a81a73af-5270-4cc0-a7f9-8024256d9d65.pptx

Education

1. RHEUMATOI

D
“ARTHRITIS”

AUDI HUSNA AFFAN

2. INTRODUCTION

The most common cause of chronic inflammatory joint disease
= Most typical features:
a. Asymmetrical polyarthritis and tenosynovitis
b. Morning stiffness
c. Elevation of the erythrocyte sedimentation rate (ESR)
d. Appearance of autoantibodies that target immunoglobins in the serum
= It is a systemic autoimmune disease and changes can be widespread in a
number of tissues of the body
= RA tend to die younger than their peers as a result of the effects of chronic
inflammation on a number of organ systems
= Chief among these is early ischemic heart disease secondary to the effects of

inflammation on the cardiovascular system.

3. EPIDEMIOLOGY

= Affects | -3% of the population world wide
= With a peak prevalence between the ages of 30 and 50 years

= Women are affected 3 or 4 times more commonly than men

4. CAUSES

= Important factors in the evolution of RA are:
a. Genetic susceptibility
b. An immunological reaction; possible involving a foreign antigen,
preferentially focused on synovial tissue

An inflammatory reaction in joints and tendon sheaths

a 9

The appearance of rheumatoid factors in the blood and synovium

o

Perpetuation of the inflammatory process

En

Articular cartilage destruction

5. PATHOLOG

= RA is a systemic disease but the
most characteristic lesions are seen
in the synovium or within
rheumatoid nodules.

= The synovium is engorged with new
blood vessels and packed full of
inflammatory cells

6. PATHOLOGY

0006

= Before RA becomes clinically apparent the immune pathology is already

beginning.
= Raised ESR, C-reactive protein (CRP), and RF may be detectable years
before the first diagnosis.

7. PATHOLOGY

9090

= Early changes are:
a. Vascular congestion with new blood vessel formation
b. Proliferation of synoviocytes
c. Infiltration of the sub synovial layers by polymorphs, lymphocytes and
plasma cells.

= There is thickening of the capsular structures, villous formation of the

synovium and a cell-rich effusion into the joints and tendon sheath.

8. Persistent inflammation causes joint and tendon destruction.
Articular cartilage is eroded.
At the margins of the joint, bone is also eroded by granulation tissue invasion

and osteoclastic resorption.

Similar changes occur in tendon sheaths, causing tenosynovitis.
Partial or complete rupture of tendons.

Swelling of the joints, tendons and bursae.

9. PATHOLOGY

9909

= Combination of articular destruction, capsular stretching and tendon rupture

leads to progressive instability and deformity of the joints.
= The inflammatory process usually continues but the mechanical and
functional effects of joint and tendon disruption now become vital.

10. = Early feature (synovitis)

l. Most commonly affected MCPJ and PIPJ, wrist, tendon sheaths around

the joints (wrist — feet — knee — shoulder)
II. Bilateral symmetrical polysynovitis
III. Pain, fusiform swelling, stiffness, loss of mobility

IV. Constitutional symptom:

a. LOA, LOW, malaise and low grade fever

b. Tenosynovitis

12. CLINICAL FEATURES

= Late feature (DESTRUCTIVE)
I. Spread to other joint — wrist, ankle, knee, shoulder (in order of frequency)
II. Morning stiffness (more than 30 min) — improve with activity

III. Activity of daily living will be affected — quality of life affected

13. RA Is Characterised by Synovitis and
Joint Destruction

NORMAL RA

14. More later (DEFORMITY)
I. Pain, deformity, instability, decreased ROM

II. Joint deformity — movement restricted and painful
* Thumb — Z-deformity
= Fingers — Swan neck deformity/ Boutonniere’s deformities, ulnar

deviation

Wrist — radial and volar displacement

= Elbow - limited extension

Shoulder - limited abduction
= Knees — swollen, flexion an vulgus

* Toes — clawed

15. Deformities in RA

P Boutonniere &
Ulnar Deviation pr Swan neck
7 ' \ deformities

Joint
Subluxation
(wrist/MCPI)

Muscle Wasting

Fous The Peer Teshing Salen net se for ae or mislead

16. i sia
uz” deformity - ii
Radial deviation of

wrist, ulnar

deviation of digits

Hyperextension of
PIP, flexion of DIP
Boutonniere
deformity — Flexion

of PIP, extension of
DIP

17. The natural history of rheumatoid arthritis

isease: nodules, lung, eye, vasculitis, etc

18. DIAGNOSIS

* Mostly clinical:

L

Il.

Il.

IM

Bilateral, symmetrical Rheumatoid subcutaneous nodules
aI

polyarthritis =
Involving proximal
joints of hand or feet
Present for at least 6
weeks

Confirmed with

subcutaneous nodules

or periarticular

erosions on x-ray

19. EULAR RHEUMATOID ARTHRITIS CLASSIFICATION CRITERIA

2010 ACR/EULAR classification criteria for RA
A score of 26/10 is needed to classify RA

Metas etal. Art tas Mera. 2010:63:2569:2581
‘Aleta et al nn Rheum Diu. 2010, 1520-158

20. HEMATOLOGICAL

l. FBC- normocytic hypochromic anaemia (due to abnormal erythropoiesis
from chronic inflammation), WBC

2. Inflammatory markers- ESR, CRP elevated (its use as indication of
disease progression monitoring, treatment response)

3. Rheumatoid factor(RF)- anti-IgG auto Ab 80% will have it

4. Anti- cyclic citrullinated peptide(CCP) Ab

21. JOINT ASPIRATION
cz — > —
Ge SS ==

Synovial fluid — table I

Light straw [Meter

greenish
dear |Mild turbid jopaque

22. IMAGING

= For disease monitoring, treatment response.
= EARLY STAGE(SYNOVITIS)
Soft tissue swelling, periarticular osteopenia
= LATER STAGE(DESTRUCTIVE)
Juxta- erosions, narrowing of joint space
= ADVANCE STAGE(DEFORMITY)

Articular destruction and joint deformity

23. INVESTIGATION

IMAGING
hand Y Sehe |

+ X-ray hand roveats the
early changes at

Bone

erosion

tadiocarpal and
intercarpal joints.
+ Subluxations at the Ist

5 MCP and IP joints
7 cause the classical
Bone “Hitch-hiker's”
displacement deformity.
Figure 1

Figure 2

24. MANAGEMENT

= There is no cure for rheumatoid arthritis

= Aim to delay the progression of the disease, alleviate symptoms, reduce
functional limitation

= Supportive and palliative

25. MEDICATION

1. NSAIDs
= Ibuprofen, indomethacin, COX-2 inhibitors like celecoxib and

valdecoxib (reduce inflammation and relieves pain)

2. Analgesics

= Morphine and acetaminophen (reduce pain)

3. Glucocorticoids or prednisolone

= Prescribed in a small dose to slow joint damage caused by inflammation

26. SURGERY

= Improve quality of life

= Synovectomy
“When one or two joints are affected more severely than others, this
procedure is used to reduce the amount of inflammatory tissue by removing
the diseased synovium or lining of the joint. It may result in less swelling
and pain and the slowing or prevention of further joint damage

= Arthroscopic Surgery
“Thin tube with a light at the end inserted into the joint through a small
incision. It is connected to a closed-circuit television and we can see the
extent of the damage in the joint. Tissue samples taken, remove loose
cartilage, repair tears, smooth a rough surface or remove diseased synovial
tissue. Itis most commonly performed on the knee and shoulder

27. MEDICATION

4. Disease Modifying Antirheumatic Drugs (DMARD)
= There are used with NSAIDs and/or prednisolone to slow joint
destruction caused by RA over time. Examples are methotrexate,
injectable gold, penicillamine, azathioprine, chloroquine,

hydroxychloroquine, sulfasalazine and oral gold.

5. Biologic Response Modifiers
= These drugs directly modify the immune system by inhibiting proteins
called cytokines, which contribute to inflammation. Examples of these
are abatacept, etanercept, infliximab, adalimumab, and anakinra.

6. Protein — A Immunoadsorption Therapy
= This is not a drug, but a therapy that filters the blood to remove
antibodies and immune complexes that promote inflammation

28. SURGERY

" Osteotomy
+ Literally meaning, “to cut bone,” this procedure is used to increase stability by
redistributing the weight on the joint. Osteotomy isn’t often used with RA
because there are other options available besides cutting the bones.

* Joint Replacement Surgery or Arthroplasty
«e This is the surgical reconstruction or replacement of a joint. Successfully used
to help people who otherwise might be in a wheelchair, joint replacement
surgery involves the removal of the joint, resurfacing and relining of the ends of
bones and replacing the joint with a man-made component. This procedure is
usually recommended for people over 50 or who have severe disease
progression. Typically a new joint will last between 20 and 30 years

= Arthrodesis or fusion
* This procedure fuses two bones together. While it limits movement, it does
decrease pain and increase stability of the joints in the ankles, wrists, fingers,
toes and spine.

29. TREATMENT

.

Onset of disease
o NSAIDs/analgesic

o Exercise

Early ( 1% 6-12 month )

o NSAIDs, analgesic, low dose corticosteroid
Disease modifying drug

Physiotherapy

o

a

o

Splintage

+ Progressive erosive (1-5 years)

o Disease modifying drug

o Splintage

o Surgical management ( synovectomy, arthroscopic surgery ), late ( 5-20 years)
o Reconstructive surgery ( arthrodesis, osteotomy, arthroplasty)

30. COMPLICATION

= Fixed deformities

= Muscle weakness

* Infection

= Spinal cord compression

= Systemic vasculitis

= Amyloidosis- Renal failure