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RA.ppt
1. Drugs used in joint diseases
Dr Sanjeewani Fonseka
Department of Pharmacology
2. OBJECTIVES
• List the classes of drugs that are used in
the treatment of RA
• Describe the mechanism of action,
pharmacokinetics and adverse effects of
the above drugs
• Explain the basis of disease modifying
drugs
• Explain the basis of drug treatment of OA
and gout
11. Disability in RA
• Most of the disability in RA is a result of
the INITIAL burden of disease
• People get disabled because of:
– Inadequate control
– Lack of response
– Compliance
• GOAL: control the disease early on!
12. Drugs for RA
• Nonsteroidal anti-inflammatory drugs
(NSAIDs)
• Disease-modifying anti-rheumatic drugs
(DMARDs)
– Synthetic
– Biologic
• Glucocorticoids
37. Leflunomide
• Competitive inhibitor of dihydroorotate
dehydrogenase (rate-limiting enzyme in de
novo synthesis of pyrimidines)
• Reduce lymphocyte proliferation
38. Leflunomide cont
• Oral
• T ½ - 4 – 28 days due to EHC
• Elimination hepatic
• Action in one month
• Avoid pregnancy for 2 years
39. Side effects of leflunomide
• Hepatotoxicity
• BM suppression
• Diarrhoea
• rashes
44. BIOLOGIC THERAPY
• Complex protein molecules
• Created using molecular biology methods
• Produced in prokaryotic or eukaryotic cell
cultures
45. Biologics
• Monoclonal Antibodies to TNF
– Infliximab
– Adalimumab
• Soluble Receptor Decoy for TNF
– Etanercept
• Receptor Antagonist to IL-1
– Anakinra
• Monoclonal Antibody to CD-20
– Rituximab
46. Tumour Necrosis Factor (TNF)
• TNF is a potent inflammatory cytokine
• TNF is produced mainly by macrophages and
monocytes
• TNF is a major contributor to the inflammatory
and destructive changes that occur in RA
• Blockade of TNF results in a reduction in a
number of other pro-inflammatory cytokines (IL-
1, IL-6, & IL-8)
51. Drugs for RA
• Nonsteroidal anti-inflammatory drugs
(NSAIDs)
• Disease-modifying anti-rheumatic drugs
(DMARDs)
– Synthetic
– Biologic
• Glucocorticoids
52. Glucocorticoids
• Potent anti-inflammatory drugs
• Serious adverse effects with long-term use
• To control the diaseas
• Indications
– As a bridge to effective DMARD therapy
– Systemic complications (e.g. vasculitis)
58. Goals of Treatment
• Control pain and swelling
• Minimize disability
• Improve the quality of life
• Prevent progression
59. NSAIDs
• Tend to avoid for long-term use
• Indomethacin should be avoided for long-
term use in patients with hip OA
–associated with accelerated joint
destruction
60. • Read – different classes of NSAID that
can be used in OA
61. Topical NSAIDs
• Effect was not apparent at three to four
weeks
• Topical NSAIDs were generally inferior to
oral NSAIDs
• Topical route was safer than oral use
• Topical Diflofenac (1% gel or patch)
71. Colchicine
Colchicine- reduces pain, swelling, and
inflammation; pain subsides within 12 hrs
and relief occurs after 48 hrs
Prevent migration of neutrophils to joints
75. URICOSURIC AGENTS
• Probenecid
• Increased secretion of urate into urine
• Reverses most common physiologic
abnormality in gout ( 90% pt.s are
underexcretors)
83. OA
• Pain relief
• Glucosamine Sulfate
• Hyaluronic acids injections
• Surgery
84. TREATMENT OF GOUT
• Colchicine, NSAID, steroids – acute attack
• Allopurinol- decreases the production of uric
acid
• Probenecid - prevent absorption of uric acid in
the tubules of kidney
85. OBJECTIVES
• List the classes of drugs that are used in
the treatment of RA
• Describe the mechanism of action,
pharmacokinetics and adverse effects of
the above drugs
• Explain the basis of disease modifying
drugs
• Explain the basis of drug treatment of OA
and gout
