rheumatoid arthritis presentation
TRANSCRIPT
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Prepared by:
ASYA'ARI BIN ARIF
RASHEEDI JUZAIMIE BIN JUSOH
MUHAMMAD AFIQ BIN MOHD RAZALI
NUR NADIATUL NABILA BT AHMAD SAIFUDDIN
RHEUMATOID
ARTHRITIS
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DEFINITION
RA is a systemic , chronic
inflammation disease affecting many
tissues
principally attacking the joints toproduce nonsuppurative proliferative
synovitis
3 to 5 times more common in women
than men
peak incidence : 2nd to 4th decades of
life
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EPIDEMIOLOGYAND HISTORY
Gender Women are two-to-three times more likely than men to develop
rheumatoid arthritis. The exact cause for this is not known, but
it may be related to the hormone, oestrogen
Age
Rheumatoid arthritis can develop at any age but it is more
common in older people. It is most likely to be diagnosed in
people between 40 and 60 years of age
.
Family history
Although rheumatoid arthritis is not a hereditary disease,certain genes can make a person more susceptible to it. This
means that people with close relatives who suffer from
rheumatoid arthritis have a higher than usual risk of developing
it themselves because they may have inherited the same
genes. However, they are still more likely not to get the disease
than to get it.
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.
Family history
Although rheumatoid arthritis is not a hereditary disease,
certain genes can make a person more susceptible to it.
This means that people with close relatives who suffer fromrheumatoid arthritis have a higher than usual risk of
developing it themselves because they may have inherited
the same genes. However, they are still more likely not to
get the disease than to get it.
Smoking
People who smoke have a higher risk of developing
rheumatoid arthritis than those who do not.
Picture of people of different races
In Europe and North America, rheumatoid arthritis affects
0.51% of the population in total. However, it is much more
common in Native Americans (affecting over 5%) and less
common in African and Asian people. This suggests that
there are genetic factors involved in the development of the
disease.
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CAUSES
The cause of rheumatoid arthritis is unknown.
Even though infectious agents such as
viruses, bacteria, and fungi have long been
suspected, none has been proven as the cause
It is believed that the tendency to develop
rheumatoid arthritis may be genetically
inherited
Environmental factors also seem to play some
role in causing rheumatoid arthritis. For
example, scientists have reported that smoking
tobacco increases the risk of developingrheumatoid arthritis.
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MORPHOLOGY
A)Articular Lesion
The most severe form
Present as symmetric arthritis,affect small joint of
hand,feet,ankle,knees,wrists,elbows and
shoulders.
Typical in proximal interphalangeal and
metacarpophalangeal
Frequent in cervical spine
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1. Joint
- synovium becomes grossly edematous, thickened and
hyperplastic(bulbous fronds)
-Histologic features:
i. Dense perivascular inflammatory cell infiltrate(form
lymphoid follicle) in synovium composed of CD4+ T Cell,
B cell,plasma cell,dendritic cells and macrophage.
ii. Increased vascularity due to angiogenesis and
vasodilation.
iii. Aggregation of organizing fibrin on synovial surface and
float in joint space as rice bodies
iv. Accumulation of neutrophils in synovial fluids and along
synovium surface.
v. Increased osteoclast activity in the underlying
bones,leading to synovial penetration and bone erosion.
vi. Pannus formation
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Villous hypertrophy of the synovium is seen, forming large papillary projections
on the surface. These are characterized by proliferation of the synoviocytes and
aggregates of inflammatory cells within the villous stroma.
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At higher magnification ,subsynovial
tissue containing a dense lymphoid
aggregate is seen
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The region of the synovial lining that erodes into the bone, which is known as the pannus,
contains macrophages, fibroblasts and osteoclasts, which contribute to the cartilage and bone
destruction76. The sublining region of the rheumatoid joint is replete with blood vessels, which
are important for delivering inflammatory cells to the joint, such as monocytes and lymphocytes.
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B)Extra-Articular Lesion
Nonspecific inflammatory changes seen in bloodvessels(acute vasculitis) , lung
,pleura,pericardium,myocardium,lymph
nodes,peripheral nerves and eyes.
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1. Skin (rheumatoid nodules)
Most common cutaneous lesion
Arise in region of the skin that are subjected
to pressure,including the ulnar aspect of the
forearm,elbows,occiput and lumbosacral area.
Less common form in the
lungs,spleen,pericardium,myocardium,heart
valves,aorta and other viscera.
Microscopically: the centre of nodule consist
of area of fibrinoid necrosis surrounded by a
prominent rim of epithelioid
histiocytes(activated macrophage) and
numerous lymphocytes and plasma cells.
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A closer view showing the central necrosis on the left
side of the photomicrograph, with successive layers of
palisading macrophages and lymphocytes (to the right
of the necrosis).
Necrotizing granuloma surrounded by palisading histiocytes
and foreign body giant cell (black arrow)
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Rheumatoid Nodules. Rheumatoid nodules commonly form near the extensor surface
of the elbow. They can be fixed to the underlying periosteum or can be freely mobile
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2. Blood Vessels (Rheumatoid vasculitis)
Developed in high risk in affected individuals with
severe erosive disease, rheumatoid nodules and
high titers of rheumatoid factors .
Characterized by inflammatory destruction of small
and medium-sized blood vessels primarily due to leukocyte migration and resultant
damage.
Development of red spots on the skin as a result.
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PATHOGENESIS
-The joint inflammation is immunologically mediated
- The initiating agent/s are not yet understood- Proposed that it is initiated by activation ofCD4+ helper
T cells
- The activated T cells produce cytokines that :-
a)A
ctivate macrophages and other cells in the jointspace, releasing degenerative enzymes and other
factors that perpetuate inflammation..
b) Activate B cells, resulting in the production of
antibodies, some of which are directed against self-
antigens in the joint.
- The rheumatoid synovium is rich in both lymphocytes-
and-macrophage-derived cytokines.
- Activated T cells in RA lesions have also been shown
to express impressive amounts of cytokine called
RANKligand .
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The role of antibodies in the disease is suspected
from a variety of experimental and clinicalobservations .
About 80% of patients have serum IgM ( and less
frequently IgG ) autoantibodies that bind to the Fc
portions of their own (self) IgG
These autoantibodies are called rheumatoid factor (RF )
Genetic variables in the pathogenesis ofRA are
suggested by the increased frequency of this disease
among first-degree relatives and a high concordance
rate in monozygotic twins
There are also associations of HLA DR4 and
polymorphism in the PTPN22 gene with RA
There are elusive infectious agents whose antigens
may activate T or B cells.
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Articular surface (top) shows loss of articular cartilage
beneath pannus overgrowth
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The inflammation associated with RA can lead to
fibrosis (arrow) and fusion of the joint (ankylosis)
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SYMPTOMS & SIGNS
Come & go.
Primarily affects joints, others are known
When active several symptoms can be
acknowledged
- fatigue
- loss of energy
- lack of appetite
- muscle and joint aches
- stiffness
During flares- joints frequently become red,
swollen, painful, and tender.
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In rheumatoid arthritis, multiple joints are usually
inflamed in a symmetrical pattern
Occasionally, only one joint is inflamed.
Chronic inflammation can cause damage to body
tissues, including cartilage and bone.
is a systemic disease, its inflammation can affect
organs and areas of the body other than the joints.
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DIAGNOSIS
Imaging x rays, ultrasound,MRI Stage I
no damage seen on X-rays, although there may be signs of
bone thinning
Stage II on X-ray, evidence of bone thinning around a joint with or
without slight bone damage
abnormalities of soft tissue around joint possible
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Stage III
on X-ray, evidence of cartilage and bone
damage and bone thinning around the joint
joint deformity without permanent stiffening orfixation of the joint
extensive muscle atrophy
abnormalities of soft tissue around joint
possible
Stage IV
on X-ray, evidence of cartilage and bone
damage and osteoporosis around joint
joint deformity with permanent fixation of the
joint
extensive muscle atrophy
abnormalities of soft tissue around jointpossible
Blood test
rheumatoid factor
sedimentation rate
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TREATMENT
First-line medication
NSAIDs
NSAIDs are medications that can reduce tissue
inflammation, pain, and swelling
NSAIDs have side effects
Example ofNSAIDs aspirin (acetylsalicylate)
Corticosteroid medications
more potent than NSAIDs
useful for short periods during severe flares of
disease activity or when the disease is not
responding to NSAIDs
Have serious side
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Second-line or "slow-acting" drugs
Disease-modifying anti-rheumatic drugs or
DMARDs
These medicines may take weeks to months to
become effective.
DMARDs can promote remission.
Chemically synthesised DMARDs:
azathioprine
D-penicillamine
gold salts
methotrexate (MTX)
sulfasalazine (SSZ)
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PROGNOSIS
Disability
Daily living activities are impaired in most
individuals.
After 5 years of disease, approximately 33% of
sufferers will not be working. After 10 years, approximately half will have
substantial functional disability
Mortality
Estimates of the life-shortening effect ofRA vary;
most sources cite a lifespan reduction of 5 to 10
years
RA sufferers suffer a doubled risk.