Rheumatology Flashcards
sx of arthritis clinically
Cardinal Features:
- Pain
- Swelling
- Redness
- Heat
Tenderness
Stiffness
Crepitation
Functional Impairment
number of joints affected
Mono - arthritis
Oligo - (2-4) joints
Pauci - 5
Poly - 6+ joints
characteristics of RA
- chronic
- disease course may begin 10 years before the “onset”:
- initial onset: RF+, Anti-CCP+, increased CRP
- pre-symptomatic phase: synovial inflammation
- disease onset: pain, inflammation, fatigue, damage
peak age: 25-45 years, more women, improves during pregnancy **
** majority of morbidity is d/t complications: heart disease, infection, immune complex malignancies **
Clinical Features:
- major hand deformities: have “ulnar deviation” and swelling in the PIPs
- joints space narrowing and erosions along with osteopenia in areas of inflammation symmetrically
- systemic manifestations are varied!
immunopathogenesis of RA
Type III Hypersensitivity (Immune complex deposition): RA is a localized immune complex disease
- inflammation is driven by acute phase reactants like CRP, fibrinogen and others - –> the greater the inflamm. the less viscous the plasma is and cells rapidly fall out of suspension
- CD4 T cells are activated by APC –> stimulate B cells to form RF and anti-CCP.
- immune complexes made of RF and anti-CCP form inside the joint –> sets off complement and activates inflammation
- complement is consumed in the RA joint and activates PMNs
- complement fixates along the cells, resulting in further inflammation
- can determine inflammation from C’ fixation
- T cells then react with the complement layed down, MAC causes destruction along with TNFalpha from macrophages
(TNF-α upregulates adhesion molecules on endothelial cells, promoting leukocyte influx into the joint. It also stimulates the production of other inflammatory mediators, such as interleukin 1 (IL-1), IL-6, and granulocyte-macrophage colony-stimulating factor (GM-CSF))
NOTE: TNFalpha is a major mediator in RA!!!!
tx: anti-inflammatory drugs
TNFalpha, IL-1, IL-6, CRP
- TNFalpha, IL1, IL6 and CRP are ALL pro-inflammatory cytokines seen in RA
ACR criteria for ddx RA
At least 4 criteria must be fulfilled:
- Morning stiffness lasting > 1 hour *
- Swelling in 3 or more joint areas *
- Swelling in hand joints *
- Symmetric joint swelling *
- Rheumatoid nodules
- Rheumatoid factor
- Erosions or osteopenia on hand x-rays
- Must be present > 6 weeks
- none of them are occasional sx
RA vs OA
RA: symmetric involvement
- most damage done is in the joints of the fingers, particularly the MCP and PIPs (NO DIPs)
- lots of damage is knees, wrists, ankle, feet, MTPs
- less damage done in elbow, AC, shoulder, C-spine
- ** seen in morning, decreases with activity!! ***
OA: weight bearing joints
- more degenerative, in DIPs
- involves larger joints such as the shoulder, knee, hip, PIPs, DIPs, L-spine, cervical spine
- ** seen with INCREASED activity!!!! **
pannus joint
- inflammation w/in the joint, looks like “ragged red fibers”
- T cells and lymphocytes have taken over the joint space, and a lot of cellular debris that is densely packed
- these appear as big swollen, erythematous joints
two best modailities for ddx RA
- Ultrasound (cheapest!)
- increased capillary permeability, results in increased fluid.
- US enhances fluid imaged
- better to ddx level of inflammation
- can see erosions present along with fluid in white lines - MRI
- utilizes H+ ion in order to image: detects fluid that is present
- areas of swelling or inflammation are white d/t fluid present in the joint space
- can detect synovitis and vascularity
** both best for ddx, level of inflammation, synovitis, tenosynovitis and extent of erosion
plain radiographs are not best way to determine the inflammation present
- water is the reason that U/S and MRI work
- Conventional X-ray radiography can be useful in the diagnosis of RA if erosions or juxta-articular osteoporosis are present, but is of little value for detecting synovitis, tenosynovitis, or soft tissue inflammation
extra-articular manifestations of RA: skin changes? organ changes? bone changes? vascular changes?
- Rheumatoid Nodules: bumps in the skin (always RF+)
- Sjogren’s Syndrome: Sicca sx (dry eyes, dry mouth, vaginal dryness, tracheo-bronchial dryness)
- +SS-A and SS-B - Felty’s Syndrome (rheumatoid arthritis, splenomegaly and neutropenia. )
- Vasculitis: microhemorrhages in fingernails, small vessel vasculitis
- Rheumatoid Lung
- Cardiac Disease
- Neuoromyopathy/ myelopathy
- Inflammatory Eye Dx: scleritis, and scleromalacia (“necrotizing scleritis”)
- Osteoporosis: see increased kyphosis of spine
- Lymphadenopathy
- Hyperviscosity
- Cryoglobulinemia
- Dermatologic
- Amyloidosis
two reasons for myelopathy of in RA of the cervical spine
- transverse ligament of axis begins to fail –> results in translation of atlas on the axis
- Nerve impingement b/w C1 and C2
Sx of spinal cord damage:
- Diminished motor power in arms & legs
- Severe neck pain often radiating to the occiput
- Dysesthesias of the fingers & feet
- A “marble sensation” in the limbs & trunk
- Jumping legs, due to spinal automatism
- Disturbed bladder function
lab findings in RA?
Rheumatoid Factor + (Ab directed against Fc portion of IgG –> makes immune complexes)
Anti – CCP Antibody +
ANA +
Elevated ESR or CRP
CBC: Anemia Thrombocytosis Hyperglobulinemia Leukopenia/Granulocytopenia
Glucose in body fluids – very low
- high level of anti-CCP along with high levels of anti-RF = 96% chance of having RA
Note: Value of RF is good tool for ddx and severity
- high titer = good predictor of erosiveness
- but ESR may be better predictor of severity of RA
Both tests are highly specific for RA (91% and 96%, respectively), and the absence of both markers is predictive of non-RA in approximately 80% of patients. However, neither marker is particularly sensitive. (only 39% of patients with early RA have both present)
tx for RA?
Two Goals:
- alleviate pain
- slow rate of joint damage
pharmacologic is most effective in early and late phase of RA
- NSAIDs (mainstay of tx):
- don’t halt degree progression
- have high toxicity, may be costly - Corticosteroids:
- chronic use assoc. w/ many side effects
- should only be used for acute flare-ups - DMARDs: Disease modifying antirheumatic drugs
- discontinuation rate is high
- need for continued monitoring
- delayed onset of action
ex: Methotrexate, Leflunomide, HCQ, sulfasalazine - Biologic Agents: $$
- opportunistic infections are major SE (TNF-alpha blockers) - Analgesics ***
- absolutely necessary to control pain and improve fn.
** also encourage PT/OT, weightloss , exercise, rest, splints, etc.
“swan neck” vs. “Boutonniere” deformity
- boutonniere: joint inflammation along the extensor hood - results in breaking of extensor hood and the finger becomes flexed at the PIP joint, extended at DIP
swan neck: enthecitis rupture, tendon pulls out of tip of finger, have flexed DIP
** both are seen in RA!!
screening for RA?
high RF = gives severity of disease – more likely in developing vasculitis
Cyclic citrullinated peptides: CCP test = screening test for RA,
** best test
- when have Anti-CCP positive and RF positive it increases the specificity
- absence of both tests is predictive of non-RA
Highly specific, lower sensitivity:
- neither marker is very sensitive, but if have markers then its specific (high positive predictive value)
- only 63% of patients with early RA are positive for either IgM RF or anti-CCP antibodies and 39% of patients with early RA are positive for both markers
ESR and C-reactive protein (CRP) — two markers of acute phase response — do not discriminate well between RA and non-RA arthritis in patients with early arthritis and are not regarded as predictive of persistent, erosive RA
ACR remission criteria for RA?
- AM Stiffness < 15 minutes
- No fatigue
- No joint pain
- No joint tenderness or pain on ROM
- No Soft Tissue Swelling in joints or tendon sheaths
- ESR 2 consecutive months
two etiologies for developing OA?
- Progressive deterioration & loss of articular cartilage, leading to loss of normal joint structure & function
Primary:
- Aging or Idiopathic
- Genetic: Nodal O.A.
Secondary:
- Due to disorders that damage joint surfaces
Clinical features of OA? major contrast b/w OA and RA?
OA:
- most common arthrotpathy, seen in older age
- deep achey pain
- primary pathology involves cartilage!
- defect in repair
- ** non inflammatory **
- involves active enzymatic factors
- multi-factorial etiology
OA is noninflammatory, its a degenerative disease vs. RA which is inflammatory!!!
- RA involves synovium, OA involves the cartilage and is noninflammatory
- OA is an enzymatic degredation of joint space rather than immune degredation!!
- morning stiffness is indicative of RA!
pathology of OA joint
= Progressive deterioration & loss of articular cartilage, leading to loss of normal joint structure & function
- *2 principle mechanisms initiate O.A.
1. Damage to normal articular cartilage by physical forces (macro or microtrauma) - Chondrocytes react: Release degredative enzymes and Inadequate repair response
- Fundamental defective cartilage fails under normal joint loading
- Type II collagen gene defect (Ochronosis)
- Ochronotic Cartilage (pigmented and defective)
Pathologic characteristics:
- altered chondrocyte function:
- loss of cartilage, thinning
- subchondrial bone thickening and sclerosis
- remodeling of bone
- marginal spurs: osteophytes
- cystic changes in subchondral bone
- mild reactie synovitis
subsets of OA
- Generalized O.A.
- Nodal O.A.
- Heberden’s nodes (DIPs swelling)
- Bouchard’s node (PIP swelling) - Spondylosis
- translation of bone, resulting in neuro problems - Erosive O.A.
- on Xray, see lucency and holes filled w/ fluid - Inflammatory O.A.
- see swollen joints - Diffuse Idiopathic Skeletal Hyperostosis (DISH)
- increased bone spurs - Chondromalacia patellae:
- see increased Q angle in knees
- see shredded appearance of patella, rides on the medial aspect of the chondyle
Heberden’s vs. Boushard’s nodes
- nodal osteoarthritis in hands -
Heberdens nodes: DIP
Bouchard’s nodes: PIP
1st CMC joint: base of thumb
Osteophyte vs. Syndesmophyte
= “bone spurs”
- osteophyte: chronic irritation results in spondylosis, see bone spur formation that looks like teeth or clam shell on either side (seen in OA)
- can see downward pointing osteophytes in the C-spine
- syndesmophyte: from inflammatory disease, ligaments ossify, resulting in appearance of bamboo spine - seen more in ankylosing spondylitis
spondylosis
- seen in OA: causes back pain
- results from degenerative OA of joints between the center of spiral vertebra and neural foramina –> results in space becoming narrowed and compression of nerve
Spine (spondylosis) involves disc degeneration & facet involvement
- Cervical
- Thoracic
- Lumbar
- Spinal Canal Stenosis
- DISH
Side note:
- Pars interarticularis fails:
1. spondylolysis: pars bridge fails
2. spondylolisthesis: L5 translates on S1 d/t spondylolysis
- Pars interarticularis fails:
management of OA
- pain control, improve function, enhance health/quality of life, avoid Rx with related SE’s
- no cure to OA!
- education, weight reduction, PT/OT
- NSAIDs/ analgesics
- SMOADs (structure modifying anti-osteoarthritis drugs) - ex. MMPI, doxycycline
relationship of OA with CPPD
- THINK CALCIUM PYROPHOSPHATE JOINT CRYSTALS WHEN INFLAMMATORY OSTEOARTHRITIS FAILS TO RESPOND!!!!
- think pseudogout, if not responding to normal OA tx
- will see CPPD depsoition in joints, along with hooked osteophytes and positive bifrengence
risk factors of OA?
Age Obesity Genetics Gender: women have more problems Menopause
Local factors: Muscle Strength Joint proprioception Repetitive use Configuration of joint Trauma
presentation of OA?
Joints involved:
- pain in lumbar spine, knee, hip, Cervical spine, PIPs/DIPs, first metatarsophalaneal (MTPs)
- Knees are most common lcoation!!!
- in spine see spondylosis: involving disc degeneration and facet involvment
Sx of OA:
- Insidious onset
- Joint pain associated with movement
- Limitation of motion/ function
- Minimal stiffness after rest
- Referred pain
- Acute flares suggest another diagnosis
- Systemic symptoms are rare
Physical Signs:
- bony changes at joints
- creptius
- no inflammation within the joint, or seen w/in fluid
- instability
- limited ROM
- joint line tenderness
- spasm or atrophy of adjacent mm.
why is OA painful?
- not pain in cartilage, rather the things surrounding it -
Cartilage is avascular & aneuritic: Synovitis Joint capsule/ligament stretching Periosteal irritation from osteophytes Trabecular microfractures Muscle spasm Intraosseous hypertension
OA Labs/DDx testing?
- No specific diagnostic test:
- ESR and RF are appropriate for age
** synovial fluid is class 1 (non-inflammatory)**
Xrays (best tool):
- cartilage loss/joint space narrowing
- subchondral sclerosis
- osteophytes at joint margins
- subchondral cysts
What is commonly seen on Xray?
- narrowed joint space,
- osteophytes,
- increased density of sub - chondral bone
- bone cysts
DISH
- disease associated with OA
Diffuse Idiopathic Skeletal Hyperostosis – osteophytes go wild (but remember, non-inflammatory) - see lots of bone spurs!
- exuberant osteophytosis of spine/spans > 3-4 vertebral segments
- preservation of disc spaces
- ***ligamentous calcification
- > 5 yoa
- M > F
- **associated with DM
- ant. cervical osteophytes - - dysphagia
cause:
- osteoblasts start to ossify and cause tendons to become bone, results in tons of osteophyte production
Commonly seen…
- T spine is the best place to look for DISH
- upward pointing lumbar osteophtres are characteristic of DISH
- ligamentous calcification at entheses
- foot and ankle entheses
- see “candle wax ossification” - DISH seen most often on the right!
NOTE: if have dextracardia, then will have left sided DISH
environmental factors of OA?
- fluoride
- synthetic retinoids (Accutane)
- IGF-1
- obesity/metabolic conditions
essentials of ddx of OA?
Commonly secondary to other articular disease
A degenerative disorder without systemic manifestations
Pain relieved by rest; morning stiffness brief; articular inflammation minimal
X-ray findings: narrowed joint space, osteophytes, increased density of sub - chondral bone, bone cysts
cholesterol crystals
- rare
- lipid crystals DO polarize light: shine all difft. colors (like Lisa Frank)
- can be seen in lipid laden joint effusion or RA and chronic infection
