ANTI-

INFLAMMATORY

PRESENTED BY:

GROUP 3 BSN 2-D

GENERAL OBJECTIVES

After 1 hour and 30 minutes discussion, the BSN 2D will be

able to comprehend about the following:
• Explain the Pathophysiologic basis of the five cardinal
signs of inflammation.
• Compare the action of various nonsteroidal
antiinflammatory drugs (NSAIDs).
• Explain the use of disease-modifying antirheumatic
drugs (DMARDs).
 INFLAMMATION
• Is a response to tissue injury caused by the release
of chemical mediators that trigger both vascular
response and the migration of fluid and cells –
leukocytes, or white blood cells – to the injured site.

• The chemical mediators are histamines, kinins, and

prostaglandins.
 CHEMICAL MEDIATORS

Histamines Kinins Prostaglandins

• Vasodilation • Vasodilation
• Vasodilation
• Increase permeability • Increase permeability
• Increase permeability
• Chemotaxis • Enhance chemotaxis
• Pain perception • Pain perception
• Induced fever
 INFECTION
• Is caused by microorganisms and results in
inflammation, but not all inflammation are caused
by infections.

• Other causes of inflammation include trauma,

surgical interventions, extreme heat or cold, and
caustic chemical agents.
 PHASES OF
INFLAMMATION
 VASCULAR PHASE DELAYED PHASE

• Is associated with vasodilation and • Occurs when leukocytes infiltrate the

increase capillary permeability during inflamed tissue.
which blood substances and fluid leave
the plasma and go to injured site.
CARDINAL SIGNS OF
INFLAMMATION
• REDNESS
• SWELLING
• HEAT
• PAIN
• LOST OF FUNCTION
 REDNESS
• 1st Phase of inflammation

• Blood accumulates in the area of

tissue injury.
 SWELLING
• 2nd Phase of inflammation

• Plasma leaks into the interstitial

tissue at the injury site.
 HEAT
• 3rd Phase of inflammation

• Caused by blood accumulation and

may result from pyrogens.
 PAIN

• 4th Phase of inflammation

• Caused by tissue swelling and

release of chemical mediators.
LOSS OF FUNCTION
• 5th Phase of inflammation

• Because of the accumulation of fluid

at the tissue injury site and because
of pain, which decrease mobility at
the affected area
 TISSUE INJURY VASOCONSTRICTION
(momentary)

RELEASES OF CHEMICAL MEDIATORS

(histamines, kinins, prostaglandins)

DILATED INCREASED CAPILLARY PAIN FEVER

ARTERIOLES PERMEABILITY
(vasodilation)
PAIN
SWELLING: EDEMA (nerve endings and HEAT
(fluid and cell accumulation) swelling) (vasodilation)
REDNESS:
ERYTHEMA
(blood congestion)
LOSS OF FUNCTION
 ANTIINFLAMMATORY AGENTS

ASPIRIN PROSTAGLANDIN INHIBITORS

• Inhibit the biosynthesis of prostaglandin • Affects the inflammatory process

and are therefore called prostaglandin • Commonly called antiinflammatories or
inhibitors inflammatory drugs
 ANTIINFLAMMATORIES

01 02 03

Relieve pain (analgesic) Reduce elevated body Inhibit platelet aggregration

temperature (antipyretic) (anti-coagulant)
 NONSTEROIDAL ANTIINFLAMMATORY DRUGS (NSAIDs)

• Used to decrease inflammation and pain
• It includes aspirin and aspirin-like drugs
• These drugs may be called prostaglandin
inhibitors
• NSAIDs are not suggested for use in
alleviating mild headaches and mildly
elevated temperature
• NSAIDs that can be purchased over the
counter (OTC) are ibuprofen and naproxen
NSAID DRUGS THAT REQUIRE A
PRESCRITIPON
• Celecoxib
• Meloxicam
• Oxaprozin
• Nabumetone
• Sulindac
• Ketorolac
 SIX GROUPS OF NSAIDs
1 2 3

Salicylates Para-chlorobenzoic acid Propionic acid

derivatives derivative

4 5 6
Selective COX-2
Fenamates Oxicams
Inhibitors
ANTIINFLAMMATORY
AGENTS:
NONSTEROIDAL
 INDICATIONS MECHANISM OF ACTION
Diclofenac Inhibition of prostaglandin synthesis by
Mild to severe pain; rheumatoid inhibiting COX-1 and COX-2
Sodium arthritis, osteoarthritis, migraine

PHARMACOKINETICS ADVERSE REACTIONS

Rapid: PO Anemia, lacrimation, ocular hypertension,

xerophthalmia, blurred vision, keratitis,
CONTRAINDICATIONS dermatitis
• Patients with a history of increased
cardiovascular risk
• Patients undergo bypass graft surgery of
coronary artery
 SALICYLATES-

ASPIRIN comes from the family of salicylates derived from salicylic acid
↪also called Acetylsalicylic acid (ASA)
• ASPIRIN is the oldest anti-inflammatory agent
• Adolf Bayer developed aspirin in 1989
• Most frequently used anti-inflammatory agent before ibuprofen
• ASPIRIN is a prostaglandin inhibitor that decreases inflammatory
process
• ASPIRIN and other NSAIDs relieve pain by inhibiting the COX (Cyclooxygenase) enzyme
 MEMBRANE PHOSPHOLIPIDS

PHOSPHOLIPASE A2
STEROIDS
(PLA2)

ARACHIDONIC ACID
• COX-1
X

5-
• COX-2 O

LO
C

X
PROSTAGLANDINS LEUKOTRIENS
 COX-1 and COX-2

COX- COX-2
major source of1physiological selectively induced by inflammatory
prostaglandins stimuli

upon inhibition, it produces the undesirable effect of upon inhibition, pain and fever are
decreasing protection to the reduced and inflammation is suppressed
stomach lining
 USES OF COX-1 & COX-2 INHIBITORS
COX-1 COX-2
enzyme enzyme
COX-1
• Protects stomach lining
• Decreases fever
• Promotes platelet aggregation

CELL COX-2
• Triggers pain and
inflammation
USES OF COX-1 & COX-2 INHIBITORS
Aspirin and NSAID’s

INHIBITS COX-1
block block • Loss of stomach lining
protection = ulcer
COX-1 COX-2
INHIBITS COX-2
• Reduces pain
CELL
• Suppresses inflammation
USES OF COX-1 & COX-2 INHIBITORS
COX-2
inhibitors

block COX-1
• Protects stomach lining
• Promotes blood clotting
COX-1 COX-2

COX-2
CELL • Reduces pain
• Suppresses inflammation
 COX-1 and COX-2

• COX-2 inhibitors approves by the US Food and Drug

Administration (FDA)
are celecoxib, meloxicam, and nabumetone

• Many researchers believe that COX-2 inhibitors may

prevent types of cancer such as
colon cancer.
 First- Generation
NSAIDs: Salicylates
Aspirin
INDICATIONS
to reduce pain, inflammatory symptoms,
fever, decrease inflammation for osteoarthritis
and rheumatoid arthritis; arterial
thromboembolism
PHARMACOKINETICS
PO; well absorbed from GI tract; ;
have a short half life; metabolized
in the liver; excreted in urine
MECHANISM OF ACTION ADVERSE
REACTIONS
inhibits prostaglandin synthesis,
hypothalamic heat regulator center, and tinnitus, hearing loss, hypokalemia,
platelet aggregation. proteinuria, metabolic acidosis,
cerebral edema, seizures/intracranial
bleeding
DRUG-TO-DRUG INTERACTION
may interact with anticoagulants/other
NSAIDs like ibuprofen and naproxen ;
not with oral hypoglycemic drugs
CONTRAINDICATIONS
Hypersensitivity to salicylates or NSAIDs
Caution: renal/hepatic disorders, gout, alcohol
abuse, anticoagulant therapy, GI bleeding
history
NURSING INTERVENTION PATIENT
TEACHING

• Observe/Assess • Advise
• Monitor • Suggest
• Provide • Instruct
• Inform
• Evaluate
 First- Generation
NSAIDs: Salicylates INDICATIONS MECHANISM OF ACTION

For mild to moderate pain, osteoarthritis, and inhibition of tissue cyclo-oxygenases

Diflunisa rheumatoid arthritis (Cox-1 and Cox-2)

l
ADVERSE REACTIONS
PHARMACOKINETICS
rash, headache, nausea, diarrhea,
PO
dyspepsia, GI bleeding, abdominal
pain, elevated hepatic enzymes, and
hearing loss
CONTRAINDICATIONS
Hypersensitive to Aspirin
Salicylate Derivatives INDICATIONS MECHANISM OF ACTION

For ulcerative colitis and rheumatoid prostaglandin synthesis

Sulfasalazine arthritis

ADVERSE REACTIONS
PHARMACOKINETICS
PO headache, dizziness, rash, anorexia, nausea,
abdominal pain, vomiting, dyspepsia, and
oligospermia

CONTRAINDICATIONS
Allergic to sulfonamides or aspirin
 PARA-CHLOROBENZOIC ACID
• Potent prostaglandin inhibitor
• Used for rheumatoid arthritis, gouty arthritis, and osteoarthritis
• One of the first NSAIDs introduced was Indomethacin
• Indomethacin is very irritating to the stomach and should be taken with food.

TWO OTHER PARA-CHLOROBENZOIC

ACID DERIVATIVES:
• Sulindac
• Tolmetin
Para- Chlorobenzoic INDICATIONS MECHANISM OF ACTION
Acid (Indoles) To mild to severe pain, acute gout, inhibits the synthesis of prostaglandins
tendinitis, , arthralgia, ankylosing
Indomethacin spondylitis, and arthritis

ADVERSE REACTIONS
PHARMACOKINETICS
• PO dizziness, headache, nausea, vomiting,
• rapidly absorbed from the constipation, dyspepsia, and arthritis
gastrointestinal tract
CONTRAINDICATIONS
Allergic to Aspirin
Para- Chlorobenzoic INDICATIONS MECHANISM OF ACTION
Acid (Indoles) For arthritis, bursitis, ankylosing Inhibition of prostaglandin synthesis
spondylitis, gout, and tendinitis
Sulindac

PHARMACOKINETICS ADVERSE REACTIONS

Dizziness, headache, rash, dyspepsia, nausea,
Absorption: Rapid given PO vomiting, diarrhea, abdominal pain,
constipation, and elevated hepatic enzymes

CONTRAINDICATIONS
• Acetylsalicylic acid (aspirin) allergy
• Hypersensitivity
Para- Chlorobenzoic INDICATIONS MECHANISM OF ACTION
Acid (Indoles) For mild to moderate pain, Prostaglandin synthetase inhibition
rheumatoid arthritis, and
Etodolac osteoarthritis

PHARMACOKINETICS ADVERSE REACTIONS

Dizziness, weakness, dyspepsia, nausea,
PO diarrhea, abdominal pain, flatulence, and
pyrosis

CONTRAINDICATIONS
• Patients with known
hypersensitivity
 PROPIONIC ACID DERIVATIVES
• The propionic acid group is a relatively new group of NSAIDs.
• Drugs in this group are highly protein bound, drug interactions
might occur
• Better tolerated than other NSAIDs

Ibuprofen
is most widely used propionic acid NSAID

Five other propionic acid agents:

Fenoprofen calcium, Naproxen, Ketoprofen,
Flurbiprofen, Oxaprozin
 Propionic Acid
INDICATIONS MECHANISM OF ACTION
Derivative to reduce inflammatory process and relieve pain; anti-
Inhibits COX-1 and COX-2 by blocking
inflammatory effect for arthritic conditions; to reduce
arachidonate binding

Ibuprofen
fever, dysmenorrhea, headache

PHARMACOKINETICS PHARMACODYNAMICS ADVERSE REACTIONS

PO; well absorbed from GI tract; highly PO: Onset: 30min- 1hr; Peak: GI bleeding/perforation/ulcer, tinnitus,
protein bound; have a short life; 2-4hr; and seizure
metabolized in the liver; excreted in Duration: 6-8hr
urine; some in bile

CONTRAINDICATIONS
Hypersensitivity, coronary artery bypass graft surgery
DRUG INTERACTION
increased bleeding time with oral anticoagulants, increased
effects of phenytoin, sulfonamides, warfarin; decreased effect
with aspirin; may increase severe side effects of lithium

NURSING INTERVENTION PATIENT TEACHING

• Observe • Advise
• Report • Alert
• Monitor • Direct
• Provide • Warn
• Inform
Propionic Acid
INDICATIONS MECHANISM OF ACTION
Derivative
For mild to moderate pain,
• Cyclooxygenase Inhibitor
Fenoprofen osteoarthritis, and rheumatoid
arthritis
• Prostaglandin synthesis

Calcium
PHARMACOKINETICS ADVERSE REACTIONS
• Absorption: Rapidly absorbed Drowsiness, dizziness, rash, headache,
• Distribution: highly bound to weakness, pruritus, dyspepsia, nausea,
albumin constipation, palpations, tinnitus, and peripheral
• Metabolism: T 1/2- 3 hours edema
• Excretion: Renal excretion
CONTRAINDICATIONS
Patients who have shown hypersensitivity to
Fenoprofen calcium
Propionic Acid
INDICATIONS MECHANISM OF ACTION
Derivative
For mild to moderate pain,
Cyclooxygenase Inhibitor
Fenoprofen osteoarthritis, and rheumatoid
arthritis
Sodium
PHARMACOKINETICS ADVERSE REACTIONS
• Absorption: Rapidly absorbed Dizziness, blurred vision, insomia, and
• Distribution: highly bound to rheumatoid arthritis
albumin
• Metabolism: T 1/2- 3 hours
• Excretion: Renal excretion
CONTRAINDICATIONS
Patients who have shown hypersensitivity to
Fenoprofen sodium
Propionic Acid
INDICATIONS MECHANISM OF ACTION
Derivative
For mild to moderate pain,
Inhibition cylooxygenase-2
Ketoprofen osteoarthritis, and rheumatoid
arthritis

PHARMACOKINETICS ADVERSE REACTIONS

Rapid: PO Headache, insomnia, nausea, dyspepsia,
diarrhea, flatulence, abdominal pain, and
constipation

CONTRAINDICATIONS
Patients who have shown hypersensitivity to
ketoprofen
Propionic Acid
INDICATIONS MECHANISM OF ACTION
Derivative
For mild to moderate pain,
• Blocks Arachidonate binding
Naproxen osteoarthritis, and rheumatoid
arthritis, ankylosing spondylitis, and
• Inhibit both Cox-1 and Cox-2

gout

PHARMACOKINETICS ADVERSE REACTIONS

Rapid: PO Pharyngitis, dyspepsia, influenza, elevated
hepatic enzyme, edema, GI bleeding

CONTRAINDICATIONS
• Hypersensitivity to NSAID medications
• ASA or NSAID-induced asthma
• Pregnancy
Propionic Acid
INDICATIONS MECHANISM OF ACTION
Derivative
Osteoarthritis and rheumatoid
Inhibition of cylooxygenase
Oxaprozin arthritis

PHARMACOKINETICS ADVERSE REACTIONS

Rapid: PO Edema, dizziness, drowsiness, confusion, GI
bleeding
CONTRAINDICATIONS
• Peptic ulcer or other GI diseases
• Chronic liver disease
• Diabetes mellitus
• Pregnancy
 FENAMATES (Anthranilic Acids)
• Include potent NSAIDs used for acute and chronic arthritis conditions.
• Decrease prostaglandin synthesis by inhibition of COX-1 and COX-2
• Patients with a history of peptic ulcer should avoid fenamates

Other side effects include:

Edema
Dizziness Two fenamates:
Tinnitus Meclofenamate sodium monohydrate
Pruritus Mefenamic acid
Anthranilic Acids
INDICATIONS MECHANISM OF ACTION
(Fenamates)
Mild to moderate pain, dysmenorrhea
Inhibiting the synthesis of prostaglandins
Meclofenemate

PHARMACOKINETICS ADVERSE REACTIONS

Rapid: PO Dizziness, rash, abdominal pain, flatulence, and
pyrosis

CONTRAINDICATIONS
Patients with known hypersensitivity to
meclofenamate sodium
Anthranilic Acids
INDICATIONS MECHANISM OF ACTION
(Fenamates)
Mild to moderate pain, dysmenorrhea
• Binds the prostaglandin synthetase
Mefenamic Acid receptors COX-1 and COX-2
• Inhibiting the action of prostaglandin
synthetase

PHARMACOKINETICS ADVERSE REACTIONS

Rapid: PO Chest pain or discomfort, nausea or vomiting,

trouble breathing
CONTRAINDICATIONS
Patients with previous serious skin reactions to
NSAIDs
 OXICAMS
• Indicated for long-term arthritic conditions such as RA and
osteoarthritis
• Decrease prostaglandin synthesis by inhibition of COX-1 and COX-2
• Are well-tolerated and their major advantage with other NSAIDs is
their long half-life

Two oxicams:
Piroxicam
Meloxicam
 Oxicams INDICATIONS MECHANISM OF ACTION
inhibition of tissue cyclooxygenases (Cox-1
Piroxicams Osteoarthritis and rheumatoid
arthritis
and -2) leading to a decrease in synthesis of
pro-inflammatory prostaglandins

PHARMACOKINETICS ADVERSE REACTIONS

Rapid: PO Rash, pruritus, anorexia, constipation, GI

bleeding
CONTRAINDICATIONS

• Known hypersensitivity
• History of asthma
 Oxicams INDICATIONS MECHANISM OF ACTION
inhibition of tissue cyclooxygenases (Cox-1
Meloxicam Osteoarthritis and rheumatoid
arthritis
and -2) leading to a decrease in synthesis of
pro-inflammatory prostaglandins

PHARMACOKINETICS ADVERSE REACTIONS

Rapid: PO Edema, abdominal pain, eructation, arthralgia

CONTRAINDICATIONS
Patients with previous serious skin reactions to
NSAIDs
 SELECTIVE COX-2 INHIBITORS
• Cyclooxygenase-2 (COX-2) inhibitors, second generation NSAIDS
• Most NSAIDs are nonselective inhibitors that inhibit COX-1 and
COX-2
• Selective COX-2 Inhibitors are the drugs of choice for patients
with severe arthritic conditions who need high doses of an anti-
inflammatory drug
• Celecoxib, is classified as COX-2 inhibitor
• Nabumetone and Meloxicam are similar drugs that can be used;
however they are not considered true COX-2 inhibitors
 Celecoxib
Nonsteroidal antiinflammatory: COX-2 inhibitor

CONTRAINDICATIONS Therapeutic Effects

Hypersensitivity, coronary bypass surgery, renal/hepatic
failure, angina, hypertension, dysrhythmias, heart failure,
cardiac disease, dehydration, peptic ulcer disease, GI
bleeding, anticoagulant therapy, alcohol abuse, peripheral
vascular disease, older adults
Used to treat osteoarthritis and rheumatoid arthritis: Relieves
moderate-severe dysmenorrhea pain: for ankylosing, and
migraine

PHARMACOKINETICS Pharmacodynamics
Absorption: well absorbed in the GI tract PO: Onset unknown
Distribution: Protein Binding - 97% Peak: 3h
Metabolism: t1/2: 11.2 h Duration: unknown
Excretion: Primarily in feces
 Celecoxib
Nonsteroidal antiinflammatory: COX-2 inhibitor

Drug-Lab-Food Interactions
Drug: Decreased effect of ACE inhibitors, increased INR and
GI bleeding with warfarin and SNRIs, may increased toxicity
with lithium, fluoroquinolone may increase risk of seizures
fluconazole and ketoconazole increase celecoxib levels

Adverse Reaction
GI bleeding/obstruction/ulcer/perforation, hypertension, hearing loss, dyspnea
tendon rupture, hypo-hypernatremia, tinnitus, thromboembolism
Life-threatening:
Anaphylaxis, angioedema, bronchospasm, renal/hepatic failure, aplastic
anemia, agranulocytosis, leukopenia, pancytopenia, thrombocytopenia,
Stevens-Johnson syndrome
Use of NSAIDs in Older
Adults
• Treat pain associated with inflammation
caused by Osteoarthritis, Rheumatoid
Arthritis, and neuromuscular disorders.
• With the use of NSAIDs, GI distress is four What are the downsides when
times more common in adults
taking NSAIDs chronically?

• NSAIDs affect the cardiovascular, GI,

renal, and respiratory systems.
 Corticosteroids
• A therapeutic agent used to treat allergic and inflammatory disorders by suppressing the
inflammatory process at the injured site.

• Common corticosteroids such as prednisone, prednisolone, and dexamethasone are frequently

used as inflammatory agents.

• It has a half-life of more than 24 hrs

• It comes in many forms, such as tablets, injections, inhalers, and sometimes topical creams and
ointments.

• Common side effects of corticosteroids are high blood pressure, increase in blod sugar,
psychiatric problems (long term), weight gain.
 Disease Modifying Anti-Rheumatic Drugs
(DMARDs)
• Includes immunosuppressive agents, immunomodulators, and antimalarials.

• Used for treatment of Rheumatoid Arthritis, osteoarthritis, psoriatic arthritis, severe psoriasis,
ankylosing spondylitis, Crohn's disease, and ulcerative colitis.

• DMARDs may take 6-12 weeks to begin to have an effect.

 Immunosuppressive Agents
• are use to treat refractory RA, arthritis that does not
respond to antiinflammatory drugs. In low doses,
selected immunosuppressive agents have been effective
in the treatment of RA.

Immunomodulators
• Treat moderate to severe RA by disrupting the
inflammatory process and delaying disease progression.
Interleukin1 (IL-1) receptor antagonists and tumor
necrosis factor (TNF) blockers are two groups of drugs
classified as immunomodulators.
MECHANISM OF ACTIONS
MECHANISM OF ACTIONS
 PHARMACOKINETICS OVERALL ADVERSE EFFECTS

IV and Subcu: Gulimumab, Abatacept, Tocilizumab CNS: Dizziness, Headache,

Subcutaneous: Anakinra, Etanercept, Adalimumab,

Seculinumab, Canakinumab, Sarilumab, Ixekizumab, Fever, sore throat, painful
Certolizumab pegol urination, diarrhea, hypertension,
cough
IV: Infliximab, Rituximab, Tocilizumab

Dermatologic: Rash, Swelling,

PO: Leflunomide, Tofacitinib, Apremilast, Baricitinib,
Upadacitinib Bruising, tingling
 CONTRAINDICATIONS
Golimumab : Diseases such as bacterial sepsis, tuberculosis Tocilizumab: Patients have liver problems
(TB), and fungal and opportunistic infections have been Secukinumab: Children, pregnancy and lactation,
reported. congestive heart failure, multiple sclerosis,
Anakinra: patients on concomitant immunosuppressants or premalignant condition Upadacitinib: Patients with
with impaired immune systems. any known hypersensitivity.
Etanercept : Patience with sepsis.
Canakinumab: Should not be administered to
Infliximab, Rituximab, Adalimumab: Active and severe
patients during an active infection.
infection.
Sarilumab, Baricitinib: Patients with chronic
Leflunamide: Severe hepatic impairment due to
kidney disease.
hepatotoxicity.
Tofacitinib: Patients who are at high risk for pulmonary
embolism.
 DRUG TO DRUG INTERACTIONS

Adalimumab, certolizumab, etanercept, infliximab, Secukinumab

canakinumab, golimumab • risk or severity of adverse effects can be increased
• TNF blockers when Chloramphenicol is combined with
Secukinumab.
Abatacept, Anakinra, Cyclosporin, Leflunamide
Sarilumab
• Weakens the immune system
• The therapeutic efficacy of AstraZeneca COVID-
19 Vaccine can be decreased when used in
Tofacitinib combination with Sarilumab.
• Increase immunosuppressive activities
Baricitinib
Tocilizumab, Apremilast, Upadacitinib • not recommended in combination with other JAK
• Increase severity of adverse effects inhibitors, biologic DMARDs, or potent
immunosuppressives.
INFLIXIMA
( REMICADE)
B
 INFLIXIMAB

• Is a targeted disease modifying anti-rheumatic drug that is used to reduce inflammation produced
by the body.

• In certain diseases the immune system is over active, this can target healthy tissues such as joints.

MECHANISM OF ACTION

• Binds to TNF and blocks it from attaching to TNF receptors on synovial cell surfaces
• Reduces infiltration of inflammatory cells and delays inflammatory process
DRUG CLASS

Immunomodulator: Tumor necrosis factor blocker

INDICATION CONTRAINDICATION
S S
• Severe chronic plaque psoriasis • Hypersensitivity to infliximab, murine
• Psoriatic arthritis proteins, or any other component of the
• Moderate to severe rheumatoid arthritis
product
• Moderate to severe ulcerative colitis in
patients who have failed conventional therapy
• Moderate to severe Crohn's disease in patients
• Do not administer doses greater than 5
who have failed conventional therapy mg/kg to patients who have moderate to
severe heart failure
 PHARMACODYNAMIC DRUG
S INTERACTIONS
IV: Onset : RA : 3-7 d; Crohn
May decrease effectiveness of vaccines;
Disease: 1-2 wk
concurrent immunosuppressiveness may increase
Peak: UK
risk for infection or adverse effects
Duration: RA: 6-12 wk; Crohn
Disease 8-8-48 weeks

PHARMACOKINETI
CS
Absorption: UK
Distribution: UK
Metabolism: t 1/2 : 8- 9.5 d
EXCRETION: UK
 ADVERSE
REACTION

• Severe infections, hypo/hypertension, chest pain, dsypnea, seizures, bone fractures, anemia, pulonary edema,
bradycardia, GI obstrusction, antibody formation

• LIFE THREATENING: Bronchospasm, leukopenia, neutropenia, pancytopenia, hymolytic anemia,

thrombocytopenia, hepatotoxicity, Stevens- Johnson syndrome
 NURSING PATIENT
INTERVENTION TEACHING
• Obtain
• Monitor • Keep medical appointments
• • Regular sched of lab tests
Flush
• Advice to avoid live vaccines while
• Deliver
tatking infliximab
• Administer
• Discontinue
 ANTIMALARIA
LS

Antimalarial Drugs may be used to treat RA when other methods of

treatment fail. The mechanism of action of antimalarials in suppressing RA
is unclear.

The effect may take 4 to 12 weeks to become apparent. Antimalarials are

usually used in combination with NSAIDs in patients whose arthritis is not
under control.
 ANTIGOUT DRUGS
GOUT
• Is an inflammatory condition that attacks joints,
tendons, and other tissues.
• Characterized by uric acid metabolism disorder
and a defect in purine metabolism.
• Common site of gouty inflammation is the hallux
(big toe).
ANTIINFLAMMATORY GOUT DRUG
COLCHICINE
• The first drug used to treat gout, it was
introduced in 1936.

• Effective for in alleviating acute symptoms

of gout, but not effective for decreasing
inflammation.
COLCHICINE
INDICATIONS PHARMACOKINECTICS PHARMACODYNAMICS
Alleviate acute Absorption PO
symptoms of gout. GI Tract Onset: 1hr
Peak: 2hr
Distribution Duration: 1hr
PB 34 - 44%
CONTRAINDICATION
Renal and Gastric Metabolism
T 1/2 - 1.7 - 31.2 hrs
disorders

Excretion
80 - 90% feces
10 - 20% urine
COLCHICINE

MECHANISM OF ACTION ADVERSE EFFECTS

• Does not inhibit uric acid synthesis. • Headache
• Does not promote uric acid • Nausea
excretion. • Vomiting
• Inhibit the migration of leukocytes • Diarrhea
to injured sites. • Fatigue
• Peripheral neuropathy
 XANTHINE OXIDASE INHIBITORS
ALLUPURINOL

• First marketed in 1963.

• Not an antiinflammatory drug.

ALLOPURINOL
INDICATIONS PHARMACOKINECTICS PHARMACODYNAMICS
Increase uric acid Absorption
excretion. GI Tract

Distribution
PB: UK
CONTRAINDICATION
Hyperuricemia and renal Metabolism
T 1/2 - 1 - 2 hrs
calculi

Excretion
80 - 90% urine
10 - 20% feces
ALLOPURINOL

MECHANISM OF ACTION ADVERSE EFFECTS

• Inhibiting the xanthine oxidase • Nausea
enzyme. • Vomiting
• Diarrhea
• Blocks metabolism of xanthine into • GI bleeding/obstruction
uric acid.
 Febuxostat
Approved by the FDA in 2009 to treat hyperuricemia
associated with gout. Has a greater risk of promoting
cardiovascular adverse events.
Antigout: Xanthine oxidase inhibitor

CONTRAINDICATIONS Therapeutic Effects

Hypersensitvity Treat gout and hyperuricemia
Caution: Mechanism of Action:
Hepatic/renal disorder, cardiac disease, stroke, chemotherapy Block hypoxanthine and xanthine to reduce uric acid
synthesis to decrease uric acid blood and urine concentration

PHARMACOKINETICS
Absorption: PO: 49% absorbed
Pharmacodynamics
Distribution: Protein Binding - 99.2%
PO: Onset unknown
Metabolism: t1/2: 5-8 h
Peak: 1-1.5 hours
Excretion: Urine (49%), Feces (45%)
Duration: unknown
 Febuxostat
Approved by the FDA in 2009 to treat hyperuricemia
associated with gout. Has a greater risk of promoting
cardiovascular adverse events.
Antigout: Xanthine oxidase inhibitor

Drug-Lab-Food Interactions
Drug: Increased effect of theophylline, azathioprine,
didanosine, mercaptopurine, pegloticase
Lab: Increased alanine aminotransferase, aspartate
aminotransferase, blood urea nitrogen

Adverse Reaction
Bradycardia, gout exacerbations, Guillain-Barre syndrome, dyspnea, chest pain, diabetes mellitus, hyperglycemia, anemia,
elevated hepatic enzymes, hyperlipidemia, hypertriglyceridemia, hypercholesterolemia, cholecystitis, rhabdomyolysis

Life-threatening:
Thrombocytopenia, neutropenia, leukopenia, pancytopenia, angioedema, hepatic/renal impairment, dysrhythmias, Stevens-
Johnson syndrome
 URICOSURICS
PROBENECID

• Is a uricosurics that has been available since

1945.

• Effective in alleviating chronic gout.

PROBENECID
INDICATIONS PHARMACOKINECTICS PHARMACODYNAMICS
Increase uric acid Absorption
excretion. GI Tract

Distribution
PB 75 - 95%
CONTRAINDICATION
Metabolism
Hyperuricemia
T 1/2 - 3 - 12 hrs

Excretion
Urine
PROBENECID

MECHANISM OF ACTION ADVERSE EFFECTS

• Blocks reabsorption of uric acid. • Dizziness
• Flushing
• Headache
• Fever
• Nausea
• Vomiting
• Anemia
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