Rheumatoid

RHEUMATOID
ARTHRITIS
By
Devalekshmi
• DEFINITION
• Rheumatoid arthritis (RA) is a chronic inflammatory disease of

unknown etiology characterized by a symmetric polyarthritis and is
the most common form of chronic inflammatory arthritis.
• RA, a systemic disease, may also lead to a variety of extraarticular

manifestations, including fatigue, subcutaneous nodules, lung
involvement, pericarditis, peripheral neuropathy, vasculitis, and
hematologic abnormalities, which must be managed accordingly.
Etiology
• Multifactorial
• Genetic – HLA gene- Variation in 3 AA in HLA DRB1 loci(position 11,71,41)
• Environmental- 1) Smoking tobacco
• 2)Infection ( viral,mycoplasma..)trigger autoimmunity in
genetically susceptible host- by modifying host protein through citrullination
• Familial-1st degree relative,monozygotic>dizygotic twins
• Gender- female: male=3:1,after menopause same incidence
Pathophysiology
CLINICAL FEATURES
• The incidence of RA increases between 25 and 55 years of age, after which it plateaus until
the age of 75 and then decreases.
• Female to male=3:1
SYMPTOMS
• The presenting symptoms of RA typically result from inflammation of the joints, tendons,
and bursae.
Pain, joint swelling and stiffness affecting the small joints of the hands, feet and
wrists in a symmetrical fashion.
• The earliest involved joints are typically the small joints of the hands and
feet(MCP,PIP,MTP)
• The initial pattern of joint involvement may be monoarticular, oligoarticular (≤4 joints), or
polyarticular (>5 joints).
• Large joint involvement occur later(knee,elbow,ankle,hip,shoulder), systemic symptoms
and extra-articular features may also occur.
ONSET
1)Acute onset= severe early morning joint stiffness lasting >1 hour
that eases with physical activity, polyarthritis and pitting
oedema(more commonly in old age).
2)Another presentation is with proximal muscle stiffness mimicking

polymyalgia rheumatica.
3) Occasionally, the onset is palindromic, with relapsing and

remitting episodes of pain, stiffness and swelling that last for only a
few hours or day.
0N
EXAMINATION
• Symmetric bilateral pain ,swelling and tenderness of the affected joints. Painful limitation
of movement. Erythema is unusual and its presence suggests coexistent sepsis.
Characteristic deformities
1) HAND
• Most commonly involved is wrist &MCP .
• DIP is usually spared. Its involvement may occur in RA, but it is usually is a manifestation
of coexistent osteoarthritis.
• Flexor tendon tenosynovitis is a frequent hallmark of RA and leads to decreased range of
motion, reduced grip strength, and “trigger” fingers.
• Flexor tendon involvement may also lead to tendon rupture, with the flexor pollicis longes-
the most common flexor tendon to be affected by RA.
Hyperextension at PIP Spindling of fingers- swelling in PIP
Flexion at DIP
Boutonnieres- Flexion at PIP,
Extension at dip
• Boxing glass appearance- Whole hand
swollen& pitting edema over dorsum.
• Dropped finger- extensor tendon
Rheumatoid granuloma & tendon
rupture
Radial deviated wrist+ ulnar deviated digits+ palmar

subluxation of 1st MCP+ HE of 1st IPJ
FEET & ANKLE
• Chronic inflammation of the ankle and midtarsal regions -
planovalgus (“flat feet”).due to loss of the longitudinal
arch dur to rupture of the tibialis posterior tendon.
Subluxation of the MTP joints of the feet

may result in ‘cock-up’ toe deformities,
causing pain on weight-bearing on the
exposed MTP heads
• Popliteal (Baker’s) cysts –in patients with knee
synovitis(increased synovial fluid), in which synovial
fluid communicates with the cyst but is prevented
from returning to the joint by a valve-like
mechanism.
• This is not specific to RA. Rupture may be induced

by knee flexion, leading to calf pain and swelling
that may mimic a deep venous thrombosis (DVT).
Large joints, including the knees and shoulders,
are often affected in established disease,
although these joints may remain asymptomatic
for many years after onset
• Spinal cord compression
• Atlanto-axial subluxation is due to erosion of
the transverse ligament posterior to the
odontoid peg-- cord compression or sudden
death following minor trauma or
manipulation.
• It should be suspected in any RA patient who
describes new onset of occipital headache, if
symptoms of paraesthesia or electric shock are
present in the arms.
EXTRA ARTICULAR MANIFESTATION
Systemic features
• Anorexia, weight loss and fatigue may occur throughout the disease course.
• Osteoporosis
• Rheumatic Nodules Sub cutaneous nodules,(2-5mm) exclusively in RF- or ACPA-positive

patients, usually in extensor tendons (& repeated trauma sites- olecranon bursa, proximal
ulna,occiput)are frequently asymptomatic but some may be complicated by-ulceration
and secondary infection.
• They consist of a central area of fibrinoid material surrounded by a palisade of
proliferating mononuclear cells. Granulomatous lesions may occur in the pleura, lung,
pericardium and sclera
Ocular involvement -most common symptom is dry eyes
(keratoconjunctivitis sicca) due to secondary Sjögren’s syndrome(K-sicca+
xerostomia+ parotid enlargement)
• Scleritis, Episcleritis can progress to Sclero malacia perforans are uncommon
but more serious and potentially sight-threatening complications (pain and
redness).
Vasculitis
• This is uncommon but may occur in
seropositive patients.
• Presentation - fatigue and fever and nail-
fold(digital) infarcts. Rarely, cutaneous
ulceration, skin necrosis and mesenteric,
renal or coronary artery occlusion may occur.
• Serositis Serositis is usually asymptomatic but may present with pleural or pericardial
pain and breathlessness. Pericardial effusion and constrictive pericarditis may rarely
occur.
• Cardiac-Heart block, cardiomyopathy, coronary artery occlusion and aortic regurgitation
have all been reported but are rare.
• Pulmonary Pleuritis- dyspnoea, chest pain, friction rub.
• Pleural effusion- exudative , increased neutrophils, monocytes seen.
• Caplan syndrome- Multiple module+ Interstitial lung disease+ pneumoconiosis(cwp /
silicosis).
• Osteoporosis is more common in patients with RA ,prevalence of approximately one-third
in postmenopausal women with RA. There is also an increased risk of fragility fracture,
with a greater risk among women.
• Neurological Nerve entrapment syndromes- Carpal tunnel(ulnar),Tarsal tunnel-(Anterior
tibial nerve),Peripheral neuropathy
• LYMPHOMA diffuse large B-cell
lymphoma, risk of developing lymphoma
increases if the patient has high levels of
disease activity or Felty’s syndrome.
• Felty’s syndrome is a rare complication of

seropositive RA in which splenomegaly
occurs in combination with neutropenia
and thrombocytopenia.
• Hematologic- Normochromic normocytic

anemia(anemia of chronic disease,drug
induced,git bleed due to Nsaids...)
• Eosinophilia, mild leucocytosis ,
thrombocytosis.
INVESTIGATIONS
• The ESR and CRP are usually raised

but normal results do not exclude
the diagnosis.
• Tests for ACPA are positive in
about 70% of cases and are highly
specific for RA
• CBC- Anemia, WBCs- increased,
normal, decreased (feltys)
• Thrombocytosis
• Serology- RF, Anti citullinated
protein antibody.
Radiography of affected joint
1. Xray
• Symmetrical involvement
• Periarticular osteopenia
• Soft tissue swelling
• Sub chrondal bone erosion- wrist ,mcp, pip,
mtp
• Narrowing of joint space
2. MRI
More sensitive than Xray- soft tissue synovitis can
be seen before joint damage detection by
xray,joint effusion also seen.
3.USG including power Doppler-

detect Erosion better than plain Xray
ACA/EULAR Criteria
TREATMEN
T
• GOALS- disease remission, rest & splinting in acute-stage,
phsysiotherapy helps in mobilization, smoking cessation, control cvs risk
factors, screen for osteoporosis.
• 1)NSAIDS-
• 2)CORTICOSTEROID
• 3)DMARDS
• 4)BIOLOGICALS
• 5)IMMUNOSUPPRESANTS
• 6)SURGERY
1.NSAIDS
• SYMPTOMATIC RELIEF-
ANALGESIC&
ANTIINFLAMMATORY
PROPERTY
• DON’T ALTER DISEASE
PROCESS
• USED WITH CONCOMITANT
USE OF DMARDS
• S/E-Gastric/peptic ulcer,renal
function impairement
• So avoid chronic use
CORTICOSTEROID
1. Low to moderate doses -to achieve rapid disease control before the
onset of fully effective DMARD therapy, which often takes several weeks
or even months.
2. 1- to 2-week burst of glucocorticoids - management of acute disease
flares, with dose and duration guided by the severity of the
exacerbation.
3. Chronic administration of low doses (5–10 mg/d) of prednisone (or its
equivalent) -to control disease activity in patients with an inadequate
response.
• Bridge therapy- to shut down inflammation rapidly and then taper dose
as DMARDS start acting.
• PULSE THERAPY – Induce remission with--Intramuscular
methylprednisolone (80–120 mg),if synovitis persists >6weeks.
• DAS28 is widely used to assess disease
activity, response to treatment and need for
biological therapy.
• It involves counting the number of swollen

and tender joints in the upper limbs and
knees, and combining this with the ESR .
• Patient’s assessment of the activity of their

arthritis on a visual analogue scale, where 0
indicates no symptoms and 100 the worst
symptoms possible.
• This data are entered into a calculator to
generate a numerical score.
• The higher the value, the more active the
disease
DMARDS
• Modify progression and disabling potential of RA.
• Eg-Methotrexate., Sulfasalazamide, Leflunomide, Hydroxychloroquine.
• Triple therapy- MTX+ SSZ+HCQ
• Methotrexate- Drug of choice
• MOA-
• Anti-inflammatory effects exerted by low dose MTX at the level of the
synovial tissue in RA---reduces monocytic cell growth and increases their
apoptosis & decreases the IL1 and IL6 secretion and increases IL1ra
production.
• Dose 2.5-7.5 mg/kg/week- single dose+ folic acid 5mg/week for toxicity
control. If no response in 4-8week- increase dose by 2.5mg-5mg/week each
month to 15-25mg/week.
Biologicals
• TNFalpha inhibitors-
a)Etarnecept- a recombinant TNF receptor fusion protein - subcutaneously -25 mg
twice weekly.
b)Infliximab is a mouse human chimeric monoclonal antibody against TNF-a-
intravenously -3-10 mg every 4-6 weeks
c)Adalimumab is a recombinant human IgG1 monoclonal antibody directed against
TNF-a --subcutaneously in a dose 40 mg every other week.
• IL Receptor blocker- Anakinra -given subcutaneously in a dose of 100 mg daily.

Tocilizumab and sarilumab are two newer agents.
• Anti CD20 ab- Rituximab- genetically engineered chimeric murine monoclonal
antibody –against CD20 molecule on B cell surface- IV -2 infusion-2 weeks apart
(refractory RA).
• JAK inhibitors Tofacitinib, baricitinib, peficitinib, and upadacitinib, can also be
used in combination with MTX or as monotherapy
• Immunosuppressant –
• Cyclophosphamide, Azathioprine -3rd line drugs- those who
doesn’t respond to 2 nd line drugs.
• Surgery-
• Failure of medical therapy
• Maintain joint function, correct deformity,improve pain,diability.
Methods=
A) Synovectomy of inflammed joint
B) Osteotomy to correct deformity,pain relief.
C) Arthrodesis of joint to relive pain in Atlanto axial joint,wrist,ankle.
D) Joint replacement , Excision arthroplasty

Rheumatoid

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RHEUMATOID

• Rheumatoid arthritis (RA) is a chronic inflammatory disease of

• RA, a systemic disease, may also lead to a variety of extraarticular

2)Another presentation is with proximal muscle stiffness mimicking

3) Occasionally, the onset is palindromic, with relapsing and

Radial deviated wrist+ ulnar deviated digits+ palmar

Subluxation of the MTP joints of the feet

• This is not specific to RA. Rupture may be induced

• Rheumatic Nodules Sub cutaneous nodules,(2-5mm) exclusively in RF- or ACPA-positive

• Felty’s syndrome is a rare complication of

• Hematologic- Normochromic normocytic

• The ESR and CRP are usually raised

3.USG including power Doppler-

• It involves counting the number of swollen

• Patient’s assessment of the activity of their

• IL Receptor blocker- Anakinra -given subcutaneously in a dose of 100 mg daily.

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