Rheumatology Flashcards
What is osteoarthritis? How is it different from rheumatoid arthritis?
Wear and tear in the synovial joints due to genetics, overuse and injury. Imbalance between wearing down of cartilage and repair by chondrocytes. RA is inflammatory, OA is not.
Diagnosed in those over 45 with activity related pain and no morning stiffness (or they do but it lasts <30 mins so doesnt count)
Give 5 risk factors for osteoarthritis.
Obesity, age, occupation, trauma, female, family history
Give 4 x-ray changes seen in OA.
L – Loss of joint space
O – Osteophytes
S – Subchondral sclerosis (increased density of the bone along the joint line)
S – Subchondral cysts (fluid-filled holes in the bone, aka geodes)
How does OA present and how is this different to RA?
Joint pain, stiffness. Worse on activity (RA = better on activity). Leads to deformity, instability and loss of joint function.
Give 5 most commonly affected joints in OA.
Think joints with lots of use.
Large joints: Hips, Knees, Sacro-iliac joints
Small: DIP, MCP, CMC (thumb/wrist)
C-spine
Give 3 findings on examination in OA and a difference with RA.
Heberden’s nodes (in the DIP joints)
Bouchard’s nodes (in the PIP joints)
Squaring at the base of the thumb at the carpo-metacarpal joint
Weak grip
Reduced range of motion
in RA you would get z-thumb/ ulnar deviation and no nodes.
How is OA managed?
Patient education
wt loss (reduce load)
PT
OT
orthotics
Analgesia:
1. pcm/topical NSAIDs/capsaicin
2. PO NSAIDS + PPI - try to avoid continuous use due to GI + renal side effects
3. Opiates - don’t work for chronic pain though
Intra-articular steroid injections - temporary reduction in inflammation and improve symptoms.
Joint replacement can be used in severe cases, esp hip and knee.
What is rheumatoid arthritis (RA)?
Autoimmune symmetrical polyarthritis causing chronic inflammation of synovial lining of joints, tendon sheaths and bursa.
Give 4 risk factors for RA.
Female, middle-age, FHx, genetics - HLADR4, HLADR1.
Describe how RF antibodies cause disease in RA.
RF= antibody (in 70% of RA patients), targets Fc portion of IgG antibody. Causes activation of immune system against patients own IgG. RF is most commonly IgM but can be any class of Ig.
What is the role of anti-CCP antibodies in RA?
Cyclic citrullinated peptide antibodies (anti-CCP antibodies) are autoantibodies that are more sensitive and specific to rheumatoid arthritis than rheumatoid factor. Anti-CCP antibodies often pre-date the development of rheumatoid arthritis and give an indication that a patient will go on to develop rheumatoid arthritis at some point.
How does RA present and how is this different to OA?
Symmetrical distal polyarthopathy, joint swelling, stiffness. (OA is asymmetrical)
Small joints of hands and feet, MCP, PIP. Can affect larger joints. Onset can be rapid or chronic.
Systemic sx eg fatigue, wt loss, flu-like illness and muscle aches occur in RA but not OA.
Improves with activity (OA worsens with activity)
What is palindromic rheumatism?
Episodes of inflammatory arthritis with joint pain, stiffness and swelling typically affecting only a few joints, last 1-2 days and then completely resolve. Having positive antibodies (RF and anti-CCP) may indicate that it will progress to full rheumatoid arthritis.
Give the 5 most commonly affected joints in RA.
PIP joints (vs DIP/heberdens node=OA) Metacarpophalangeal (MCP) joints Wrist and ankle Metatarsophalangeal joints Cervical spine Large joints can also be affected
What is atlantoaxial subluxation?
The axis (C2) and the odontoid peg shift within the atlas (C1). This is caused by local synovitis and damage to the ligaments and bursa around the odontoid peg of the axis and the atlas. Subluxation can cause spinal cord compression and is an emergency. This is particularly important if the patient is having a general anaesthetic and requiring intubation. MRI scans can visualise changes in these areas as part of pre-operative assessment.
Give 5 signs you would see on examination of hands with RA.
Palpation of the synovium in around joints when the disease is active will give a “boggy” feeling related to the inflammation and swelling. Z shaped deformity to the thumb Swan neck deformity (hyperextended PIP with flexed DIP) Boutonnieres deformity (hyperextended DIP with flexed PIP) Ulnar deviation of the fingers at the knuckle (MCP joints)
What is Boutonnieres deformity and what causes it?
Tear in the central slip of the extensor components of the fingers –> when patient tries to straighten their finger, the lateral tendons that go around the PIP (called the flexor digitorum superficialis tendons) pull on the distal phalynx without any other supporting structure, causing the DIPs to extend and the PIP to flex.
(RA)
Give 5 extra-articular manifestations of RA.
Pulmonary fibrosis with pulmonary nodules (Caplan’s syndrome)
Bronchiolitis obliterans (inflammation causing small airway destruction)
Felty’s syndrome (RA, neutropenia and splenomegaly)
Secondary Sjogren’s Syndrome (AKA sicca syndrome)
Anaemia of chronic disease
Cardiovascular disease
Episcleritis and scleritis
Rheumatoid nodules
Lymphadenopathy
Carpel tunnel syndrome
Amyloidosis
How is RA diagnosed?
Clinical diagnosis (symmetrical polyarthropathy affecting small joints)
Other Ix:
RF, anti-CCP (if RF -ve), CRP, ESR
X ray hands+ feet
USS joints - synovitis. used when findings of clinical examination are unclear.
ACR/ELAR 2010 criteria.
Give 4 changes on X ray seen in RA.
BODS Bony erosions Periarticular Osteopaenia Joint Destruction and deformity Soft tissue swelling
When should you refer someone with suspected RA to rheumatology routinely+urgently?
Routine referral –> persistent synovitis, even if negative antibodies.
Urgent –> small joints of the hands or feet, multiple joints or symptoms more than 3 months.
(NICE)
How can disease activity + response to treatment be measured in RA?
DAS28- Disease Activity Score. It is based on the assessment for 28 joints and points are given for:
Swollen joints
Tender joints
ESR/CRP result
Health Assessment Questionnaire (HAQ) measures functional ability - check at diagnosis.
Give 5 poor prognostic factors in RA.
Younger onset Male More joints and organs affected Presence of RF and anti-CCP Erosions seen on xray
How is RA managed?
MDT Steroids to induce remission NSAIDs/COX-2 inhibitors effective but balance with risk of GI bleed, use PPIs Minimal effective dose. DMARDs - 1st line = 1 of methotrexate, leflunomide, sulfasazaline, hydroxychloroquine (mild) 2nd line = 2 of the above 3rd line = methotrexate + TNF inhibitor 4th line = methotrexate + rituximab
How is RA managed in pregnancy?
Pregnant women tend to have an improvement in symptoms during pregnancy, probably due to the higher natural production of steroid hormones. Sulfasalazine and hydroxychloroquine are considered as DMARDs in pregnancy. (Methotrexate is teratogenic, avoid in both mums AND DADS)
Which biological therapies target TNF?
adalimumab, infliximab, etanercept
Which biological therapy targets CD20?
rituximab
How does methotrexate work, how is it taken, and what are the most important SEs?
Interferes with the metabolism of folate and suppresses components of the immune system.
Injection or tablet once a week. Folic acid 5mg is also prescribed once a week to be taken on a different day to the methotrexate.
Pulmonary fibrosis Mouth ulcers and mucositis Liver toxicity Myelosuppression, leukopaenia It is teratogenic (harmful to pregnancy) and needs to be avoided prior to conception in mothers and fathers
How does leflunomide work, and what are the important SEs?
Interferes with the production of pyrimidine. a component of RNA and DNA.
Mouth ulcers and mucositis HTN, peripheral neuropathy Rashes Liver toxicity Myelosuppression, leukopaenia Teratogenic - mums and dads
How does sulfasalazine work and what are the main SEs?
Immunosuppressive and anti-inflammatory, possibly to do with folate metabolism. Safe in pregnancy however women need adequate folic acid supplementation.
Male infertility (reduced sperm count. reversible) Myelosuppression
How does hydroxychloroquine work and what are the SEs?
Interferes with Toll-like receptors, disrupting antigen presentation and increasing the pH in the lysosomes of immune cells. Safe in pregnancy.
Nightmares
Reduced visual acuity (macular toxicity)
Liver toxicity
Skin pigmentation
How does infliximab work and what are the main SEs?
Monoclonal antibody to TNF. TNF is a cytokine which stimulates inflammation.
Reactivation of TB and hepatitis B
Vulnerability to severe infections and sepsis
