DMARDs
1. Rheumatoid Arthritis (RA) Overview
Rheumatology: Diseases causing inflammation of joints, muscles, ligaments, connective tissue.
Examples: OA, RA, gout, SLE, psoriatic arthritis, ankylosing spondylitis, Sjogren’s, myositis.
Pathogenesis of RA (not coming in exam)
RA is an autoimmune disease involving:
● Initiation: nonspecific inflammation
● Amplification: T-cell activation
● Chronic inflammation: cytokines TNF-α, IL-1, IL-6, IL-17 → synovial proliferation,
joint destruction
Key immune cells involved:
● T-cells (IL-15, IL-17, RANKL)
● B-cells (antibody production, antigen presentation)
Symptoms
● Systemic: morning stiffness, fatigue, low-grade fever, anorexia
● Joint: symmetric pain & swelling in MCP, PIP, wrists, MTP, knees, shoulders
Pathophysiology
● Immune system attacks joint lining → chronic inflammation
● Cytokines + metalloproteases → bone & cartilage destruction
● Progressive joint deformity; more common in women
, 2. Pharmacological Management Strategy
1. NSAIDs → fast pain relief (no disease modification)
2. Corticosteroids → fast anti-inflammatory effect
3. DMARDs → slow, but prevent joint damage (start early within 1–2 yrs as cartilage
damage & bony erosions occur in this years)
3. Classification of DMARDs
A. Conventional Synthetic DMARDs (csDMARDs)
● Methotrexate (MTX)
● Leflunomide
● Sulfasalazine / 5-ASA agents
● Hydroxychloroquine
● Azathioprine
● Cyclosporine
● Mycophenolate
● Cyclophosphamide
● Gold salts (aurothiomalate)
B. Biological DMARDs (bDMARDs)
Cytokine modulators:
● Anti-TNF: Adalimumab, etanercept, infliximab, golimumab, certolizumab
● Anti-IL-1: Anakinra
● Anti-IL-6: Tocilizumab
● T-cell costimulation blocker: Abatacept
● B-cell depletion: Rituximab
C. Targeted Synthetic DMARDs (tsDMARDs)
● Tofacitinib (JAK inhibitor)
1. Rheumatoid Arthritis (RA) Overview
Rheumatology: Diseases causing inflammation of joints, muscles, ligaments, connective tissue.
Examples: OA, RA, gout, SLE, psoriatic arthritis, ankylosing spondylitis, Sjogren’s, myositis.
Pathogenesis of RA (not coming in exam)
RA is an autoimmune disease involving:
● Initiation: nonspecific inflammation
● Amplification: T-cell activation
● Chronic inflammation: cytokines TNF-α, IL-1, IL-6, IL-17 → synovial proliferation,
joint destruction
Key immune cells involved:
● T-cells (IL-15, IL-17, RANKL)
● B-cells (antibody production, antigen presentation)
Symptoms
● Systemic: morning stiffness, fatigue, low-grade fever, anorexia
● Joint: symmetric pain & swelling in MCP, PIP, wrists, MTP, knees, shoulders
Pathophysiology
● Immune system attacks joint lining → chronic inflammation
● Cytokines + metalloproteases → bone & cartilage destruction
● Progressive joint deformity; more common in women
, 2. Pharmacological Management Strategy
1. NSAIDs → fast pain relief (no disease modification)
2. Corticosteroids → fast anti-inflammatory effect
3. DMARDs → slow, but prevent joint damage (start early within 1–2 yrs as cartilage
damage & bony erosions occur in this years)
3. Classification of DMARDs
A. Conventional Synthetic DMARDs (csDMARDs)
● Methotrexate (MTX)
● Leflunomide
● Sulfasalazine / 5-ASA agents
● Hydroxychloroquine
● Azathioprine
● Cyclosporine
● Mycophenolate
● Cyclophosphamide
● Gold salts (aurothiomalate)
B. Biological DMARDs (bDMARDs)
Cytokine modulators:
● Anti-TNF: Adalimumab, etanercept, infliximab, golimumab, certolizumab
● Anti-IL-1: Anakinra
● Anti-IL-6: Tocilizumab
● T-cell costimulation blocker: Abatacept
● B-cell depletion: Rituximab
C. Targeted Synthetic DMARDs (tsDMARDs)
● Tofacitinib (JAK inhibitor)
