opiods

PT 26 PHARMACOLOGY

� DRUGS TO TREAT PAIN & INFLAMMATION

�  Faculty: Dr. Lynn L. Olegario, FPARM

Drugs To Treat Pain

Main drugs used for their analgesic effects:

� Non-opioid (ex: NSAIDs)

� Opioids � Adjuvant Drugs (ex: anti-convulsants)

OPIATES

�  Opium, has a characteristic odor & bitter taste with its chief active ingredient : Morphine

�  Also present are

Methylmorphine (codeine), thebaine, noscapine, papaverine

�  Diacetylmorphine (heroin)

Papaver Somniferum

OPIOIDS

�  Natural Opiates �  Semi-synthetic Opiates �  Synthetic Opiates �  Endogenous Opiates �  Opiate antagonist

Opioids: Mechanism of Action

� Pre-synaptically, bind at opioid receptors inhibiting the release of substance P and glutamate

� Post-synaptically, bind at the opioid receptors, inhibiting neurons to open potassium channels that hyperpolarize the cell

OPIOID Classification

1) Strength: Weak / Strong

2) Action:

Pure Agonists Partial agonists Mixed agonists-antagonists

Opioid Classification, Strength: WEAK Opioids

�  Codeine �  Tramadol

Opioid Classification, Strength: STRONG Opiods

�  Butorphanol �  Fentanyl �  Meperidine �  Morphine �  Nalbuphine �  Oxycodone

Opioid Classification, Mode of Action

�  Agonists - opioids that mimic the effects of morphine

�  Antagonists - opioids that oppose the effects of morphine. Sometimes called morphine antidotes

�  Agonist-antagonists - opioids that mimic some effects and oppose other effects of morphine

Opioid Classification,Mode of Action: EXAMPLES

�  Pure agonists �  Morphine, hydromorphone, codeine,

oxycodone, methadone, levorphanol, meperidine

�  Agonist-antagonists �  Mixed agonist-antagonist

�  Nalbuphine, butorphanol, pentazocine, dezocine

�  Partial Agonist �  buprenorphine

�  Antagonists �  Naloxone, naltrexone

Opioid Receptors and Effects of Stimulation

Receptor Effects

mu1 analgesia, euphoria, priritus, nausea, constipation

mu2 respiratory depression, addiction, bradycardia

kappa spinal analgesia, sedation, papillary constriction

delta analgesia, mood change, nausea

sigma dysphoria, hallucinations

Opioid receptors are found in the central nervous system Below are the different types of opioid receptors

OPIOIDS: Principles of Dosing

1. Doses should be adjusted in each patient to achieve pain relief with an acceptable level of adverse effects.

2. There is no ceiling or maximum

recommended dose for full opioid agonists.

OPIOIDS: Principles of Dosing

3. Use around the clock dosing for continuous or frequently recurring pain.

4. Consider as needed dosing for dose

finding and for rescue dose.

Transitory flare of pain in patients otherwise controlled with chronic opioid therapy

Breakthrough Pain

Rescue Dose

Analgesic given in addition to the around the clock analgesic dose to relieve the

breakthrough pains

1) Spontaneous 2) Incident 3) End-of-dose failure

Time

Persistent Pain

RTC Opioid

Rescue Dose Breakthrough Pain

Preferred Treatment Routes of Administration

�  Oral route is generally preferred

�  Alternative routes needed for patients with: �  Impaired swallowing �  Gastrointestinal obstruction �  Need for rapid onset of analgesia �  Problems in managing complex oral regimen

Routes of Administration

�  Non-invasive Oral Transdermal Intranasal Sublingual Buccal

Routes of Administration

�  Invasive Parenteral Bolus: Intramuscular Intravenous Subcutaneous Parenteral infusions: IV/ SC Intraspinal: epidural intraspinal Intraventricular:

Ambulatory PCA

Opioid Effects: Degree of Tolerance Developed

High Intermediate Limited/None analgesia bradycardia miosis

euphoria, dysphoria constipation

mental clouding

sedation antagonist actions

respiratory depression

antidiuresis

nausea/vomiting

cough suppression

Adverse Effects of Opioids

o  Constipation o  Nausea/ vomiting o  Sedation o  Changes in cognition, mood or perception o  Dry mouth o  Pruritus o  Urinary retention o  Myoclonus o  Respiratory depression

22

Naloxone is given at titrated doses until patient shows signs of lightening upwith acceptable vital signs and analgesia maintained.

ANALGESIA SIDE EFFECTS

OPIOID REVERSAL

Morphine Misconceptions

�  Morphine will cause Addiction �  Tolerance to morphine s analgesic effects �  Causes dangerous respiratory depression �  Will make the patient zombie �  Hasten s death

Drugs To Treat Pain


� Non-opioid (ex: NSAIDs)


ADJUVANT ANALGESICS

�  Defined as drugs with other indications that may be analgesic in specific circumstances

�  Numerous drugs in diverse classes

Multipurpose ADJUVANT ANALGESICS

Class: Examples: Antidepressants amitriptyline,

desipramine, nortriptyline, paroxetine, venlafaxine, citalopram, others

Alpha-2 adrenergic tizanidine, clonidine agonists Corticosteroids prednisone,

dexamethasone

ADJUVANT ANALGESICS for Neuropathic Pain

Class: Examples: Anticonvulsants gabapentin, valproate,

phenytoin, carbamazepine, clonazepam, topiramate, lamotrigine, tiagabine, oxcarbazepine, zonisamide, pregabalin

Local anesthetics mexiletine, tocainide

ADJUVANT ANALGESICS for Neuropathic Pain

Class Examples NMDA receptor dextromethorphan,

ketamine Antagonists amantadine Miscellaneous baclofen, calcitonin Topical

Inflammation

Signs & Symptoms

�  dolor �  rubor �  calor �  tumor �  functio laesa

Inflammation …Pathophysiology

…response to tissue injury� dilatation of blood vessels� increased permeability & increased receptiveness of leukocytes� accumulation of inflammatory cells at site of injury.(polymorphonuclear

neutrophil leukocytes, macrophages; basophils & eosiniphils) … Inflammatory responses produced & controlled by

interactions of varied inflammatory mediators derived from leukocytes and some from the damaged tissues

Inflammation Pathophysiology:

… Inflammatory mediators include �  Histamine �  Kinins (bradykinin) �  Neuropeptides (substance-P, calcitonin gene-

related peptide) �  Cytokines (interleukins) �  Arachidonic acid metabolites (eicosanoids)


… Arachidonic acid metabolites: the Eicosanoids �  involved in the majority of inflammatory reactions

�  most anti-inflammatory therapy is based on the manipulation of their biosynthesis

�  family of polyunsaturated fatty acids formed from arachidonic acid (* Biosysnthetic pathway)


… Arachidonic acid �  Derived from phospholipids of cell membranes,

mobilized by action of enzyme phospholipase A2

�  Further metabolized by: �  By cyclooxygenase� produce classical prostaglandins , thromboxanes & prostacylin (prostanoids) �  By lipoxgenase� produce leukotrienes

Actions of the Eicosanoids in the Inflammatory Reaction

Prostanoids Actions in Inflammation

Classical Prostaglandins PGD2, PGE2, PGF2

Thromboxane A2 (TXA2)

Prostacyclin (PGI2)

•  Produce increased vasodilation, vascular permeability & edema in an inflammatory reaction; prostaglandins also sensitize nociceptive fibers to stimulation by other inflammatory mediators.

•  Platelet aggregation & vasoconstriction. •  Inhibition of platelet aggregation & vasodilatation.

Actions of the Eicosanoids in the Inflammatory Reaction

Leukotrienes Actions in Inflammation LTB4, LTC4

•  Increase vascular permeability, promote leukocyte chemotaxis (and cause contraction of bronchial smooth muscle)

Drugs To Treat Pain


� Non-opioid (ex: NSAIDs/Non-selective & Selective)


Anti-inflammatory Drugs Main drugs used for their broad-spectrum anti-

inflammatory effects:

�  Non-steroidal Anti-inflammatory (NSAIDs/Non-selective) �  COX2- Selective inhibitors �  Steriodal anti-inflammatory drugs

(glucocorticoids)

�  Exert their effect by inhibiting the formation of eicosanoids thru the enzyme cyclooxygenase

Anti-inflammatory Drugs: CHEMICAL CLASSIFICATION

�  NSAIDs/Non-selective COX Inhibitors: 1. Salicylic acid derivatives 5. Arylpropionic acids 2. Para-aminophenol derivatives 6. Anthranilic acids 3. Indole & indene acetic acids 7. Enolic acids 4. Heteroaryl acetic acids 8. Alkanones

�  Selective COX-2 Inhibitors: 1. Diaryl-substituted furanones 3. Indole acetic acid 2. Diaryl-substituted pyrazoles 4. Sulfonamides �  Steroidal anti-inflammatory Drugs (Glucocorticoids)

NSAID s

�  1900 s (mid) ; synthetic agents MOA similar to salicylates

�  Cornerstone of therapy for pain and inflammation

�  Over the counter medication (>30 billion tabs / year)

�  1/3 of elderly take NSAID s daily

�  70% report NSAID s intake at least once a week

HISTORY

�  1898 : Aspirin introduced �  1960 s : NSAIDs introduced �  Early 1970 s : NSAID inhibition of COX enzyme proposed �  1988-1992 : COX-1 & COX-2 isoenzyme hypothesized �  Early 1990 s : COX-2 gene isolated �  1994 : COX-2 enzyme characterized �  1999 : COX-2 selective inhibitors introduced

Anti-inflammatory Drugs:NSAIDs Diverse group of drugs possessing ability to inhibit both forms

of the enzyme cyclooxygenase, involved in metabolism of arachidonic acid.

Mechanism of action: •  Irreversible inhibition ?How- acetylation of the active site; example is Aspirin

•  Competitive inhibition ?How- acts as a competitive substrate; example is Ibuprofen

•  Reversible, non-competitive inhibition ?Example is Paracetamol; has a free-radical trapping action interfers with production of hyperoxidases which has a role in cyclooxygenase activity

Anti-inflammatory Drugs:NSAIDs Diverse group of drugs possessing ability to inhibit both forms of cyclooxygenase.

2 Cyclooxygenase Isoforms: •  COX1- expressed in most tissues, esp. platelets, gastric mucosa & renal musculature; involved in physiological cell signalling - most adversed effects of NSAIDs due to inhibition of COX1 •  COX2 - induced at sites of inflammation & produces prostanoids involved in inflammatory responses - analgesic & anti-inflammatory effects of NSAIDs due to inhibition of COX2

Anti-inflammatory Drugs:NSAIDs NSAIDs work by inhibition of cycloooxygenase� inhibition of prostaglandin

synthesis� therapeutic effects.

Clinical Effects : •  Analgesic effect •  Anti-inflammatory •  Antipyretic effect

•  Not all NSAIDs possess these 3 actions to exactly same extent!

Major Clinical Effects of NSAIDs Clinical Action Mechanism of Action

Analgesic action

•  A peripheral effect due to inhibition of prostaglandin synthesis at the site of pain & inflammation. •  Prostaglandins do not produce pain directly, but sensitize nociceptive fiber endings to other inflammatory mediators (bradykinin, histamine, 5-HT)� amplifies pain message. •  Most effective against pain with inflammatory component. •  Small component of central effect in reducing prostaglandin synthesis in the CNS.


Anti-inflammatory action

•  Prostaglandins produce increased vasodilatation, vascular permeability & edema in an inflammatory reaction.

•  Inhibition of prostaglandin synthesis reduces this part on the inflammatory reaction.

•  NSAIDs do not inhibit the numerous other mediators involved in an inflammatory reaction; thus inflammatory cell accumulation is not inhibited


Antipyretic action

• During fever, leucocytes release inflammatory pyrogens (interleukin-1) as part of immune system� acts on thermoregulatory center in the thalamus� increase in body temperature.

•  This effect mediated by an increase in hypothalamic prostaglandins (PGEs), the generation of which is inhibited by NSAIDs.

•  NSAIDs do no affect temperature under normal circumstances or in heat stroke.

Anti-inflammatory Drugs:NSAIDs NSAIDs work by inhibition of cycloooxygenase� inhibition of prostaglandin

synthesis� therapeutic effects.

Indications: •  Musculoskeletal & joint diseases (strains, sprains,

rheumatic problems, arthritis, gout, etc)

•  Analgesia for mild to moderate pain relief (headaches, dysmenorrhea; symptomatic relief in fever)

• 

NON-SELECTIVE NSAIDs NSAIDs and Its Effects

Chemical Class Analgesic Antipyretic Anti-inflammatory

Salicylic acids Salicylic acid derivatives

+ + +

Propionic acids Arylproprionic acids

+ + +

Acetic acids Indole & indene acetic acid

+ + ++

NSAIDs and Its Effects


Oxicams Enolic acids/ Oxicams

+ + ++

Pyrazolones Phenylbutazone

+/- + ++

NSAIDs and Its Effects


Fenemates Anthranilic acids

+ + +/-

Para-Aminophenols Para-aminol derivatives

+ + -

Anti-inflammatory Drugs:NSAIDs

Contraindications: •  NOT BE GIVEN to patients with GASTROINTESTINAL

ULCERATION or BLEEDING; previous HYPERSENSITIVITY to any NSAID

•  Caution for patients with ASTHMA & when RENAL function is impaired

Adverse Effects: •  Common esp in elderly, chronic users •  Less common, liver disorders & bone marrow suppression

• 

General Adverse Effects of NSAIDs System Adverse Effect Cause Gastro-intestinal

Dyspepsia, nausea vomiting Ulcer formation & potential hemorrhage risk in chronic users

Inhibition of the normal protective actions of prostaglandins on the gastric mucosa. (PGE2 & PGI2 normally inhibit gastric acid secretion, inc mucosal blood flow, & have a cytoprotective action)

Renal Renal damage/nephrotoxicity Promotes salt & water retention

Inhibition of PGE2 & PGI2- mediated vasodilatation in the renal medulla & glomeruli

Others Bronchospasm, skin rashes, other allergic-type reactions

Hypersensitivity reaction/allergy to drug

Preventive Measures to Reduce NSAID-Induced GI Toxicity

�  Short duration of therapy �  Lower dose �  Using antacids , PPI (i.e. omeprazole), PG-

analogue (misoprostol) �  Avoid co-therapy (coumadin , NSAIDs,

ASA ,steroids ) �  Treat H. pylori bacteria

Non Steroidal Anti-inflammatory Drugs

�  Salicylic acid derivatives - Aspirin, sodium salicylate, choline magnesium trisalicylate, salsalate, diflunisal, sulfasalazine, olsalazine

�  Para-aminophenol Derivatives - Acetaminophen

�  Indole & indene acetic acids – Indomethacin, Sulindac

�  Heteroaryl acetic acids – Tolmetin, Diclofenac, Ketorolac

�  Arylpropionic acids- Ibuprofen, Naproxen, Flurbiprofen, Ketoprofen, Fenoprofen, Oxaprozin

�  Anthranilic acids (fenamates) - Mefenamic acids, Meclofenamic acid

�  Enolic acids - Oxicams (Piroxicam, Meloxicam)

�  Alkanones - Nabumetone

- 1800 s (late); willow bark extract - formulated , introduced by Bayer - reduce fever, pain, inflammation - salicylism and other side effects

Aspirin NSAIDs: SALICYLATES

�  Pharmacological Properties 1) Analgesia- low intensity pain; from integumental structures; examples: headache, myalgia & arthralgia

2) Antipyresis- lowers body temp rapidly & effectively

3) Respiration - increase O2 consupmtion & CO2 production - directly stimulate respiratory center �hyperventilation

4) Acid-Base Balance & Electrolyte Pattern - initially respiratory alkalosis

5) Cardiovascular Effects: - therapeutic dose� no direct effect - larger doses� dilate peripheral vessels - toxic amounts� depress circulation

SALICYLATES �  Pharmacological Properties 6) Gastrointestinal Effects- epigastric distress; nausea & vomiting - gastric ulceration & hemorrhage, erosive gastritis - exacerbation of peptic ulcer symptoms

7) Hepatic & Renal Effects - cause hepatic injury; retention of salt & water

8) Uricosoric Effects- dose dependent

9) Effects on the Blood – prolongation of the bleeding time

10) Effects on Rheumatic, Inflammatory & Immunological Process - suppress antigen-antibody reactions

11) On pregnancy- not teratogenic; low birth weights; 3rd trimester: anemia, antepartum& postpartum hemorrage, prolonged gestation

12) Local Irritant Effects- keratolytic action for warts, fungal infections. Methylsalicylate for external use

SALICYLATES

�  Pharmacokinetics and Metabolism

�  Absorption: orally- rapidly; stomach & upper small intestine - plasma conc found in <30minutes - peak value reached within 1 hour

rectally- slower; incomplete

integumentary- rapid esp applied as liniments

�  Distribution: most body tissues; cross placental barrier; 80-90% of bound to plasma proteins

�  Biotransformation & Excretion - excreted in the urine - plasma half-life for aspirin is 15 min - salicylate is 2-3 hours for low doses; 12 hours for anti-inflammatory doses

SALICYLATES �  Therapeutic Uses: alleviate fever, pain & inflam Systemic uses: Sodium salicylate & Aspirin 1) Antipyresis- fever is deleterious; relief when fever is lowered - dose: Adult = 325-650 mg orally every 4 hours Children= 50-75 mg/kg/day in 4/6 div doses

2) Analgesia- nonspecific relief of pain; same dose for fever

3) Rheumatoid arthritis:Juvenile Rheumatoid Arthrtis Other Uses- prophylaxis for platelet hyperaggregability such as in coronary heart disease - for inflammatory bowel disease, as suppository - hypertensive pregnant women

SALICYLATES

�  Toxic Effects

�  Salicylate Intoxication: dose varies with preparation of salicylate - 10 to 30 grams; 4.7 gr. fatal in children

Signs & Symptoms: Salicylism - Headache, dizziness, tinnitus, difficulty in hearing, dimness of vision, mental confusion, lassitude, drowsiness, sweating, thirst, hyperventilation, nausea & vomiting - pronounced CNS disturbances; acid-base balance disturbance; hemorrhagic phenomena - an acute medical emergency! �  Aspirin Hypersensitivity- allergic reactions

SALICYLATES �  ASPIRIN ( Acetyl salicylic acid)

�  Brand Name: - Anthrom - Enteroprin - Aspec-EC - Rhea Aspirin - Aspilets - Tromcor - Astrix - United Home Aspirin - Bayer Aspirin - Cor-30 * Aggrenox - Cor-80 * Alka-Seltzer - Cortal

PARA-AMINOPHENOL DERIVATIVES: ACETAMINOPHEN

�  Pharmacological Properties: phenacetin - analgesic & anti-pyretic effects similar to Aspirin BUT has anti-inflammatory effect. Antipyretic effect due to ability to

inhibit cyclooxygenase in the brain �  Pharmacokinetics & Metabolism: Absorption- rapid, almost complete absorption from GIT - plasma conc peaks in 30-60 minutes; half-life about 2 hours after therapeutic dose; uniform distribution - binding to proteins is variable

�  Therapeutic Use: Adult= 325-1000 mg, >4000 mg/day Children= 40-80 mg/age/weight

�  Toxic Effects: Allergic reaction; hepatoxixity


�  ACETAMINOPHEN (Paracetamol)

�  Brand Name: - Acet/Acet-MS/Acet-ES - Detramol - Opigesic - Aeknil - DLI Paracetamol - Parvid - Alvedon 500 - Dolexpel - Pharex Paracetamol - Anaseran - Essendol - Baropyrine - Febrinil - Retalgan - Betanol - Flurinol - Rexidol - Biogesic - Gendol - Saridon - Bioseran - Gifaril P - Tempra - Calpol/Calpol Six Plus - Meforagesic - Tylenol

- Corgic/Corgic Plus - Naprex - Ultragesic - Crocin - Nektol - Winadol


�  ACETAMINOPHEN (Paracetamol)

�  Brand Name: * AlaxanAlaxan FR * Neozep/Neozep Forte * A-P-Histalin * Norgesic/Norgesic Forte * Bioflu * Parafon forte * Buscopan Plus * Relaxid * Decolgen Forte * Restolax * Decolgen No-Drowse * Sinutab Extra Strength/Sinutab * Decolgen Reformulated *Tuseran Forte (Reformulated) * Dolcet * Doloneurobion *Muskelax * Myracof-T * NafarinA

INDOLE & INDENE ACETIC ACIDS

INDOMETHACIN (Indocid, Infree)

�  Pharmacological Properties: anti inflammatory, analgesic & antipyretic effects similar to aspirin

�  Pharmacokinetics & Metabolism: Absorption- rapidly, almost complete from GIT - peak plasma concentration 1-2 hrs; urine excretion

�  Drug Interaction: Probenecid concurrent use increase conc

�  Therapeutic Uses: not commonly used; more effective for Ankylosing spondylitis, Osteoarthritis Gout; single dose up to 100 mg at bedtime. Combine with others

�  Toxic Effects: Gastrointestinal complaints Hematopoietic reactions- neutopenia, thrombocytopenia & rarely aplastic anemia

INDOLE & INDENE ACETIC ACIDS

SULINDAC (Clinoril) �  Pharmacological Properties: less potent as Indomethacin

�  Pharmacokinetics & Metabolism: - 90% absorbed after oral; peak plasma concentration within 1-2 hrs; excreted in urine and feces

�  Therapeutic uses: RA, OA & AS; Gout; 400 mg/day

�  Toxic Effects: less GIT & CNS side effects

ETODOLAC (Lodine) �  Pharmacological Properties: selective COX2 inhibitor

�  Pharmacokinetics & Metabolism: rapidly absorbed orally; 99% bound to plasma proteins

�  Therapeutic Uses:200-400mg for post-op analgesia, OA, RA

ANTHRANILIC ACIDS (Fenamates)

MEFENAMIC ACID MECLOFENAC FLUFENAMIC ACIDS �  Pharmacological Properties: anti inflammatory, antipyretic & analgesic properties

�  Pharmacokinetic Properties: peak plasma concentration reached in 0.5-2 hrs; excreted in urine and feces

�  Toxic Effects & Precautions: GIT & hypersensitivity reactions

ANTHRANILIC ACIDS (Fenamates) �  MEFENAMIC ACID

�  Brand name: - Acidan - Gisfen - Proxyl - Afligec - Harpinac - Ralgec - Analcid - Icelax - Revalan - Aprostal - Isagesic - Ritemed Mefenamic - Calibral - Istan - Selmac - DLI Mefenamic acid - Medianon - Sensomef - Dolfenal - Mefenax - Spegic - Eurostan - Pacimic - Tynostan - Fendal - Penomor - Zapan - Fenexan - Pharex Mefenamic Acid -Gardan - Ponstan

COX-2 SELECTIVE INHIBITORS

COX-2 selective inhibitors

GI adverse effects of non-selective NSAIDS led to development of COX-2 selective inhibitors

Aspirin

1900

Phenylbutazone

1950 1980 1995 2000

Indometacin

1990

Mechanism of action of aspirin determined

Ibuprofen Diclofenac Celecoxib

Rofecoxib

2005

Valdecoxib

Etoricoxib

Prexige®

Traditional NSAIDs

1960 1970

COX-2 identified

Naproxen

Parecoxib

Anti-inflammatory Drugs

Main drugs used for their broad-spectrum anti-inflammatory effects:

�  Non-steroidal anti-inflammatory drugs (NSAIDs)

� Steriodal anti-inflammatory drugs (glucocorticoids)

Corticosteroids - 1900 s (early) ; wonder drug; strong anti-inflammatory/analgesic

Phospholipids Phospholipase A

Arachidonic Acid

( PG, thromboxanes, prostacyclins) Lipooxygenase Cyclooxygenase (leukotrienes, bradykinin)

(-) Steroids

Steroidal Anti-inflammatory Drugs (Glucocorticoids)

Profound generalized inhibitory effects on inflammatory responses result from their effects in altering activity of certain-responsive genes.

Mechanism of action: •  Reduced production of acute inflammatory mediators ?prevent formation of arachidonic acid from membrane lipid by inducing synthesis of a polypeptide called lipocortin. ?lipocortin inhibits phospholipase A2 , the enzyme responsible for mobilizing arachidonic acid from cell membrane�inhibit formationof prostaglandins & leukotrienes

•  Reduced number & activity of circulating immunocompetent cells, neutrophils & macrophages

•  Decreased activity of macrophages & fibroblast involved in chronic stages of inflammation

Steroid Side Effects

�  Cushing's �  Osteoporosis �  Cataract �  AVN �  Hyperglycemia �  Acne �  Hirsutism �  Infection

Recommendation... Pain Management: ETIOLOGY BASE & MECHANISM BASE

(Pharmacologic Treatment) NOCICEPTIVE:

VISCERAL PAIN �  Corticosteroids �  Intraspinal local

anesthetic agents �  NSAIDs �  Cox2 �  Muscle relaxants �  Opioid via any route

Pain Management: ETIOLOGY BASE & MECHANISM BASE (Pharmacologic Treatment)

Recommendation....

NOCICEPTIVE: SOMATIC PAIN �  Acetaminophen �  Corticosteroids �  Local anesthetic either

topically or by infiltration �  Non-steroidal anti-

inflammatory drugs (NSAIDs)

�  Cox-2

Pain Management: ETIOLOGY BASE & MECHANISM BASE (PHARMACOLOGIC TREATMENT)

Recommendation...

NEUROPATHIC PAIN �  Anticonvulsants �  Corticosteroids �  Neural blockade �  NSAIDs �  Cox 2 �  Opioids via any route �  Tricyclic antidepressants

Thank You…

Documents

opiods