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RHEUMATOID
ARTHRITIS
PREPARED BY:-
MALINI.R
P1122002
PRESENTED ON : -
12/01/23
CONTENTS
Introduction
Types of rheumatoid arthritis
Stages of rheumatoid arthritis
Epidemiology
Etiology and Pathophysiology
Symptoms
Diagnosis
Risk factors
Complications
Treatment 2
Introduction
Rheumatoid arthritis (RA) is a chronic symmetrical, autoimmune disease that
involves inflammation in the lining of joints and often affects internal organs.
 Result in progressive joint destruction, deformity, and disability.
3
4
DIFFERENCE BETWEEN RHEUMATOID ARTHRITIS AND
OSTEOARTHRITIS
5
DIFFERENCE BETWEEN RHEUMATOID ARTHRITIS AND
OSTEOARTHRITIS
DISEASES RHEUMATOID ARTHRITIS OSTEOARTHRITIS
CONDITION
Autoimmune disorder Degenerative joint disorder
AFFECTS MCP AND PIP in hands DIP in hands
CAUSES Bone erosion breakdown of the cartilage
SYMPTOM
Morning stiffness usually exceeds 30
minutes
Morning stiffness usually less 30
minutes
TREATMENT
Disease-modifying medications and
biologics that target your immune
system.
Anti-inflammatory and
corticosteroid medications.
6
MCPAND PIP DIP in HANDS
7
TYPES OF RHEUMATOID ARTHRITIS
 SEROPOSITIVE RA - When anti-CCP and /or RF are detected in the blood of someone with
RA.
 SERONEGATIVE RA- If someone has rheumatoid arthritis but anti-CCP and RF antibodies
are not present in the blood.
 more likely respond to treatment.
 JUVENILE IDIOPATHIC ARTHRITIS (JIA)- JIA describes multiple types of autoimmune,
inflammatory arthritis in children.
8
STAGES OF RHEUMATOID ARTHRITIS
STAGE 1-The body mistakenly
attacks its own joint tissue.
STAGE 2- Antibodies Develop and
Swelling Worsens
STAGE 3-Symptoms Are Visible
STAGE 4- Joints Become Fused
9
EPIDEMIOLOGY
 Approximately 1% of the population worldwide is affected by rheumatoid arthritis.
 It occurs three times more common in women compared to men.
 Nearly 5% of women and 3% of men over the age of 65 years are affected by the disease.
 Rheumatoid arthritis also affects young children.
10
ETIOLOGY AND PATHOPHYSIOLOGY
11
ETIOLOGY AND PATHOPHYSIOLOGY
12
13
14
15
16
17
18
19
20
SYMPTOMS
 joint swelling may be visible or may be apparent only by palpation.
 Stiffness may precede development of synovitis.
 Extra-articular involvement may include rheumatoid nodules, vasculitis, pleural effusions,
pulmonary fibrosis, ocular manifestations, pericarditis, cardiac conduction abnormalities,
bone marrow suppression, and lymphadenopathy.
 Nonspecific prodromal symptoms fatigue, weakness, weight loss, joints ,low-grade fever, loss
of appetite, anorexia, and diffuse musculoskeletal pain, joint pain, joints that are tender, swollen
and warm, and rheumatoid nodules under the skin.
21
22
DIAGNOSIS
Laboratory abnormalities that may be seen include :-
 Complete blood count: Slight elevation in WBC count
 normocytic, normochromic anemia;
 thrombocytosis or thrombocytopenia;
 leukopenia;
 elevated erythrocyte sedimentation rate
 C-reactive protein;
 and positive antinuclear antibodies
 Erosions occurring later in the disease course are usually seen first in the
metacarpophalangeal and proximal interphalangeal joints of the hands and
metatarsophalangeal joints of the feet.
23
RISK FACTORS
 Gender
 Genetics
 and Environmental exposure (cigarette smoking, air pollutants, and
occupational).
24
COMPLICATIONS
 Permanent joint damage requiring arthroplasty
 Rheumatoid vasculitis
 and Felty syndrome requiring splenectomy if it remains unaddressed.
25
GOAL OF TREATMENT
26
 to induce a complete remission, although this may be difficult to achieve.
The primary objectives are to
 reduce joint swelling, stiffness, and pain;
 preserve range of motion and joint function;
 improve quality of life;
 prevent systemic complications;
 prevent or control joint damage
 To minimize adverse effects of treatment.
TREATMENT
Adequate rest, weight reduction if obese,
occupational therapy, physical therapy, and use
of assistive devices may improve symptoms and
help maintain joint function.
Patients with severe disease may benefit from
surgical procedures such as tenosynovectomy,
tendon repair, and joint replacements.
Patient education about the disease and the
benefits and limitations of drug therapy is
important. 27
NON PHARMACOLOGIC THERAPY
PHARMACOLOGICAL TREATMENT
A disease-modifying antirheumatic drug (DMARD) should be started within the first 3 months of symptom
onset.
 DMARDs should be used in all patients except those with limited disease.
Early use of DMARDs results in a more favorable outcome and can reduce mortality.
 First-line DMARDs include methotrexate (MTX) (7,5 to 20mg), hydroxychloroquine(400mg),
sulfasalazine(1000mg), and leflunomide(20mg).
 MTX is often chosen initially because long-term data suggest superior outcomes compared with other DMARDs
and lower cost than biologic agents. 28
PHARMACOLOGICAL TREATMENT
 Leflunomide appears to have long-term efficacy similar to MTX.
Biologic agents with disease-modifying activity include the anti-TNF agents (etanercept (25mg), infliximab (3mg/kg),
adalimumab(40mg), the IL-1 receptor antagonist anakinra(100mg), and rituximab (1g), which depletes peripheral B
cells.
Biologic agents are effective for patients who fail treatment with other DMARDs.
DMARDs that are less frequently used include azathioprine (2 to 3mg), penicillamine(250mg), gold salts, minocycline
(100mg), cyclosporine (2.5 to 5mg), and cyclophosphamide (50 to 100mg). These agents have either less efficacy or
higher toxicity, or both.
• Combination therapy with two or more DMARDs may be effective when single-DMARD treatment is unsuccessful.
29
PHARMACOLOGICAL TREATMENT
Combinations that are particularly effective include-
 (1) MTX plus cyclosporine,
 (2) MTX plus sulfasalazine and hydroxychloroquine.
Nonsteroidal anti inflammatory drugs (NSAIDs) and/or corticosteroids may be used for symptomatic relief if
needed.
corticosteroids have the potential for long-term complications.
They provide relatively rapid improvement compared with DMARDs, which may take weeks to months before
benefit is seen. 30
Thank you
32

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rheumatoid arthritis.pptx

  • 2. CONTENTS Introduction Types of rheumatoid arthritis Stages of rheumatoid arthritis Epidemiology Etiology and Pathophysiology Symptoms Diagnosis Risk factors Complications Treatment 2
  • 3. Introduction Rheumatoid arthritis (RA) is a chronic symmetrical, autoimmune disease that involves inflammation in the lining of joints and often affects internal organs.  Result in progressive joint destruction, deformity, and disability. 3
  • 4. 4
  • 5. DIFFERENCE BETWEEN RHEUMATOID ARTHRITIS AND OSTEOARTHRITIS 5
  • 6. DIFFERENCE BETWEEN RHEUMATOID ARTHRITIS AND OSTEOARTHRITIS DISEASES RHEUMATOID ARTHRITIS OSTEOARTHRITIS CONDITION Autoimmune disorder Degenerative joint disorder AFFECTS MCP AND PIP in hands DIP in hands CAUSES Bone erosion breakdown of the cartilage SYMPTOM Morning stiffness usually exceeds 30 minutes Morning stiffness usually less 30 minutes TREATMENT Disease-modifying medications and biologics that target your immune system. Anti-inflammatory and corticosteroid medications. 6
  • 7. MCPAND PIP DIP in HANDS 7
  • 8. TYPES OF RHEUMATOID ARTHRITIS  SEROPOSITIVE RA - When anti-CCP and /or RF are detected in the blood of someone with RA.  SERONEGATIVE RA- If someone has rheumatoid arthritis but anti-CCP and RF antibodies are not present in the blood.  more likely respond to treatment.  JUVENILE IDIOPATHIC ARTHRITIS (JIA)- JIA describes multiple types of autoimmune, inflammatory arthritis in children. 8
  • 9. STAGES OF RHEUMATOID ARTHRITIS STAGE 1-The body mistakenly attacks its own joint tissue. STAGE 2- Antibodies Develop and Swelling Worsens STAGE 3-Symptoms Are Visible STAGE 4- Joints Become Fused 9
  • 10. EPIDEMIOLOGY  Approximately 1% of the population worldwide is affected by rheumatoid arthritis.  It occurs three times more common in women compared to men.  Nearly 5% of women and 3% of men over the age of 65 years are affected by the disease.  Rheumatoid arthritis also affects young children. 10
  • 13. 13
  • 14. 14
  • 15. 15
  • 16. 16
  • 17. 17
  • 18. 18
  • 19. 19
  • 20. 20
  • 21. SYMPTOMS  joint swelling may be visible or may be apparent only by palpation.  Stiffness may precede development of synovitis.  Extra-articular involvement may include rheumatoid nodules, vasculitis, pleural effusions, pulmonary fibrosis, ocular manifestations, pericarditis, cardiac conduction abnormalities, bone marrow suppression, and lymphadenopathy.  Nonspecific prodromal symptoms fatigue, weakness, weight loss, joints ,low-grade fever, loss of appetite, anorexia, and diffuse musculoskeletal pain, joint pain, joints that are tender, swollen and warm, and rheumatoid nodules under the skin. 21
  • 22. 22
  • 23. DIAGNOSIS Laboratory abnormalities that may be seen include :-  Complete blood count: Slight elevation in WBC count  normocytic, normochromic anemia;  thrombocytosis or thrombocytopenia;  leukopenia;  elevated erythrocyte sedimentation rate  C-reactive protein;  and positive antinuclear antibodies  Erosions occurring later in the disease course are usually seen first in the metacarpophalangeal and proximal interphalangeal joints of the hands and metatarsophalangeal joints of the feet. 23
  • 24. RISK FACTORS  Gender  Genetics  and Environmental exposure (cigarette smoking, air pollutants, and occupational). 24
  • 25. COMPLICATIONS  Permanent joint damage requiring arthroplasty  Rheumatoid vasculitis  and Felty syndrome requiring splenectomy if it remains unaddressed. 25
  • 26. GOAL OF TREATMENT 26  to induce a complete remission, although this may be difficult to achieve. The primary objectives are to  reduce joint swelling, stiffness, and pain;  preserve range of motion and joint function;  improve quality of life;  prevent systemic complications;  prevent or control joint damage  To minimize adverse effects of treatment.
  • 27. TREATMENT Adequate rest, weight reduction if obese, occupational therapy, physical therapy, and use of assistive devices may improve symptoms and help maintain joint function. Patients with severe disease may benefit from surgical procedures such as tenosynovectomy, tendon repair, and joint replacements. Patient education about the disease and the benefits and limitations of drug therapy is important. 27 NON PHARMACOLOGIC THERAPY
  • 28. PHARMACOLOGICAL TREATMENT A disease-modifying antirheumatic drug (DMARD) should be started within the first 3 months of symptom onset.  DMARDs should be used in all patients except those with limited disease. Early use of DMARDs results in a more favorable outcome and can reduce mortality.  First-line DMARDs include methotrexate (MTX) (7,5 to 20mg), hydroxychloroquine(400mg), sulfasalazine(1000mg), and leflunomide(20mg).  MTX is often chosen initially because long-term data suggest superior outcomes compared with other DMARDs and lower cost than biologic agents. 28
  • 29. PHARMACOLOGICAL TREATMENT  Leflunomide appears to have long-term efficacy similar to MTX. Biologic agents with disease-modifying activity include the anti-TNF agents (etanercept (25mg), infliximab (3mg/kg), adalimumab(40mg), the IL-1 receptor antagonist anakinra(100mg), and rituximab (1g), which depletes peripheral B cells. Biologic agents are effective for patients who fail treatment with other DMARDs. DMARDs that are less frequently used include azathioprine (2 to 3mg), penicillamine(250mg), gold salts, minocycline (100mg), cyclosporine (2.5 to 5mg), and cyclophosphamide (50 to 100mg). These agents have either less efficacy or higher toxicity, or both. • Combination therapy with two or more DMARDs may be effective when single-DMARD treatment is unsuccessful. 29
  • 30. PHARMACOLOGICAL TREATMENT Combinations that are particularly effective include-  (1) MTX plus cyclosporine,  (2) MTX plus sulfasalazine and hydroxychloroquine. Nonsteroidal anti inflammatory drugs (NSAIDs) and/or corticosteroids may be used for symptomatic relief if needed. corticosteroids have the potential for long-term complications. They provide relatively rapid improvement compared with DMARDs, which may take weeks to months before benefit is seen. 30
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