECTIVITY COX-1 specific low dose aspirin Non COX selective inhibitors (prototypical NSAID`s) aspirin, indomethacin, diclofenac, piroxicam, ibuprofen, naproxen, mefenamic acid, ) Preferential COX-2 inhibitors nabumetone, meloxicam, nimesulide, etodolac Highly selective COX-2 inhibitors celecoxib, rofecoxib (withdrawn!), valdecoxib, parecoxib, etoricoxib, lumiracoxib
17 ACTIONS OF NSAIDS: 1. Antiinflammatory 2. Analgesic 3. Antipyretic 4. Antiaggregatory
18 NSAID`S CHEMISTRY, PHARMACOKINETICS Weak organic acids - well absorbed Protein bound, usually to albumin (drug interactions) All can be found in synovial fluid after repeated dosing
19 NSAIDS - MAIN INDICATIONS prompt pain relief rheumatoid arthritis osteoarthritis low back pain ankylosing spondylitis gout acute musculoskeletal disorders Periarthritis painful post-operative conditions pain following dental surgery treatment or prophylaxis of diseases associated with platelet hyperagreggregability (coronary artery disease, postoperative deep-vein trombosis) dysmenorrhoea and gynaecological disorders closing of ductus arteriosus Botalli
20 MAIN ADVERSE REACTIONS OF NSAIDS Epigastric distress GI bleeding Peptic ulcers bleeds/perforation Renal disfunction Renale failure acute (Acute renal failure) /chronic (analgesic nephropathy) blood pressure (edema) platelet dysfunction Agranulocytosis Hypersensitivity Prolongation of gestation and inhibition of labor.
21 ANTIPYRETIC DRUGS p-aminofenol derivatives: acetaminophen, (phenacetin) pirazolon derivatives: Metamizol, (phenazon, Aminophenazon), Propyphenazon, acid salicylic derivatives: ASA, acetylsalicylic acid (Aspirin)
22 METABOLISM OF ACETAMINOPHEN
23 FEBRILE CHILDREN Aspirin Reye s syndrome Paracetamol mg/kg b.w. Ibuprofen 7-10 mg/kg b.w.
24 SALICYLIC ACID DERIVATIVES acetylsalicylic acid (ASPIRIN) diflunisal olsalazine sodium salicylate magnesium salicylate salsalate
25 DOSES OF ASA AND PHARMACOLOGICAL ACTION anti-inflammatory action 4,0-6,0g/day anti-pyretic and analgesic actions 2,0-3,0g/day anti-platelet 75mg-150mg/day The lethal dose of ASA 20-30g
26 PROPIONIC ACID DERIVATIVES Fenoprofen (Nalfon) Flurbiprofen (Ansaid) Ibuprofen (Advil, Motrin, Nuprin, others) Ketoprofen (Orudis, Oruvail) Naproxen (Aleve, Anaprox, Naprelan, Naprosyn) Oxaprozin (Daypro)
27 ACETIC ACID DERIVATIVES Indomethacin Sulindac (pro-drug) Etodolac
28 HETEROARYL ACETIC ACIDS Diclofenac Ketorolac Tolmetin
29 mefenamic acid meclofenamate FENAMATES
30 OXICAM DERIVATIVES Piroxicam Meloxicam
31 SELECTIVE COX-2 INHIBITORS Celecoxib (Celebrex) Rofecoxib (Vioxx) Valdecoxib (Bextra) Lumiracoxib (Prexige)
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