Thursday January 28, 2000 8AM
Introduction to Clinical Medicine Dr. Ratnoff
3/9/01 at 9 am Fathy and Robb
Rheumatoid Arthritis (RA) and Osteoarthritis (OA)
Dr. Ratnoff’s lecture consisted of slides from a CD-ROM from the American College of Rheumatology (ACR), Clinical Slide Collection. In inquiring about availability of that CD-ROM, he stated that the reading assignment in Stein was more than sufficient. I will describe what the slides showed and emphasize what he did. He did mention at the beginning of class general objectives for the lecture: 1) Pathophysiology of RA and OA, 2) Clinical features of RA including extra-articular manifestations, and 3) Compare/contrast clinical features of RA to OA.
• Picture of a normal joint
o A fibrous joint capsule holds the joint together. Just under the capsule is a single layer of cells called the synovium, which is the layer that undergoes proliferation in RA (see below).
o The ends of the opposing bones each have a layer called the subchondral bone plate covered by articular cartilage, which absorbs much of the weight bearing pressure.
o Must distinguish whether joint pain is coming from inside joint or is referred from the muscles and tendons adjoining.
• 1987 ACR Classification Criteria for RA
o A positive blood test for rheumatoid factor does not definitively diagnose RA – do not base diagnosis on a lab test.
o Must have 4 of the following 7 findings (MEMORIZE)
▪ Morning stiffness that lasts at least 1 h (at least 6 wks)
▪ Swelling at 3 or more joints (at least 6 wks)
▪ Swelling in hand joints (at least 6 wks)
▪ Symmetrical joint swelling (at least 6 wks)
▪ Erosions or decalcification on X-ray of hand
▪ Rheumatoid nodules
▪ Abnormal serum rheumatoid factor
o Notice that pain is not on the list (it is assumed)
o Stiffness and swelling of joints can occur because of different conditions such as viral arthritis, but they do not persist up to 6 wks
o Thus an abnormal X-ray and positive serum finding without swelling, nodules and stiffness is not a basis for RA diagnosis.
• Classification of Function
o Class I – no limitations
o Class II – adequate for normal activity despite joint discomfort (i.e. pain and movement limitation) – most of the patients we will see
o Class III – inadequate for most self-care and occupational activities
o Class IV – bed and wheelchair confinement
• Criteria for Clinical Remission
o No fatigue, morning stiffness reduced to 15 min or less, no joint pain, no joint tenderness or pain on motion, no soft tissue swelling in joints or tendon sheath, a sedimentation rate of less than 30 in women and 20 or less in men.
o Need to be present for 2 months or more, and no extra-articular or constitutional manifestations.
o Because therapy for RA was poor, the ACR made a new criteria called ACR 20, in which a 20% improvement in symptoms is progress. Newer drugs can produce ACR 30 and ACR 40 improvements routinely.
o Do not initiate these drugs without documenting the 4 of 7 findings, because you can do serious damage.
• Stages of RA Pathogenesis
|Stage |Symptom |Finding |
|1. Antigen presentation on T cells |None |None, normal X-ray |
|2. T and B cell proliferation, angiogenesis in |Malaise, mild joint stiffness, swelling |Swelling or pain of small joint, wrist, knee, |
|synovium | |normal X-ray |
|3. Synovial fluid PMN accumulation, synovial cell |Joint pain, swelling, morning stiffness, malaise, |Warm and swollen joints, soft tissue proliferation,|
|proliferation |weakness |limited motion, soft tissue nodules, and tissue |
| | |swelling on X-ray |
|4. Pannus invasion, chondrocyte activation, enzyme |Same as 3 |Same as 3, periarticular osteopenia, synovium looks|
|activation | |big and swollen on MRI |
|5. Subchondrial bone erosion, pannus invasion of |Same as 3, loss of function, deformity |Same as 3, flexion contraction, extra-articular |
|cartilage, stretched ligaments | |disease, early erosion and joint space narrowing on|
| | |X-ray |
o Pannus invasion – synovium thickens and makes fingers that invade into the joint like a cancer
o Dr. Ratnoff went over basic immunology regarding antigen presentation by an APC (monocyte or dendritic cell) via an MHC class II molecule to a CD4+ T cell with its TCR. Must have co-stimulatory molecules on the surfaces of these two cells to also interact for T cell activation to occur.
o In RA, the antigen is unknown.
o There is no evidence for microbial influence in RA to date.
o It is difficult to identify stage 1, and that is an area of research.
• Felty’s Syndrome
o Especially malignant form of RA
o Seropositive for RA, nodules, aggressive arthritis
o In addition, have splenomegaly and granulocytopenia, the later of which causes opportunistic infections
• Dr. Ratnoff proceeded to go through a series of slides with pictures demonstrating clinical features
o Extensor tendon rupture – ball of muscle on dorsum of hand, pt can only extend certain fingers
o Fusiform changes in hand – swelling of MCP and PIP joints (not DIP joints)
o Chronic hand deformity – swelling of MCP joints, ulnar deviation of fingers, and volar sublexation (fingers pulled down towards palm), interosseous muscle atrophy, swelling and fusion of wrist
o Nodules – typically on extensor surfaces (commonly on elbow)
o Swan Neck deformity – fingers on side view look like neck of a swan - hyperextension at PIP and flexion at DIP (does not mean that DIP is involved, its because of the tendons’ action)
o Boutonniere’s Deformity – opposite of Swan Neck – flexion at PIP and hyperextension at DIP.
o Telescoping Digits – fingers have shrunken
o Carpal Tunnel Syndrome – compression of Median nerve due to swelling of the wrist, results in Thenar muscle atrophy and parasthesia in the digits
o Arthritis Mutilans – severely deformed hands
o Popliteal cysts (Baker’s cyst) – happens when knee joint becomes inflamed and pressure pushes on the popliteal fossa and a small synovial cyst forms which can enlarge and rupture. Contents will spill out and cause calf to enlarge, become red and give a Homan’s sign (which can also suggest thrombophlebitis or deep venous thrombosis)
o Protruding metatarsal heads in the feet – alleviated via surgery and/or supports
o Hammer Toes
o Subconjunctival inflammation – beginning of Episcleritis, associated with higher stage RA
o Scleral inflammation leading to scleritis then Scleral Malasia Perforans (hole in the cornea) and blindness – must use systemic steroids and cyclophosphamide, takes weeks to months, unilateral or bilateral
o Digital infarcts – at tips of fingers, caused by vasculitis, not necessarily associated with organ vasculitis
o Posterior displacement of the odontoid process at Atlanto-occipital joint and compression of the spinal cord
o Bone erosions – look like “PacMan bite” into bone, look for them in hands and not the big joints.
o Rheumatoid nodules in the lung – can look like TB or cancer, need to make clinical judgement about biopsy
o Histological slides – Synovium proliferation, no longer a single layer; slide of pannus invading joint; slide of vasculitis
• Osteoarthritis
o Patient usually over age 50
o Morning stiffness less than 30 min
o Crepitus in joint, with or without inflammation
o Bony enlargement or tenderness
o Rheumatoid Factor is low
o Synovial fluid is non-inflammatory (Dr. Ratnoff mentioned reading about synovial inflammation since we were running out of time)
• Slide showing Heberden’s nodes and Bouchard’s nodes
o Heberden’s nodes are osteophytes at DIP joints, and Bouchard’s nodes are osteophytes at PIP joints
o MCP joints are not involved in OA but DIP joints are, which is the opposite of RA
• Obstruction of Neural Foramina by Osteophytes
o Can cause nerve compression
• Slide showing Loss of Joint Space by Osteophytes in the Lumbar spine
• X-ray of the Hand
o Cardinal features are narrowing/obliteration of joint space, osteophyte formation and sclerosis as opposed to juxtaposed osteopenia in RA
• Pathophysiology of OA
o “Wear and Tear” arthritis which makes sense but does not explain Heberden’s nodes and Bouchard’s nodes. There is involvement of metalloproteinases and other enzymes that cause abnormal cartilage cycling and a familial/genetic involvement.
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