Rheumatoid Arthritis Flashcards
Rheumatoid Arthritis (RA)
one of the most common inflammatory
arthritides.
○ Chronic (>6 weeks)
○ Systemic (articular and extra-articular manifestations)
○ Symmetric involvement
Etiology of RA
The exact cause of RA remains unknown; however, there are several influences that are
factors that are suspected in the development of RA
● Genetic factors: HLA-DR4, HLA-DR1 (lesser extent)
● Environmental factors: smoking
● Autoantibodies: Rheumatoid factor (RF) and/or anti-citrullinated protein (ACPA/CCP)
autoantibodies
Pathophysiology of RA
These factors/stresses likely cause modifications peptides at mucosal surfaces, such as the
lung, gut, oral cavity, and synovial membranes. The synovial membranes become inflamed and
proliferate forming a pannus (proliferation of the synovium) that invades bone, cartilage, and
ligaments and leads to damage and deformities.
Autoantibodies can be found in sera years (e.g. up to 6-10 years) before clinical symptoms
occur. This suggests that initiating events (environmental, genetic factors, etc) may cause a
complex interaction between the innate and adaptive immune systems
Family history and RA
● Several rheumatic disorders have a strong genetic basis and tend to cluster in
families. Asking about family history of rheumatic diseases can help to build a
diagnosis.
Onset and course of RA
● RA symptoms tend to have subacute onset (occurring over weeks to months)
and is usually > 6 weeks.
Clinical Presentation of RA
● Patients suspected of RA may have recurrent low grade fevers, chills, night
sweats, and weight loss
● Stiffness in or around the joints may be noted (e.g. 1 hour before improvement)
● It is important to differentiate between Arthralgia (joint pain) and Arthritis
(joint inflammation). RA is an inflammatory arthritis (presence of synovitis).
Suspicion for RA is indicated by the presence of _____, or inflammation of
synovial membranes
synovitis,
Articular Manifestation distribution of RA
● Distribution in early disease: the wrists, metacarpophalangeal (MCP) joints,
proximal interphalangeal (PIP) joints of the hands, interphalangeal joints of the
thumbs, metatarsophalangeal (MTP) joints of the feet
● Distribution in late disease: larger joints like the ankles, knees, elbows,
shoulder
● Less common involvement: temporomandibular and sternoclavicular joints
● Nearly always spared: distal interphalangeal joints and thoracolumbar spine
Articular Manifestations - Joint
Deformities in RA
Fusiform swelling
Boutonniere deformity
Swan-neck deformity
Ulnar deviation of fingers
Hitchhiker thumb
“Piano key” ulnar head
Cock-up toe deformities
Hallux valgus (Bunion):
______: synovitis of PIP joints
which causes them to appear
spindle-shaped.
Fusiform swelling
______: flexion of the PIP
and hyperextension of the DIP joint, caused
by weakening of the central slip of the
extrinsic extensor tendon and a palmar
displacement of the lateral bands
Boutonniere deformity
______: contraction of the flexors (intrinsic muscles) of the MCPs which results in flexion contracture of the MCP joint, hyperextension of PIP, and flexion of the DIP join
Swan-neck deformity
______: subluxation of
MCP joints results from weakening of the
extensor carpi ulnaris leading to radial
deviation of the wrist causing all finger tendons
to pull the fingers ulnarly with power grasp
Ulnar deviation of fingers
______: hyperextension of IP joint
with flexion of MCP and exaggerated
adduction of first metacarpal. Causes inability
to pinch
Hitchhiker thumb
______: secondary to
destruction of ulnar collateral ligament
leading to a floating ulnar styloid.
“Piano key” ulnar head
______: dorsal
subluxations of the MTPs
Cock-up toe deformities
It is important to note that ______ can
be present with RA and may be seen on PE
osteoarthritis
● Heberden’s nodes affecting the DIP
joints
● Bouchard’s nodes affecting the PIP
joints
Extra-articular Manifestations of RA
Rheumatoid Nodules (Subcutaneous)
the most common (currently)
extra-articular manifestation
Sjogren’s Syndrome (Secondary) is also
common
Diagnostic Labs for RA
Autoantibodies:
● Rheumatoid Factor (RF), anti-CCP (CCP)
Inflammatory markers:
● Erythrocyte Sedimentation Rate (ESR), C-Reactive Protein (CRP)
Adjunct labs:
● CBC, CMP
● ANA by IFA, Comprehensive ANA panel, Chronic Hepatitis Panel (Hepatitis C
and Hepatitis B)
● With consideration: Uric Acid, CPK, SPEP
Labs for RA diagnosis
● Labs
○ RF, CCP, ESR, CRP
● Imaging
○ X-ray, US, MRI
● Joint fluid aspiration testing
In rare instances a synovial
biopsy will be used in the
diagnosis of RA.
Anti-Malondialdehyde-Acetaldehyde Antibody (MAA) and RA
● This new autoantibody is associated with the development of RA
similar to RF and CCP
● Elevations of MAA are associated with high levels of CCP
○ Elevations in CCP are associated with the development of RA
■ Months up to 18 years per some literature
○ Elevations in MAA are associated with the development of RA
■ 2-3 years prior
known risk factors for the development of RA
● Smoking, Silica
○ PTSD and RA (Vets being exposed to “burn pits” while during
active duty have been see to develop RA)
Synthetic / Traditional DMARDs
● Methotrexate (MTX)*
● Leflunomide (Arava)*
● Sulfasalazine*
● Azathioprine (Imuran)
● Hydroxychloroquine (Plaquenil)*
● Cyclosporine
● Minocycline
Biologic and Small Molecule DMARDs
● Infliximab (Remicade)
● Adalimumab (Humira)*
● Etanercept (Enbrel)
● Golimumab (Simponi / Simponi Aria)
● Certolizumab (Cimzia)
● Abatacept (Orencia)
● Tocilizumab (Actemra)
● Sarilumab (Kevzara)
● Rituximab (Rituxan)
● Tofacitinib (Xeljanz)
● Anakinra (Kineret)
