Introduction, Aetiology, Pathophysiology, Clinical features, Diagnosis, Treatment of Rheumatoid Arthritis

1. BY – Sakshi Joshi
RHEUMATOID
ARTHRITIS

2. TABLE OF CONTENTS
PATHOPHYSIOLOGY &
CLINICAL FEATURES
03
INTRODUCTION &
OVERVIEW
01 ETIOLOGY
02
DIAGNOSIS &
TREATMENT
04

3. INTRODUCTION
01

4. INTRODUCTION
Rheumatoid Arthritis (RA) is a chronic multisystem disease of unknown cause .
• Its is a common disease having peak incidence during 3rd to 4th decade of life.
• It has 3-5 times more preponderance in females.
• Onset is insidious followed by fatigue; weakness; stiffness, swelling and pain of
joints of hands, wrists and feet .
• It’s most prominent manifestation is inflammatory arthritis of peripheral joints,
and systemic include haematologic, pulmonary, neurological and cardiovascular
abnormalities.

5. ETIOLOGY
02

6. Rheumatoid arthritis is a heterogeneous disease, which can be, based
on data combining genetic risk factors and autoantibodies, sub-
classified into ACPA-positive and negative RA.
Smoking is thus far the most important environmental risk factor
associated with the development of RA
The causes of RA are still unclear, even though important progress has
been made in recent years. In particular, our understanding of the
immunological changes in the pre-disease phase and in the earliest
phases of arthritis has improved considerably, as has the granularity to
which we can now dissect the cellular composition of the tissues at the
site of inflammation..
ETIOLOGY

7. Abnormalities in the cellular and humoral immune response lead
to the occurrence of autoantibodies, most notably rheumatoid
factors (RF) and antibodies against post-translationally modified
proteins (Anti-modified protein antibodies (AMPA) that comprise
antibodies against various modifications such as citrullination
(ACPA), carbamylation (aCarP) and acetylation (AAPA) as well
as the immigration of T and B-lymphocytes into the synovium.
There is also an intense activation of the innate immune system
with highly activated cells of the monocyte/macrophage system in
the tissue sites involved.
ETIOLOGY

9. PATHOPHYSCIOLOGY &
CLINICAL FEATURES
03

10. What goes wrong in the body?
Is triggered by an
interaction between
RA
Immune protein like
Human Leukocyte
Antigen
HLA DR1 & HLA DR2
Genetic Factors
 Cigratte smoke
 Intestinal pathogen
Environmetal Factors

11. Environmental Factors can
cause modifications of our own
antigens

12. Citrullination is a process in
which amino acid Arginine gets
converted in amino acid Citruline

13. ■ Antigens get picked by Antigen Presenting Cells (APCs)
Lymph Nodes
activate
CD4 T helper cells
 T-helper cells activate B cells proliferate & Plasma Cells
differentiate
 Plasma cells produce specific auto-antibodies against self antigens

16. Antigens are picked by
APCs & get carried to
Lymph Nodes to activate
CD4 T-Helper cells

20. Pannus damages the
cartilage & other soft
tissues & erode bone.

22. Baker or Popliteal Cyst
In the knee joint, a one-way valve can form, which gets filled from the
swollen knee filling the semi-membranous bursa.
Synovial sac gets so swollen that it bulges posteriorly into the popliteal
fossa, creating a synovial fluid filled cyst.

24. Extra-articular Manifestations :-
Non-Organ specific, symptoms of inflammation –
o Fever
o Low appetite
o Malaise
o Muscle Weakness
Organ specific –
o Rheumatoid Nodules
o Increase in risk of Atherosclerosis
o Anemia
o Interstitial Lung Fibrosis
o Pleural Effusions

27. Why do we see symmetrical
arthritis in RA?
Fibroblasts-like synoviocytes (FLS) when activated –
they can migrate from joint to joint.
So, they can migrate from the hand joint on one side
to hand joint on other.
This is why we see symmetry.

28. Link with DENTISTRY
Porphyromonas gingivalis causing Gingivitis
New research shows link between Rheumatoid Arthritis &
Periodontal ( gum) disease.

29. Commonly affected joints are –
 Metacarpophalangeal (MCP)
 Proximal inter-pharangeal (PIP)
 Metatarsopharngeal (MTP)
As the disease worsens, Large joints start to effect –
 Shoulders
 Elbows
 Knees
 Ankles

30. During ‘Flares’ – sudden worsening of disease.
The affected joints get extremely swollen, warm, red &
painful.
Overtime, joints become really stiff especially in the
mornings or after periods of long inactivity.
* Remission – is a period when patients have NO
symptoms of RA

31. Boutonniere or Buttonhole
Deformity
Ulnar Deviation
Opposite to Buttonhole
DEFORMITIES
Swan Neck deformity

32. DIAGNOSIS
04

33. The Diagnostic criteria is as follow:-
1. Morning stiffness.
2. Second Arthritis of 2-3 joint areas
3. Arthritis of head joint
4. Systematic arthritis
5. Rheumatoid nodules
6. Serum Rheumatoid Factor (RF)
7. Radiographic changes –
a. joint involvement
b. serological test
c. acute phase reactant
d. duration of symptoms

35. a) Radiographic features
1. periarticular osteopenia
2. uniform symmetric joint space narrowing
3. marginal sub-coronal erosion
4. joint sub-luxation
5. joint destruction
6. collapse
b) Ultrasound detect early soft tissue lesion
c) MRI has greater sensitivity to detect synovitis and marrow changes.
d) Elevated APRs (ESR, CRP)
e) Thrombocytosis
f) Leukocytosis
g) ANA 30 to 40%
h) Inflammatory Synovial fluid
i) Hypoalbuminemia
Other abnormal abnormalities:-

37. 1.Antibodies that recognise FC protein of IgG
2.Can be IgM ,IgG IgA
3.85% of patients with RA over first two years can become RF positive
& negative RF may be repeated 4 to 6 months for the first 2 years
disease in some patient may take 18 to 24 months to become super
positive .
4.Prognostic value with high titer of RF in general tend to have poor
prognosis more extra-articular manifestation
Rheumatoid factor (RF) :-

38. Serum anti CCP antibodies:-
The presence of serum and anti CCP antibodies has about the
same sensitivity as serum RF for the diagnosis of RA.
However, its specificity approaches 95%.
*A positive test for anti CCP antibodies is the setting of an early
inflammatory Arthritis is useful for distinguish RA from other
arthritis.
*There is some incremental value in testing of presence of both RF
and anti CCP as same patient with RF and positive for RF but
negative for anti-ccp and vice versa.
*The presence of RF and anti CCP antibodies also has prognostic
significance with anti CCP antibody showing the most value for
getting worse outcomes.

40. 1.According to National centre for biotechnology information
United States National library of medicine human studies have
shown that the association of P gingivilis infection with our a
patient and individual at higher risk of RA animal studies also
demonstrate that P gingivalis infection facilitated the development
and progression of destructive arthritis.PG wireless is the only
known prokaryotic organisms that contain enzyme
peptidylarginine deiminase (PAD) which is essential for general of
citrullinated autoantigen. It has a great promise to provide
therapeutic target for prevention and treatment of RA disease
affecting 1 to 2% of population worldwide.
1.
How Microbiology is linked to
Rheumatoid Arthritis

41. According to the British journal of rheumatology it published a paper
called Microbiology will give the real answer to Rheumatoid Arthritis by
Dr DK Ford states that rheumatoid arthritis main not primarily generic
disease immunopathology kal processor close to the heart of lesion what
rheumatoid establishment sings to a forgotten is that antigen specificity is
the fundamental of immunology observation of non antigen-specific
phenomena are unlikely to result in definition of real cause this study of
non specific receptors of immune cells of non specific immunome orders
and non specific mitogen response is not likely to explain why previous
healthy MS Smith began her writers at 40 age had resumption after 5
years later. here the link the sexually acquired reactive arthritis is a
sequel of genetic infection with at least two well defined sexually
transmitted infections disease so this can be curb.
2.
How Microbiology is linked to
Rheumatoid Arthritis

42. How Microbiology is linked to
Rheumatoid Arthritis
According to another paper of microbiology society the gut microbes
could lead to onset of Arthritis this research was conducted in University
of Leeds investigated that composition of gut microbiome in people at
higher risk of to avoid Arthritis the gut microbes is a complex community
of bacteria and other microbes that aside and that an important role in
health and well-being.the fecal sample collection from 25 people did not
have Arthritis but had identify as at a risk due to having non-specific
musculoskeletal pain and testing positive for anti citrullinated peptide
antibody is a ACPA in .The microbial composition of these microbiome
was determined and compared with healthy control samples.at high risk
individual had higher number of bacteria found in their gut including
Helicobacteracea and Bifidobacteriacae.
3.

43. How Microbiology is linked to
Rheumatoid Arthritis
According to the journal of oral microbiology the rheumatoid arthritis and
periodontal disease have shown similar physio pathological mechanism
such as chronic inflammation with adjacent bone resorption in an
immunogenetics susceptible host .The oral micro organism for
Porphyromonas gingivalis triggers the factors for RA. And patients with
RA have more severe and frequent PD .they have been reports
regarding the detection of antibodies against periodontal bacteria while
other studies have identified periodontal bacterial DNA in serum and
synovial fluid of Arya patient and have exploded the possible pathways
of transport of periodontal bacteria DNA. So there is a strong evidence of
of association between both the diseases.
4.

44. TREATMENT
04

45. There is NO cure for RA, but treatments can improve
symptoms and slow the progress of the disease.
It can be done by medications, therapy and surgery
and Disease-modifying treatment has the best results
when it is started early and aggressively.
TREATMENT

46. MEDICATIONS
 NSAIDS and coxibs- effective in relieving the joint pain,
stiffness of RA and reduces fever.
Example- Ibuprofen , Naproxen ,Aspirin, Celecoxib,
Piroxicam,etc.
 Corticosteroids- Reduce inflammation in RA.
Example- Betamethasone, Cortisone, Prednisone,
Dexamethasone,etc.
 Immunosuppressants- These drugs fight off the damage
caused by RA.
Example- Cyclosporine, Azathioprine,etc.

47. MEDICATIONS
Disease-modifying anti-rheumatic drugs (DMARDs)- act
mainly through inhibition of inflammatory cytokines.
Example - Methotrexate,Sulfasalazine,Hydroxychloroquine
,leflunomide, minocycline.Azathioprine, gold(intramuscular or
oral), Hydroxychloroquine and Penicillamine are used less
frequently

48. SURGERY
 Arthroplasty - surgery to repair or replace a joint.
 Joint replacement- Removing a damaged joint
and inserting a new, functioning one its place.

49. THERAPIES
▪ Physical therapy - Restores muscle strength and function
through exercise.
▪Streching - Streching exercises can improve flexibility and
improve physical function.

50. MEDICAL PROCEDURES
Arthrocentesis - Using a syringe to collect fluid from around
a joint. Also called joint aspiration.

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