SBJ-2 Osteoarthritis and Rheumatoid Arthritis

Terms	Definitions
Osteoarthritis 7 million Americans	What accounts for more disability among seniors than any other disease?
No systemic, inflammation is mild, if at all present.	Systemic symptoms of osteoarthritis?
Progressive degeneration of hands, spine, weight-bearing joints Hands: DIPs, PIPs, 1st CMC AC shoulder, C/T/L Spine Hips, cysts in superior acetabulum Knees 1MTP	What joints are typically affected by osteoarthritis?
Osteoarthritis	What is the most common articular disorder?
Obesity Heredity Age Previous joint trauma Smoking Certain occupations (with usage of the joint)	Risk factors for osteoarthritis?
Present, but usually <30 minutes	Morning stiffness characteristics with OA?
Associated with OA, it involves any period of prolonged rest that results in joint stiffness	What is the "gel phenomenon"?
AM stiffness <30 minutes Joint pain / tenderness worse with activity, better with rest Crepitus (crunchy feeling) Bony swelling (Heberden's and Bouchard's nodes) Functional impairment (like decreased fine motor movement) Periarticular muscular atrophy	Clinical signs of OA?
Non inflammatory synovial fluid High viscosity Clear and yellow WBC < 1-2 k	Lab findings in OA?
Osteophytes (bone spurs) Non uniform joint space narrowing Subchondral cysts (e.g. in the superior acetabulum of the hips) Malalignment	XR findings in OA?
Cartilage degeneration at point of maximal stress, with a non-uniform, focal joint space narrowing.	Primary problem in OA?
Swelling of articular cartilage, and then breaking down articular cartilage which then thins and softens. Cartilage loss leads to subchondral bone sclerosis, trabecular compression, reactive bone deposition. Synovial fluid leaks into underlying bones, forming cysts Endochondral ossification	After cartilage degeneration, what can happen with OA?
Both are slides of articular cartilage. Top is cross-section through normal hip cartilage, with abundant mucopolysaccharide Bottom shows degenerative changes in the articular cartilage indicative of OA. Hypercellularity, low MPS (pink)
DIP joint slide, showing irregular bony hypertrophy. The joint is trying to repair itself in the setting of OA, with no active inflammation
Heberden's nodes, seen in OA. If you push on these bony budges, these might be tender. They usually become non-tender in time. This is basically bony proliferation, in which proliferation of the bone kind of attempts to keep the joint from moving.
Synovial cyst seen in the setting of OA-derived Heberden's nodes. Not inflammatory.
Bouchard's nodes (bony proliferations surrounding the PIPs). Also seen here are Heberden's nodes	What is the cursor pointing to?
Bone spurs (osteophytes) of the DIPs (Heberden's nodes), with irregular joint space narrowing. PIPs also have ireregular joint space narrowing. Also seen here are subluxation of the 1st MCP All in the setting of OA	What is abnormal
Osteophytes Bone sclerosis Bony compression Irregular joint space narrowing All in the setting of OA
Seen in the setting of erosive OA Gull wing deformity, with osteophytes. Periarticular osteopenia is not present (thinning of bones around a particular joint)
Hip changes seen in the setting of OA Bone sclerosis of the right and especially the left hip. Left hip almost has obliteration of the joint space.
OA hips, advanced, very much so on the left. Complete obliteration of joint capsule, with bony growth and sclerosis.
Oral NSAIDs, ASA, Acetaminophen Glucosamine condroitin (nutritional supplement) Limbrel (Flavocoxid) - OTC Viscosupplementation (hyaluronic acid injections, qWeek for up to five weeks) Topical capsaicin Diclofenac patches Lidocaine patches Narcotics (esp low dose, Tramadol) Steroid injections	Medications available for OA?
Joint replacement (esp. knees and	Surgery available for OA?
PT for muscle strength, range of motion Medical unloader braces Assistive devices	Therapy available for OA?
Weight reduction Exercise	Lifestyle changes that would help with OA?
Capsaicin Diclofenac patches Lidocaine patches	Patches /topical drugs available for OA?
Chronic systemic, autoimmune, inflammatory disorder	What is Rheumatoid Arthritis, in a nutshell?
Synovial tissue becomes inflamed, and proliferates, forming pannus. These pannus invade bone, cartilage, and ligaments	Primary disease process in RA?
Symmetric synovitis (typically bilateral, and across the joint itself) Bony erosions at the joint margins There are also many extraarticular manifestations: (see other slides)	Signs of RA?
35-45 years old 1/3 after the age of 60	Peak age of RA?
1% of world pop F:M 3:1	Prevalence and sex disparities in RA?
Functional limitation and 30% of patients lose of work within the first five years due to functional impairment (although this is getting better)	Progression of RA?
Synovial tissue	What is the primary target of the autoimmune inflammatory process that happens in RA?
Edema Angiogenesis Hyperplasia of synovial lining and inflammatory infiltrates	Signs of early stage RA?
Massive hyperplasia of type A synovial cells Subintimal mononuclear cell infiltration Extensive infiltration by plasma cells, macrophages, lymphocytes Pannus formation	Signs of late stage RA?
Subintimal mononuclear cell infiltration: plasma cells, macropahges, lymphocytes. Late stages of RA	Cell types seen in RA, and when along the course of disease?
Normal on left RA on right
Slide showing normal synovium Synovial cells are basically a few cell layers deep
Synovitis in the setting of RA Thickening of the layer, with lots and lots of cells (almost looks like granulation tissue). This is before the formation of pannus
Pannus, formed from the synovium, in the setting of late stage RA. Cartilage is starting to invade.
Soluble TNF receptor IL-10 IL-1 receptor antagonist	What cytokines are considered anti-inflammatory in the setting of RA?
TNFalpha IL-1 These are produced in excess of IL-10 and other anti-inflammatory chemical seen in the setting of RA	What cytokines are considered inflammatory in the setting of RA?
DIPs, thoracic and lumbar spine Large joints involved later in the disease process	What joints are spared in early RA?
Small joints in hands and feet: MCPs MTPs PIPs Usually joints are affected bilaterally	What joints are hit hardest in RA?
MCP 90-95% Wrist 80-90% PIP 65-90% Knee 60-80% MTP 50-90% Shoulder 50-60% Ankle/subtalar 50-80% Cervical spine 40-50% Hip 40-50% Elbow 40-50% Temporomandibular 20-30%	Most commonly affected joints in RA?
Fusiform swelling seen in RA Soft-tissue swelling is an early finding in rheumatoid arthritis and usually appears as typical fusiform or spindle-shaped enlargement of the proximal interphalangeal joints. The second and third fingers of this patient are most involved. These proximal interphalangeal joints are tender and have a limited range of motion. If you push on this, it will be very boggy and squishy. Totally unlike OA
A woman with long standing rheumatoid arthritis has soft tissue swelling and subluxation of the metacarpophalangeal joints. The right thumb shows hyperextension of the interphalangeal joint (a Z deformity). Both ring fingers have Boutonniere deformities with flexion of the proximal and hyperextension of the distal interphalangeal joints.
Soft tissue swelling over the ulnar styloid.	What is ulnar styloid prominence in the setting of RA?
Feature of RA. Weakening of the central slip of the extensor tendon, and palmar displacement of the lateral bands	What is Boutonniere deformity?
Feature of RA. Contraction of the flexons of the MCPs	What is a Swan Neck deformity?
Hand deformities seen in RA. MCP swelling with lateral deviation. You can also see swelling along the ulnar prominence
Swan neck hand deformity seen in RA Also Boutonniere deformity seen in the pink (slipping of tendon sheets seen underneath).
Arthritis Mutilans, seen in very severe RA. Medications can prevent this kind of disease, but we still see this presented. One feature of this is that the ulnar styloid has basically been eroded down and away.
Cock up or Hammer toe deformity, can be a feature of RA
Uniform narrowing of the joint capsule at the knees, this can be a feature of RA. No sclerosis No bone spurs
Rheumatoid nodules Vasculitis Fragility Pyoderma gangrenosum	Skin manifestations of RA?
Scleritis Episcleritis Iritis Keratoconjunctivitis Sicca Scleromalacia perforans	Eye manifestations of RA?
Pleural effusions Interstitial lung disease Bronchiolitis obliterans Rheum nodules Vasculities	Pulmonary manifestations of RA?
Pericarditis Pericardial effusion Vasculitis Valve disease Conduction defects CAD	Cardiac involvement of RA?
Osteoporosis Osteopenia	Other bone manifestations of RA?
Skin (e.g. Rheumatoid nodules) Eye Lungs Heart Bone Neurologic Hematopoietic Kidney	Extra-articular RA manifestations typically affect what systems?
Entrapment neuropathy Cervical myelopathy Mononeuritis multiplex (vasculitis) Peripheral neuropathy (CTS, TTS)	Neuro manifestations of RA?
Anemia Thrombocytosis Lymphadenopathy Felty's syndrome (triad of RA, splenomegaly, neutropenia)	Hematopoietic manifestations of RA?
RA Splenomegaly Neutropenia	What is the triad of Felty's syndrome?
Amyloidosis Vasculitis	Kidney manifestations of RA?
Rheumatoid nodule, seen in the setting of RA. Extensor surface of elbows, you can see these on other joints and tendons. Rubbery, firm sort of nodule.
Scleromalacia perforans This is basically thinning of the sclera, with the uvea trying to poke through
White males	Who usually gets a RA-associated lung manifestations?
Vasculitis associated with RA
Sjogren's syndrome seen in the setting of RA. Dry eyes, dry mouth, parotid enlargement. (Sjogren syndrome is an autoimmune disorder in which the glands that produce tears and saliva are destroyed, causing dry mouth and dry eyes. However, the condition may affect many different parts of the body, including the kidneys and lungs.)
Biologic agents, new class of therapies of cytokine blockade.	What newish drug type has drastically changed outcomes and morbidity of RA?
NSAIDs Steroids (oral or intraarticular) Disease Modifying Anti-rheumatic Drugs (DMARDS) Biologics (Enbrel, Humira)	Drug classes used for RA?
Over the long term, potential for kidney, liver, and GI toxicity	Problems with using NSAIDs for RA
Many, many side effects if using these long term	Problems with using steroids for RA?
Liver, BM toxicity	Problems with using Disease Modifying Anti-rheumatic drugs for RA?
Potential for reactivation of latent TB, infections	Problems with using biologic agents for RA?
MTX Sulfasalazine Gold sodium thiomalate Hydroxycholorquine sulfate Cyclosporine Leflunomide	Examples of DMARDs?
Methotrexate (7.5-25 mg PO, SC, or IM once weekley). Used typically orally. Also used: Sulfasalazine Leflunomide Not really used: Cyclosporine	Gold standard go to DMARD for RA? What other ones are actually used?
No liver or kidneys Possible retinal toxicity	Problems with using Hydroxychloroquine sulfate for RA
Gold sodium thiomalate	DMARD with the most toxic effects?
Hydroxychloroquine sulfate (but yes to possible retinal toxicity)	DMARD with the least toxic effects?
Anti-TNFalpha (Infliximab) Anti-CD20 (Rituximab) Anti-IL1 (Anakinra) Costim mod that inhibits T-cell activation (Abatacept) Anti-IL6 (Tocilizumab)	Main biologic classes used for RA?
Anti-TNFalpha. Given q6-8 weeks for RA	What is Infliximab?
Anti-TNFalpha SQ qW	What is Etanercept?
Anti-TNFalpha SQ qOW	What is Adalimumab?
Anti-TNFalpha This is pegylated, so we can give it SQ qMonth	What is Golimumab?
Anti-TNFalpha 2SQ qMonth	What is Certolizumab?
Anti-CD20 Infusion at Day 1/15	What is Rituximab?
Anti-IL1 SQ qDay, so not very popular	What is Anakinra?
Biologic drug: Costim modulator that inhibits T-cell activation Infusion/SQ at day 1, then SQ qWeek	What is Abatacept?
Anti-IL6 biologic Infused q4 weeks	What is Tocilizumab?
RA has erosions, osteopenias, etc. Also more likely to be symmetric OA has spur formation, osteophytic growth, sclerosis etc. Both have cysts and narrowing of the joint space. (RA may have osteophytes and sclerosis, but not as likely)	Bone involvements in RA vs OA?
RA: 25-50 OA: after age 40	Age of onset: RA vs OA?
RA: MCP, PIP, not TL spine OA: DIP, PIP, LS spine	Joint differences between RA and OA?
OA You see bone formation at the DIPs You also see that the MCPs are pretty well preserved.	OA or RA?
OA A lot of sclerosis. not very uniform throughout the joint itself.	OA or RA?