Rheumatoid Arthritis

Arthritis
“arthro” = joint
“itis” = inflammation
“Arthritis can affect babies and children, as well as people in the
prime of their lives”
• Rheumatoid arthritis is an autoimmune disease in which the
normal immune response is directed against an individual's own
tissue, including the joints, tendons, and bones, resulting in
inflammation and destruction of these tissues.

•Commonest inflammatory joint disease seen in clinical

practice affecting approx 1% of population.

•Characterized by persistent inflammatory synovitis leading to

cartilage damage, bone erosions, joint deformity and disability.
 Anatomy of the Joint

Articular/hyaline cartilage
-acts as a shock absorber
- allows for friction-free movement
- not innervated!
Synovial membrane/synovium
-secretes synovial fluid
-nourishes cartilage
-cushions the bones
 Overview
 Age: Any age, commonly 3rd to 6th decade
 Female: male 3:1
 pattern of joint involvement could be:-
1) Polyarticular : most common
2) Oligoarticular
3) Monoarticular
 Morning joint stiffness > 1 hour and easing with physical activity is
characteristic.
 Small joints of hand and feet are typically involved.
 Clinical Manifestations

 Articular

 Extra-articular
 Articular manifestation

 Pain and swelling in

affected joint
aggravated by
movement is the most
common symptom.

 Morning stiffness ≥1
hr
 Joints involved -
 Relative incidence of joint
involvement in RA
 MCP and PIP joints of hands & MTP of feet 90%
 Knees, ankles & wrists-
80%
 Shoulders- 60%
 Elbows- 50%
 TM, Acromio - clavicular & SC joints-
30%
 Joints involved in RA
 Don’t forget the cervical spine!!
Instability at cervical spine can lead to
impingement of the spinal cord.

 Thoracolumbar, sacroiliac, and distal

interphalangeal joints (DIP)of the hand are
NOT involved.
PIP Swelling
Ulnar Deviation, MCP Swelling,
Left Wrist Swelling
 Extra-articular

manifestations
Present in 30-40%
 May occur prior to arthritis
 Patients that are more likely to get are:
 High titres of RF/ anti-CCP
 HLA DR4+
 Male
 Early onset disability
 History of smoking
Extraarticular Involvement
 Constitutional symptoms ( most common)
 Rheumatoid nodules(30%)
 Hematological-
 normocytic normochromic anemia
 leucocytosis /leucopenia
 thrombocytosis
 Felty’s syndrome-
 Chronic nodular Rheumatoid Arthritis
 Spleenomegaly

 Neutropenia
 Respiratory- pleural effusion, pneumonitis ,
pleuro-pulmonary nodules, ILD
 CVS-asymptomatic pericarditis , pericardial
effusion, cardiomyopathy
 Rheumatoid vasculitis- mononeuritis multiplex,
cutaneous ulceration, digital gangrene, visceral
infarction
 CNS- peripheral neuropathy, cord-compression
from atlantoaxial/midcervical spine subluxation,
entrapment neuropathies
 EYE- kerato-conjunctivitis sicca, episcleritis,
scleritis
 Rheumatoid nodule
•These are small subcutaneous nodules
present at the extensor surfaces of hand,
wrist, elbow and back in rheumatoid
arthritis patients.

•Characteristics feature of rheumatoid

arthritis

•A marker of disease activity

•Canbe present even if other features of

rheumatoid Arthritis are absent
Laboratory investigations in RA
 CBC- TLC, DLC, Hb, ESR & GBP

 Acute phase reactants

 Rheumatoid Factor (RF)

 Anti- CCP antibodies

 Rheumatoid Factor (RF)
 Antibodies that recognize Fc portion of IgG
 Can be IgM , IgG , IgA
 85% of patients with RA over the first 2 years become RF+

• A negative RF may be repeated 4-6 monthly for the first two year of
disease, since some patients may take 18-24 months to become
seropositive.
• PROGNISTIC VALUE- Patients with high titres of RF, in general,
tend to have POOR PROGNOSIS, MORE EXTRA ARTICULAR
MANIFESTATION.
 Causes of positive test for RF
 Rheumatoid arthritis
 Sjogrens syndrome
 Vasculitis such as polyarteritis nodosa
 Sarcoidosis
 Systemic lupus erythematosus
 Cryoglobulinemia
 Chronic liver disease
 Infections- tuberculosis , bacterial endocarditis, infectious
mononucleosis, leprosy, syphilis, leishmaniasis.
 Malignancies
 Old age(5% women aged above 60)
Anti-CCP
 IgG against synovial membrane peptides
damaged via inflammation
 Sensitivity (65%) & Specificity (95%)
 Both diagnostic & prognostic value
 Predictive of Erosive Disease
 Disease severity
 Radiologic progression
 Poor functional outcomes
 Acute Phase Reactants
Positive acute phase reactants () Negative acute phase reactants ()
Mild elevations – Albumin
– Ceruloplasmin – Transferrin
– Complement C3 & C4
Moderate elevations
– Haptoglobulin
– Fibrinogen (ESR)
– 1 – acid glycoprotein
– 1 – proteinase inhibitor
Marked elevations
– C-reactive protein (CRP)
– Serum amyloid A protein
 Elevated APRs( ESR, CRP )
 Thrombocytosis
 Leukocytosis
 ANA
 30-40%

 Inflammatory synovial fluid

 Hypoalbuminemia
 Radiographic Features
 Peri-articular osteopenia
 Uniform symmetric joint space narrowing
 Marginal subchondral erosions
 Joint Subluxations
 Joint destruction
 Collapse

 Ultrasound detects early soft tissue lesions.

 MRI has greatest sensitivity to detect synovitis and
marrow changes.
Diagnostic Criterias
 ACR Diagnostic Criteria (1987)
 Description
 Morning stiffness

 Arthritis of 3 or more joints

 Arthritis of hand joints

 Symmetric arthritis

 Rheumatoid nodules

 Serum rheumatoid factor

 Radiographic changes

 A person shall be said to have rheumatoid arthritis if he or

she has satisfied 4 of 7 criteria, with criteria 1-4 present for
at least 6 weeks.
 2010 ACR/EULAR Classification Criteria
 a score of ≥6/10 is needed for classification of a patient as having definite RA
 A. Joint involvement SCORE
 1 large joint 0
 2−10 large joints 1
1−3 small joints (with
or without involvement of large joints) 2
 4−10 small joints (with or without involvement of large joints) 3
 >10 joints (at least 1 small joint)†† 5

 B. Serology (at least 1 test result is needed for classification)

 Negative RF and negative ACPA 0
 Low-positive RF or low-positive ACPA 2
 High-positive RF or high-positive ACP 3

 C. Acute-phase reactants (at least 1 test result is needed for classification)

 Normal CRP and normal ESR 0
 Abnormal CRP or normal ESR 1

 D. Duration of symptoms
 <6 weeks 0
 ≥6 weeks 1
Management
Goals of management
 Focused on relieving pain
 Preventing damage/disability
 Patient education about the disease
 Physical Therapy for stretching and range of motion
exercises
 Occupational Therapy for splints and adaptive devices
 Treatment should be started early and should be
individualised .
 EARLY AGGRESSIVE TREATEMNT
Treatment modalities for RA
 NSAIDS
 Steroids
 DMARDs (Disease Modifying Antirheumatic
Drugs)
 Immunosuppressive therapy
 Biological therapies
 Surgery
Systemic Lupus Erythematosus
(SLE)
Systemic Lupus Erythematosus
 Chronic multisystem inflammatory
autoimmune disease
 Complex interactions among many
factors including
 Genetic
 Hormonal
 Environmental
 Immunologic

,
Systemic Lupus Erythematosus
 Affects
 Skin
 Joints
 Serous membranes
 Pleura
 Pericardium

 Renal system
 Hematologic system
 Neurologic system

,
Systemic Lupus Erythematosus
 Characterized by an unpredictable
course with alternating exacerbations
and remissions
 Most common in women of childbearing
years
 More common in African Americans,
Asian Americans, Hispanics, and Native
Americans than in whites

,
Etiology and Pathophysiology
 Etiology is unknown
 Most probable causes
 Genetic influence
 Hormones
 Environmental factors
 Certain medications

,
Etiology and Pathophysiology
 Overaggressive autoimmune
reactions directed against
constituents of:
 Cell nucleus
 Single- and double-stranded DNA
 Antibody response related to B- and
T-cell hyperactivity

,
Clinical Manifestations
 SLE is extremely variable in severity
 Ranges from a relatively mild disorder to
rapidly progressive disease affecting
many organ systems
 Most commonly affects skin, muscles,
lining of lungs, heart, nervous tissue,
and kidneys

,
Multisystem Involvement of SLE
Clinical Manifestations
 Dermatologic
 Cutaneous vascular lesions
 Most commonly in sun-exposed areas
 Oral/nasopharyngeal ulcers
 In up to 33% of cases
 Alopecia
 Butterfly rash
 Occurs in 50% of cases

,
Butterfly Rash of SLE
Clinical Manifestations
 Musculoskeletal
 Polyarthralgia with morning stiffness
 Arthritis
 Swan neck fingers
 Ulnar deviation
 Subluxation with hyperlaxity of joints
 Increased risk of bone loss and fracture

,
Swan Neck Deformity

,
Clinical Manifestations
 Cardiopulmonary
 Tachypnea
 Cough
 Pleurisy
 Dysrhythmias
 Fibrosis of SA and AV nodes
 Pericarditis
 Accelerated CAD
 At risk for coagulation disorder

,
Clinical Manifestations
 Renal
 Lupus nephritis
 Manifests in about 40% of cases within 5
years of onset
 Ranging from mild proteinuria to
glomerulonephritis
 Primary goal in treatment is slowing the
progression

,
Clinical Manifestations
 Nervous system
 Generalized/focal seizures
 Peripheral neuropathy
 Cognitive dysfunction
 Disorientation
 Memory deficits
 Psychiatric symptoms

,
Clinical Manifestations
 Hematologic
 Formation of antibodies against
blood cells
 Anemia
 Leukopenia
 Thrombocytopenia

,
Clinical Manifestations
 Infection
 Increased susceptibility to infections
 Defects in ability to phagocytize invading
bacteria
 Deficiencies in antibody production
 Immunosuppressive effect of many
antiinflammatory drugs
 Infection is a major cause of death

,
Multiple
Sclerosis
 “What does MS mean to you?”
2.3 million
people

“Fighting for my
future”
“I may not look sick on
the outside, but on the
inside it’s like my body
is trying to kill me” ”World Map.” Clicker Clipart

“An uncertainty about

tomorrow”
“It's Multiple Sclerosis Week! Tell Us What MS Means to You.” National Multiple Sclerosis Society, main.nationalmssociety.org/site/MessageViewer?em_id=68686.0&dlv_id=86366&s_AffiliateSecCatId=1&pw_id=10481.
Cellular processes, symptoms, and disease progression
help create treatment options.
What is Multiple Sclerosis?

“Multiple Sclerosis Myelin Sheath Cartoon.” Gene.

“Multiple Sclerosis.” Genentech, www.gene.com/patients/disease-education/multiple-sclerosis?topic=multiple-sclerosis.

MS is an Autoimmune Disease.

“Blood Brain Barrier.” Bioninja.

 The immune system causes permanent damage
to glial cells and neurons.
KILL
T-CELL ER
T-
CELL
BLOOD BRAIN BARRIER

“Clinical Progression of Multiple Sclerosis.” Khan Academy, Khan Academy, www.khanacademy.org/science/health-and-

medicine/nervous-system-diseases/multiple-sclerosis/v/clinical-progression-of-multiple-sclerosis.
Multiple Sclerosis causes changes in
saltatory conduction.

Rose, John W., et al. “Lectures: Pathology.” Multiple Sclerosis,

library.med.utah.edu/kw/ms/path.html#1.
 What are the Symptoms of Multiple Sclerosis?
BALANCE and
COORDINATI
ON
VISUAL
PROBLEMS
FATIGUE

MUSCLE PAIN
and TINGLING

“Black person.” Pixabay.

“Gray Person.” Clicker Clipart.

Agamanolis, Dimitri. “Demyelinative Diseases, Chapter 6.” Neuropathology: An Illustrated Interactive Course for Medical Students and Residents, neuropathology-web.org/chapter6/chapter6aMs.html.
 How does MS Progress?
Relapsing Remitting
MS
Severit
y

“Orange MS Ribbon.” Pinterest.

“Clinical Progression of Multiple Sclerosis.” Khan Academy, Khan Academy, www.khanacademy.org/science/health-and-

medicine/nervous-system-diseases/multiple-sclerosis/v/clinical-progression-of-multiple-sclerosis.
Tim
e
 Treatment options target the symptoms, not the source…

“Corticosteroids.” Healthy Place.

“Physical Therapy for MS.” Behance.

Mayo Clinic Staff. “Multiple Sclerosis.” Mayo Clinic, Mayo Foundation for Medical Education and Research, 4 Aug. 2017,
www.mayoclinic.org/diseases-conditions/multiple-sclerosis/diagnosis-treatment/drc-20350274.

And we still have a lot of progress to make.

Where do we go from here?

CURE!