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
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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 up
with acceptable vital signs and analgesia
maintained.
ANALGESIA SIDE EFFECTS
OPIOID REVERSAL
Morphine Misconceptions
Morphine will cause Addiction
Tolerance to morphines analgesic effects
Causes dangerous respiratory depression
Will make the patient zombie
Hastens death
Drugs To Treat Pain
Main drugs used for their analgesic effects:
Non-opioid (ex: NSAIDs)
Opioids
Adjuvant Drugs (ex: anti-convulsants)
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)
Inflammation
Pathophysiology:

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)
Inflammation
Pathophysiology:
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
Main drugs used for their analgesic effects:
Non-opioid (ex: NSAIDs/Non-selective
& Selective)
Opioids
Adjuvant Drugs (ex: anti-convulsants)
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)
NSAIDs
1900s (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 NSAIDs daily
70% report NSAIDs intake at least once a week
HISTORY
1898 : Aspirin introduced
1960s : NSAIDs introduced
Early 1970s : NSAID inhibition of COX enzyme
proposed
1988-1992 : COX-1 & COX-2 isoenzyme
hypothesized
Early 1990s : 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.
Major Clinical Effects of NSAIDs
Clinical Action Mechanism of Action
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
Major Clinical Effects of NSAIDs
Clinical Action Mechanism of Action
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
Chemical Class Analgesic Antipyretic Anti-
inflammatory
Oxicams
Enolic acids/
Oxicams
+ + ++
Pyrazolones
Phenylbutazone
+/- + ++
NSAIDs and Its Effects
Chemical Class Analgesic Antipyretic Anti-
inflammatory
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

- 1800s (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
PARA-AMINOPHENOL DERIVATIVES:
ACETAMINOPHEN
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
PARA-AMINOPHENOL DERIVATIVES:
ACETAMINOPHEN
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
- 1900s (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 membraneinhibit
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