Rheumatoid arthritis is a chronic autoimmune disease characterized by inflammation of the joints that can lead to long-term joint damage and disability. It is caused by the immune system attacking the synovial membrane and joint lining, causing swelling and stiffness. Common symptoms include pain, swelling, and stiffness in the small joints of the hands and feet. While the exact cause is unknown, genetic and environmental factors are believed to play a role. Treatment focuses on reducing inflammation and preventing further joint damage through medications, physical therapy, exercise, and sometimes surgery.

1. RHEUMATOID
ARTHRITIS/DISEASE
BY:
Ms.Keerthi Samuel,
Asst.Professor,
Vijay Marie CON

3. INTRODUCTION
• Rheumatoid arthritis is a chronic disease characterized
by periods of disease flares and remissions with an
unknown cause.
• In RA multiple joints are involved but not always
symmetrical.
• It affects all the ages.
• Damage to the joints occurs early and doesnot correlate
with the severity of symptoms.
• The rheumatoid factor is an antibody that can be found
in the blood of 80% people with rheumatoid arthritis.

4. DEFINITION
■ Rheumatoid arthritis is an autoimmune disease caused
by chronic inflammation of unknown etiology marked by
symmetric , peripheral polyarthritis which results in joint
damage &physical disability.
■ It is a progressive disease of synovial lining of
peripheral joints characterized by symmetrical
inflammation leading to potentially deforming polyarthritis.
It is the most common systemic inflammatory disease
characterized by symmetrical joint involvement

5. INCIDENCE
■ New cases of RA are typically two to three ties higher
in women than men.
■ People with a genetic component ,inherited traits are
at higher risk.
■ Acc to CDC from 2013-2015 an estimated of
54.4million US adults annually were affected.
■ 49.6% of people above 65 years, 41.3 million Non-
Hispanic whites are affected.
■ Adults aged 18 years or older who are overweight or
obese report doctor-diagnosed arthritis more often
than adults with a lower body mass index (BMI)

6. ETIOLOGY ■ Unknown cause,Believed that it is hereditary.
1. ENVIRONMENTAL INFLUENCES : Such as
infection, trauma,
2. GENETIC MARKERS: HLA-DR4 triggers RA.
Such factors are not considered as diagnosis
because half of the people who posses this
antigen donot develop RA
3. ANTIGEN DEPENDENT ACTIVTION OF T
LYMPHOCYTES: leads to proliferation of
synovial memebrane. Activation of pro
inflammatory cells from the bone marrow ,
cytokinins and auto antibody production.
ENVIRONMENTAL FACTORS
GENETIC MARKERS
ANTIGEN DEPENDENT ACTIVATION
OF T LYMPHOCYTES
ANTI-CITRULLINATED PROTEINS
TUMOR NECROSIS FACTOR (TNF)
SYNOVITTIS

7. ETIOLOGY 4. ANTI-CITRULLINATED PROTEINS: these are
peptides highly specific for RA
5. TUMOR NECROSIS FACTOR: IL-1,IL-6 and
growth factors propogate the inflammatory
process, and agents found to alter these
cytokines reduces pain and deformity.
6. SYNOVITIS- hallmark in pathogenesis of RA.
Synovium proliferates abnormally ,groeing into
the joint space and into the bone forming a
PANNUS. The pannus migrates to the articular
cartilage and subchondral bone leading to
destruction of cartilage, bone tendons and blood
vessels.
ENVIRONMENTAL FACTORS
GENETIC MARKERS
ANTIGEN DEPENDENT ACTIVATION
OF T LYMPHOCYTES
ANTI-CITRULLINATED PROTEINS
TUMOR NECROSIS FACTOR (TNF)
SYNOVITTIS

8. ETIOLOGY 4. ANTI-CITRULLINATED PROTEINS: these are
peptides highly specific for RA
5. TUMOR NECROSIS FACTOR: IL-1,IL-6 and
growth factors propogate the inflammatory
process, and agents found to alter these
cytokines reduces pain and deformity.
6. SYNOVITIS- hallmark in pathogenesis of RA.
Synovium proliferates abnormally ,groeing into
the joint space and into the bone forming a
PANNUS. The pannus migrates to the articular
cartilage and subchondral bone leading to
destruction of cartilage, bone tendons and blood
vessels.
ENVIRONMENTAL FACTORS
GENETIC MARKERS
ANTIGEN DEPENDENT ACTIVATION
OF T LYMPHOCYTES
ANTI-CITRULLINATED PROTEINS
TUMOR NECROSIS FACTOR (TNF)
SYNOVITTIS

9. PREDISPOSING FACTORS
1. GENDER: women before the menopause are affected three
times more often than men. After the menopause the frequency of
onset is similar between the sexes, suggesting an etiological role
of male sex hormone. The use of oral contraceptives delay the
onset of disease but has no effect on RA
2. FAMILIAL: Increased incidence in first degree relatives and high
risk in monozygotic twins (15%)than dizygotic twins (3.5%). It
affects families for many generations.

10. PATHOPHYSIOLOGY
TRIGGER
INFLAMMATION
JOINT AND TISSUE
DESTRUCTION

11. PATHOPHYSIOLOGY
I. TRIGGER
■ The combination of etiological factors
sends a trigger to the body to create
antibodies – known as autoantibodies that
seek out joint linings.
■ These autoantibodies include rheumatoid
factor (RF) and anti-cyclic citrullinated
peptide antibody (anti-CCP).
II.INFLAMMATION
■ This results in the production of chemicals
being released including tumour necrosis
factor alpha (TNF-α), Interleukin (IL)-1, IL-
6, IL-8, transforming growth factor beta
(TGF-β), fibroblast growth factor (FGF)
and platelet-derived growth factor (PDGF).
■ Increased levels of cytokines are present.
Cytokines play a central role in the
perpetuation of synovial inflammation.

12. PATHOPHYSIOLOGY
III.JOINT &TISSUE DESTRUCTION
■ These chemicals inflame and damage the body’s cartilage, bone,
tendons, and ligaments which causes extravasation of leucocytes.
■ HYPERPLASIA of the synovial membrane with extensive
angiogenesis.
■ There is an increased number of both type synoviocytes and is
infiltrated with immune and inflammatory cells: particularly
macrophages, B- and T-lymphocytes, plasma cells and dendritic cells.
■ The persistence of the chronic inflammatory response in conjunction
with ongoing joint destruction (is finding in many patients with RA
despite the use of effective anti-inflammatory agents and disease-
modifying drugs).

13. STAGES OF RA
I. SYNOVITIS
■ Stage 1 is early stage RA.
■ Many people feel joint pain, stiffness, or
swelling. During Stage 1,
■ there is inflammation inside the joint.
■ The tissue in the joint swells up. With no
damage to the bones, but ,synovium, is
inflamed.
■ Can progress to bone erosion

14. STAGES OF RA
II. PANNUS FORMATION
■ Moderate stage RA.
■ Synovitis causes damage to the joint cartilage. When
cartilage is damaged, there will be pain and loss of
mobility.
■ Range of motion in the joints may become limited.
■ Inflammation and exuberant proliferation of the
synovium leads to formation of pannus and destruction
of cartilage, bone, tendons, ligaments, and blood
vessels. Basically, the hypertrophied synovium is
called PANNUS

15. STAGES OF RA
III. FIBROUS ANKYLOSIS
■ Stage 3, it is considered severe.
■ damage extends not only to the cartilage but to the bones due
to increased friction between the bones. Pain and swelling
increases causing FIBROUSANKYLOSIS with bone erosion.
■ Fibrous ankylosis is a fibrous connective tissue process which
results in decreased range of motion. Symptoms present as bony
ankylosis, in which osseous tissue fuses two bones together
reducing mobility, which is why fibrous ankylosis is also known as
false ankylosis.
BONEANKYLOSIS
FIBROUSANKYLOSIS

16. STAGES OF RA
IV. BONY ANKYLOSIS
■ At Stage 4, there’s no longer inflammation in the joint.
■ This is end-stage RA, when joints no longer work.
■ In end-stage RA, people may still experience pain,
swelling, stiffness, and mobility loss. There may be
reduced muscle strength. The joints may become
destroyed and the bones fused together (ankylosis).
■ Bony ankylosis is the union of the bones of a joint by
loss of articular cartilage, resulting in complete
immobility.

17. STAGES OF RHEUMATOID ARTHRITIS

18. CLINICAL FEATURES ■ Early rheumatoid arthritis tends to affect smaller joints first
— particularly the joints that attach your fingers to your
hands and your toes to your feet later spreads to the
wrists, knees, ankles, elbows, hips and shoulders leading
to POLYARTHRITIS.
■ Swollen, warm, tender and stiff joints limits movements
particularly early in the morning on waking or prolonged
inactivity.
■ The deformities seen are:
– Buttonhole deformity
– Subluxation of metacarpophalangeal joint/ULNAR
DRIFT
– Z thumb deformity
– Swan neck deformity
– Hammer toe deformity
– Arthritis mutilans
1. JOINT

19. 'Z deformity' may occur in
rheumatoid arthritis. It is seen at
the thumb and consists of
hyperextension of the
interphalangeal joint, and fixed
flexion and subluxation of the
metacarpophalangeal joint
Swan-neck
deformity/BOUTONNIERE
DEFORMITY/BUTTON HOLE
is a bending in (flexion) of the
base of the finger, a
straightening out (extension)
of the middle joint, and a
bending in (flexion) of the
outermost joint.
Swollen,red, tender joints

20. A hammer toe or contracted
toe is a deformity of the
muscles and ligaments of
the proximal interphalangeal
joint of the second, third, or
fourth toe causing it to be
bent, resembling a hammer
Ulnar deviation, also known
as ulnar drift, is a hand
deformity in which the swelling
of the metacarpophalangeal
joints causes the fingers to
become displaced, tending
towards the little finger.
Arthritis mutilans is a rare
medical condition involving
severe inflammation damaging
the joints of the hands and feet,
and resulting in deformation and
problems with moving the
affected areas; it can also affect
the spine

21. CLINICAL FEATURES ■ The rheumatoid nodule or NECROTIZING GANULOMA,
which is sometimes in the skin, is the most common non-
joint feature .The typical rheumatoid nodule may be a few
millimetres to a few centimetres in diameter and is usually
found over bony prominences, such as the elbow, the heel,
the knuckles, or other areas that sustain repeated
mechanical stress.
■ Nodules are associated with a positive RF (rheumatoid
factor) titer, and severe erosive arthritis.
■ Rheumatoid vasculitis can thus commonly present with
skin ulceration and vasculitic nerve infarction known
as mononeuritis multiplex. The most common
presentation is due to involvement of small- and
medium-sized vessels
2.SKIN

22. CLINICAL FEATURES
■ Sweet syndrome is a rare disorder characterized by
fever and the sudden onset of a rash, which consists of
multiple tender, red or bluish-red bumps or lesions.
These lesions usually occur on the arms, legs, trunk,
face or neck. In some cases, additional systems of the
body can become involved including the
musculoskeletal system such as inflammation of the
joints (arthritis).
■ Diffuse alopecia areatais seen in RA.
2.SKIN

24. DIAGNOSTIC TESTS
1.RHEUMATOID FACTOR:
■ Found in60% of patients with RA. however 5% of healthy
individuals will have elevated levels of RF.
■ If initially negative the test can be repeated in 6-12
months.
■ RF is not an accurate measure of disease progression.
2.ERYTHROCYTE SEDIMENTATION RATE:
■ They are markers of inflammation ad are usually elevated
in RA.
■ It helps to indicate the activity of the disease but they
don’t indicate the severity of the disease.

25. DIAGNOSTIC TESTS
3. ANTICYCLIC CITRULLINATED PEPTIDE
ANTIBODIES(ACPA):
■ These are found in patients with RA and useful
in predictive erosive disease.
4.RADIOGRAPHIC EXAMINATION:
■ This can reveal the extent of bone erosion and
cartilage loss.
■ An MRI can detect proliferative pannus

26. OTHER BLOOD TESTS
■ C- Reactive protein
■ Complete blood count
■ Renal function test – uric acid
■ Liver enzymes and other immunological tests
like anti nuclear antibodies.
■ Elevated ferritin – can be a sign of RA and
seronegative RA.

27. EULAR
-(European
League against
Rheumatism)
If the score is greater than or equal
to 6 it indicates definite
rheumatism.

28. MANAGEMENT
■ GOALS:
– to control inflammation
– relieve pain, and
– reduce disability associated with RA.

29. MANAGEMENT
Medical management
Physical and occupatonal therapy
Surgical management
Cognitive therapy
Natural therapy

30. MEDICAL MANAGEMENT
1. NSAIDS – NON STEROIDAL ANTI INFLAMAMTORY DRUGS:
 Commonly used to treat RA.
 They help to manage chronic pain, inflammation and swelling.
 They do not slow down the disease. Most people with RA also take other types
of medications, such as methotrexate or biologics, to help prevent further joint damage.
EX: Aspirin, celecoxib, diclofenac, ibuprofen, ketoprofen, ketorolac
MECHANISM OF ACTION: They block cyclic oxygenase enzymes which cuts pain and
stiffness.
SIDE EFFECT: Increased BP, gastric irritation , headaches, anemia, rash, tinnitus, heart attack
and stroke.

31. MEDICAL MANAGEMENT
2. DMARD’S: DISEASE MODIFYING ANTI RHEUMATIC DRUGS:
• Commonly used are methotrexate, hydroxychloroquine, sulfasalazine.
• Anti-cytokine agents: anti TNF drugs include infliximab
• IL-1 receptor antagonist : which depletes peripheral B cells. Ex: rituximab.
3.IMMUNOSUPPRESIVE AGENTS:
• Less frequently used.
• Ex: Azathioprine, D- penicillamine, Gold (auranofin), cyclophosphamide, cyclosporin
4.COMBIANTION THERAPY:
• Cyclosporine + methotrexate
• Methotrexate + Sulfasalazine and hydroxychloroquine.
5.GLUCOCORTICOIDS: low dose prednisolone

32. PHYSICAL AND OCCUPATIONAL THERAPY
■ For people with RA, physiotherapy may be used together with
medical management. This may include cold
and heat application, electronic stimulation, and hydrotherapy.
■ Physiotherapy promotes physical activity. In RA, physical activity
like exercise in the appropriate dosage (frequency, intensity, time,
type, volume, progression) and physical activity promotion is
effective in improving cardiovascular fitness, muscle strength, and
maintaining a long term active lifestyle. Physical activity
promotion according to the public health recommendations should
be an integral part of standard care for people with RA and other
arthritic diseases.

33. SURGICALMANAGEMENT
ARTHROPLASTY/TOTAL
JOINT REPLACEMENT
OPEN/ARTHROSCOPIC
SYNOVECTOMY
RECONSTRUCTIVE HAND
SURGERY

34. SURGICALMANAGEMENT-
ARTHROSCOPY
■ It is a type of joint surgery in which a thin tube with a light
source (called an arthroscope) is inserted into the joint
through a small incision (cut) in the skin, allowing to see
the inside of the joint.
■ Instruments are inserted through other small cuts to
work on the joint. Surgery will not cure rheumatoid
arthritis or stop the disease's progress. But it may
improve function and provide some pain relief.

35. SURGICALMANAGEMENT-
SYNOVECTOMY
■ Synovectomy surgery is done to remove inflamed joint
tissue (synovium) that is causing unacceptable pain or is
limiting your ability to function or your range of motion.
Ligaments and other structures may be moved aside to
access and remove the inflamed joint lining.
■ Following knee synovectomy, knee will be immobilized in a
removable cast. And physical therapy is started after 1 to 2
days. Synovectomy does not cure the disease. But it may
relieve symptoms temporarily.
■ There may also be a loss in the range of motion of the joint,
or the inflammation in the joint may return.

36. SURGICALMANAGEMENT-ARTHRODESIS
■ Also known as arthrodesis, joint fusion is a surgical
procedure for the treatment of severe arthritis pain. It
involves fusing together the bones in your aching joint to
create one solid bone. The fused bone is often more
stable and results in decreased pain.
■ Ankle fusion may also be carried out to treat a severe foot
deformity, like club foot, high-arched or flat foot which has
damaged the ankle joint or made it unstable.

37. SURGICALMANAGEMENT-ARTHRODESIS
■ It can take up to three months before you’re walking again
after surgery. This can be a frustrating and difficult time,
especially if you’re used to being active. Most people resign
themselves to weeks of hobbling around on crutches.
Fortunately, there are now some alternatives which can
make the process a lot easier for you.
Here are the main options(RECENTADVANCEMENT)
■ Conventional Crutches
■ Knee Scooters or “KneeWalkers”
■ Hands-FreeCrutch:The iWALK 2.0

38. SURGICALMANAGEMENT-
JOINT REPLACEMENT
■ The definitive treatment for advanced joint destruction in the late
stages of rheumatoid arthritis can be successfully treated with
total joint arthroplasty. Total knee arthroplasty has been shown to
be a well-proven modality that can provide pain relief and
restoration of mobility for those with debilitating knee arthritis.
■ The knee is one of the most commonly affected joints in patients
suffering from chronic rheumatoid arthritis (RA)
■ In advanced disease, when synovectomy is of no benefit, total
knee arthroplasty (TKA) has proven to be the most successful
intervention that reduces knee pain and improves physical
function in RA
■ Total hip replacement is another option

39. COGNITIVE THERAPY
■ This review concludes that cognitive behavioral therapy (CBT)
is the most efficacious treatment for pain management in RA;
however, there are indications that mindfulness may have
particular benefits for patients with a history of
depression. CBT is most effective when administered early in
the course of the disease especially to manage chronic pain.
■ One of the major challenges is ensuring access to effective
interventions for patients, particularly early on in the course of
the disease, with a view to preventing physical and
psychological morbidity.

40. NATURAL THERAPY

41. RECENT ADVANCEMENTS
■ IMMUNO ADSORPTION APHEREIS:
■ Immunoadsorption is a selective apheresis method for the
removal of specific antibodies and immune complexes, leaving
other plasma components and obviating the need for plasma
replacement.
• Extracorporeal immune adsorption of plasma over columns
containing inert silica matrix and covalently attached
staphylococcal protein is done.
• Used in patients who failed other therapies.
• Used in join pains, swellings