slow acting anti-inflammatory drugs ). by prof. azza el-medany dr. osama yousf
TRANSCRIPT
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Disease –Modifying Antirheumatic drugs
Slow Acting Anti-inflammatory Drugs )
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BY PROF.
AZZA EL-MEDANY
DR.
OSAMA YOUSF
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OBJECTIVES
At the end of the lecture the students should
Define DMARDsDescribe the classification of this
group of drugsDescribe the general advantages &
criteria of this group of drugs Describe the general clinical uses
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o Know some examples of drugs related to DMARDS.
o Describe the mechanism of action , specific clinical uses , adverse effects &
contraindications of individual drugs.
OBJECTIVES ( Continue)
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General FeaturesLow doses are commonly used early in the
course of the diseaseUsed when the disease is progressing & causing
deformities ( they stop the progress of the disease )
Used when the inflammatory disease is not responding to NSAIDs
Can not repair the existing damage , but prevent further deformity
Have no analgesic effectsSlow onset their effects take from 6 weeks up to
6 months to be evident
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General Clinical Uses
Treatment of rheumatic disorders
Combination therapies are both safe & efficacious
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Hydroxychloroquine Mechanism of action :
Stabilization of lysosomal enzyme activity
Trapping free radicals
Suppression of T lymphocyte cells
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PharmacokineticsRapidly & completely absorbed following
oral administration.
Has a very large volume of distribution
Penetrates into C.N.S. & traverse the placenta
Metabolized in liver
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ContinueSome metabolic products retain
antimalarial activity
Both parent drug & metabolites are excreted in the urine
The excretion rate is enhanced in acidic urine
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Pruritius
GIT upset
Discoloration of nail beds & mucous membranes
Irreversible retinal damage
Adverse Effects
Headaches
Blurred vision
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MethotrexateImmunosuppressant drug
Response to methotrexate occurs sooner than for other slow acting drugs.
Doses of methotrexate are much lower than those needed in cancer chemotherapy
Given once a week
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Mechanism of action
Inhibition of polymorphonuclear chemotaxis
Inhibition of T-Cells ( cell-mediated immune reactions)
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Nausea
Liver cirrhosis
Mucosal ulceration
Acute pneumonia –like syndrome
Adverse Effects
Cytopenias
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Tumor necrosis factor –α
(TNF-α ) blocking agents
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Infliximab
A chimeric antibody ( 25% mouse, 75% human)
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Mechanism of action
Binds to human TNF-α resulting in inhibition of macrophage & T cell function
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InfliximabGiven as IV infusion over at least two
hoursHalf-Life 8-12 days Given every 8 weeks regimen.Elicits up to 62% incidence of human
antichimeric antibodies.Concurrent therapy with methotrexate
decreases the prevalence of human antichimeric antibodies
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Adverse effects
Infections
Upper respiratory
tract infections
Activation of latent
tuberculosis
Pancytopenia
Infusion reactions
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Comparison between NSAIDs & DMARDs
DMARDs NSAIDsSlow onset of actionArrest progression of the
diseasePrevent formation of
new deformityUsed in chronic cases
when deformity is exciting
Rapid onset of actionNo effect Can not stop formation
of new deformityUsed in acute cases to
relief inflammation & pain
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SUMMARYDMARDs are used mainly in chronic cases of
rheumatoid arthritis , when the disease is progresssing and forming deformity.
They do not remove the existing damage but prevent further formation of deformities.
They have no analgesic effect.
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SUMMARY ( Continue)They are slow in onset needs weeks to
manifest their effects .
Hydroxychloroquine acts mainly through suppression of the activity of lysosomal enzymez and trapping free radicals .
Its main adverse effects is irreversible retinal damage & hepatic toxicity.
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CONTINUEMethotrexate acts mainly through
suppression of phagocytic cells & T cells
Its adverse effects are bone marrow depression & mucosal ulceration
Infliximab is a chimeric TNF-α blocking agent.
Given with methotrexate to reduce antichimeric effect
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CONTINUEIts main adverse effects are upper respiratory
tract infections & reactivation of latent TB,
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CONTINUEMethotrexate acts mainly through
suppression of phagocytic cells &