RHEUMATOID ARTHRITIS (RA):
PHARMACOLOGY OF DRUGS
1. Introduction
Rheumatoid arthritis is a chronic, systemic, autoimmune inflammatory disease characterized
by:
Symmetrical polyarthritis
Synovial inflammation → pannus formation
Cartilage destruction and bone erosion
Pathophysiology (Key targets)
Activation of T-cells
Release of pro-inflammatory cytokines:
TNF-α, IL-1, IL-6
Activation of B-cells → autoantibodies (RF, anti-CCP)
Increased prostaglandins & leukotrienes
📌 Goal of therapy:
Reduce inflammation
Relieve pain
Prevent joint damage
Maintain function
2. Classification of Drugs Used in RA
A. Symptomatic Relief
1. NSAIDs
2. Glucocorticoids
B. Disease-Modifying Antirheumatic Drugs (DMARDs)
1. Conventional (Synthetic) DMARDs
2. Biologic DMARDs
3. Targeted Synthetic DMARDs (JAK inhibitors)
, 3. NSAIDs in Rheumatoid Arthritis
Examples
Ibuprofen
Naproxen
Diclofenac
Indomethacin
Celecoxib (COX-2 selective)
Mechanism of Action
Inhibit cyclo-oxygenase (COX-1 & COX-2)
↓ Prostaglandin synthesis → ↓ pain & inflammation
Role in RA
Provide symptomatic relief only
Do NOT alter disease progression
Adverse Effects
Gastric irritation, ulcers
Renal toxicity
Cardiovascular risk (COX-2 inhibitors)
📌 Important: NSAIDs are adjuncts, not definitive therapy.
4. Glucocorticoids
Examples
Prednisone
Prednisolone
Methylprednisolone
Mechanism of Action
Bind intracellular glucocorticoid receptors
↓ Transcription of inflammatory genes
↓ Cytokines (TNF-α, IL-1, IL-6)
↓ COX-2 expression
PHARMACOLOGY OF DRUGS
1. Introduction
Rheumatoid arthritis is a chronic, systemic, autoimmune inflammatory disease characterized
by:
Symmetrical polyarthritis
Synovial inflammation → pannus formation
Cartilage destruction and bone erosion
Pathophysiology (Key targets)
Activation of T-cells
Release of pro-inflammatory cytokines:
TNF-α, IL-1, IL-6
Activation of B-cells → autoantibodies (RF, anti-CCP)
Increased prostaglandins & leukotrienes
📌 Goal of therapy:
Reduce inflammation
Relieve pain
Prevent joint damage
Maintain function
2. Classification of Drugs Used in RA
A. Symptomatic Relief
1. NSAIDs
2. Glucocorticoids
B. Disease-Modifying Antirheumatic Drugs (DMARDs)
1. Conventional (Synthetic) DMARDs
2. Biologic DMARDs
3. Targeted Synthetic DMARDs (JAK inhibitors)
, 3. NSAIDs in Rheumatoid Arthritis
Examples
Ibuprofen
Naproxen
Diclofenac
Indomethacin
Celecoxib (COX-2 selective)
Mechanism of Action
Inhibit cyclo-oxygenase (COX-1 & COX-2)
↓ Prostaglandin synthesis → ↓ pain & inflammation
Role in RA
Provide symptomatic relief only
Do NOT alter disease progression
Adverse Effects
Gastric irritation, ulcers
Renal toxicity
Cardiovascular risk (COX-2 inhibitors)
📌 Important: NSAIDs are adjuncts, not definitive therapy.
4. Glucocorticoids
Examples
Prednisone
Prednisolone
Methylprednisolone
Mechanism of Action
Bind intracellular glucocorticoid receptors
↓ Transcription of inflammatory genes
↓ Cytokines (TNF-α, IL-1, IL-6)
↓ COX-2 expression
