A 70 yr old female presents with right sided groin pain. Sometimes the pain radiates to the anterior thigh. She denies stiffness lasting longer than 30 min when she wakes up in the morning but finds that the pain is aggravated by ongoing activity. She enjoys gardening and says that she has to rest more often to obtain pain relief. What investigation would be diagnostic for her disease?
This patient likely has OA. A radiograph would allow for diagnosis with the following 4 hallmark features:
- Joint space narrowing
- Subchondral sclerosis (subchondral bone is more dense and doesn't have as much give; appears white on Xray)
- Subchondral cysts
- Osteophytes (small boney projections at the joints; body is trying to increase surface area in order to decrease the force per unit area of the joint)
Other investigations might include blood work with normal CBC and ESR, CRP, negative RF and ANA. The synovial fluid would be clear, pale yellow, and <25%PMN.
The knee radiograph of a 68 yr old female shows joint space narrowing, subchondral sclerosis, subchondral cysts and osteophytes. What are her treatment options?
OA Treatment - currently no treatment alters the natural history of OA
- Weight loss (minimum 5-10lb loss) if overweight
- Physiotherapy: heat/cold, low impact exercise program
- Occupational therapy: aids, splints, cane, walker, brace
- Oral: acetaminophen/NSAIDs, glucosamine +/- chondroitin +/- MSM
- Joint injections: corticosteroid (repeated injections not recommended if you are trying to preserve the joint), hyaluronic acid
- Topical: capsaicin, NSAIDs
- Realign = osteotomy
- Obliterate = fusion or excision
What is happening physiologically in degenerative joint disease (OA)?
Degenerative Joint Disease (OA)
- NOT the same as normal aging
- Chondrocytes cannot repair dammaged cartilage
- Damaged articular cartilage heals with fibrocartilage
- Increased water content
- Decreased number of chondrocytes
- Decreased proteoglycan content
- Disrupted collagen
There is a deterioration of articular cartilage due to local biomechanical factors, which leads to joint trauma and release of proteolytic and collagenolytic enzymes. OA develops when cartilage catabolism > synthesis. Abnormal local bone metabolism further damages joint and a synovitis may occur secondarly to cartilage damage resulting in effusions.
Describe some of the classic findings of a patient with OA in their hand.
OA of the Hand
- DIP involvement = Herbeden's nodes = osteophytes = enlargement of the joints
- PIP involvement = Bouchard's nodes
- CMC involvement = thumb squaring
- 1st MCP (other MCPs are usually spared)
What is the difference between ostoearthritis and osteonecrosis?
Osteoarthritis - inflammation of joints results from multiple factors 1) joint integrity, 2) genetic predisposition 3) local inflammation 4) mechanical forces 5) cellular and biochemical processes
Osteonecrosis - decreased blood supply to bone causing death of the bone and marrow cells which leads to mechanical failure of the joint
What are the risk factors for osteonecrosis?
Osteonecrosis RFs: VITAMIN
Vascular: Sicle cell disease
Infection/Inflammation: viral and bacterial; SLE
Trauma: fracture, dislocation
Metabolic: EtOH, Gaucher's Hyperlipidemia
Neoplastic: Multiple myeloma, Irradiation-induced
A 72 yr old female presents with an unstable but painless knee. Her story describes decreased proprioception around the knee as well. She has a history of diabetes mellitus. What is the likely diagnosis?
- Unstable and painless
- No proprioception around the joint
- Usually lower extremities (foot)
- Can have open ulcers
- Xrays show severe destruction of both sides of the joint
- Causes: DM (most common), syphilis, leprosy, spina bifida, syringomyelia
- Jointa aspirate can have hemarthrosis
- can be diffciult to differentiate from infection but the bone scan usually shows no increase in uptake
Neuropathic arthropathy (or neuropathic osteoarthropathy), also known as Charcot joint (often "Charcot foot"), refers to progressive degeneration of a weight bearing joint, a process marked by bony destruction, bone resorption, and eventual deformity. Onset is usually insidious.
A 56 yr old female presents complaining of stiffness and joint pain. She says that in the morning it takes her over half an hour to get out of bed due to stiffness. She describes pain in the PIP joints of both hands as well as both knees. The patient says that 3 months ago she would hike Grassi Lakes every Saturday she has since stopped this activity due to fatigue on a regular basis. She does find that walking does provide some relief though. On PE you note that both the her PIP joints are swollen and tender. Her knees are warm. What investigations would you complete to confirm your diagnosis?
This patient has RA. RA is mainly a clinical diagnosis: history, PE, GALS. However, investigations would be as follows:
- RF + (80% sensitivity) but may not be present at onset of symptoms
- anti-CCP +: sensitivity ~80% but more specific; may precede the onset of symptoms
- Increased disease activity is associated with decreased Hb (anemia of chronic disease), increased platelets, ESR, CRP and RF
- Xrays may be entirely normal at onset
- First change is periarticular osteopenia, followed by erosions
- U/S, MRI may be used to image hands to detect early synovitis and erosions
A 56 yr old female presents complaining of stiffness and joint pain. She says that in the morning it takes her over half an hour to get out of bed due to stiffness. She describes pain in the PIP joints of both hands as well as both knees. The patient says that 3 months ago she would hike Grassi Lakes every Saturday she has since stopped this activity due to fatigue on a regular basis. She does find that walking does provide some relief though. On PE you note that both the her PIP joints are swollen and tender. Her knees are warm. What are the treatment options for this patient?
- Goal: remission or lowest possible disease activity
- The key is early diagnosis and early intervention with DMARDs, "window of opportunity" = trtmnt within first 3 mths of disease may allow better control/remission
DMARDs (Disease Modifying Anti-Rheumatic Drugs) and Biologics: standard for care and should be started ASAP
- Trtment is based off of disease severity and prognostic factors
- Methotrexate is the gold standard (potential toxicities: GI, hematologic, hepatic, pulmonary, teratogenic, renal)
- Add ons: hydroxychloroquine, sulfasalazine, leflunomide
- Biologics: indicated if inadequate response to DMARDs (ex. azathioprine, infliximab, etanercept, adalimunab, abatacept, rituximab, tocilizumab)
Reduce inflammation and pain: NSAIDs and corticosteroids
- Prednisone may be used as a bridging therapy
- Intra-articular injections
- Give Ca2+ and Vit D, and bisphosphonates if long term use (>3mths)
What deformities might be present in an RA patient on PE?
- Signs of mechanical jt damage: loss of motion, instability, deformity, crepitus, joint deformities
- Swan neck deformity, boutonniere deformity
- Ulnar deviation of MCP, radial deviation of the wrist
- Hammer toe, mallet toe, claw toe
- Flexion contracture
- Limited shoulder mobility
- Carpal tunnel syndrome
- Baker's cyst (presents similar to DVT); outpouching of synovium behind the knee
What are the potential extra-articular manifestations of RA?
Extra-Articular Manifestations of RA
- Ocular: scleritis
- Skin: cutaneous ulcers, palpable purpura, rheumatoid nodules
- Pulmonary: pleural disease (chest pain, dyspnea), interstitial lung disease (dyspnea, cough)
- Vascular system: small vessels, accelerated atherosclerosis (RA is an independe RF for CAD)
- Neurological system: peripheral nerves, median nerve (Carpal tunnel)
- Sjogren's Syndrome (secondary): dry eyes, mouth, lung or vagina (late stage)
- Amyloidosis: protein deposits, renal complications
What disease is characterized by the following diagnostic criteria?
These are the diagnostic criteria used for SLE
- Malar rash: classic "butterfly rash", sparing of nasolabial folds, no scarring
- Discoid rash: may cause scarring due to invasion of basement membrane
- Serositis: pleuritis or pericarditis
- Oral/nasal ulcers: usually painless
- Arthritis: symmetric, involving >2 small or large peripheral joints, non-erosive
- Photosensitivity: skin rash in reaction to sunlight
- Arthritis: symmetric, involving >2 small or large peripheral joints, non-erosive
- Neurologic disorder: seizures or psychosis
A 20 yr old African-American female presents with arthralgias of both knees. Her HPI describes general fatigue, and weight loss. On PE you notice oral ulcers, and livedo reticularis of the skin. What investigations would assist in making a diagnosis?
This patient's story has you thinking SLE. Investigations for SLE are as follows:
- ANA + (98% sensitive)
- ENA +
- anti-dsDNA (associatd with nephritis) and anti-Sm (95-99% specific)
- anti-dsDNA titer and serum complement are useful to monitor treatment response in patients who are clinically and serologically concordant
- anti-dsDNA increases and C3 and C4 decrease with disease activity
- APLA Ab may cause increased risk of clotting and increased aPTT
- Anemia of chronic disease
- Urinalysis: proteinuiria, hematuria, pyuria, casts (if lupus nephritis)
A 28 yr old female is meeting with you, a family physician, to discuss a recent spontaneous abortion and her wishes to try to get pregnant again. Her previous history reveals a history of migrane headaches and you note that a recent clotting study revealed an elevated aPTT. What syndrome do these factors lead you to be suspicious about?
Antiphsopholipid Ab Syndrome
- Multi-system vasculopathy manifested by recurrent thromboembolic events, spontaneous abortions and thrombocytopenia
- Often presents with migraine type headaches
- Circulating APLAs interfere with coagulation cascade
- Manifestations of APLA: thromboembolic events, spontaneous abortions, thrombocytopenia, associated with livedo reticularis, migrain headaches
- Primary APLA; absence of other disease
- Secondary APLA: connective tissue disease, malignancy, drugs, infections (HIV, TB, Hep C)
A 50 yr old female presents with dysphagia. She describes progressive difficulty swallowing; starting with difficulty swalling solids and now liquids. What rheumatic disease would be on your differential diagnosis?
Scleroderma - a non-inflammatory autoimmune disorder characterized by widespread small vessel vasculopathy and fibrosis
- Idiopathic vasculopathy (not vasculitis) leading to atrophy and fibrosis of tissues
- Intimal proliferatin and media mucinous degeneration = progressive obliteration of vessel lumen resulting in fibrotic tissue
What is the most common joint pattern of psoriatic arthritis?
- Most common pattern is asymmetric oligoarthritis
- arthritis of DIP joints with nail changes
- Psoriasis may develop before or after onset of arthralgias
- 15-20% of patients will develop joint disease before skin lesions appear
- Treatment: NSAIDs, steroids, DMARDs, biologics
True or False. Reactive arthritis is self-limiting.
True (most of the time)
- Following an infectious episode in the GI or GU tract:
- GI: Shigella, Salmonella, Campylobacter, Yersinia species
- GU: Chlamydia, mycoplasma
- Clinical triad: arthritis, conjunctivitis, urethritis/cervicitis
- Self-limited, typically 3-5 mths; chronic in 15-20% of cases
What are the differences between Gout and Pseudogout?