This document provides an overview of rheumatoid arthritis (RA), including its definition, incidence, risk factors, clinical presentation, investigations, diagnosis, and treatment. RA is a chronic inflammatory disease that primarily affects the joints, most commonly in the hands, feet and wrists. It occurs in around 3% of adults and is more common in females. Genetic and environmental factors are involved in its pathogenesis. Clinically, it presents with symmetric joint swelling, stiffness, and can involve extra-articular structures. Investigations include blood tests and x-rays. Treatment aims to control symptoms, prevent joint damage, and involves medications like DMARDs and biologics, as well as physical therapy and surgery.

1. Presented by
Prof.Dr. Nahla Mohamed
Gaballah
Professor & Head of Rheumatology and
Rehabilitation Department

2. Definition:
Rheumatoid arthritis (RA) is a
chronic systemic inflammatory disease
primarily involving the joints, most
commonly the small joints of the hands &
feet and progress in systemic fashion to
involve synovial joints all over the body.

3. Incidence:
The disease occurs in
approximately 3% of the adult
population.
Sex distribution:
3 females:1 male.

4. Age:
Most commonly middle –aged
adults between 30-40 years, but many
occur at any age group.
If it occur before 16 years old, its called
Juvenile Rheumatoid Arthritis(JRA)
(STILL’SDISEASE).
Also, it may begin after the age of 50 years
(ELDERLY RA) which usually takes more
benign course.

5. AETIOLOGY
There is no specific aetiology .BUT
,there are several predisposing or
initiating factors that predispose to
the occurrence of the disease .

6. Genetic factor:
The association of RA and the humen
leukocyte antigen (HLA antigens DR1 and
DR4) is well established.
Also, RA patients possess HLA DR2
considered an indicator of good prognosis.
On the other hand seropositive erosive
diseases are more likely in HLA DR3.
There is a higher prevalence of RA in the
first degree relatives and in monozygotic
twins.

7. Infectious agents:
Microbes are the most triggering
agents of the disease in genetically
predisposed individuals.many bacterial
organisms such as diphetroid and
mycoplasma.
Also virus such as Epstein Barr virus
considered as a potential etiologic agent
for RA .

8. Hormonal factor:
Higher incidence of the disease
occurs in female about (70%).
The incidence is lower in females taking
contraceptive pill, also remissions of
disease activity commonly in pregnancy
which occur due to the association with
alpha 2 glycoprotein which is
immunosuppressive and the immuno
modulating properties of female sex
hormones.

9. Auto immunity:
RA is one of the autoimmunes
disease in which the antibodies are
produced against normal IgG of self .

10. PATHOGENESIS
One or several antigens will activate T
cells which becomes the first major
amplification step in the pathogenesis of
RA. colonel expansion of T cells will
drive B lymphocytic proliferation and
production of antibodies including
rheumatoid factor (RF).

11.  This immunological events causes
inflammation of the synovial membrane
(synovitis).
 So the synovial membrane becomes
thickened ,hyperplastic, hyperaemic ,
oedematous and proliferate to form villi
filling the joint space produce (Pannus)
which released damaging chemicals into
synovial fluid so ,erode the cartilage.

12. Normal Early RA
Soft tissue swelling
due to:
- Synovitis
- Effusion
- Capsule thickening
Established
RA
Chronic
RA
- Cartilage erosion
- Bone destruction
- Subluxation
Bone
Synovial
membrane
Articular
cartilage
Periarticular
osteoporosis
Pannus
Erosion of
cartilage
Pathogenesis of RA

13. CLINCAL PICTURE
Onset: - mode of onset: Insidious
Acute precipitated
by physic trauma.
-Pattern of onset: -monoarticular
- Pauciarticular
- Oligoarticular
- Polyarticular
Course: - progressive
-regressive
-remission and exacerbation

14. Duration.
Sequence of joint involvement
Morning stiffness: difficulty in movements
of joints due to accumulation of
inflammatory metabolites at nights due to
immobilization of joints.

15. A-Articular manifestations:
 Any synovial joints all over the body can
be affected but the classic presentation
are affection of small joints of hands, feet
and wrists.

16. RHUEMATOID HAND AND WRIST:
Early:
The hand feels stiff,swollen,difficulty in
making a fist and lifting things.
-Fusiform swelling of the finger .
-Swelling of the second and third MCP with
filling in hollows between knuckles.
-Extensor tendon sheath swelling .

17. Early RA: Fusiform swelling of proximal
interphalangeal joints PIP of both hands

18. -Swelling on dorsal aspect of wrist.
-Triggering of fingers.
-Carpal tunnel syndrome.
-Prominent ulnar styloid (piano sign)
-Wasting of small muscles.

19. Late:
The characteristic rheumatoid deformity
including:
*Swan neck deformity:
flexion of DIP and MCP joints with
hyperextension of PIP joint
*Boutonniere deformity(button hole
deformity):
Flexion of PIP, MCp joints with
hyperextension of DIP joint

20. Swan neck deformity
Button hole deformity

21. *Z-shaped deformity of the thumb:
Flexion of MCP of the thumb with
hyperextension of IP joint(from the
patient need to pinch).
*Radial deviation of the wrist
*Ulnar deviation of MCP
*Rupture extensor tendons (dropped
fingers)

22. A
B
(A) MCP swelling with ulnar deviation
(B) Swelling of the wrist

23. Late RA

24. B-extra- articular manifestations:
1-Rheumatoid nodules: occur in 15-20% of
RA patients usually subcutaneous over
the extensor surface of elbow , over bony
prominences such as head , sacrum and
Achilles tendon.
They are usually mobile but they may
bound to the periosteum and they have
certain characteristic pathological pattern
. they may be single or multiple , may
decrease in size with treatment but do
not disappear .

25. It is associated with positive rheumatoid
factor and their prescence indicate poor
prognosis .
They may appear around fingers called
intra cutaneous and even may appear in
the internal organs such as heart ,lung.

26. 2-Anaemia:
 It present in patients with active RA its
usually normocytic normochromic
anaemia ,it may occur as a result of blood
loss or marrow suppression by drugs or
as a part of felty syndrome (variant of
RA).

27. 3-Lymphandenopathy :
The nodes are soft,mobile non tender
(one or two) it is diagnostic for felty
if it is associated with
splenomegaly ,anaemia, positive RF
and leucopenia.

28. 4-Osteoprosis:
Early localized periartciular
osteoporosis in x-ray film.
Late generalized osteoporosis as a
result of immobilization and drugs
used.

29. 5-Eye involvement:
 In the form of episteritis (common
and self limiting),
 keratoconjunctivitis sicca(sjogen’s
syndrome),
 Scleritis occur in severe systemic RA
with vasculitis.

30. 6-Lung involvement:
Lung is a common site of extra-articular
involvement in RA in the form of
pleurisy, pleural effusion .
*Rheumatoid nodues in the lung.
*Interstitial fibrosis.
*Rheumatoid
pneumoconiosis(Caplan’ssyndrome).

31. 7-Heart involvement:
in the form of pericarditis pericardial
effusions ,nodules in the conducting
system and on the valves.
8-Neuromuscular involvement.
9-Renal and liver involvement.

32. “LABORATORY INVESTIGATIONS”
-Complete blood picture (C.B.C).
-Erythrocyte sedimentation rate(ESR).
-C-reactive protein titre.

33. -Rheumatoid Factor :
 Detected by latex fixation test or Rose
waeler method. Positive in 75-80% of RA
patients but can be only detected in 5 %
of normal population,
 Its titre may decrease with the
improvement of the disease activity,but
it never turn negative and the
controversy is true as it can changed
from negativety(early) towards
positivety

34.  Anti- Cyclic Citrillunated Peptide
(CCP) antibody:
 It has high diagnostic specificity for RA
and used recentely in the new criteria for
diagnosis of earlyRA.
 It provide prognostic information on the
severity of the disease.

35. DIAGNOSIS
The American Rheumatism Association
criteria (ARA) for diagnosis of RA:
1-Morning stiffness lasting to at least one
hour before maximal improvement
2-Symmetric arthirits
3-Arhititis of 3 or more joint area out of 14
joint areas
(PJP,MCP,wrist,elbow,knee,ankle,MTP
joints) Rt and Lt side.
4-Arthiritis of one joint area below the wrist

36. 5-Subcutaneous nodules
6-Positive serum rheumatoid factor
7-Radiological changes
A patient is said to have RA if satisfied at
least 4 of the above 7 criteria
Criteria 1 to 4 must be present for at least 6
weeks

38. Treatment
The “goal of treatment “is to control pain
and inflammation, prevent joint damage
and disease disability which can be done
by:
1-Education to the patients and their
families about the native of the disease
2-Rest (short periods of bed rest mainly in
the acute stage) and splints for the
inflamed joints

39. 3-Disease modification through the
suppression of inflammation and the
immunologic process by using immune
suppressive drug therapy (once the
disease has diagnosed the use of the
immune suppressive drugs(DMARDS)
should be started such as :

40. Methotrexate: 10-25 mg i.m/ week, it has
rapid onset of action (4-6weeks), safe
and not expensive.
Leflonamide (avara): can be used in
patients intolerant to methotrexate with
oral loading dose of 100 mg daily for 3
days followed by maintainance dose of
10-20 mg daily.

41. Sulfasalazine (salazopyrine): tablet 500 mg
starting by one then gradually increased
to four tablets daily.
Antimalarial drugs such as dagrenol giving
as one tablet daily
Azathioprine,Gold(myocrisin),cyclosporine

42. Most patients respond well to combination
therapy such as methotrexate and
antimalarial.
However , we can use steroid as a bridge
therapy until the immune suppressive
drugs start its action ,while NSAIDS (non
steroidal anti inflammatory drugs) are
used to decrease the pain only and not
stop the pathological progression or
rheumatoid disease.

43. 4-Anticytokine therapy:
It is newly developed targeted therapy ,
highly effective for control disease
activity and prevention of structural
damage ,it is highly indicated in patients
with active disease not controlled by
DMARDS but it has very high cost such
as:

44. Anti-TNF alpha e.g Etanercept 25 mg twice
weekly S.C or 50 mg once weekly.
Infliximab (Remicade) intravenous infusion
at 0,2,6 week then every 2 months 3-5 mg
/week.
Adalimumab (Humira) 40 mg every two
weeks S.C.
Anti –IL 1 receptor antagonist e.g
Anakinra.

45. 5-Maintenance of join function and
prevention of deformity by physical
therapy in the form of regular active
exercises after heat application ,maintain
the strength of muscle ,assisted active or
active range of motion to the joints and
avoidance of positions of deformity by
using splints.
6-Repair of joint damage if it will relieve
pain or facilitate function (joint
replacement therapy) arthroplasty.

46. TThhaannkk yyoouu